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PRACTICE OF MED CINE.
Epirep sy Dr. Ht von ZIEMSSEN,
PROFESSOR OF CLINICAL MEDICINE IN MUNICH, BAVARIA,
VOL. XIIL
DISEASES OF THE SPINAL CORD
AND
MEDULLA OBLONGATA.
BY
Pror. WILHELM HEINRICH ERB, of Heidelberg, Baden.
Translated bp
EDWARD G. GEOGHEGAN, M.D., of London; EDWARD W. SCHAUFFLER, M.D., of Kansas City ;
DAVID F. LINCOLN, M.D., of Boston; and JOHN A, McCREERY, M.D., of New York.
ALBERT H. BUCK, M.D., New Yorks,
EDITOR OF AMERICAN EDITION.
NEW YORK:
WILLIAM WOOD AND COMPANY,
' 27 GREAT JONES STREET.
1878. 3 “9
Lh ' * gnterea scor dir to Act of Congress, in the year 1878, by
WAN _ WILLIAM WOOD & CO.,
In the Office of the Librarian of Congress, at Washington.
ALL RIGHTS RESERVED.
CONTENTS.
PAGE
INTRODUCTION..... C=) ots shes eae A 40,4 ene eel Terre Mie wenses ane mines eae oe
PAMEOIMIORS SMEROGUCUION. oc ccc cesses ccectscruetsbebeanes ERS eee 7
IM as 06 sc con siec' st vewaealen bei ath Gin dining ale a eek ed 7
MN 5 5 5g ecinin'e ov 0 0100.05.64 URES OED CUM G Repke ce beneds 33
Bibliography..... Cw hia di0:5) 0,64 CK.0 Oe SER Ee Eee hai oe ea oe « 33
NN aa d'6 04 5, 0 0 a 6.0.4 .64:0:4 dee AMO Re vag STAD 40:0 ba wee 39
DEOUOE CODGUCHOR. 6 ci icc csc ccc ccccccncs oi SRLS MUTE Ca Wi ia's: Siamk 6 oid burs 37
Co-ordination of movements..... PPT re ORR Sr 39
» Vaso-motor paths and Centres... ..... cs cncccccvessvcevcecvececs ua ends 42
Trophic centres and paths............... aA ahs <ca.0 as oe cae ee 44
en SEE a eso does 00060 ca 0.0 0eedigibh Dee wi ake ato Sania so £0
EE SIE TOD, Sa a's 9:06 6,0 Sap MCRAE Ne Geese bee cideebee 51
Centres and paths for the innervation of the viscera......... re se . 52
General Symptomatology........... oe tsee eee ee Raenke vaca we hye ote 66
ON CE MUNEMEINEIAET os 5. 50s boned REM MMMEMR PERN SS Coens acpbaeéce 66
Diminntion of sensory action, anzsthesia....... + eer . 67
Exaggeration of sensory action ........ceeccecccccsccececs i sacsiveerale 73
Disturbances of motility........ TE on a ee ae go ian
Diminution of motility, weakness and paralysis ..............0ee.e08 79
Imperfect co-ordination of movements, ataxia.............eeeeseeee 83
Various characteristic gaits...... Case MEMS Ubi n <5: ¢,0i0 016 bao ese axata A 96
Increase of motility-spasm............0cceeeecece Af ER ok Parry tS
Alteration in the velocity of the motor conduction..............-.55 104
Electric reaction of the motor apparatus..........ccecccececccccees 105
Disturbances of reflex activity............+. Ate Puranas a eee 6 oe sake maue
Vaso-moitor disturbances ............- COMP MN A ch PNK CRs a0 ¥0.x 00060068 111
TROPIC CISGULOANOES, 6.0.0.6 0 ccc wccccesssneece Src > dea Ratdis et uice Base, 6 9a 113
Disturbances in the urinary and sexual apparatus,........ Ro Bintee tas ace ~» 129
Disturbances of digestion and defecation .............+...+ hear eassna tet ee
Disturbances of respiration and circulation.................+. ey Tet ee 140
Disturbances of the oculo-pupillary fibres, the various cerebral nerves,
and the brain itself..... er ae > SAR ae Shean nop dae Cems 141
General Etiology ............ dcveeuee ee aha siowiew aie 146
PROUIEOMASEICG CUBDOMGION, 65 ccc ccs wd nt wese oregon ee cd srcncrccsensescoees 146
iv CONTENTS.
PACE
Sexual excesses and irregularities. .........ssseeecseesesees Jasin tee 147
Influence of age and SCX...... csc cece e cet cnet ene t en neescenenees 150
General disturbances of nutrition ......... eee ere ee eee ener eee eseeeees 151
Propagation of neighboring morbid processes .....+..++..eeserseeeeeeee 151
Exposure to Cold. ... cs csc ce cet ee ede c erence cctececceresesccecenes coe AOE
Disturbances of circulation, excessive exertion and psychical influences .. 102
Poisoning and the local development of various infectious diseases..... .. 153
AGULG THRGABOS, 6, ica deceeevisseets voce she tarhes ve csanene i she 153
Irritation and disease of peripheral organs............. cece eee ee eceees 154
General Diagnosis... ......seteesccceccccsececsceesccesscsscveserse ae eee 155
General Therapettics.. 2... ies cscs cee stivsgescee cecense cesses 6 sme osname 160
External remedies. ......-..2cccsceeee abies $53 Ss Seen ee nec s . 162
GEE higavisas >» ccindueyes eee Sake Winoin’s «8 bbw 9 9-30 3:3 ap ole a . 162
WAPINGES 6p nds v.0c'S sland oe SSI RE OR ERENT 163
Bataa . . is.00's 303 caer eae tiie cie.y aie el og wo 9 eer e's. ik <a 164
Climate ......... ay ates wwe ea & aR SeNeies ee owen see 6950 eae 175
WlOOtri gh «os oss6vcee ee ROE e sie bh Aes co ee 0s coc ckbeses sabe eee mann 178
Blood-letting and derivatives .........cc cece sce c ec cc eect ence ences 185
Eixtergal FYIGhOUG ., geo pip s4 5 cetke's oo 40 0d hele'es 3 Pee oes oe
Internal remedies....... Seb ap iee eas icaeipa,n'b's 06 8s 90> aun oy oo ‘oe Se
Symptomatic remedies and methods, .........0..2cccecccecccecene soe a
General method: of Tle... a. oh outer sews cee oe ne bwese cegele eens esce aUe
DISEASES OF THE MEMBRANES OF THE SPINAL CORD.......-...-.eeeeeeeeeeeee 199
Hyperzemia of the Meninges and the Cord itself... . 22.0.2... cece eee eee ees 199
Bibliography... ss ..s0c8 sak aped 6'b'e-0b dame eh bb bode een en 199
Etiology and pathogenesis......... No.0) Wa cern BS DEWIES +4520 5 Rea . 200
Pathologioal qnatomy,.... 2... .0c0as ses sen scsee sadees de aes <a eeie ne 202
AFPUPCOMACOLORY 6... osc oven vcs eeg so.nle'd © enh pigin Sip Snip ge-atetl eit pie een 203
BUM 5 <0. a n'n's.0 00 0 6s 0 4,0's 050 e 0.0 W5-0 WS aaeislogs oki anne Te eee e see . 206
ATORUIDONG 65... 5 ws'c o'ss00 4 06 0yls'ebelkivcethe Sapa element snag Was naan 207°
peemmngoal Hemorrhage. ........s0rcseck acum ¥oamble see savas ¢ es 0i5 eee 208
Bibliography .....0+0sssevtkans ee «Meehan ee ee Wow the ee eee . 208
Biology and pathogenesis. .......cccnteus hares sshvsud whose ts MeeOIEe 209
Pathological anatomy........sescseccccccoss s\éed boo oka s Va¥ ee Saale 210
Symptomatology..............06- She kde se 08 6 Gavediely & wate «(6356 sien ann 211
Course and termination. . 2.5 06.0.5 canscivns sub he scdeupal s bne4 sag ne 213
PASAFIOMIG = 6556405 ci <¥n'o\s's ot beee set CEGLBROS ES So RELA. s SINE So tee ee 214
Prognosis and treatment.............0-sseeeeeeees (so eee sap eeee er
Inflammation of the Spinal Dura Mater .........0.ccccecccccccenccevcesces 216
» PIDMOPEABEY 5 co on ues cseecayiseus-eh ou ck SANs ss ee 216
Pachymeningitis Spinalis Externa.........ccscccecesssscoctvstecsaavee 217
Pathological ‘anatomy... ... 2... ¢essciicaaews pees dus 33550 Tee 218
PYM PHOMALOLOTY fc... oo ss sie vn bone PRAPE wba ess conta cena . 219
RPSMNN fg a 5s aces pile 6.2 po Seals tte SPE PO . 220
Prognosis and. treatment... 7 Vospeacke visi oes + son. ca damn eeeene <iaoe ae
CONTENTS. Vv
PAGR
Pachymeningitis Spinalis Interna. ........0.ccscccscceserccccccececs oe al
Etiology and pathological anatomy... ........ccececcceseessececces 222
DUAMOOTABEM ORY. , « s 00.65 sas chssderdse tar ed ener vies Helge Os ee" bb ace 223
Diagnosis, prognosis, and treatment...........:cccccecccccesceees 225
Inflammation of the Spinal Pia Mater............. na ad OREO CUS UR DAO vos 226
IMI ota c oe ond eras ESE e: CERO eet eRe ab teees 226
I EU 6 do Ceo: divi e.6 ve aw OSS ROMOMETEAK DITO de eee Ree Se cor 229
PE clatdarnideuweid ds avr tees end A eUeUT AU aes Silev dd eves eons 229
GOR BERUOTO GS 0 15555-0750 we oslie PONE R Na TESS EVN Wn Ge ctwds 231
Symptomatology .......scccecsssecceeces ie 1 ee eee oe 234
Course, duration, termination, .......0.ccievcecuscevecenceseveses 244
UE lel rcieteiviaieabsia a sro o-se'e.orol o'sinre- org oe RRM Eels ORC ele dW UeN de 5 e's 245
ORM rer todas ec ererdd'arase'e sree elwewowweaegaetee ms Pra aides Rvlees c 247
eR ea v-at u's'0'shaneaw'n er eies die ale OVO RMON A PUREE RUN eeededes 248
RU ANON A OBI aha? o'5/<lsr0'e- aie's'0'e v'n'a'ciele'e'od MONRE OED SOM eee nwese eenes 252
MMIMIND Tr ry lod cte 0's" c'a''s s'ele'va'c'ee ieee wedged dale Paw ere ew ate bbs vie 252
PRP ROOPICRMENALODY 666 oe ccc seer eee ser eiwe ered sv avecccusse 253
ee OS TE PEELE RE ERO OLE Ee LR TOE 255
Mes MATAGIOM, TOOUIG 0). 0's 0 0 ce ces ccea eee eect eb ce eb ee eee cee 257
NE SPL TEPOE OL TCPP ULCER EERE TE Ls Eee 258
TNE tarsi), 'o'a'a'e's's's e's v's Cw elle ema ae ee cs ewe ekerongs 259
MN SIEM Ps lo a'e'e'siss'e eo 0s Voce hd CEMREREE Tas ee dee Seas cae 260
Tamors of the Spinal. Membranes... . ..-.-.. 0... vec sclsc eect eee cctcessescce 262
EIEN Dina 5,'55*s"0re aoa s'e'y' ew v oislerelp ian et Sh wots Sey «oe sles wones 262
Pathological anatomy..............+.+ ovo GlubththieaicteN reed beees veces 264
UMMM, FF Data ehe fala stereha'sre)s 0s 0c ce* ect bw CME eOU Cees eee eons ¥uoevene 268
ONO irae os 5:5 '0'e'oe srn'ctale eile AW MEO Weis cr se sceeces 268
Course, duration, termination. .......0. cide rece cce ete ccccceenees 273
SRRAEEE ALAS vis bos uss Dorcds VCS eee UN EDOM Ea ee vou scene dec as 274
MMM INNORNUA Tat 'alwA Bic’ se b's oc 0's Mev ticeneieh eb ale eee wees Ate ee 276
Addendum.......... ABA NuTa'c ao! 'o's’'s’a-'e'etw'eile wlehoareet Pees EWE CUD teed s 277
Anatomical Changes in the Spinal Membranes, without clinical signifi-
SN a Re ALI Raretivg vs oer » « o'c-0- 0st uh RS AMMEN a and etesols UNC ONT US Se vas 277
DE TAPE ATs OOD 6.60 0c:8 se owceementdvedes sess eceuele cdeeeuceds 279
Introduction ..... PRN Cay 6.00.0 004s ébe UAE ER DREMEL SW hicls o> 610 bsiwd aoe 279
Pee ONE SEMEL. wc 5 5c oo oe v0 vic DON EDE RHEE CE Sone ecertbbaleee 5 tae OOO
hc herein 0: <-wae 005s WHR ae eA FO WER ULES Tee os 280
PINE MNO OI 8 glans Sate o'4:cic'e 0 vo :0 oan ww See eUeees odlee cles a ae 281
URL cco igre: 0's es 4 liane sn oie ORE Datialale «0's 281
Pathogenesis and etiology......... shee UR oe TORN CER TEOE CT ee woe 282
ROME UATE i 6 0:a ic 0r<-0'e sige OMe TRE TSEC Medawhes odode 285
NSE) 0p cave ok ass SAUER Ee OS AUT ES la eve nes buese 286
Sere MNEBEION., CELMINAGON..... « ccis ab ORAe & Aes lassan scene ccdWecseda cde 288
TIT no a vo: «: ansyasins tsi 6 RARER eh x-4. SONS ORS N TIES Mole 10 2 289
EMA MINU. Ne Seats ears ab) 4 vin 061.04: 8pcai-4 16 Se ROIE & CUS" 55 devel sdercseeesore 290
CONTENTS.
Spinal Apoplexy........-eseeeeereeeceetereees TTT ey ey Sean
Bibliography... ...---eeeeeeeecereeeeceeereereeees eee ebn <n
Pathogenesis and etiology...-.+++++++seeeees Ook s oe eisic Cs tea eae .
Pathological anatomy. .......+eeeeeseeeceeeeee ee ceseeeesseeeecceeees f
Symptomatology ......--seeeeceeeereeeeeeeecs $v ele o¥isie oalele lee nal os
Course, duration, termination... .....s.ceereessec cece cece cceneece ecees
Diagnosis. .........ceeeeceeeseeceeecee Fakaisleue i ert ryey AP a
Prognosis and treatment..........+- meinen on'6 sts ¥o.0 0s 0 sles So ee
Wounds of the Cord, .. 0... ccncccccdscscdarsonstewaswesseeusveeeu as > sane
Bibliography... ......cecceecesescees os Caw aloudetnes eet er
BtiOlO gy... 0. ce secs ese cccvnsccsssencevaes inwicislee'aig Mine ato cae ocean
Pathological anatomy. .......000.cccsoeesscrccepsceacecsves see oon
Symptomatology ..........+eeeeees EE Pe POE jv owe male
Course, duration, termination..... Paw wies 02. p:siy wines eer cereccesece ve
Diagnosis and PrognoSisS......cc.scecccccccssecsvcece > viavelaiece 5 eI ey
TYCGDIONG x5 0509.5 0s cae ee A SES alee bond bb re Pore rr erste se
Slow Compression Of thie: Conds ...is5s0.0.00c0.08e 6aelides tees iss eee eee wa
AORLADOY Us evan k a9 000 oat 8s ork oe Late haneres teen «cae
Btiology and pachogeiweain, 5. 2 ose s ocyn es ibe hess soe evele aes Oee eee ar
Pathological anatomy... . <0 ss6i4s.c02 0000.00.09 0.0+,0'0.0, 00,0 4¢008%a 6 ae
Symptomatology ...........e2e0e ey er RE Py Tere ojalan iwi ¢s vies
Course, duration, termination...........s.ccececescces oustnen gee cane
DOORN SS 5's..505 2 ¥09% 8 6 vec eme hee Saueaenaae Ter Lite oie
Prognosis....... epee Sebo $C Oa RECUR EEa IO) Sa ceanntes ass Ve vasa
SS ROMINOINE A 5 cin 5 i's po et He RFES ReaD ERE EER ipod pen ad as dene eee Pee
Concussion of the Spinal Cord............cce cc eeeceeees 4 sip eaehatee ob sco ;
FUGUOSTADDY.... si o:o-0espvasakede bees apne on awe « ockes same
BUlology,.and pathogenesis... . .o 4 ss et s0sidiewwine oe aewee blew ean $5. 65min
Pathological anatomy............+6. eee eee en 9 4p se vata Series cea
Symptomatology ..........ceeeseseees Soa tee eo) Re hvevaesaus rer
BRUNE ss d.oiycs V5 400000. 0s'n 0 aoa ee ae ae ee vs ws peso 90/00
PTOGROME.. cise ces sss éliaats oad tania WIT OC rire
PRORUNONG. . cose ccns.ones op 00th skeen Rona er eNinn ee reer :
Soma) TeritatiOn, 605. casa cscs a vecteiss iis hw. ae OAS 0 beck am ues lean
PMDRORTADDY.. ..5 600 6d: acc CREE aS EES Oe nvr
Etiology..... EP iatesiag des bee ane diane Cee wo Se eb eles Mi - koe aeae .
Symptomatology ..........cccccecceces ‘oisarepilamnat PTET ii “
Course, duration, termination.,..... PROPER TE Sento ‘
CRROMR Sib thek srk sans 2 5 oo caw) reir ry rer 6 ¥.0:0 eiarplh a eipté are eRe
Prognosis .and treatment... ........sccsccccesssescece oo lees SUheEnEE wa
Spinal Nervous Weakness.............. verry rr ro agiaws sxtnes
Bibliography...........-. sbwts Eoaeak pin ea Mae ere ee Tee
Re See SIO ie, on weRUn.o-4.0-0 wie © 6's a ke ble wae eee
Symptomatology .............0.e008 hae ae TEESE eh nw at aera
Course, duration, termination......... Pe eee vy
CONTENTS. vii
PAGE
NS hawins sf uheves esas tee s SERA TKEGRT 43 CRAP TAGE OATTESS 378
Prognosis........ ED ss 5 5. An Ra MER INR GT Ata a hed ciéee eek 6s 379
Treatment..... EGR oa) 6+) REM ER See ae eT eb ed 66 a8 semen dese oosce COU
(Translated by David F. Lincoln, M.D.)
PAPO 60s eeied veececeas PD PYVETTERET TET | pe eea be ee eeaideaeed is Teas ve . 382
Bibliography. ....ccccscssses 084.0403800 erie ss Miteres dyeee 382
Introduction.......... Sie ow opie Sele SAME Wig e elon sage wae wo 4.6 383
GOES os 6 6 44 ces oe Pee sN Vise voces CAEMERET EVN Se daus Oe code a bias . 385
PAPOUGIE-OUUR oo dicta cocic de eiadccevenceneddnee Op) ee ES ee ee 387
Bilology and. pathogenesis. 2.0.6.5 ccc ceteceeecs beta dececssceceeces 388
PREROIOGION ORASOIIG oo occ ccc cco censdstd tes MnO ese Ce neercesine’s 391
Symptomatology. .......cccssccecccsccees SC PEMERE SVT Ube ves oweccee 402
Course, duration, termination,.... ee yy it eee RE 414
PON curck ue Sabwuweeks.d 563050650080 BUN eU Oeebes 3’ es ee 418
NUN uh deve dda PE s6694 6544045 Sea ce SUE ERRED Ne MERE EC a@es’ oes 420
MPPMUOE Cane aidedisncssactecesisade 1 CR ee vis ere eeiae Webs vs 422
ENE aaa Aa hres vie'uv ioe vv'eds 6 0.GURREBEREIS UU ce elec eebee 6 ve 426
PEMURT GUA DALROPONOEIS «6 o ocie ocicic cs selenide delet eece velsccceseessece 427
Pathological anatomy..............e0. CERAPEAURET Ne Odea dele waages 429
NON oo al hc di ctelc wa ececetsn WaldcttaRelWele's ccc Wee's ceeeiay 438
Course, duration, termination.......... Satin SE UHOR EN He ud ka'd ceo eelwes 448
Different forms of chronic myelitis........... DRE Wid 6s 6s-0)e'e'a 0% pre 449
EMORROMB ES iodo eee wdatseds vedede ens sa wre "eG fC ee 453
Prognosis ..........4 Fede asegads Deed CRP MEEM RecA o ees daw vs whetesia 456
TYOREMENL... 0600 eies eves oc eae ato ew atarale PuNME Vena cWelee cae eves 457
NMS ich GE 65 Wns Nd's 2:44 do 6546501 CoRR ERROR ER RUG bel Oe Secs colecee 467
ORLA TINT . oie\ ein’ 'ahe'esie vid tba ee ORR WE EEE TURE US ced ci wowace 467
Pathogenesis.............06. 6 00. do so telnet nab eroyle ss rey Pre ore 468
INE MEROUING «0.4: 6:0! 0's v0! u 'e'sie' a s:atalotetbbelpialtiel eleieis"e'e'e'sieglevece oes eese 470
SUNN ah gt para pian siara'é-0's'e'0\ 0's ests aaa Mua eeadce de dtc kbube coe 470
Diagnosis, prognosis, treatment. ........cccc cece cece ccc ccccccccccccces 471
Multiple Sclerosis. ........6.cccccceees Per rt yee Ree V Wikis '<warccmauctes 472
BOER INOY ata) sto ooo orale ve e-v ail Omabsletdldtd Tabaicteiccle dows veld ove cess 472
CO Be a ie erry VRE A eee 473
Etiology and pathogenesis. ..........0.ceeceecceecs Dawes ebaoulad ewe Wreds 475
i ORORNORL GROOT 5055) «.0's'<! 00:0 n'n'sievis stealpiabsiefaeiale 6:0 00 Web baleleccdceUee ac 477
See MAI ORAM O GT hasnt ae <i! 6:< aie: «'e ein orslaretchelalabtiareteds' we’ a ais Kena Res betes . 483
(Translated by John A. McCreery, M.D.)
RPeRN, CUPRINORT, COTMINALION, ....:5...5.<:4-c:saionmicicaiarerecccreocaecciceuisthelccdess 505
Diagnosis. .... Freer agescns banenGeantas Bah a .cine sc cwwscwesceiduaeddees 507
eR MMNINN atcha ue spisiawisisiew sieves Sue HuMiseha wan er che alee s eV hk oe 512
viil CONTENTS.
PAGE
Tabes Dorsalis..........00+eeceeeee recor ed aed ade a2 baoecéd ccene ote hen
Bibliography... ...... 26sec cece ec cee eee ebtteraterecccececsene 513
History... cc cece cece cece cece cece cnc ceetstetacssemecscceertinas 517
Etiology and pathogenesis.......-++0++ sere rece eeeeeeee cence tees - 522
Pathological anatomy........++.++++-++ Sa ki Raise © sine eee os sea 531
Symptomatology ... 0.6... ec ee ere e eee e eee e etter eee ee eee senecseeeees 540
Course, duration, termination............. Gen delas 64. nih ania: a oo
Theory of the disease.......2.-eeeeeereees cp t/a.0's egos eats a re 599
PNG ioc ois 0.00 erp evndeedocaeee se sakna ak tse os awed a ds= eee 603
DG 6 as n.d & o. 0)ojn nasty smruecntin Serene Ric knack bein RO 6eds aan
i Pntammeish | .8 5s do maa ke mann aelh > Jy a.by> visbie, sb ha htied Sa ‘odes Ue
Spasmodic Spinal Paralysis. .......ceececccccseccsceessccesece 60écds cee . 620
Bibling wap Py’ sx...c x0.s ass new esln's ain's9.0 0 tails ssi 04s kde ee 620
Introduction and history.......... aLks d'b pe bibe Dawe oe Owen . 621
Etiology and: pRihogememias in ch iene bts sleis asin Oc 0 Kaen ee ae os widest eee - 624 .
Pathological anapomyivs < asi sae sca t9e 5.000 Fos no 200+ opts algae nn 625
Course, duration, termination......... abv 90,6 ,0.0010 6 1io2 tee ee 635
Theory Of the Gisease rs «ais. < 26. <.0,00,0)0:5,0,0'o/a cm hina § as Cdee else es pe 636
Complications... 6.5.44 0s deivas 0? e290 OT Pe ee eee ‘eae reer
PAOAMOMIR. Fo oS ce cib andor sip eee ie bo dle RW RW Sid RSs Ra Rai 642
PEOGWOSI, © osiiso. 3. <.o.m0 0. ose piomjeo sie 6.5.40 Moki AF Rpg aA ls MEINE . 644
TLOGIINOND, 5 ic.s<c = d5.0.0.0 0 wes oie RS oe Lee Wertiercc 645 ©
Hemiplegia et Hemiparaplegia Spinalis..........0cc cc ceccesecccccccescsces 646
Bibliography. ..... > os vueawlwe spike ee bs LNe bees ... 646
BEINGGEY 2 oo. 5 600 0.004010 Kble Aah s waipia emp eawnee oe ees SE ee . 646
Etiology and pathological anatomy. ..........ccesccccccsssecesecsscecs 648
Symptomatology, ,....--..0-09.8sp se cpee eee poounes oleae tele 649
Pathologiea! physiology... <1... +4<<0anassshe.ceeees gage eee = sss eae
Course, duration, termination. ........:.5450p00ss shwaeeww sedan osael .-.-- 660
TOON 5 54 aay jee + 6aay Fare ce Si 55eN pte oh Ba Nee Bie. See raed see 661
Ie a a ps 0 0100 .5:0/8 st ee ee gids Feleota oes dewe Oa
BP TORGUIONG 6 as.0.6.5:4.0.040 9 > 200) > Ra RO ERD aiedeee os sqeveele enn
Poliomyelitis-Anterior Acuta. .......<. +00» dees a@bvel sauce Wrlgees osio'sis ee
Diblioptaphy ... .. <5 i isetkenceen aad n eb eee bane Se -.-. 663
History..... Reise MPT fe ere voc ws COS . 664
Definition. .... sch: wR D8 ©, 551k Se eee isseodaaa vin hte . 666
Etiology and pathogenesis. ..........sss 000s cede agtesuionss neve uae teow) ee
Pathological anatomy........ alah aie Pee CRT me OE Ty ne 670
PFOA TOMB oS ois os 5 9.0 a0 38 Seb ea eee eG ee bb «entree ‘pee om
The poliomyelitis anterior acuta in children...... Dis tives ae tguene . 681
The poliomyelitis anterior acuta in adults............
Course, duration, termination...........ccccccccccccccscecevces A 701
Diagnosis 5 a wdrclis\eiside yo» da suis oo Bettie aaa eranis ch oiacciennee ie 703 at
TRQQO OMB 0255 5.5 uses os oe once digs teh MMe ats buds -0.2.<icoregsiadg ae 706
ROTA, 5 iso wa 0h 5s ios bosses Rew eens vais pals canes iy Te
CONTENTS. 1x
, PAGE
Poliomyelitis Anterior Chronica...... GUM CUERRAALRG BARR CECE Te MERTON ES 8 0 712
PO TREN ile 6:0 s:0:dnicre ee OREN RAMEE Te CEN NS NG Ua ewe'e'sa'e'ee owielewe 713
EE Sale LCE de 4 a.0<'< cds ew ernie ea MEET ACAR VU CCCR onic esas Cad eeee 714
PUMGRORIORL BUBLOUNY 6 5 5 6 o.cc 5s os cet ate See Cbts op oes Hides Std ew saceceee 716
Se RON vig. aie's's,s va. e/o sicle set SOUMEAERE Pa Ap aee CUO SISSY COs recess 717
MED ilald niu COOKE Wala. 6.0.00: ¢-« v eciciciadibemanuedaa + anieeat Taal 6 oo 728
Prognosis,.....+. BERECED «4.94 44 00.0 tte PR EERMOMECE SOO a Te MEO ea es cacese's 731
Doe bie e Misa se 4.00 8 6.050. weeks ORRMEM MINEO EONS WenlWatctereedas 731
DRPAR EES AGCORTORE BCUIAS 6 6:56.00 5 owe c ccncsaisevembneeene ss eW UUs vececcoes 732
NOIMNS a a didiek & wns. 9 de 6.6 ke CEMA eee eee als «nes ceciels 732
Co RR ea oO aan i a ed 732
MtiOlowy- ANd PAthoOWONeris, . ..6.....0 000 eeesecins Maaalae Hea elo e.s Mhewbaid ds 735
BROMO IOAL BHRUOUNY 6 i's 6.6 oie a ce cece vergistn sigma eure lls ed se eecece 736
EP EERE rk. Oo i es 737
Diagnosis......... Se eer or 2d a 743
en aie Wisk ya: <is 01% 0 <.0 «= 0 0 scene DO ee 745
Treatment...... ou oT 6 ae Sean UAAe OR OTORAT waiedies neces 746
Intramedullary Tumors......... Ct Nic o.n's 6.0. cine EC POP RMEPT IS anole ence 747
Bibliography......... gc 6.0 ose cede e® + da nedaiiens< .- 147
IONS, DEMNINS B io. 5 oss. 5 koe oo oc oc cm eee ae baveceescccece 748
Etiology.......<... “hr RE? SE eee Wa eRe MAS eee x cia, nase 752
NN CLG go:dia o10, «.uc.e/n oie oa dae wena e ed eislnwie «ea decdien 753
Diagnosis......... PUN patiieid ne medecea eee” ahs TOS ES oe ae 755
Prognosis and treatment...... seceneceeveeeees rere eee Milan sicsenes 756
Secondary Degenerations, ............0c cece ceeece DU Paledis <.cidie eievig eae 757
Bibliography......... ere. ee Coe 757
PEON Pe awe Wehives <eeceer Sew en's eA DERG ULS Wa a dee occlaw seis 758
Etiology and pathogenesis. .... dt dsl ASPEN UTM CceDeeeeccses 759
POMORMIOD ANELOINY | oo eiic 5 coi css sede cdeewedde eet ee be ov bles Ueewes 767
NS UST SET ee ee PTET EE OA ee eee 774
Diagnosis. .....6.6.00 Te TERE R TEER eR AE REE Ee 776
PE TOQNOBIBS P0865 58 6d das PUPTeTETe eT. ee Od) Se ate 777
UROMUINORG! 5655.6 852 esa eed ic os ccs edweed Oe EP ee ee ee 778
Deformities and Malformations..; . ..... cesecaleavwccsdectsccedccecccceccece 779
ECON Foicies 63 0 5 v0 ts oe EAM EREEW ERs Cee ees Ubu eces 779
CPOHGUEE CIUGMNGRUONE S255 oi i os oc 6) ONE ad ete ee ae Ob dene OUR elee de one 779
‘SS yetoms Of Spink DIGGS, ; . iia cundawesdecese clei oOo. es Sieeeec eae 787
PROMS retire bess ccces cect chambeeeaeanetes bee ee eg eS ae 790
eS eee ee eee Cee 791
AMUVONMMLG dS odd dd ode: k salve Wiel hd aR MES bw RSD oa kee ee 791
Mare G2 Doubtful Diccases . . oo. .... sc cew eee enees Si iilaed ered Mes ce bees 794
NRT NER Ni sana vscinns'an he RI es Delle exe waliekiaed 795
OOO 6.4 9.0 v.52. 00 0 cd ada aeRRa MORE D eee WO aes WE WU CeK US os 795
Pathogenesis and pathological anatomyw............... cee ee eee eee 796
Symptomatology... ......ce cece eee PE CPR LAE RROD Oa ele see 800
CONTENTS.
PAGE
Saltatory Spasm...........-eeeeeee Bea rere yowe ee dso bbe Seog boule ne
Bibliography. ........-++:- sc uduateneean cements oa'e bodes Sak ee
Symptomatology ......--seeseeeeeee eect ete eeenenees aay Sree . 801
WEAMOIV occcewnn sc secce ca easy tanaee deed vba ee ..... 806
PROMIMONES.. ois vb cces ec ccesensantuese ceiee os sceecceeuwade ns oes vee OS
Tonic Spasms... .......scccescccccceweccccccccscosceteseneens sooeee) GUE
DURANT... 1... <2 aneveernenrece utes sevees er .. 808
Symptomatology ..... ua eed bemeeen bs lp ceed ce itslswe 65a aesrn nnn 809
OTe ok 05is:0 scinv pein wavalaia eoemen anon delet ale tees aaa Pee
PORES | 6 i6.c od.n's viv noe Gus enlire Shiccise ted esueee dive «2 see
Intermittent Spinal Paralysis............. iindessveweese hee os ose SeeEe . 814
Bibliography ........... Sg bin'd w 0.0 wib'v <ab'pin's aves a Sala a ea 814
Symptomatology......... PE inte ata: fis dyoveib dn ace PE i . 815
Diagnosis: 2s: <0-newwn I eel eh dacksin ache Save. ow ieligih anes ihn ee cs see
Treatment......... pe ee Siande nip escacal «sas deo sens 817
Toxic Spinal Paralysis.......... ea ebadsre’ eis Wen Ue eet <<a eee . 816
Bibliography......... Bx ahi Ga at's week occa inl wae ma 00.0 Oe
General OTGRENOS 6 < ckas be Seatac seiae daujanegh eriveriee . 818
Paraplegia dependent on Idea............. occ diseases ce ldbe 0 eu 819
Biblingtaphy ac. cckasecakes caicr Sins ve dpb lea idee Wake oss bese ee
NOH ioc: ccca said 204 pho hve eae OTe Mieke tp andeibeia Son eA aie alien ows tem 6b
Symptomatology . «. .\..-csrecenacasecaces 0:06 © ¢0'e'wieb bie od’ ae 819
Diagnosis... 0:6. 60. PT He PRIOR PET TE ee --. S21
THOGGINGEE....0.6 0: «ccs. as:d'ssaonalaterneejecklne Ate Ren a ote watt wate ori
(Translated by Edward W. Schauffler, M.D.)
DISEASES OF THE MEDULLA OBLONGATA......ccscciccscccccscvceccsess: + aoe
Anatomical Introduction........... ov -«, 6:4 oS Aube bw pata pamela ee: -o+. 825
BiGIONTAMNY «s s.cnus canna 62 Aa eka eee 5 ala ahe"ots<s 916 aR .- 825
Physiological Introduction...............- Rane dene eige ve 0 6's nee ee 851
DiPUOSTADDY 5. sss ss.cs.v0 utp bo amie 6 ob oie Se ee ioaes ee
Motor conduction........... os Raeeee Sats vaaidintk da erlene ja mecpaeied . 853
Sensory conduction ....,....s+sisesiyes ss Msi See eaeReS dna ieee .. 854
The respiratory centres............. pe yee rere. ce 648 $3 ore 857
Centres for the cardiac movements..... ee ae Rs at 5's Stews keel ose ee
WORIOR OF MMOOR Foci o's a cada ccc nee eeeeiee becarok to bsg atniraill oadiee oe-eeleeae
Centre of deglutition.......... TS ree Os o harewea ee Ree --- 860
VINEE ROO Ss vawigs ccdlcgh OR eeEe VT ee? cometh keink eb qelomeae 861
Nutritive centres for certain nervous regions............+ és Mews és s'ee
Centres for certain secretions............ ak eit ae toa waeDt oa ceed sem
Pathological Introduction............cccccccceevecesevecs rrr ons. wen 863
Hypereemia and Hemorrhage ....5.........ccceccccceces ayit-s he ea c+ ane ... 865
Bibliography .:. «. os «<A Goma ee ee hawk vias Me ey Pe 865
Etiology and pathogenesis............ padie Se nwie dds 0 A e'enw whe 8 pa ee
CONTENTS. Xl
PAGE
Pathological anatomy............ Teemheeess daaaascue ae Kiln eSaee Pe Te . 867
Symptomatology .........eeee0. Peitee Ban tak Wah eds colnk eS ak cise se 868
NEES ae didads ¢0s.ccawe ees DEED aeRME Aaa bake sts ohe des eetaces 874
PTOGNOMB, o's o's oe c's al ekiale’s b cétventns Shadeanrs TO RPP ARAS ERP AS ioe ERS 87
ee Pecan ac nc'cp 6:6 can GedeMee et CaKET SWE bin de 0 vdieebe beces 875
OSES Sorter rai si. cine Diameaet 04366465 00ty b's heen 80
Bibliography. .........s0 Pade Pp ES APE eee Piscabes te6c 876
PPORONIE BEEL WUOLOGY sos ka c's c clasarenabaweres'ss Ssaeeestbbaedcece 877
Pathological anatomy............e0e0 cuawem elas Dba cehin Kae aa AA 0: (desea, ae
PU TMDLOMBUOLORT yin vccecesdccscccaceccsens RRR E Id Oh he heise as aes 0 ad,s 880
Diagnosis..... eee aa ta th es.de 60s 4.65,06Ke Bs dice sce Mead 884
DECC CREO SEN eC hGe a os 5.0.60 006 00.0 ace a eeeme tO Se 886
Treatment..... PRetn deinen aed 05-00 < 6:66. 02-4i Meee esa Miniolalve dineleals 887
Injuries and Wounds........ big ease 64 osn ccc cn eieeeae AoE Oe 887
Bibliography ........ os at o'e csi. « pea eee EES MeaAihee's d50 9.68 887
Pathogenesis and etiology...........sseeeees Rekha ails A MNGal es Gelks: 0.084. 888
Pathological anatomy...... Rekdsicccnes ¢¢chaaeeeenaeecran iad ecis 891
Symptomatology ..... Le OE OP Re 893
ree ites Tae cad 6.06 6 0 0.04.6 cee MMNEISA ? 0.0100 Sais ew en sins 897
Ne adie le wins Ghandi bn + 00 04 64nd tS ORDO hse ais ch eind mals As 899
ES Reelin Gua, bcd ebdcie cc ce srebes Pepe ey a Ringside oc paths caked 909
Acute Bulbar Myelitis...... ~ eee Sickie. 00.0: <'w: 0:0 i RRM heLatae a 0 8 ave, aa, SATS 900
Sa ain s oc + 60 6.05 HAMMER E GSE Rescveceanewe 900
NN ea ced Wait kd pdieo.dnlss cecccesa coud SUM EMR A eleie-ce os eccetias 901
Pathological anatomy...........ceesceeses SNEED Sh 4 60.4.0 '00iso 0 0 901
Symptomatology .........c.cceeeeee PP ore 2 reer 902
UNIMON ways a'0,9 eas Reales b kiss 0 0c Sessa Nat oe AAR ate Tae 904
Rn Gis e's4 0 6°65 6 1g MOR Es 2s dike «alee a'e'9 one 904
NNT a caine CV deee CXS 2s ac ccce cackes TRRRREN Wiss wediecsee0edewiec . 904
Progressive Bulbar Paralysis ............eeee00: RMR Es 46 iu ods awaaen 905
Ei dig a's s\s'os 5 3 <6. 6dM eee ba wkd sec ks ws cede 905
se i Se >) ee 906
Pathogenesis and etiology. ............-seeeeees US SS ore ee 908
SP nr ne ee 910
Symptomatology...... DUKE 6 t.s.06 06 4 o CEM U Rd bb eek oes shaee eee 915
RPOMIEN, CAUERAACNLS CORIMIDAUION..... 060 o:c ree eeeeniwe cere sccccscsstewseces 933
SPOTNMONIAOUNY dali be oecencssce cess canenate RP es BAe 933
eC SNE COMORES Con, ss 00 00 cs wae RME Nels a0 pele cue cig ewaseee 938
NING Corviad Mae veil. osc 6s sa-ee TNL Ad Win o'c.esen Wie mide.w ess. 0. 939
Prognosis..... Pee EAE Gnd os 0.0 6 kb EIN i oie « avars viele ooh 00 ewera on 942
Treatment..... PAGE RED ales v.0 ¥:0.4 Ridh RMR RS bo «beled nels yeeedews ease 943
Other Chronic Diseases.............0e00+0. EMG Rea spe bech.os wanaiovs «2 947
RIOT a os:é 65s 500 he VeMSRMEMN DS v.60 SI Sia Wekowunaleeus . 947
NOU MIOUPO Sa ese. vs cnc encevebeaad _ Ver p neecen aie ghee sa M17
NM MOMS Oh. o's 0d ss 'nldn 4 ROW ORIEN SO lb a6¥ bbs evinces Saw ehes es . 949
ere eeerereses
; Ae
_Bibgphyvvnrvneesesenee Mojase!
a: a Ft
MMe ce cay sac ee 9S) a- 8% ie oe ie
(Translated by Edward G. Geoghegan, M.D.)
DISEASES
OF THE
SPINAL CORD AND ITS ENVELOPES.
ERB.
NPR OoOD UG Rae N:
Our knowledge of the diseases of the spinal cord is rapidly
extending. This numerous, important, and interesting class of
maladies, long neglected, is at present receiving the profound
attention of various classes of observers, and the labors bestowed
upon it are bearing fruit in many ways.
This improvement forms but a part of the general forward
movement of the last twenty or thirty years, in which special
pathology has shared equally with other branches of scientific
medicine. There are, however, three sources from which our
knowledge of the diseases of the spinal cord has been especially
enriched.
First in order, and most important, stands the improvement
in the experimental physiology of the spinal cord, which has
been made within the period of twenty or thirty years. The
study of this subject has led to extremely remarkable and
important results, many of which yet remain a matter for con-
troversy or doubt. Unexpected, even insurmountable difficul-
ties, have risen to obstruct what we at first thought an easy
quest; but these difficulties have served only as incentives to
deeper and fuller investigations, which have proved abundantly
fruitful of isolated facts, often of the greatest value in path-
ology.
The improved methods of pathologico-anatomical examina-
tion have been equally important in developing our knowledge
of the diseases of the cord. Although in use for little more than
ten years, they have been constantly receiving improvements,
and have already added greatly to our knowledge and compre-
4 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
hension of the facts. By their means many diseases have been
discovered, whose existence was not even suspected by those
using the former imperfect methods of examination; through
them a hitherto unknown degree of exactness in localizing dis-
ease has been rendered possible, and we have learnt to refer nu-
merous morbid phenomena to definite local changes in the cord.
Conjoined with physiological research and an improved, intel-
ligently directed method of clinical examination, the study of
pathological histology has thrown great light upon the general
pathology of the spinal cord, and has led to the most interesting
conclusions in respect to pathological as well as physiological
processes.
Finally, we may mention the progress of therapeutics, which
has lent the impulse of a new interest to the study of many
forms of disease of the spinal cord. We have lately learnt to
cure a number of such diseases, formerly thought incurable; or,
at least, we have been enabled to improve the prognosis in many
such. This we mainly owe to the science of electro-therapeu-
tics, which has made so many contributions to the pathology
of the nervous system ; not a few of the advances that have
been made in spinal pathology are associated with the names of
electro-therapeutists. Nor is balneo-therapeutics (the scientific
aspect of which has greatly improved of late) less deserving -
credit in this respect.
The diseases of the spinal cord have thus come to furnish a
most attractive and interesting field for scientific research, and
one most fruitful of important practical results; we can say that
the progress made in its cultivation has been of late years —
extremely satisfactory.
And yet it must be stated with emphasis, that we only stand
at the beginning of a successful development of the subject, and
that an extremely large amount of work remains to be done.
We cannot help seeing that the rich results of physiological
research are still very defective and uncertain in many essential
points; the results, indeed, often change from day to day with
each new method and new observer, and they are far from always
possessing that degree of exactness and trustworthiness to which
physiological research would lay claim. The excessive difficulty
INTRODUCTION. 5
of the subject explains why it is that in many points we have
perhaps not yet reached the root of the matter.
Nor is it less certain that the researches and results of path-
ological anatomy are still far from trustworthy, that the points
thoroughly explained are but few, and that the general patho-
logical significance of the commonest and most important morbid
processes in the spinal cord is not yet clear. The impossibility
of observing with exactness all the characters of a fresh spinal
cord, the errors and uncertainties attending the examination of
hardened specimens, and finally, the undeniable fact that these
researches have given us no information at all in regard to not a
few diseases, or stages of diseases, of the cord—these circum-
stances ought to make us very cautious about viewing these dis-
eases as if their key were held by pathological anatomy alone.
Practical experience, finally, shows us that the treatment of
diseases of the cord is still without hope in many respects. The
number of desperate cases which mock at all kinds of treatment
shows us,with continually fresh emphasis, how much remains to
be discovered and achieved.
All the more encouraging is the way in which the work is
going forward. Numerous investigators are busy with the phys-
iology and pathology of the spinal cord ; every day brings fresh
discoveries, new additions to our knowledge, a broadening and
clearing of our views.
It is obvious that it is extremely hard to write a text-book
of diseases of the spinal cord in the midst of this crowding
rapidity of growth of knowledge. It is perhaps impossible to
state in any decided terms the daily changing position of our
knowledge; and a dogmatic statement like the present, com-
pelled as it must be to shun the prolixity of a monograph, and to
refrain from the thorough discussion of debatable questions,
’ requires every species of caution in its presentation.
The preceding remarks will make it sufficiently plain why we
consider the clinical point of view as the most important one at
the present time. We write for the practising physician, who
encounters the actual diseases from day today. For him it is
important that a description shouldspossess unity and clearness,
and should give him something to work by. We have therefore
6 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
laid the chief stress upon the clinical presentation, in making
which we have rested mainly upon the basis of pathological
physiology, bestowing meanwhile a due share of attention upon
pathological anatomy.
One thing more should be added. After long deliberation,
we have decided that the special descriptions of disease should
be preceded by a general account, which has grown to a great
size, but will not, we hope, be found superfluous or worthless.
The anatomical introduction, the brief statement of the macro-
scopic and microscopic anatomy of the cord and its membranes,
with a synopsis of the physiology of the cord, which we have
placed first, are justified by the facts that these things are indis-
pensable to the understanding of the diseases ; that they mostly
escape the memory of the practising physician in the course of
time; that they have to be sought in text-books and journals
which are not often possessed by practising physicians, and that,
even in such works, they are not always treated with regard to
the pathology, nor even with a proper understanding of the
latter.
An account of the general symptoms seemed to us most
desirable in aiding the student to understand the pathological
phenomena, and in saving repetitions and explanations in the
special division of the work. We have, therefore, taken pains to
present in this part a brief and clear account of researches in
physiology and pathological anatomy, and of clinical observa-
tions, pointing out by the way the chasms which exist in our
knowledge.
Finally, it seemed not undesirable to describe the general
treatment, especially as regards electro-therapeutics and balneo-
therapeutics—very important branches, which, at the present
time, have hardly received a connected scientific treatment ;
although, even here, we have had to point out many defects and
obscurities—perhaps more than had been anticipated.
—-_ —a— ~~ ie
SS
L. Anatomical Introduction.
Cf. Longet, Anat. et physiol. du syst®me nerveux. German transl. by Hein. 1847.—
Koelliker, Mikroskop. Anatomie. Handb. der Gewebelehre, 5. Aufl.—Stilling,
Neue Untersuchungen iiber den Bau des Riickenmarks. 1857.—Bidder und
Kupffer, Untersuch. tiber die Textur des Riickenmarks u. s. w. 1857.—Schroe-
der van d. Kolk, Bau und Function der Medulla spinalis und oblongata.
Braunschweig, 1859.—G@oll, Denkschrift der med.-chir. Gesellsch. des Cantons
Ziirich. 1860.—Frommann, Untersuch. iiber die normale u. pathol. Anatomie
des Riickenmarks. 1864.—Deiters, Untersuch. tiber Gehirn und Riickenmark
des Menschen u. s. w. 1865.—M. Schultze in Stricker’s Handb. der Gewebelehre.
—Gerlach, ibidem.—Henle, Handb. der Anatomie. IIL Bd. 2. Hilfte.— Wundt,
Physiologische Psychologie. Leipzig, 1874.—-C. Lange, Ueber chron. Riicken-
marksentziindung. Kopenhagen, 1874; see Schmidt’s Jahrb. Bd. 168. p. 238.
1875.—Leyden, Klinik der Riickenmarkskrankheiten. I. 1874.—Huguenin, Allg.
Pathol. der Krankheiten des Nervensystems. 1873.—Boll, Histiologie und His-
tiogenese der nery. Centralorgane. Arch. f. Psych. und Nervenkrankheiten. IV.
p. 1. 1874.—Schiefferdecker, Beitr. zur Kenntniss des Faserverlaufs im Riicken-
mark. Arch. f. Mikroskop. Anatomie. X. 1874; and numerous other authorities.
The spinal cord is suspended in the vertebral canal, hanging
almost free, and with a considerable degree of mobility.
It is unnecessary to describe the vertebral canal in this place.
As points of practical importance, it may be stated that its ante-
rior wall is perfectly firm and solid, being composed of the bodies
of the vertebra, with the interposed disks of cartilage, while its
posterior and lateral walls have numerous vacant spaces, which
are only filled up by ligaments and other soft parts, as nerves,
blood-vessels, etc. The lateral spaces (intervertebral foramina)
exist along the entire canal; the posterior, on the contrary (inter-
vertebral fissures), are distinctly marked in no place, except in
the cervical region—particularly at the two uppermost vertebre
—and again from the tenth dorsal vertebra downward, especially
in the lumbar part. Throughout the greatest part of the dorsal
8 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
vertebral column these fissures are completely closed by the ver-
tebral arches, which cover each other like the tiles of a roof,
From this it is manifest what portions of the cord’ are most
exposed to external injuries.
The cord and its envelopes are far from filling up the entire
canal; and this circumstance protects the cord from injurious
pressure in the most movable parts of the column, namely, the
cervical and lumbar regions. The width of the canal varies; it is
greatest-in the regions of the neck and loins, least in the dorsal
region, especially from the sixth to the ninth dorsal vertebra ;
within the sacrum it rapidly diminishes. The shape of its trans-
verse section is nearly circular in the dorsal region, while in
the cervical and lumbar regions it is drawn out laterally, and
assumes nearly the form of an obtuse-angled triangle, with its
basis directed forward ; in the sacrum it has the form of a half-
moon, with the convexity directed backward.
The length of the cord is much less than that of the canal.
Its extreme tip (the end of the conus terminalis) lies in adults at
or near the boundary between the first and second lumbar ver-
tebre. iehst’* asserts that a difference exists between the sexes
in this respect; in men, the lower edge of the first, in women,
the lower edge of the second lumbar vertebra forming the extreme
limit of the cord. |
It is a matter of some practical importance to be able easily
to distinguish the different regions of the canal, in order to define
with accuracy the location of a given disease; this is done by
palpation and counting the spinous processes. Thus, we easily
recognize the spinous process of the second cervical vertebra,
and that of the seventh (vertebra prominens), from which points
the separate processes can easily be counted by palpation. It is
not so easy to recognize the spinous process of the twelfth dorsal
by the insertion of the twelfth rib. |
The greatest part of the cavity of the canal is lined with a
hard periosteum, covering the bony walls in every part.
Within the canal, the cord is covered, first, by a cylindrical
1 Spinal cord : the term will be thus used henceforward,
? Centralbl. f. d. med, Wissensch. 1874. No. 47.
ANATOMICAL INTRODUCTION. 9
fibrous sac of wide dimensions, the dura mater spinalis, which
begins at the foramen occipitale magnum, to the edges of which
it is firmly attached, and terminates by contracting itself around
the filam terminale, finally losing itself in the periosteum of the
coccyx. The outer surface of the dura is not closely connected
with the walls of the canal, but is separated from them by a
loose, moist, connective tissue, with abundance of fat, which
envelops every part of the dura in a layer of greater or less
thickness. The inner surface of the dura is smooth and shining,
and covered with several layers of pavement epithelium. The
neurilemma of the nerve-roots which perforate the sac of the
dura unites with the tissue of the latter.
The dura is supplied with arterial blood by the vertebral,
intercostal, and lumbar arteries ; its venous blood passes off by
veins which form large plexuses in the loose cellular tissue of the
anterior and posterior surfaces of the dura, connected with the
external vertebral plexuses. Numerous nerve-fibres are supplied
to the tissue of the dura and the periosteum of the canal.
The pia mater spinalis, the so-called vascular coat, lies much
closer to the cord. It envelops the cord in the closest manner
from top to bottom; it forms an exactly fitting cylindrical sheath
for the cord, containing the blood-vessels that belong to it, and
closely united in every part with it ; it sends numerous sheath-
like processes into the interior of the cord, which divide into
many branches, spreading in all directions among the nervous
elements of the cord, forming a framework for the support of
these elements, and imparting to the cord a due degree of firm-
ness; the largest of these processes, easily visible to the naked
eye, lies in the anterior median fissure of the cord, while a
smaller one is seen in the posterior fissure ; but numberless finer
processes pass into the substance of the cord from the entire
periphery of the pia.
The pia mater is a membrane of connective tissue of consider-
able toughness and firmness ; it consists almost wholly of waved
connective tissue, is extremely rich in blood-vessels (which will
be further described in speaking of the blood-supply of the cord),
and is also rich in nerves, which originate from the posterior
roots. Often, especially in old people, the pia is strikingly rich
10 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
in pigment, so as to have a light gray or brownish tint; this is
commonest at the cervical part, and is by no means always path-
ological.
The pia is joined to the dura on either side by from twenty
to twenty-three processes of a three-cornered shape; they are
arranged in two perpendicular rows, one on each side of the
cord, with their bases inserted into the pia, and their points into
the dura. They constitute the ligamentum denticulatum.
The pia accompanies the filum terminale to the end of the
canal, and is there united with the dura and the periosteum of
the coccyx.
Between the dura and the pia lies the arachnoid. Henle
describes it as an unusually loose, watery, areolar tissue, which
becomes compacted in the direction of the dura to a connected,
delicate, resistant layer (arachnoid proper), while its inner por-
tion passes directly into the tissue of the pia. Between the inner
and the outer thickened layers (viz., the pia and the arachnoid)
there exists, therefore, a loose areolar tissue, which is designated,
and with propriety, as subarachnoid tissue.
The fluid which this tissue contains in abundance is of great
importance, and forms that part of the cerebro-spinal fluid
which is contained in the spinal canal. It is clear, contains but
a small amount of solids, and appears poor in microscopic
elements. Its quantity in the adult amounts to about sixty
grammes, but varies considerably. It exists under a certain
positive though moderate pressure. When the dura is pierced
and the arachnoid also injured, it flows off.
The function of this fluid is, without doubt, that of protect-
ing the cord from mechanical injuries ; by keeping it floating in
a fluid, it preserves as equal a pressure as possible, and perhaps
also regulates the circulation and the pressure in the blood-
vessels. A sudden evacuation of this fluid in cases of injury to
the dura is followed by serious disturbances, which are, how-
ever, doubtless due in part to cerebral implication.
The spinal fluid is not in a state of repose, but, as Quincke'
has recently given exact proof, is constantly undergoing a
' Zur Physiologie der Cerebrospinalfliissigkeit. Reichert’s und Du Bois-Reymond’s
Archiv. 1872. Heft 2.
ANATOMICAL INTRODUCTION. 11
double motion: first, it moves to and fro in the subarachnoidal
tissue, under the influence of respiration ; and second, it is con-
tinually secreted under a definite pressure by the blood-vessels,
and as continually passes off by certain channels into the
lymphatic vessels. These channels for the spinal fluid are
chiefly situated in the nerve-trunks which leave the spinal canal.
It is obvious that these motions in the spinal fluid may be of the
greatest importance in the propagation of morbid meningeal
processes, in the removal and transportation of inflammatory
and other products.
The spinal cord (medulla spinalis) is a cylindrical cord, some-
what flattened in front for a great part of its length, and not in
every part of equal thickness. It does not nearly fill the sac of
the dura, but is closely wrapped by the pia. After removal of
the attached roots, it is easy to discern two swellings, the cervi-
cal enlargement and the lumbar enlargement. While the thin-
nest part of the cord, that in the dorsal region, has a transverse
diameter of about 10 mm., and a sagittal diameter of about 8
mm., the cervical enlargement measures 13 or 14 by 10 mm., and
the lumbar enlargement 12 by 9mm. The diameter of the upper
cervical region remains about 11 or 12 mm.
The spinal cord begins where the medulla oblongata termi-
nates, but without any sharp line of demarcation. Its upper-
most limit is best placed just above the point of exit of the first
pair of cervical nerves, lying at about the height of the upper
edge of the posterior arch of the atlas. Its conical tip (conus
terminalis) is situated opposite the body of the first or second
lumbar vertebra. The lumbar enlargement reaches from the
beginning of the conus terminalis upward to the tenth dorsal
vertebra; the cervical enlargement, from the second dorsal
upward to near the middle of the cervical column, at the third
or fourth vertebra. The lower end of the conus terminalis is
prolonged into the filum terminale, which reaches to the end of
the canal. The average length of the cord is from 35 to 40 cm.
The consistency of the cord varies somewhat in individual
cases ; in the perfectly fresh state it is quite tough and elastic,
and easy to cut; its cut surface is fhen smooth, and seldom
pushes over the edges; shortly after death it begins to grow soft
12 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
and deliquescent, and thus offers much greater obstacles to
examination.
Besides these features, we observe in the cord a number of
grooves, which, even when seen from without, give a hint of the
internal construction of the cord.
On the somewhat flattened anterior aspect, we find the ante-
rior median groove running down the whole length of the cord,
which, sinking into the cord, forms the broad fissura longitudi-
nalis anterior,' reaching nearly to the centre of the cord, and
containing a large process of the pia mater.
On the posterior aspect a similar groove runs from top to
bottom, the posterior median groove, which, in like manner,
sinks to a fissura longitudinalis posterior,” directed in the sagit-
tal line towards the centre of the spinal cord. This fissure also
contains a process of the pia mater, though a much smaller one,
closely attached to the adjacent walls of the fissure.
These two fissures divide the cord in two symmetrical lateral
halves, which are united by a narrow bridge composed of the
white and gray commissures. The anterior fissure is broader
than the posterior, but shallower.
After these fissures, the first thing to observe are the nerve-
roots which leave the cord, arranged in a double row, one on
each side. The posterior root-fibres lie in a perpendicular line
above one another, and form an almost continuous row, which
maintains a given distance from the posterior median fissure, but
gradually approaches it as they descend. If all the root-fibres
are removed, their points of exit form a sort of longitudinal
groove, called the swlcus lateralis posterior, or posterior lateral
fissure.
The anterior root-fibres do not leave the cord in a single row,
but are scattered over a stripe about 2 mm. broad, on the anterior
portion of each side of the cord. Their distance from the ante-
rior median groove is also definite, but by degrees becomes less.
When the root-fibres are removed, this stripe is plainly marked,
and is designated as the anterior lateral fissure—swleus lateralis
anterior. |
! Anterior median fissure of Quain,
® Posterior median fissure of Quain,
ANATOMICAL INTRODUCTION. 13
In the upper half of the cord another fissure or groove is
visible, lying about half-way between the posterior median and
the posterior lateral fissures, and designated as the sulcus inter-
medius posterior.
These fissures are commonly used to bound the regions of
the white substance of the cord. In each lateral half, the white
mass lying between the anterior median and the anterior lateral
fissure is called the anterior column ; the mass lying between
the anterior and the posterior lateral fissure is called the lateral
column ; and the white matter between the posterior lateral and
the posterior median fissure is named the posterior column.
In the upper division of the cord, this posterior column is again
divided by the sulcus intermedius posterior into two columns,
which are genetically quite distinct (Pierret), and which claim a
very special significance in pathology; the median portion of the
posterior column, adjacent to the posterior median fissure, is
called the wedge-shaped colwmn of Goll, or funiculus gracilis
(zarter Strang); while the lateral portion, which adjoins the
posterior lateral fissure, is called /wniculws cuneatus (Keilstrang).
Most of these divisions of the white mass of medulla are more
or less arbitrary ; the finer anatomy of the cord recognizes only
the sharp division of the anterior and posterior median fissures.
Pathological facts, however, not only justify the above division
of the posterior cords, but permit a division, not sharply made,
into owler and inner anterior column, and posterior and ante-
rior lateral column.
The anterior and posterior nerve-roots arising from each lat-
eral half of the cord converge, and, after uniting, pierce the dura
and pass to the intervertebral foramina; the posterior root of
each spinal nerve enlarges to a ganglion (ganglion spinale) before
entering the foramen, while the anterior root passes by this gan-
glion and unites farther on with the posterior root to form a
spinal nerve. The distances between the origins of roots being
less than those between the intervertebral foramina, the lower
roots are compelled to take a more and more oblique course in
order to reach the foramina; those from the conus terminalis run
almost parallel, forming a bundle of*nerves descending within
the sac of the dura mater, named cauda equina.
14 ERB.—DISEASES OF THE SPINAL CORD ‘AND ITS ENVELOPES.
This is nearly all that can be seen upon external inspection
of the cord.
In studying the inner structure of the cord it is necessary,
above all, to attend to cross-sections ; they give the best infor-
mation, and by mentally joining the results of the various sec-
tions for the whole length of the cord, a correct idea is gained of
the peculiarly complicated columnar structure of the cord.
In any section we may make we recognize first a division into
two substances: the central gray or gray-reddish mass, irregu-
larly defined, and of a peculiar shape, generally resembling that
of the letter H, called the gray substance ; and a peripheral
white mass surrounding the gray, filling in the irregular outlines
of the latter, and giving to the whole the form of a cylinder,
called the white substance. The latter is divided into the above-
named columns by the fissures and the nerve-roots, a division
which, in the lateral parts, is distinct only upon the surface, and
does not extend clearly into the mass of the white substance.
When we look closely at a section of the cord, we discover in
its centre a fine canal, often filled with tissue elements or patho-
logical products—the canalis centralis. This canal opens up-
ward into the fourth ventricle; at the lower end of the cord, at
the tip of the conus terminalis, it expands to a small cavity—the
ventriculus terminalis lately described by Krause ‘—which again
opens into the cavity of the filum terminale.
The central canal is surrounded by a partly gray and partly
white mass, which joins the two halves of the medulla; the gray
portion of this bridge, in which the central canal lies, is behind,
and is called the gray or posterior commissure ; the white. por-
tion lies in front, borders directly upon the anterior median fis-
sure, and is called the white or anterior commissure. See Fig.
2, 7 and g.
From this median region the gray matter extends in consid-
erable mass and peculiar form into each half of the medulla.
Its anterior part is rounded and broad, and pushes towards the
antero-lateral column ; its posterior part is narrower and more
pointed, and points directly to the posterior lateral fissure ; it
1 Centralbl. f. d. med. Wiss. 1874. No. 48.
ANATOMICAL INTRODUCTION,
15
bounds the posterior columns externally, and separates them
from the lateral columns.
are connected ; they are bounded outwardly
by a line, which is, in general, concave on its
outer side. But this line is irregularly pressed
outward in many places by projecting masses
of gray matter, and has scarcely the same
form in any two sections. See Fig. 1.
The anterior rounded part of the gray sub-
stance is called the anterior cornu, or, better,
when considered as extending through the
entire length of the cord, the anterior pil-
lar; the posterior acute portion is called
the posterior cornu, or, better, the posterior
pillar. Subsequent examination will show
that the gray substance differs very much in
‘elementary composition at different heights.
This may be seen, without the aid of a mi-
croscope, by observing that the form of the
transverse section of the gray matter differs
extremely in different sections of the cord, as
a glance at Fig. 1 will show.
The section made in the dorsal region is
the smallest, and most resembles a Roman H,
with its fore limbs rounded and its hinder
ones pointed (Fig. 1; 4 and 5); in the cervical
and lumbar enlargements it is much thicker,
is provided with rounded horns, swelling into
heads, and is enlarged by deposits of various
shapes (Fig. 1; 2, 3, 6, 7). There is no doubt
that these enlargements of the spinal cord
are chiefly, if not exclusively, due to the in-
crease in the gray substance.
In many portions of the cord various pro-
cesses are seen to leave the lateral portions of
the gray matter, usually containing bundles
The two parts of the gray substance
Ge
Fie. 1,
Sections of the human spi-
nal cord taken at different
heights. Magnified */,°
1. Upper cervical portion.
2,3. Cervical enlargement.
4, 5. Dorsal portion,
6,7. Lumbar enlargement.
8. Conus terminalis.
of nerve-fibres, which radiate to varigus depths in the white
matter ; these processes meet and form a kind of network, which
16 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
encloses separate portions of the white columns, rendering the
outer boundary of the gray matter very uneven and jagged.
These gray bundles of fibres are called processus reticulares.
They are most marked at the boundary between the anterior and
posterior cornua (Fig. 2, p). In the cervical and upper dorsal
part of the cord a triangular prismatic process projects from the
basis of the anterior cornu in front of these reticular processes
into the lateral column, which has been designated the tractus
intermedio-lateralis (Fig. 2, 0).
BS
s,
%,
oo”
i
‘
'
Pd
of
o
Fie. 2.
Semidiagrammatic section of the cord about the lower part of the cervical enlargement. Magnified o/..
a. Anterior median fissure, 0, Posterior median fissure. ec. Anterior column. d, Lateral column. e. Pos-
terior column. ff. Goll’s.wedge-shaped column (Zarter Strang). g. Funiculus cuneatus. A. Anterior roots.
i. Posterior roots. k. Central canal. /. Sulcus intermedius posterior. m. Anterior pillar (cornu), 7.
Posterior pillar (cornu). 0. Tractus intermedio-lateralis. yp, Processus reticulares. q. Anterior or
white commissure, 7. Posterior or gray commissure. 8, Clarke’s column or columna vesicularis.
An exact idea of these forms is only to be gained by the
repeated examination of good sections from the hardened cord,
under various powers of the microscope.
All the unevenness, indentations, faults in the contour of the
gray matter, are filled out by the white substance, which sur-
rounds the gray in a layer of various thickness like a cloak, and
gives to the cord its external form of a more or less perfect cylin-
der. The mass of white substance diminishes slowly but per-
ceptibly in the downward direction (Gerlach); it disappears
wholly at the commencement of the filum terminale.
ANATOMICAL INTRODUCTION, 17
The white substance is traversed by numerous radiating septa
of various degrees of fineness, and by the nerve-roots, which
cross it from the gray matter to the surface in a similar radiating
manner. ‘The septa are connected by numerous branches, which
divide up the field of white substance into numerous rhombic
districts vf various size, in which the nerve-fibres of the white
substance are contained. The septa and septula thus compose a
fine and complex network, enclosing the vessels of the cord and
the nerve-fibres.
At its outer border, just under the pia mater, the white sub-
stance is again enclosed by a very fine layer of gray. This sur-
sounds the white substance like a thin overcoat, accompanies the
processes of the pia which enter the cord, and separates the
nerve-bundles proper from the septa; it sends out from the septa
numerons offshoots, which penetrate among the nerve-fibres and
envelop each one completely. Most later observers are agreed
in considering that this substance is almost, if not entirely, com-
posed of the connective substance of the cord (neuroglia).
Comparing now the sections with each other, we obtain the
following plastic view of the structure of the cord:
Its nucleus is formed by a pillar of gray matter which tra-
verses the whole length of the cord. This may be approximately
compared with a channelled column of somewhat irregular form,
perforated by a fine canal in its centre, and possessing four chief
projections and four intervening depressions. This pillar is thin
and slender everywhere, but is made thicker by accessions of
new matter in the cervical and lumbar regions.
Its forward projections are rounder, broader, more massy,
forming the anterior cornua; its posterior projections are sharp-
er, more slender, narrower, forming the posterior cornua. The
nerve-roots pass off from each of the four projections in the form
of fringes.
Of the four depressions, the anterior and posterior are the
deeper, smoother, and more regular; the two lateral are shallower
and less regular; their bases are made irregular everywhere by
the deposition of gray masses, by projections and knobs upon
the pillar ; in parts they are wholly filled up, and here and there
a longitudinal ridge comes out into them.
VOL. XIIL—2
18 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The white substance is as it were pressed into these chan-
nels, as when a soft clay is used to fill up the flutings of a
pillar and smooth over its irregularities. Being smoothed off
exteriorly, these white masses finish the round outline of the
column. The white substance may also be conceived of as com-
posed of long strings or ribbons which fit exactly into the exist-
ing cavities and spaces, and are laid into the channels of the
central gray pillar.
The whole is then covered in with a fine gray mantle, which
closely embraces the cord, as does the pia mater.
Blood-vessels and lymphatics of the cord. The tissue of the
cord is rich in blood-vessels; the gray substance possesses an
especially rich capillary network. All the blood-vessels arise
from the pia; they pass into the cord through the processes
of the pia, and, following their ramifications, send an abundant
network of capillaries into the gray and white substance.
The arteries of the pia originate in the vertebral arteries.
Each vertebral artery gives off an anterior and a posterior spinal
artery. The two anterior spinal arteries unite in a single stem,
which runs down along the whole length of the cord without
much loss of diameter to the conus terminalis; this arteria
impar is reinforced at the level of each pair of nerve-roots by
small arteries which originate in the intercostal and lumbar
arteries, and pass through the intervertebral foramina with the
nerve-roots ; on the other side it distributes numerous fine twigs
to the pia and cord, and finally, at the foot, it forms two anas-
tomoses with the posterior spinal arteries.—The posterior spinal
arteries, one on each side, run down underneath the posterior roots,
with each pair of nerves receiving fine branches of communi-
cation from the intercostals, and sending off numerous fine twigs
to the pia and the cord.
It therefore seems plain that the pia mater and cord are
principally nourished by the vertebral arteries, and next to them
chiefly by the intercostals.
The capillaries of the cord discharge their blood directly into
two central venous trunks, lying to right and left of the cen-
tral canal within the gray commissure (Fig. 2), and running the
whole length of the cord. By their numerous horizontal con-
ee —_— — -
ANATOMICAL INTRODUCTION. 19
nections they distribute their blood to the outer veins of the
cord; of these the greatest and most important is the vena
mediana spinalis anterior, which runs the whole length of the
cord, lying behind the anterior spinal artery in the anterior
median fissure. Down the posterior median fissure runs the
vena mediana spinalis posterior, which increases gradually in
size as it descends. Numerous venous networks, which also
increase in calibre as they descend, unite these external veins
to each other. The latter transmit their blood (through branches
which run with the nerve-roots and pierce the dura) to the
great spinal plexuses, which lie in the loose fatty tissue sur-
rounding the dura, and anastomose with the outer vertebral
plexuses, etc.
Regarding the lymphatic passages in the cord, little is known
exactly. The perivascular lymph-spaces first carefully described
by His (and since more fully by Boll and Adler—see Archiv f.
Psychiatrie u. Nervenkr. Bd. IV. and V.), are said also to exist
in the cord. They stand in connection with a large lymph-space,
lying between the pia and the cord, from which the lymph is
carried through the lymphatics of the pia. According to
Schwalbe the subarachnoidal space is also a lymph-space, but
not directly connected with the perivascular lymph-spaces of the
cord.
Finer structure of the cord. The cord is composed of very
various tissue-elements, for the exact histological description of
which we refer to hand-books of histology; as regards the finer
structure of the important nervous elements, compare the article
by M. Schultze in ‘‘Stricker’s Manual of Histology.’’ In this
place only a brief sketch can be given.
Nervejibres, both medullated and non-medullated, occur in
the spinal cord. All these are completely destitute of Schwann’s
sheath, or, at all events, it has not been demonstrated by the
present methods of research. The medullated fibres compose the
greatest part of the white substance and the anterior commis-
sure; they occur of very various diameter, the thickest being
- found in the anterior columns; the Funiculi graciles contain only
slender fibres. In all, the axis cylinder may plainly be seen in
20 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
cross-section, and its diameter is nearly proportioned to that of
the medullary sheath. The finest medullated fibres are found in
the gray matter, of which they form a preponderant element.
They pass in all directions through the gray matter, both isolated
and in bundles, and frequently dividing up. The non-medul-
lated fibres, analogues of the naked axis cylinders, are only
found in the gray matter, in which they ramify to a very great
extent; their finest branches unite to form a close mesh-work,
which, with the ganglion-cells, is especially characteristic of the
gray substance (Gerlach). And a few bundles of larger fibres
with medullary sheaths, originating in the nerve-roots, pass
through the gray substance for short distances.
The cellular nervous elements, the ganglion-cells, are found
almost exclusively in the gray substance, and are the component —
which most strikes the eye; when they are found in the white
substance, they are almost always single, and close to the gray.
They are large, multipolar cell-bodies, sometimes visible to
the naked eye; they have no envelope, their nucleus is large,
with a distinct glistening nucleolus, and they usually contain an
accumulation of pigment granules. They are remarkable for
their numerous radiating processes, almost all of which ramify
abundantly (protoplasm processes), while one process (the nerve-
process) remains smooth and undivided, and after a longer or
shorter course receives a medullary sheath and becomes a medul-
lated nerve-fibre. This undivided process is, therefore, also
called the axis cylinder process.
According to Gerlach, not every ganglion-cell possesses a nerve-process, but
many are connected with the fine network of nerve-fibres only through the ramifica-
tions of their protoplasm processes ; among such, the smaller forms of cells occurring
in the posterior cornua are especially named. These cells, therefore, are connected
with nerve-fibres only through the intervention of the fine network of nerves. Boll,
however, doves not consider that the existence of this kind of cells is sufficiently
established.
The size of the ganglicn-cells in the cord, like their form, is
very variable. They are found small, medium-sized, and large.
By far the largest are found in the anterior cornua, with a great .
number of processes; the smallest, more of a spindle shape, in
ANATOMICAL INTRODUCTION, 21
the posterior cornua ; those of medium size and a more rounded
form, in the so-called columns of Clarke.
They lie in groups and heaps, forming, in various parts of the
gray substance, actual columns of cells extending for a consider-
able distance in the cord; they are especially abundant and
definite in their distribution in the gray anterior cornua, while
in the posterior cornua they occur but sparingly and in quite
irregular arrangements.
The attempt has often been made to establish a close relation between the
form and size of the ganglion-cells and their functions. Jakubowitch first stated
expressly that the larger cells with many processes, in the anterior cornua, are
motor cells, while the smaller should be regarded as sensitive, and the smallest, of a
spindle shape, as sympathetic (vaso-motor). Other observers have made similar
hypotheses, and, more especially of late, a trophic action has been ascribed to the
ganglion-cells, upon the basis of pathological facts. Of all this only so much
appears certain: that the large cells with many processes in the anterior cornua are
most intimately related to the motor apparatus; but what these relations are, and
how they are expressed in the form and size of the cells, in their position and
grouping, is quite unknown at present; nor is anything whatever known with cer-
tainty regarding the existence, position, form and size of ‘‘ sensitive,” ‘‘ vaso-motor,”
“trophic,” “reflectory,” “automatic” ganglion-cells, although many pathological
facts recently collected seem to give us at least a starting-point for the solution of
these problems.
The nervous fibres and cells, which are certainly the most
important components of the cord, are enveloped in a basement
substance of connective tissue, the so-called neuroglia, which
gives support and firmness to the cord. This substance radiates
inward from the pia in numerous septa, bearing the blood-vessels,
which break up into a great number of branches, and finally
form a very delicate network in which the nervous elements are
embedded. The gray cortical layer and the greatest part of the
trabecular network proceeding from it, a great part of the gray
substance (especially that which is commonly named the sub-
stantia gelatinosa), and the entire supporting framework of the
white substance, are composed of this neuroglia. In regard to
its finer structure, the opinions of the best authorities (Koelliker,
Frommann, Gerlach, Henle, Boll, Ranvier, C. Lange, and others)
are still divided, as the difficulty of investigating this tissue is
very great. All observers agree that the neuroglia consists
92 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
chiefly of a network of fibres very closely interlaced, embedded
in a more or less abundant finely granular basement substance,
and containing numerous nuclei, granules and cell-elements.
But, as regards the significance and the exact character of these
fibres and cells, a great deal of controversy still exists. Some
consider the fibres as elastic (Gerlach), others as more like con-
nective tissue (Henle, Ranvier), others as the processes of cells
(Kélliker, Boll, C. Lange); and the interpretations of the inter-
jacent cellular and nucleoid structures are equally various.
Boll has very recently given a careful description of the neu-
roglia, which is different from previous ones. He states that its
sole component is a form of multipolar connective tissue cell,
composed of countless fine processes, not ramified; and a nucleus.
These cells envelop the vessels in the septula, like sheaths, then
branch off from the sheaths, and at last form by themselves the
septula which embrace the single nerve-fibres and groups of
fibres—as finely woven twigs embrace the upright staves of a
basket, or as the fingers of the two hands may be woven into a
kind of tube. These peculiarly shaped cells, characterized
especially by their numerous unbranched processes, are called
Deiters’ cells or the spider-cells of Jastrowitz, and are often
particularly easy to see in pathological specimens of the cord.
Among their processes there lies a small quantity of a granular
interfibrillary substance. Their nuclei, according to Boll, are
what Henle calls ‘‘ granules’’ (Kérner). An essentially similar
description of the neuroglia is given by C. Lange.’
Very recently, Ranvier has presented another view, according
to which the connective tissue of the spinal cord is quite analo-
gous to the interstitial connective tissue of the peripheral nerves.
It is said to consist of numerous fine fibrillary bundles of con-
nective tissue, not anastomosing, but crossing in many directions,
and at the points of crossing there lie flat nucleated connective
tissue cells.” It is not necessary here to decide these difficult
histological points; it is enough to know that the entire spinal
cord, both white and gray matter, is permeated by a fine-meshed
' See Virchow-Hirsch’s Jahresbericht for 1873, Bd. II. p. 76, and Schmidt's Jahrb.
Bd. 168. p. 239. 1875.
* Centralblatt f. d. med. Wiss. 1874. No, 31.
mira
a i a i ee Bi el
J . -
OE ———— a ee ee - i ee Peay ae | Se ae hye
cross-section, in transverse sections
ANATOMICAL INTRODUCTION, 23
structure of connective tissue, consisting chiefly of fine fibrils in
which numerous nuclei are embedded, and surrounding in the
closest manner the nervous fibres and cells.
If Boll’s view should turn out to be the true one, the * granules” of Henle would
at last receive their right interpretation. They have been looked upon in all pos-
sible lights: as young connective-tissue cells, as young nerve-cells, as lymph-cells,
as wandering colorless blood-cells without prospect of future advancement, etc.
But it cannot be denied that not a few structures resembing cells and nuclei are
found in the cord, whose exact interpretation is not easily made out.
The arrangement of the histological elements of the spinal
cord is extremely complicated, and it is very hard to make it out
accurately in all its details and in all parts of the cord.
Very simple by comparison is the structwre of the white
columns. They contain the framework of connective tissue in
its simplest and most perspicuous
arrangement ; it is composed of the
neuroglia with the vessels inclosed
by it, contains a few multipolar
ganglion-cells, and embraces in its
meshes the nerve-fibres, sometimes
singly, sometimes grouped in bun-
dles of several (Fig. 3).
The large majority of these fibres
runs parallel to the long axis of the
Fra. 3.
A piece of the transverse section of the
7 white substance of a lateral column. Neu-
cord, for which reason they almost roglia, with Deiters’ cells embedded in it,
embraces the nerve-fibres, which are cut
alway s present their well-known across, and are seen with distinct axis-cylin-
ders. Magnified 23“,
of the cord. But the longitudinal bundles by no means always
maintain an exactly parallel direction among themselves; they
deviate from it in many ways, cross here and there at acute
angles; often weave into each other, or are seen to change their
place in the cross-section by degrees, moving towards the centre
or the circumference of the cord, forward or backward.
A certain number of fibres, however, run across the white
columns in a more or less exactly horizontal direction. Such are
especially the entering fibres of the roots, which run in broad
bundles at the level of the section, 6r only a little off from it.
They pass more or less directly from the cortex to the gray
24 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
pillars [cornua]. The anterior roots mostly reach the gray
anterior pillars in the shortest and straightest path, while the
bundles of the posterior roots are much interlaced after entering
the cord, and pass through a devious and irregular course before
reaching the gray posterior pillars. The fibres of the white
commissure are horizontal.
Finally, there are a few oblique fibres and bundles in the
white columns. They are partly root-fibres, which do not take
a directly horizontal course to the gray substance, but first pass
obliquely upward or downward in the white substance for a
certain distance, and then bend to enter the gray; and partly
fibres which, leaving the gray matter in a horizontal direction,
change to a perpendicular. This arrangement is especially
frequent at the surface of contact between the lateral columns
and the gray matter, where an abundance of fibres leave the gray
and turn upward or downward in the lateral columns. It is,
however, doubtful (although recently reaffirmed) whether root-
fibres run directly up or downward in the white columns, with-
out first having passed the gray substance; this is affirmed of
some bundles of fibres in the posterior roots.
The structure of the gray columns (cornua] is considerably
more complicated, and has not yet been examined in at all a
satisfactory way. Two kinds of gray matter are usually distin-
guished in it, plainly recognizable and separable by the naked
eye, namely, the spongy and the gelatinous substance.. Their
distribution upon the surface of a cross-section is very une-
qual. The spongy substance composes the chief mass of the
gray columns, while the gelatinous substance forms only a semi-
lunar cap over the tips of the posterior cornua, of greater or less
thickness (substance of Rolando), and surrounds the central
canal in a moderately thick layer. A prismatic column, situated
at the boundary between the anterior and posterior cornua
laterally from the posterior commissure, and close to the apex
of the white posterior column, has been considered by many
entitled to rank as a special formation in the cord; it is the
columna vesicularis, now best known as Clarke's column (Fig.
2, s). This formation, rich in ganglion-cells, is found only in the
dorsal part of the cord, beginning at the upper end of the lum-
ANATOMICAL INTRODUCTION. 25
bar enlargement and ending at the lower part of the cervical
enlargement.
Careful examination shows that probably the largest part of
the gelatinous substance belongs to the neuroglia. It consists
of the finely granular substance before described, which, how-
ever, in this situation is traversed by a few of the finest fibres of
connective tissue, and contains a remarkable number of nuclei
(glia-cells). It is traversed by many bundles of fine nerve-fibres,
running in gentle curves from behind forward in various courses.
These bundles originate in part from the posterior root-bundles,
in part from the posterior columns, and probably also from the
lateral columns. Besides, the gelatinous substance is traversed
by vertical bundles, parallel with the long axis of the cord, which
are especially distinct in the lumbar cord, and occupy principally
the middle and the anterior parts of the gelatinous substance.
In them large nerve-cells are rarely found, and the fine network
of nerve-fibres discovered by Gerlach is said to be also wanting.
The spongy substance is far more complex in structure. It
consists of a mixture of fine fibres and bundles of fibres, seem-
ingly inextricable, crossing in all directions, which resolve
themselves into fine networks of fibres, only to recompose them-
selves in the former aspect of bundles of fibres; at the same
time they contain numerous multipolar ganglion-cells, arranged
in definite groups. The fine nerve-fibres select the spongiosa for
the seat of a repeated ramification, and their branches unite to
compose a network of excessive fineness, discovered by Gerlach.
Very similarly, the protoplasm processes of the multipolar cells
form with their ramifications a fine network ; and it is extremely
probable, although not yet certainly proved by direct observa-
tion, that the fine bundles of nerve-fibres and the ganglion-cells
communicate at numberless points through the medium of this
network.
Boll has confirmed Gerlach’s discovery in all points, and has added to his state-
ments another, to the effect that this fine network of nerve-fibres is not merely
distributed through the entire gray substance, but can also be followed through the
septa of the white substance into the gray corfjcal layer. From this it would
follow that this remarkable and important network is universally distributed
through the cord.
26 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Schiefferdecker has very recently attempted to follow out
with somewhat more minuteness the incredible medley of nerve-
bundles in the cord, and to ascertain the course of the principal
ones. The most important result of his investigations—and it is
hard to apply either physiologically or practically—is that, so
to speak, al/ parts of the gray and some parts of the white sub-
stance are placed in the most universal and manifold mutual
connection by the various networks of nerve-fibre ; the entering
nerve-roots form connections with all the groups of ganglion-
cells ; the latter are mutually joined by strands of fibres of their
own, and send forth bundles of fibres to the white columns; and
all parts of each half of the cord stand in connection with all
parts of the other half; while, finally, higher and lower seg-
ments of the cord are joined by vertical fibres.
The spongiosa is crossed in many places by vertical ascending
bundles of fibres ; this is especially the case in the neighborhood
of the white substance, where bundles detach themselves from
the white columns, enter the gray matter, and after a short dis-
tance return to the white. This is most developed in the proces-
sus reticulares. The longitudinal commissures in the gray sub-
stance, just mentioned, appear in transverse sections as vertical
bundles of fibres.
The groups of ganglion-cells in the gray substance are
highly interesting. Their number and mode of distribution in
the anterior and posterior cornua vary. They can be seen excel-
lently, with their processes and ramifications, in cross and longi-
tudinal sections. Repeated observations have shown that their
nerve-process is directly transformed into a medullated nerve-
fibre, and, in the case of the great cells of the anterior cornua,
that the fibre passes directly into the anterior roots and mingles
with their bundles of fibres ; but this has been shown in the case
of but few cells, and in most the nerve-process takes other
directions, of which the object is chiefly unknown. It is further
demonstrated with certainty that the protoplasm processes of
the ganglion-cells break up by repeated ramification into a fine
network of nerve-fibres (Gerlach, Boll, Schiefferdecker), and it is
probable that this network stands directly connected with the
finest nerve-fibres and their ramifications.
ANATOMICAL INTRODUCTION, 27
Most of the ganglion-cells are found in the anterior cornua ;
in the cervical and lumbar enlargements, especially, a great
number of them are seen in every transverse section. Their dis-
tribution is not the same in all parts of the cord, but distinct
groups can be made out in most sections. First, a medial
group, adjacent to the anterior and inner border of the anterior
cornua, often broken up into smaller groups; next, a lateral
group, situated in the anterior external portion of the anterior
cornu (Fig. 4, A, a 6), and containing a great many cells;
Fre. 4,
Semi-diagramatic transverse sections of the gray substance of the cervical (A) and lumbar enlargement
(B), to show the situation of the ganglion-cells. Magnified !2/,* Aa, medial group; », antero-lateral ;
¢, postero-lateral group: d, columna vesicularis, Ba, medial group; a’, group first appearing in the lumbar
region, perhaps belonging to the medial; }, antero-lateral; c, postero-lateral group. In the posterior cor-
nua, only a few scattered ganglion-cells.
besides which, there is found in the cervical and upper dorsal
portion, in the tractus intermedio-lateralis, a third group of very
large multipolar cells, which may be designated as the postero-
lateral group (Fig. 4, Ac). To the latter corresponds a simi-
larly situated group in the lumbar region; but in this part of
the cord the division into sharply defined groups is less dis-
tinct, and the cells are distributed more or less irregularly over
28 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the greater part of the section of the anterior cornua (Fig. 4, B).
The arrangement of these groups of cells in different sections is
extremely variable, and the number which can be distinguished
is sometimes greater, sometimes less.
All these groups are found throughout the length of the
anterior gray matter, forming literal columns of cells. Amongst
the groups, and through the whole mass of the anterior cornua,
many single ganglion cells with more than one process are
found, more or less abundant in different sections. Even in the
white columns in the neighborhood of the anterior cornua, a few
sporadic cells occur.
In the gray posterior cornua the principal column of gan-
glion cells is the columna vesicularis. Its situation and extent
is described above. It consists chiefly of closely-crowded fine
nerve-fibres, mostly vertical in their course ; but there are fibres
which run in all possible directions, establishing connections
between Clarke’s columns and the other groups of ganglion cells,
the anterior and posterior root-fibres, etc. Among these fibres
there lie many pretty large nerve-cells, mostly spindle-shaped,
with their long axes in a vertical direction, and provided with
numerous protoplasm-processes ; a nerve-process has not yet
been demonstrated in connection with them. In cross-section
the cells of Clarke’s columns mostly appear roundish. Their
size increases towards the upper and lower ends of the cord.
Besides these, the posterior cornua contain only a few nerve-
cells scattered over the entire section. A large multipolar cell is
seldom found; the most part are of the smaller sizes, and are
distributed irregularly and in very variable quantities among the
spongy tissue of the posterior cornua. Nerve-processes have not
been certainly demonstrated in connection with them; but the
part they take in the formation of the fine network of nerve-
fibres may be considered as established.
The central gray substance, which unites the four gray col-
umns and encloses the central canal, chiefly consists of a finely
granular and finely fibrillated mass (neuroglia, gelatinous sub-
stance), containing many cell-bodies or nuclei. This substance
is traversed by a fine network of nerve-fibres with broad meshes
(Gerlach), and also contains bundles of fibres, of greater or less
ANATOMICAL INTRODUCTION. 29
thickness, passing from one-half to the other of the spinal cord,
before and behind the central canal, sometimes taking the direct
transverse course, and sometimes ascending and descending
obliquely (gray fibres of the anterior and posterior commis-
sures).
The white commissure consists almost entirely of nerve-fibres
with dark contour, most of which run in a horizontal plane,
decussate at an acute angle, and pass from one lateral half of the
cord to the other, diagonally from front to rear. But a few
bundles ascend obliquely, and immediately assume a perpendic-
ular direction. The white commissure first connects the gray
columns of one. side with the anterior columns (white) of the
opposite side (Gerlach), as the bundles of fibres which leave the
former pass upward in the latter ; it further connects the various
cell-groups in the gray columns with one another, and finally, it
contains fibres which traverse the gray substance and pass into
the white lateral columns.
The central canal is a very narrow passage, often obliterated
or occluded, presenting a roundish or elliptic, sometimes a tri-
angular transverse section. It is lined with a ciliated cylindrical
epithelium, and its wall is formed of dense undulated connective
tissue of extremely fine fibrous structure (ependyma). It is
bounded externally by the central gray substance, and is filled
with a fluid, probably identical with the cerebro-spinal fluid.
Anatomical data concerning the connection between the histo-
logical elements, and the course of the fibres in
the spinal cord.
Many studies have been made by anatomists, with a view to
unravelling the connection between the separate elements of the
cord, the course of the entering root-fibres, their connection with
other fibres, and with the ganglion cells, and finally, their ulti-
mate destination, or their continuation to the brain. Unspeak-
able trouble and toil have been devoted to these examinations ;
absurdly small and trifling have been the results; hardly any-
thing is established with certainty, and the liveliest controversies
30 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
are still kept up upon almost all points. But every fresh exam-
ination reveals fresh complications of the course of the fibres,
which reduce the attempt to disentangle and follow them out
almost to an impossibility ; and the deeper we go into the finer
structural relations of the cord, the plainer it becomes that a
separation and isolation of the individual groups of fibres or cells
is not what is sought or reached, but rather a connection among
them, as universal and complete as possible. This naturally
renders it extremely hard to reach the desired goal.
We shall here attempt to state, as briefly as possible, what
may at present be regarded as somewhat certain, and likewise,
what may be regarded as at least probable. For all details and
further explanations we refer to the works of Stilling, Clarke,
Koelliker, Frommann, Gerlach, Deiters, Goll, Henle, Boll, Schief-
ferdecker, and others.
The following points seem at present pretty well established :
That all, or at least by far the greater part, of the nerve-roots
pass straight to the gray substance, and enter it ; this is certainly
true of the anterior roots, but perhaps not of some small portion
of the posterior root-fibres.
That a large number of these entering root-fibres unite with
the ganglion cells or their processes; this also seems quite cer-
tain for the anterior roots, but is still doubtful in respect to the
posterior.
That numerous fibres pass from the gray substance.into the
antero-lateral columns, especially the lateral columns, bend up-
wards, and in the white columns take the direction towards the
brain. Some of these nerve-fibres, leaving the anterior gray
columns, pass into the white commissure and thence into the
anterior white column of the other side of the cord (decussation
within the cord), in which they probably run to the brain.
Others pass into the lateral columns, in which they run up into
the medulla oblongata, and finally decussate in the pyramids.
That numerous fibres from the posterior gray columns enter
the posterior white columns (and the posterior regions of the
lateral columns ?) where they bend upwards and run further in
the direction of the brain.
That the ganglion cells of the gray substance are mutually
ANATOMICAL INTRODUCTION. 31
connected by numerous processes in the most complicated man-
ner, both in the anterior and posterior cornua of each lateral
half, and by means of the commissures which join the two lateral
halves with each other; that moreover, processes of these gan-
glion cells pass, some directly into the root-fibres, and some into
the white columns, where they assume a vertical direction.
That of the fibres which enter with the posterior roots, a part
pass horizontally directly forward, and lose themselves in the
fine network of nerve-fibres, or reach the ganglion-cells of the
anterior cornua; while another part runs upward or downward
at the side of the posterior gray column, then bends again, and
at last enters the gray substance.
That the fine nervous network, and the nerve-bundles which
by their resolution compose it, and the bundles which are recom-
posed from it, serve to connect the groups of ganglion cells in all
possible directions, with each other, with the entering root-
fibres, with the white columns of both sides in the sagittal, trans-
verse and vertical directions.
The following statements may be regarded as more or less
probable, but not at present certainly proved :
That after the root-fibres enter into certain ganglion cells,
processes from the same cells_pass directly into the white sub-
stance (going from the anterior cornu into the antero-lateral
column, from the posterior cornu into the posterior column and
the posterior part of the lateral column) ; in the white substance
they ascend directly to the brain.
That individual fibres of the anterior and the posterior roots
meet each other in certain cells of the gray substance.
That a few bundles from the anterior roots merely traverse
the gray substance, going thence directly into the anterior parts
of the lateral column, and there bending upward. Their signifi-
cance is not yet clear.
That the posterior root-fibres first enter into the fine network
of nerve-fibres, in the gray posterior columns, and that the con-
nection with the ganglion cells is accomplished through this
network (Gerlach).
That each single ganglion cell, by means of its branching
processes, passes into a fine network of nervous fibres, from
32 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
which larger medullated fibres are again developed (connection
of the cells with the nerve-fibres).
That the network of nerve-fibres into which the posterior root-
fibres break up is in continuous communication with the network
of nerve-fibres in the anterior gray columns; that from this latter
network numerous fibres originate, which cross the median plane
in the gray commissure, and then ascend toward the brain, some
in the vertical bundles of the posterior cornua, some in the pos-
terior columns (total sensory decussation in the cord ?). The gray
substance, therefore, seems to be much more intimately connected
with the posterior nerve-tracts (through the fine network) than
with the tracts which prolong the anterior nerve-roots.
That from Clarke’s columns bundles of fibres pass out into
the lateral columns.
That the medial parts of the posterior columns (so-called
fasciculi graciles) have by their development and structure a
special significance, which is at present entirely obscure. Pierret
considers them as a great longitudinal commissure, intended to
bring various parts of the gray substance into mutual connec-
tion.
All these results are defective and inadequate in the highest
degree ; they hardly permit us to form an exact idea of the com-
plicated course of the fibres. In general, we can only infer from _
all this that the root-fibres which pass from the peripheral nerves
into the cord first enter the gray substance, where they have
their first termination ; that they next, after many ramifications
and connections, leave the gray substance and pass up the white
columns to the medulla oblongata. This process is repeated step
by step at the entrance of every new pair of roots.
But this scanty result gives us no information regarding the
precise direction of the single fibres, none regarding their connec-
tions, none regarding the physiological significance of the several
groups of fibres. Anatomy can at present give us no certain
information upon these points; we must expect it rather from
the most scrutinizing physiological research. ‘The next section
will be devoted to explaining the paths of conduction in the cord,
as at present understood through the aid of physiology and the
equally important aid of pathological anatomy.
PHYSIOLOGICAL INTRODUCTION, 33
Let it only be remarked in this place, that the anatomical
formation of the cord, which we have just attempted to sketch,
is somewhat modified in its uppermost region by the accession of
some new parts. We refer to the origin of the accessorius,
whose roots are seen leaving the lateral column as far down as
the fifth and sixth cervical vertebree. Within the cord they can
be followed to the ganglion cells of the postero-lateral cell group
of the anterior cornu.
In analogy with this, the so-called ascending root of the
trigeminus can be followed in the cervical cord to about the level
of the third cervical vertebra in the form of a large bundle of
fibres, which is in relation with the substantia gelatinosa of the
posterior cornu, and gradually passes into it.
Finally, in the uppermost part of the cord, the decussation
of the pyramids produces a sort of substantia reticularis—a
manifold interweaving of the bundles of fibres—which is visible
in the middle of the anterior half of the cord. _
Concerning the further course in the medulla oblongata of the
nerve-paths which leave the spinal cord, see further on, under
the proper heading.
II. Physiological Introduction.
Cf. Longet, Anatomie et physiologic du systtme nerveux; German transl. by Hein,
1847.—Schiff, Lehrb. der Physiol. des Nervensystems. Lahr, 1858-59.—
Centralbl. f. d. med. Wissensch. 1872. No, 49.—Brown-Séquard, Experim. and
clinical researches on the physiol. of the spinal cord, etc. Richmond, 1855.
Course of lectures on the physiol. and pathol. of the central nervous system.
Philadelphia, 1860.—Sanders, Geleidingsbanen in het ruggemerg. Groningen,
1866.— Wundt, Physiologic, 1873. 3. Aufl. ; Physiol. Psychologie. Leipzig, 1874.
—Hermann, Grundriss der Physiologie. 2. Aufl. 1874.—Zeyden, Klinik der
Riickenmarkskrankheiten. I. 1874.—Also innumerable articles in Reichert and
du Bois-Reymond’s Archiv, Virchow’s Archiv, Pfitiger’s Archiv der Physiologic,
Zeitschr. f: wissensch. Zoologie, Zeitschr. f. rationelle Medicin, Moleschott’s
Unters. z. Naturlehre, the Monatsberichte of the Saxon Academy, Brown-
Séquard’s Journal de la physiol. de 'homm®, etc., the Archives de la physiol.
norm, et pathol., etc.
VOL. XIII.—3
34 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The simple fact that traumatic destruction of the cord at any
place, or its experimental section, completely suspends the sensi-
tive, motor, and vaso-motor connection between the brain and the
periphery of the body, was sufficient to prove that the channels
for maintaining this connection lie in the spinal cord; in making
a step beyond this it became necessary to employ a great variety
of experiments to establish with accuracy the course and the
situation of these various channels. In order to accomplish this,
physiology has made colossal efforts, and has produced a series
of most valuable studies, incomplete though they be in many
respects. Of late years, pathology has contributed not a little
to enlarge our knowledge of the physiology of the cord.
Unfortunately, the physiological as well as the pathological
methods of investigation, and especially those of pathological
anatomy, are still very imperfect. In the experiments by section,
which are the most frequently employed, the effect of the
primary shock and of the secondary inflammation are hard to
separate from that of the simple severing of the channels of con-
duction ; secondary degeneration also frequently occurs, and
disturbs the result of the experiment. This manifestly gives
rise to uncertainty and confusion in the statement of results,
which is increased. by the difficulty of obtaining from animals
exact objective reports of the disturbances of function. In man,
on the contrary, it is comparatively easy to ascertain in patho-
logical cases the nature, the degree, and the extent of the dis-
turbance of function; but it is less easy, and in fact, quite a mat-
ter of chance, to obtain for anatomical investigation exactly the
right stage of the disease, and it is harder still to find the histo-
logical changes defined exactly and beyond a question. This
must always be borne in mind, that we may not suffer ourselves
to repose in too great confidence of the value of our knowledge.
In the following paragraphs we shall attempt to present a
brief summary of what is established in the physiology of the
cord, or at least, that which is probable, and capable of being
used by the pathology of our day.
ee ee
PHYSIOLOGICAL INTRODUCTION. 35
Sensory Conduction in the Spinal Cord.
All the impressions received by peripheral sensitive nerves?
are conducted to the spinal cord by the posterior roots; they
pass first into the gray substance, and thence are conducted into
the posterior columns and a part of the lateral columns, in which
they ascend to the brain.
The principal channel for sensations of touch, pressure, tem-
perature, tickling and the like, is to be sought in the white
posterior columns.
Section of the white posterior columns destroys the sensation of touch perma-
nently in the regions situated posteriorly to the section (Schiff); but it does not
annihilate every sensation, as a hyperesthesia, especially in respect to painful
impressions, continues for a time, gradually disappearing. It is not yet determined
whether there exist separate paths of conduction for the different varieties of the
sense of touch, but Brown-Séquard maintains this view and supports it by weighty
pathological facts; he supposes these paths to lie mostly in the gray substance.
The latest experiments of Woroschiloff (in Ludwig’s laboratory) are of great interest ;
they seem to show that the lateral columns are of far more importance in conduct-
ing sensation than has hitherto been supposed. But these experiments are confined
to the lumbar cord of the rabbit, and cannot yet be made the basis of more general
conclusions. They appear to show that each lateral column contains sensory fibres
for both legs; the more important seem to decussate.
The sensation of pain is conducted chiefly or exclusively by
’ the gray substance.
Schiff makes section of the posterior columns destroy the sense of touch, but
not that of pain; while section of the entire gray substance, leaving the posterior
columns intact, destroys the sense of pain, and leaves that of touch (the condition
known in pathology as analgesia).
The presence of the network of nerve-fibres shown by histology, hardly permits
us to explain these facts by the assumption of separate paths of conduction; hence
Wundt (Physiol. Psychologie, p. 117) has proposed the hypothesis of different
excitability of white and gray matter; the gray requires, in order to produce a
reaction, a much higher and more intense irritation than the white ; but when the
reaction occurs, its intensity is all the greater, and produces pain. If, therefore, the
gray substance alone remains for the purposes of conduction, more powerful irrita-
+.
—_
' According to Brown-Séquard, the paths for the ‘‘ muscular sense” lie in the ante-
rior roots,
386 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
tions are usually required ; and when sensation is produced it is more violent—that
is, painful; but if the white columns alone are retained, the irritation quickly
reaches a degree at which sensation is produced, but never goes so far as to produce
pain.
The gray matter conducts sensation even after the section of
all the white columns; it does this in its entire section and in
every part of it, although it is quite inexcitable under direct irri-
tation, and is, therefore, designated as @esthesodic substance
(Schiff). In this sense the white substance, with the exception
of the posterior root-fibres which traverse it, was supposed to be
also eesthesodic ; the experiments of Engelken, Fick, and Ditt-
mar, however, seem to have finally settled that the paths of sen-
sation which have once passed through the gray substance of the
cord are still excitable.
The anterior and the greater part of the lateral columns have
nothing whatever to do with the conduction of impressions of
sensation. |
The conduction of sensory impressions decussates in the cord
soon after the root-fibres enter it; this decussation seems to be
pretty complete in the dorsal and cervical medulla of man
(Brown-Séquard, Schiff). The decussation of the sensitive paths
is certainly complete in the medulla oblongata.
Whether the paths of all the kinds of sensation decussate is not yet fully deter-
mined; according to Schiff’s later statements those for the sense of touch do not;
according to Brown-Séquard, those for the muscular sense also do not. The latter
author also says that the channels for the various kinds of sensation decussate at
different heights. Miescher found decussation of the centripetal (sensory) fibres
from the sciatic, which produce a reflex increase of the blood-pressure. The fact
of the sensory decussation in the cord is established beyond any reasonable doubt
by numerous pathological observations. |
The isolated conduction of the separate sensory impressions
can only be explained (in view of the fine network) by supposing
that certain tracks in the conductive substance offer less resist-
ance than others, and are, therefore, habitually employed. Such
tracks are probably constituted by the fibres which pass directly
from the network of nerve-fibres into the posterior (lateral) col-
umns and pass upward in the latter to the brain; these, under
normal circumstances, offer least resistance. The further exten-
’
. a ee ae ee ane
PHYSIOLOGICAL INTRODUCTION. 37
sion of powerful sensory impressions, or the conduction which
continues to take place after interruption of the principal chan-
nel, is readily explained by reference to the network.
In the same way is explained the transference of powerful
irritation to neighboring or distant sensitive tracks, producing
the associated sensations; they require only a diminution of
resistance in certain channels, or an increase in the strength of
the irritation.
A retardation of the conduction of sensation occurs when the
posterior columns are entirely cut, and only a part of the gray
substance remains ; the more the gray substance is diminished, the
more distinct is this retardation (Schiff); this fact may very well
be used to explain that retardation of the conduction of pain
which not infrequently occurs in pathological cases.
In regard to the position of definite sensory paths in the
cord, physiology informs us that in the case of the lower extrem-
ities these paths lie at first in the lateral columns, and do not
enter the posterior columns till a higher point; the posterior
columns of the lumbar cord are said to contain only the nerves
of touch for the pelvic region, sexual organs, perineum, and
anal region.
Motor Conduction in the Spinal Cord.
This subject has by no means been examined in all points.
The principal line of conduction for voluntary movements
passes from the brain into the cord, through the decussation at
the pyramids, and probably to a still greater extent through
other routes of decussation in the medulla oblongata and pons.
The motor (voluntary) paths do not further decussate in the
cord, but remain upon that side which belongs to the half of
the body destined to receive the nervous influence.
Most of the paths for voluntary motion probably run down
in the lateral columns, enter the gray substance at different
heights, form connections, through the network of nerve-fibres,
with the large multipolar ganglion cells, and pass through
their axis-cylinder processes into the ‘Anterior roots. The fibres
for voluntary motion all lie in the anterior roots; these roots,
38 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
however, contain other fibres which possess a different physio-
logical function.
Section of the posterior columns and the entire gray substance does not destroy
the voluntary movements of the portion of body lying behind the point of section.
Section of the antero-lateral columns and the entire gray substance destroys all vol-
untary motion in the corresponding parts. Section of the anterior and the lateral
column lessens voluntary motion for only a short time, and motion returns the
quicker, in proportion as the gray substance is retained. In regard to the function
of the anterior columns proper we are still greatly in doubt; they do not seem to
aid in voluntary motion; they are supposed to carry fibres, for the most part,
whose function is to transmit reflex impulses originating in the brain (Huguenin);
they also bear fibres which experience one more decussation in the cord, and pass
through the anterior commissure into the gray anterior column of the other side.
In these points, also, Woroschiloff's experiments (upon the lumbar cord) have
brought new and unexpected facts to light, which ought, however, to be applied
with extreme caution. Motor baths for both legs are contained in each lateral
column; the more important of these, those which produce reflex action, co-ordina-
tion, etc., seem not to decussate.
Even after section of the antero-lateral columns, a translation
of motor impulses to the posterior half of the body is possible
through the gray substance, and even through certain limited
portions of it. This substance is inexcitable under a great va-
riety of stimuli, at the same time that it conducts the impulses
of motion ; it is therefore kinesodiec (Schiff). This is by no means
true of the longitudinal fibres of the antero-lateral column;
they are not kinesodic, as is affirmed by many physiologists,
who seek to derive all the phenomena of motion which occur
when the antero-lateral columns are irritated, from irritation of
the root-fibres which traverse them; the experiments of En-
gelken and Fick leave not the slightest doubt that the anterior
(lateral?) columns of the cord are as truly excitable as any
other nerve-fibre.
The isolated conduction of individual motor impulses, like
that of the sensory excitations, is explained by the supposition
that of the many channels which are open some offer less re-
sistance, and therefore are usually selected. But even in this
region many translations to other tracts (associated movements)
occur, either because the normal paths are not sufficiently
PHYSIOLOGICAL INTRODUCTION. 39
used, or because the resistance offered by other paths is dimin-
ished, or because the irritation is increased in force.
As respects the position of certain motor paths in the cord,
we will here mention the statements of Schiff, that the lateral
columns of the upper cervical portion contain those for the
muscles of respiration, and that cutting them destroys perma-
nently the movements of respiration on the same side. But this
is denied by others. Woroschiloff found in the lumbar cord
of the rabbit the motor paths for the foot and leg below the
knee lying towards the outer circumference of the lateral col-
umn, and those for the thigh more towards the middle.
Co-ordination of Movements.
The spinal cord plays a considerable part in this important
function, and disturbances of co-ordination of movement are not
at all rare in spinal disease; for these reasons, and in view of
the numerous unsettled controversies connected with the mat-
ter, we feel ourselves bound to give a careful statement of the
difficulties which surround it.
What is meant by. co-ordination of movement, is not difficult
to define ; it consists in the tnmnervation of a large number of
muscles simultaneously, each with a different but appropriate
degree of force, for the purpose of attaining a given object of
motion.
A little close inspection will reveal the fact that muscular motions, even those
which look simple, as lifting a burden or throwing a stone, are really quite complex,
and involve a large number of muscles; still more is this the case in the more com-
plicated acts of writing, piano-playing, gymnastic feats, and the like.
The manner in which this wonderful mechanism regulates
the co-ordination of movements, and the methods it takes to
accomplish its results, can best be seen by observing children
or persons who are learning to perform any complex motion,
as writing or piano-playing.
In the new-born child but few co-ordinate acts seem pre-
pared for; the movements of respiration, of sucking, crying, and
swallowing, and perhaps those of the eyes, are performed imme-
40 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
diately. All other co-ordinated motions must be learnt with
pains and by a thousand attempts, as is the case with standing,
walking, running, and especially speaking, and later, writing
and all sorts of skill in the use of the hands. The apparatus for
co-ordination seems to be ready formed, but not to be in readi-
ness for full use ; it attains full development by use and varied
practice. It is conceivable and probable that the frequent use of
the nervous paths (in the fine network ?) in certain directions by
degrees overcomes the resistance along these lines, until at last
their employment becomes almost a matter of course.
The process which takes place when co-ordinated movements
are being learnt, may be somewhat as follows: The will sends
down an impulse, and the part of the central apparatus which it
first reaches is that which presides over the association and
co-ordination of the single impulses of motion. This takes place
under the constant supervision of the sight (in the case of speech,
of hearing also), and of the peripheral sensations of the skin and
muscles ; which convey a conscious impression of the correctness
or inaccuracy of the movements, and enable the person to apply
to them the proper corrections. By continued exercise and
repetition the movements become more and more perfect, and
may thus reach a high degree of precision.
When co-ordination has once been acquired, and the motor
paths concerned have been sufficiently trodden, the complicated
movements take place quite automatically, in response to a simple
impulse of the will, aided by the apparatus for co-ordination.
A supervision by the sight or the sense of touch is then no longer
needed. This clearly appears from the fact, that after a little
practice we can execute the most complicated motions with a
swiftness and sureness which prove that they are not at all con-
trolled by any active and defining regulative sensation—as when
we grasp at a certain object, throw at a mark, leap over a ditch,
play the piano in the most rapid time, etc. We therefore are
able so to determine in the central organ the arrangement and
force of the various processes of innervation, and by the aid of
the will and the co-ordinative apparatus so to bring them to pass,
that a completely ordered movement is the result. At any rate,
this is the way in which most co-ordinate movements are per-
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PHYSIOLOGICAL INTRODUCTION. 41
formed, when once they have been sufficiently practised and
learnt, as walking, running; grasping, writing, speaking, etc.
The question as to the anatomical seat of the centres of co-or-
dination and the centrifugal paths belonging to it, is not com-
pletely settled. According to the latest researches (among which
those of Goltz are of especial importance) it appears that the
proper centres of co-ordination lie in the brain only. The cor-
pora quadrigemina, thalami optici, and cerebellum are the organs
which seem to take the most prominent part in the co-ordination
of movement.
In the spinal cord there seem to be no such centres, although
the undoubted fact that orderly reflex movements may be evoked
from the cord is sufficient proof that combined movements, serv-
ing definite purposes, can be arranged in the cord. But the
point we are here interested in is the co-ordination of voluntary
movements, which has little to do with the apparatus for these
reflex actions.
It seems, upon the whole, that the spinal cord contains only
those paths of conduction which lead the co-ordinative impulses
to the muscles, which, therefore, place the cerebral centres of
co-ordination in connection with the anterior roots.
In what part of the cord these co-ordinative paths lie, and in
what manner they enter into connection with the motor paths, is
at present wholly unknown. Pathological facts, to which we shall
come later, permit us to suspect that these paths are to be sought in
the white posterior columns or in their immediate neighborhood ;
and in order to supply the connection with the various nerve
paths the fine network of nerve-fibres may also be called in play.
But the physiological researches of Woroschiloff—which, how-
ever, refer only to the lumbar medulla—show that the co-ordina-
tory paths lie in the middle third of the lateral columns, in the
hollow between the anterior and posterior cornua. This agrees
with a statement by Schiff, that the symptoms of ataxia may
be produced in the lumbar cord by lesion of the lateral columns.
In the closest connection with the co-ordination of movements
we may here speak briefly of the processes which enable us to
retain the equilibrium of the body. In the execution of this
function a large number of accurately and finely co-ordinated
42 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
muscular contractions are concerned, which continually alter the
centre of gravity of the body in such a way that its equipoise is
kept and the body remains upright. For this purpose a con-
stant oversight by the senses appears to be necessary, to inform
us of the position of the body in space and of the posture and
position of the parts of the body. The oversight is exercised
partly by the sensibility of the soles of the feet, the joints, the
muscles, the skin, etc., partly by the sense of sight, and perhaps
also by the semicircular canals of the labyrinth of the ear. These
centripetal stimuli, constantly in activity, are converted in the
central organ into definite co-ordinated movements, which pre-
serve the equilibrium of the body. The co-ordinating centre
which preserves the balance of the body is supposed to lie
in the corpora quadrigemina and the thalami optici. The con-
ductive paths appertaining to it lie in the spinal cord, of course,
with the exception of those which come from the organs of sight
and hearing. The sensory paths for this function are situated,
without doubt, in the posterior columns and the gray substance ;
the situation of the centrifugal paths is unknown.
Vaso-motor Paths and Centres in the Spinal Cord.
These have been the object of much and repeated investiga-
tion down to the most recent time. Cutting the cord at any
point produces a transitory but very considerable dilatation of
all the arteries below the point of section ; irritation of the cord,
on the contrary, produces a contraction of the arteries below the
point of irritation. From this we may infer that vaso-motor paths
run in a centrifugal direction in the cord. They are said to be
chiefly contained in the lateral columns, and in part, probably
in the gray matter also; they are supposed to decussate for cer-
tain parts of the body, especially for the vessels of the thigh and
trunk (Schiff). This statement, however, is denied (von Bezold).
The centres of vaso-motor innervation certainly lie in the cord
and medulla oblongata. It has hitherto been generally assumed
that the chief centre lies in the medulla oblongata; but the
researches of Goltz, Schlesinger, Vulpian, and Mor. Nussbaum
have now established beyond a doubt that vaso-motor centres are
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PHYSIOLOGICAL INTRODUCTION. 43
found throughout the length of the cord as far down as the lum-
bar region. It is from these centres that the tone of the vessels
is re-established when they have been dilated after section of the
cord. The wound at first inflicts a shock, with temporary paral-
ysis ; hence the dilation which directly follows the section. As
soon as the centres have recovered, the vessels return to their
normal volume; every fresh section of the cord at a lower point
produces the same series of phenomena. A continued, or even
a permanent paralysis of the vessels may occur, but only when
the entire cord is destroyed ; in this case the irritation of peri-
pheral sensory nerves no longer produces a reflex contraction or
dilatation of vessels, in the way observed when the lumbar cord,
including the vaso-motor centres, is intact.
But even when the lumbar cord is totally destroyed, the ves-
sels of the posterior half of the body are neither permanently nor
wholly paralyzed ; the original dilatation gradually diminishes,
and the cutaneous temperature, at first considerably increased,
sinks again to the normal point or beneath it. The same is the
case after section of the sciatic nerve. These facts have com-
pelled us to suppose that the vessels also possess a peripheral
gangliar apparatus, like that of the heart, which preserves their
tone and keeps them at a certain degree of dilatation, even when
they are cut off from all connection with the nerve-centres.
Goltz* has recently attempted to refer all the vaso-motor phe-
nomena which occur during the various experiments in section
of the nerve to irritation of vaso-dilator nerves. These, when
irritated by the cut, he supposed to act upon the peripheral
ganglia like a sort of nerve of arrest, paralyzing their activity,
and thus producing a lax condition of the vessels. According
to this view the cord contains only that class of vaso-motor cen-
tres which cause dilatation of vessels. In spite of the elaborate
defence of this position—which is also held by Vulpian—it has
not proved sound, and a further series of researches, made
by Putzeys and Tarchanoff in the laboratory of Goltz, has again
shaken the theory of vaso-dilator nerves.” They refer the symp-
.
! Pflueger’s Archiv. Bd. IX. 8. 174.
? Centralbl. f. d. med. Wissens. 1874. No. 41.
44 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
toms to a great exhaustibility and an excessive stimulation of
the vaso-motor paths, which result in immediate dilation of the
vessels, preceded regularly by a brief period of contraction.
The vascular tonus, therefore, is under the influence of cer-
tain very complicated sets of apparatus; those of the peripheral
nerves come first, but are subordinated to the centres in the
spinal cord, so that when the latter are excluded, the former
require some time to develop their entire activity and to restore
the tone of the vessels. This increase of the activity of the peri-
pheral ganglionic apparatus is perhaps favored by the increased
influx of blood which occurs after the spinal centres have been
excluded. A similar relation may exist between the spinal
centres and the vaso-motor centres in the medulla oblongata.
It is not known where the vaso-motor centres in the spinal
cord are situated: probably in the gray anterior pillars. The
vaso-motor nerves which come from these centres mostly lie in
the lateral columns; they leave the cord in the anterior roots ;
those destined for the head come from the cervical cord, those
for the upper extremities from the upper dorsal, those for the
pelvis and lower extremities from the lower dorsal and the lum-
bar cord; the abdominal viscera receive their vaso-motor nerves
through the splanchnic, and the uro-genital apparatus from the
lumbar nerves. ,
Trophic Centres and Paths in the Spinal Cord.
Physiology is entirely in doubt respecting the existence and
the mode of action of trophic nerves. Pathological facts, in
numbers, have continually pointed to the existence of some
such trophic influence, coming from the nervous centres ; but no
generally accepted basis for a doctrine of the trophic nerves and
their functions has ever been established. We may therefore
confine ourselves to a few remarks, and avoid a close discussion
of this section of the general pathology of the spinal cord.
The influence of the nervous system upon the processes of
secretion is probably no longer doubted, in view of what we
really know concerning the secretion of saliva. It is palpable
that these processes have the very closest analogy with processes
ya
PHYSIOLOGICAL INTRODUCTION. 45
of nutrition. That the nutrition of most of the peripheral parts,
the nerves, muscles, bones, joints, skin, hair, nails, etc., depends
in many respects upon the spinal cord seems to follow from
numerous pathological facts which have been collected by
Charcot. These observations show that many and various
trophic disturbances—both those of an inflammatory and gan-
grenous nature, and also simple atrophy and degeneration—
occur in all the parts named when their nervous connection with
the spinal cord is cut off, or when the latter itself is affected in
certain ways and in certain regions.
The nature of these trophic influences and the routes which
conduct them are in most points problematic. The proper cen-
tres for these influences are probably the ganglion-cells, espe-
cially those of the gray anterior pillars. The routes over
which the trophic influences are conveyed to the periphery run
in the motor and sensory nerves ; but it is questionable whether
there exist for the purpose special trophic nerve-fibres, or
whether the motor and sensory fibres themselves assist in con-
veying trophic influences. At all events, no special trophic
nerves are anatomically demonstrated at present.
Respecting the position of the trophic centres for special
tissues, something is known, but most is obscure. Those for
Sensitive nerves seem to lie in the spinal ganglia, as found by
Waller and confirmed by Schiff. There are numerous and well-
established pathological facts in favor of this view, as degenera-
tion of the posterior roots, with unimpaired nutrition of the
peripheral sensitive nerves, in cases by Charcot, Vulpian,
Schueppel, and others.
The trophic centres for motor nerves and muscles doubtless
lie in the anterior cornua, and are usually supposed to exist in
the large multipolar ganglion-cells. In the same situation,
according to pathological facts, the centres of nutrition for bone
and joints are probably to be found (see Infantile Spinal Paraly-
sis). But the centres of nutrition for the skin and its adnexa
are probably elsewhere ; they are apparently to be sought in the
central gray substance or the posterior columns, their nerve-
>
' Clinical Lectures on Diseases of the Nervous System.
46 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
fibres leaving the cord with the posterior roots; perhaps they
exist in the spinal ganglia also.
Further research is required in order to determine all this.
The experiments of Eichhorst and Naunyn’ have lately shown
that the spinal cord contains the means of self-maintenance and
self-nutrition. |
Reflex Action of the Spinal Cord.
The production of reflex movements—i. e., the direct trans-
ference of sensory excitation to motor paths, unassisted by the
intelligence and the will—may be assigned without contradiction
to the gray substance. All spinal reflex acts—i. e., all reflex
acts which occur after the brain has been severed from the spinal
cord—require, without doubt, the aid of the gray substance of
the cord to produce them. These results are confirmed by a
great variety of physiological experiments and by numberless
pathological facts.
In spite of this, we are not yet entirely clear in regard to the
reflex apparatus, and the precise course taken by the excitation
which produces the reflex action; yet it is pretty certain that
ganglion-cells constitute the proper apparatus for producing
reflex action, and that it is in them that the transference of
centripetal sensory excitation to centrifugal motor paths takes
place ; experiments show, further, that the entering root-fibres
must connect with ganglion-cells very soon after passing into
the gray substance.
The centripetal paths, which convey a stimulus inward, lie
beyond a doubt in the posterior roots ; those which convey forth
a stimulus, the centrifugal, or motor, lie in the anterior roots ;
but of that which lies between these two routes, and its histo-
logical structure, we are not well informed. We may, however,
guess that there are branch conductors given off both from the
sensory and from the motor paths at various points within the
spinal cord, which meet each other at certain ganglia and groups
of ganglia (reflex centres), and enter into conductive communica-
1 Arch. f. experiment. Path. u. Pharmak. II. p. 242.
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PHYSIOLOGICAL INTRODUCTION, 47
tion with each other ; but these conductors may be supposed to
be connected by means of the fine network of nerves with all
tother possible paths in the gray matter, up to a great distance
from their proper seat, so that a reflex motor excitation, origi-
nating from a single point, may be diffused more or less exten-
sively. The reflex excitation may therefore pass to many or
even all of the motor paths; but, as a rule, it passes to but
a few, and often to but a single one.
There exist numberless paths, with very various resistances
to conduction ; those which present the least resistance are first
occupied. If the strength of the irritation is increased, or the
resistance within the reflex paths is diminished, the reflex
movements are correspondingly increased in extent.
In harmony with this complication is the fact, that the time
required to carry out the reflex conduction is many times
(according to Helmholtz 11-14 times) greater than that required
for simple motor conduction.
The degree of reflex irritability differs very much in different
persons; in many, all possible reflex acts can be produced with
the greatest ease, while in others this is very difficult, or impos-
sible. Various physiological conditions, many poisons, and espe-
cially pathological conditions, have the power to modify the
reflex irritability to a considerable extent.
The first and ordinary consequence of a brief sensory irrita-
tion is a simple brief contraction of the muscles, or a more
prolonged tetanic contraction ; subsequently repeated convulsive
jerks also occur; Freusberg’ and Goltz’ have lately observed
reflex actions that intermitted rhythmically, following a single
or continued irritation ; in the higher degrees of excitation the
muscular contractions become more and more extended, and
almost the entire musculature may at last take part in the reflex
action, as occurs in many forms of general spasm.
The way in which the reflected actions increase in extent,
while the irritation is increased, has been carefully studied by
Pflueger, who found the following results: The excitation, pass-
.
1 Reflexbewegungen beim Hunde. Pflueger’s Archiv. IX. p. 358.
? Ueber die Functionen des Lendenmarks des Hundes, Ibid. VIII. p. 460.
48 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
ing from a sensory fibre, is first transferred to motor fibres on
the same side and the same level of the cord; next it passes to
the symmetrically situated fibres of the other side, but in a some-
what weaker degree; then motor fibres in other sections of the
cord are attacked, first those lying above toward the medulla
oblongata, and afterwards those situated lower down; finally,
general reflex contractions of the great part of the muscular
system occur.
The reflex actions are not always simple movements; more
or less complicated movements occur, which may even have the
appearance of adaptation to a certain end (movements of self-
defence, of flight, and the like), in which cases there doubtless
exists a simultaneous excitation of several motor paths, which
are associated in the cord for certain purposes, or are united by
habit. There are, however, actual series of motions, motions
with a proper sequence, which serve a given purpose ; such are,
for instance, the rhythmic twitching of the hind legs, described
by Freusberg, the processes concerned in defecation, etc. These
cases are sometimes instances of a stimulus to new motion,
originating in the first reflex action; or they are cases of the
stimulation of entire centres, which govern various physiological
acts at once.
Reflex actions may be originated by stimulus applied to any
sensitive part of the body. Cutaneous reflex actions are the best
known, originating in stimulation of the skin ; the most sensitive
regions in this respect are the sole of the foot, the face, the front
of the belly, the inner surface of the thigh. Irritation of the skin
excites in different persons more or less generalized reflex actions,
which are strictly obedient to Pflueger’s laws of reflexion.
The tendinous reflexions, lately described by Westphal’ and
myself,* are of great importance in pathology. The tendon of
the quadriceps and the ligamentum patelle, the tendo-Achillis,
and the triceps tendon in the upper arm, are the best points for
demonstrating these reflex actions, as yet only observed in man.
They are caused only by mechanical irritation (light tapping
1 Ueber einige Bewegungserscheinungen an gelihmten Gliedern. Arch. fiir Psych.
u. Nervenkrankh, V. p. 803. 1875.
2 Ueb, Sehnenreflexe bei Gesunden und bei R.-M.-Kranken. Ibid. V. p. 792.
PHYSIOLOGICAL INTRODUCTION. 49
with the finger or the percussion hammer), are very easily dis-
tinguished from the cutaneous reflex actions, and are strictly
confined to the muscles and groups of muscles belonging to
these tendons. Similar reflex actions can be originated, at least
in cases of pathological increase of excitability, from the peri-
osteum of many bones, from fasciz and articular ligaments.
Westphal’s article, containing a great quantity of interesting and valuable mate-
rial bearing on the phenomena in question, appeared after I had written the above.
He gives the name of “lower leg phenomena” to that which I denominated the
tendo-patelle reflex action, and the name of ‘‘foot phenomenon” to the reflex clo-
nus which occurs when the foot is passively moved in dorsal flexion (to be described
in the section on general symptomatology under ‘Increase in Reflex Activity’’),
The article shows that Westphal does not consider these as reflex acts, but believes
that the muscular contractions are produced directly by mechanical stretching and
shock of the muscular substance. The fact that this is most easily produced at the
tendon depends on the facility with which the fibres of the muscle can be mechani-
cally irritated all at once, by pulling the tendon. Westphal, therefore, considers
the phenomenon as due to a direct irritation of muscle, and compares it in patho-
logical cases with abnormal states of muscular tension and contraction.
We ought, I think, to have very convincing grounds for abandoning the theory
which lies next at hand, with its numerous physiological analogies, especially when
the positive reasons for the alternative theory are so very few. I can by no means
admit the existence of such reasoris, as opposed to the reflex theory of these pheno-
mena. Moreover, a great number of positive facts, which I have since collected,
and which can easily be proved, even upon many well persons, are so decidedly in
favor of the reflex theory, and against the theory of direct muscular irritation, that
all my doubts are completely put to rest. I will mention only a few of these briefly.
In many patients, the quadriceps reflex action can be produced by moderate tap-
ping on a large part of the free surface of the tibia. Tapping on tendons in places
where firm substance underlies them (e. g., tendon of the tibialis posticus under the
malleolus) produces the reflex action. In both these cases, all mechanical action
upon the muscle is avoided. We can produce the effect upon the biceps femoris (in
patients) by taking up the tendon in our fingers, in an entirely relaxed condition,
and pinching it a little while; this succeeds, even if the tendon just above the
pinched part is held firmly with the other hand. The reflex action of the supinator
longus can be produced from the lower end of the radius. I saw in one case a
reflex contraction produced in the deltoid when the capitulum ulne was lightly
tapped, and onein the triceps brachii when a spot near the c. ulne was tapped. In
all these cases the experiments were carefully repeated, to show that. the reflex action
did not originate in the skin, and that no mechanjeal shock, transferred to the dis-
tant muscle, could have been the cause. In hemiplegic patients, when the patellar
tendon of one side is tapped, we often see twitching of the adductors of the other
VOL. XIII.—4
50 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
side. Ina case of compression of the lumbar cord the tendo-patellx reflex action
was absent; when the motility returned, the reflex action also appeared—a proof
that the integrity of the conduction to the central organ is requisite. In tabes
we often find the tendo-patelle reflex action wholly absent, while the mechanical
excitability of the quadriceps is retained or even exaggerated.
But the question has since been attacked experimentally, and, as it seems to me,
has been decided beyond a doubt. FF. Schultze and P. Fuerbringer! have made a
series of experiments, all favorable to the reflex theory. It appeared, first, that in
rabbits and dogs the phenomenon of the tendo-patelle is a quite constant occur-
rence, and has remained unknown to physiology only because it has never been
looked into; the reflex act can be produced with especial ease and distinctness
from the exposed tendon. The experiments were associated in some instances with
section of the spinal cord, in others not ; they were modified in the greatest variety
of ways by section of the nerves and muscles, poisoning with curare, etc., and their
uniform testimony was to the effect that the muscular phenomena in question cannot
be due to a direct action through the tendon, but depend on a reflex operation, the
mechanism for which, in the case of the lower extremity, is situated in the lower
segments of the spinal cord; and lastly, that a reflex act originating in the skin can-
not possibly be the cause.
The last statement leads by anticipation to the observation of Joffroy * that these
phenomena, at least in pathological cases, are essentially due to irritation of the
skin, while the irritation of the tendon plays only a subordinate part. Joffroy
brings many instances in which irritation of the skin produced the phenomenon of
reflex clonus of the muscles of the calf, to be described below. I have repeatedly
seen this. - I have, however, convinced myself that this also is due simply to a sec-
ondary irritation of the tendon. In such cases, every cutaneous irritation of the
foot produces a reflex dorsal flexion of the member, and this suffices to originate a
reflex clonus, exactly as passive dorsal flexion would produce it. Whether or not
there are cases in which the spasmodic tremor can be originated directly from the
skin, I must for the present leave undecided.
It remains to be said, that O. Berger is decidedly in favor of the reflex theory,
upon the ground of such facts as I have mentioned.*
We may therefore with propriety introduce the name of “‘ tendinous reflexion”
for this phenomenon.
Our view is decidedly sunported by C. Sachs’ very recent demonstration of
nerves in the tendons, which can hardly have any other than a sensitive function.*
It is also known, and has lately been confirmed by Freus-
berg’s data, that numerous reflex actions may originate from the
1 Centralbl. f. d. med. Wiss. 1875. No. LIV.
? De la trépidation épileptoide du membre infér., etc. Gaz. méd. de Paris, 1875
No. 33 et 35.
3 Schles. Gesellsch. f. vat. Cult. Medic. Sect. Sitzg. v. 23. Juli, 1875.
# Die Nerven der Sehnen. Reichert und Du Bois’ Archiv. 1875. p. 402.
Swe aS ee StS ae eee see | ee
—
ae
—— ee o
7 Ter Ree
-
ee rea
PHYSIOLOGICAL INTRODUCTION, 51
viscera, as the bladder, rectum, anus, the intestines (dependent
on their degree of fulness), etc. Freusberg has, finally, tried to
show the probability that reflex actions may also be originated
from sensitive nerves in muscles, by twitching and stretching
them. All these matters find their parallel in human pathology.
We have hitherto spoken almost exclusively of reflex actions
which affect the voluntary striped muscle. But it is easy to
show that reflex actions may extend to all the centrifugal phe-
nomena, and that such actions play a most prominent part in the
occurrence of many phenomena of movement; we would call to
mind the reflex processes which are so essential to the discharge
of feeces and urine, to the movements of the stomach and intes-
tine, to erection and ejaculation, to the movements of the uterus ;
the reflex production of the secretion ; and lastly, the important
reflex processes which occur in the blood-vessels, and are carried
out through the vaso-motor paths.
Inhibition of Reflex Action.
The experiments upon reflex action have also shown that the
irritation of certain parts may give rise to an inhibition or sup-
pression of spinal reflex acts. And it appears that this effect
may be produced as follows :
First, a powerful arresting influence proceeds from the brain
(Setchenow). Daily experience shows that we can suppress
many reflex acts by the aid of the will; but this relates only to
such acts as stand under the general control of the will, and can
be performed by a voluntary effort. Experiments show that
separation of the brain from the cord considerably increases the
spinal reflex actions ; such a separation is in fact always made
when the reflex processes have to be studied. It is further
shown that irritation of certain parts of the brain (in frogs, the
so-called optic lobes) lessens the spinal reflex acts, and retards
them, or entirely puts an end to them. The paths of conduction
for these inhibitory influences from the brain are thought to lie
in the white anterior columns.
Inhibition of reflex acts can also be produced from the peri-
phery. Numerous physiological experiments within the last few
52 ERB.—DISEASES OF THE SPINAL CORD AND-ITS ENVELOPES.
years have shown that the spinal reflexions can be arrested and
completely suppressed by irritation of sensitive nerves (Lewis-
son, Setchenow, Nothnagel, Goltz, Freusberg). A great variety
of sensitive paths may be used by this function ; the inhibition
takes place with most certainty from the skin, whether by power-
ful irritation of a limited spot, or by slight irritation of large
surfaces; it may also be originated by irritation of the sensory
nerve-trunks, of the sensitive muscular nerves, or of the viscera
(e. g., by distention of the intestines and stomach). The paths
used in the production of these processes of inhibition lie, with-
out doubt, in the posterior roots.
We have, however, nothing but conjecture to aid us in form-
ing an idea as to how these acts of inhibition come to pass in the
cord itself. We know that the reflex acts are arrested when the
sensory cells of the reflex arc receive impressions simultaneously
from other sensory districts—central or peripheral. ‘‘The sus-
ceptibility of certain centres to impressions which give rise to
the reflex act is lessened, when these centres receive impressions
from other nerves at the same time”’ (Goltz). It is quite obvious
that this statement is not an adequate explanation. Ferliaps
there exists a special inhibitory apparatus in the cord.
Centres and Paths for the Innervation of the Viscera.
The innervation of the heart, apart from the centres situated
within, itself, is dependent on certain centres in the medulla
oblongata. As regards the part taken by the cord in the ex-
tremely complicated innervation of the heart, there still exists a
difference of opinion. It is thought that the exciting centre for
the movements of the heart is situated, partly or wholly, in the
‘upper cervical region, and that the paths which lead from it run
downward for some distance in the cord, after which they reach
the sympathetic by various routes, thence passing to the heart.
Irritation of the paths in the cervical cord is said to accelerate
the activity of the heart.
As regards those roots of the accessorius, which originate low
down in the cervical cord, it is not yet clear how important they
may be in the innervation of the heart. But the cord possesses
al
= al
PHYSIOLOGICAL INTRODUCTION. 53
a powerful influence on the movements of the heart, through the
vaso-motor innervation ; it is well known that irritation or paral-
ysis of the vaso-motor nerves exercises a great influence upon
the rate and the force of the heart’s action.
The activity of the organs of respiration is also dependent
on the respiratory centres in the medulla oblongata, Recent
investigations by P. Rokitansky* seem to show that there exist
respiratory centres, analogous to the vaso-motor, in the upper part
of the cord, whose function becomes more distinct after the cord
is severed from the medulla oblongata.
The paths which conduct the excitation from the centres of
respiration to the muscles of respiration are said to be all con-
tained in the lateral columns of the cervical cord and upper dor-
sal cord. This view has lately been maintained by Schiff against
the attacks of Brown-Séquard and others.
The cord seems to have a great influence upon the movements
of the digestive tract. All these movements (swallowing, peris-
tole of the stomach and intestine) are reflex in their nature, and
are probably produced by centres situated in the cord. On the
other hand, the cord has also a reflex inhibitory power over these
movements. Thus Goltz’? has demonstrated an inhibitory influ-
ence exercised by the cord upon the movements of the cesophagus
and the stomach, and states further, that destruction of the cord
produces extensive and active peristaltic action of the bowel, and
causes diarrhoea. It is much to be wished that we possessed
* more accurate investigations into these relationships, and into
the seat of the centres and paths.
The evacuation of the rectum is produced by a more compli-
cated mechanism, as follows: The contents of the intestine enter
the rectum, producing a reflex peristaltic action of the latter;
the centre for this reflex act is situated in the lumbar cord. The
pressure of the contents against the place of exit probably at
first excites the tonicity of the sphincters by reflex action, and
interferes with evacuation. At the same time the sensitive nerves
give notice to the consciousness of the approach of an evacuation,
>
_
1 Untersuch. tb. d. Athemnervencentra. Wien, med. Jahrb. 1874. I S. 30.
® Pfliiger’s Archiv. VI. 1872.
54 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
and the influence of the will can be invoked to strengthen the
contraction of the sphincter and prevent the occurrence of dis-
charge for awhile. If the reflex contraction becomes stronger,
or if the sphincter is voluntarily relaxed, the discharge takes
place. It is aided by the action of the abdominal compression
(straining), which is either voluntary, or, in case of severe irri-
tation of the mucous membrane of the rectum (tenesmus), is
directly reflex. The passage of the masses of feeces through the
anus provokes those rhythmic reflex contractions which Goltz‘
has described, the reflex centres for which must also be sought
in the lumbar cord. These contractions close up the rectum.
The centres for all these processes lie in the lumbar cord; the
paths from the centres to the rectum lie in the sacral nerves and
the sympathetic plexuses. And as the sensory and motor paths
which ascend from the rectum through the cord to the brain (the
position of which in the transverse section is not yet exactly
known), are also concerned in the process of faecal evacuation, it
is easy to see how many points there are whence pathological
disturbances in the process of evacuation may originate.
Quite analogous conditions are found in the evacuation of
urine, the disturbances of which are so extremely common in
diseases of the cord. According to Goltz’ new and admirable
investigations,* the normal process is as follows: the increasing
fullness of the bladder produces an increasing irritation of the
walls ; by this sensory irritation a reflex contraction of the detru-
sor is occasioned through the agency of a centre located in the
lumbar medulla ; at the same time the impulse to urinate reaches
the consciousness, when the evacuation may be prevented by
voluntary contraction of the sphincter vesice, or of the urethral
muscles which act as sphincters, until the vesical muscles become
fatigued and the impulse to urinate diminishes. The. tonus of
the sphincter may also, perhaps, be increased reflexly by the
entrance of the first drops of urine into the urethra. After some
time fresh and more powerful contractions of the detrusor occur,
until at last the sphincter is overpowered, or is voluntarily
1 Pfliiger’s Archiv. VIII. 1873.
® Ueber die Functionen des Lendenmarks des Hundes, Ibid. VIII. p. 474.
PHYSIOLOGICAL INTRODUCTION. 55
relaxed, when the evacuation takes place ; it can be hastened by
the action of abdominal straining, either voluntary, or, if the
impulse to urinate is very strong, of a reflex sort; and is con-
cluded by a few rhythmic contractions of the urethral muscles.
The act of evacuating the bladder is, therefore, purely reflex
in its nature; the centre for its accomplishment lies in the lum-
bar medulla.
After section of the dorsal medulla the evacuation takes place in a perfectly
regular way, whenever the bladder has reached its normal point of fullness, or the
wall of the bladder is irritated in some other way. The complete paralysis and
cessation of evacuation which appears to occur during the first days after the
operation, depends on the concussion (Erschiitterung) of the lumbar medulla and
paralysis of its centres which the operation brings about. These centres usually
recover in a short time, and resume their functions.
The evacuation is excited by sensory irritations, the most
active of which is irritation of the wall of the bladder itself by
distention and pressure from its contents ; but irritation of the
anal region may also provoke the discharge. The sensory and
motor nerves of the bladder, which form the paths for this reflex
process, leave the lumbar medulla along with the roots of the
sacral nerves (probably the third, fourth, and fifth), and pass
with them, either directly or through the sympathetic plexuses,
to the mucous membrane and the muscles of the bladder and the
urethra.
There are, however, other motor and sensory paths, which lead
upwards in the spinal cord from the bladder to the brain. Budge
has succeeded in producing contractions of the bladder by stimu-
lating the cord as high up as the pedunculi cerebri; the paths
are supposed to lie in the anterior columns of the cord. It
requires no proof to show that the routes for the voluntary exci-
tation of the sphincter and the urethral muscles also run through
the cord to the brain. ‘
In spite of this, the will seems to exercise no direct influence
upon the contraction of the detrusor. The voluntary discharge
which we can produce without the presence of the impulse to
urinate, is probably brought about by*relaxing the sphincter,
and bringing a powerful abdominal pressure to bear upon the
walls of the bladder, which gives rise to a reflex contraction of
56 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the detrusor (Goltz). But that by an involuntary reflex action
originating in the brain the reflex mechanism of the lumbar
medulla may be brought into activity, and an evacuation pro-
duced, is shown by the cases in which psychical impressions are
followed by sudden discharge of urine; also by the fact that
certain ideas are capable of calling out the desire to urinate, or
of increasing it considerably. The paths in the spinal cord
which serve for the propagation of this class of impressions may
be excited by irritating the cord itself, and contractions of the
bladder produced.
Itis a matter of daily observation, and hardly needs to be
mentioned, that inhibitory processes exist in the case of the
mechanism of urination, as of all other reflex actions.
The correctness of the above statements can easily be shown
by careful observation of one’s own person, and is fully con-
firmed by pathological facts. We should, however, be careful’
to observe that disturbances in the function may originate, not
only in the centre in the lumbar cord, but also in the sensory
and motor paths which unite the bladder with this centre on the
one hand, and with the brain on the other. The relations may
certainly be very complicated.
Very similar conditions are met with in the processes of erec-
tion and ejaculation, which also depend mostly upon the spinal
cord, and which have received fresh light from the observations
of Goltz (1. c.).
The erection of the penis is brought about, according to
Eckhard’s investigations, by direct irritation of the so-called
nervi erigentes, which originate in the sacral plexus and are dis-
tributed in the corpora cavernosa. The process is now universally
regarded as an act of inhibition, exercised by the nervi erigentes
upon the ganglionic apparatus of the vessels of the penis (Lovén) ;_
this causes a relaxation of the vascular tone, and a powerful
influx of blood into the corpora cavernosa, hc produces the
erection.
This irritation of the nervi erigentes occurs in the reflex way
also ; the centre for this reflex act lies in the lumbar cord (Goltz), —
1 Beitr. z. Anatomie und Physiologie. Giessen. Bd. III. IV. und VII.
PHYSIOLOGICAL INTRODUCTION. 57
for itis very easy to produce reflex erections in dogs after section
of the dorsal medulla.
This reflex act is produced with most certainty by irritation
(slight friction) of the skin of the penis and glans, or of the skin
of the lower abdomen and perineum; by irritating the bladder
or rectum, by introducing the catheter, and probably also by
irritation of the testes, by over-fullness of the seminal vesicles, ete.
The reflex act can be arrested or suppressed, either by power-
ful peripheral irritations or by cerebral influence. Complete
destruction of the lumbar cord renders it impossible.
The brain also possesses a certain influence upon the occur-
rence of erections; but this is not a direct influence of the will,
for erections cannot be thus produced. But erections can be
produced by loose thoughts, by stimulation of the fancy, by
looking at things which excite sexual appetite. This appetite is
known to be located in the brain; from the cerebral centre, the
mechanical reflex centre in the lumbar cord may receive the excit-
ing impulse. The paths which convey this excitation from the
brain to the lumbar cord must lie in the spinal cord. In fact,
Eckhard has succeeded in producing erections by irritation of
the spinal cord, as high as the pons and pedunculi. The same is
the case in many diseases of the spinal cord. The portion of the
transverse section of the cord which contains these paths is not
yet known.
Quite the same processes are passed through in e/aculation ;
for this also is a simple reflex act having its centre in the lumbar
cord. It seems, however, to require for its production a some-
what longer and more powerful irritation. The nerve-paths
probably lie chiefly in the sacral plexus.
‘ The spinal cord has also an influence upon the uterine con-
_ tractions. The motor nerves of the uterus lie in the spinal cord,
and may be followed, by irritating them, up into the medulla
oblongata (W. Schlesinger’). Uterine movements may also be
provoked reflexly from the sciatic nerve. The centre for these
movements does not lie exclusively in the medulla oblongata, as
was formerly thought, but such centres may be demonstrated in
1 Ueb. d. Centra der Gefiiss- u. Uterusnerven. Wien. med. Jahrb. 1874. I. p. 1.
58 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the whole length of the cord (Schlesinger). The chief centre for
the production of labor-pains lies in the lumbar cord, according
to Goltz." After division of the dorsal medulla the reflex acts
proper to copulation, and those of labor and birth take place in
a normal manner. The processes of ovulation, of development
of the pregnant uterus and the lacteal glands, the development
of the impulses which are associated with reproduction, suffer
no visible impairment from this operation.
Nasse has observed in the human subject, after crushing of
the cervical medulla, a normal performance of the act of partu-
rition.
The innervation of the iris is also in part dependent on the
spinal cord. The motor-paths for the dilatator pupille lie in
the cervical and upper dorsal cord. Irritation of this region
produces dilatation of the pupil; it has therefore received from
Budge the name of centrum cilio-spinale. According to Salkow-
ski (Dissert. Kénigsb. 1867), this centre lies much higher up,
namely, in the medulla oblongata. The motor-fibres which pass
from it run downwards in the cord without decussating, pass out
with the anterior roots of the lower cervical and upper dorsal
nerves, go thence into the cervical sympathetic, and then to the
eye. Section of these fibres causes contraction of the pupil. The
same route is taken by the vaso-motor paths for the head and
external ear.
The influence of the cord upon the various processes of secre-
tion in the body has been very little studied. It is probable
that there exists such an influence upon the secretion of sweat
and saliva, and doubtless also upon the production of semen and
ovulation, the secretion of the digestive fluids, etc. But at pres-
ent we are not in possession of exact knowledge in respect to
these points.
The only positive facts of this sort that we possess are those
furnished by Eckhard? in regard to the secretion of urine, who
says that section of the cervical cord produces a complete and
‘I Pfliiger’s Archiv. Bd. IX. p. 552.
® Untersuchungen tiber Hydrurie. Beitr. zur Anatomie und Physiologie. Bd. V. p.
147. 1870.
7 c
A re ri - a » ae + Dee
PHYSIOLOGICAL INTRODUCTION, 59
permanent arrest of this secretion. Eckhard infers from his
experiments the existence of a centre for exciting the secretion
‘of urine, situated at the level of the rhomboid fossa; the excitor
paths which pass downwards from this centre leave the cord by
the upper dorsal nerves; there are also inhibitory paths for the
secretion of the urine, located in the splanchnic nerve. The
qualitative changes in the urine, which are so common in affec-
tions of the spinal cord, are probably due in great part to stag-
nation of the urine in the paralyzed bladder, and to the decom-
posing influences of secondary disease of the bladder.
The theory of muscular tonicity needs only a very short
mention. It has called forth a great deal of investigation, but
can hardly be applied in pathology. We understand by the
term muscular tonus, a constant mild innervation of the striped
muscles by a stimulant influence proceeding from the spinal
cord. Later investigations have shown that this is probably in
substance nothing more than a weak reflex excitement, which
originates in sensory stimulation of the skin, muscles, joints,
and other parts, and is chiefly produced by the action of chang-
ing the position of the members of the body.
In connection with this point stands the much discussed
question of the influence of the- posterior roots on the excitabil-
ity of the anterior. While some physiologists (Harless, Cyon,
Steinmann, etc.) state with perfect confidence that the excitabil-
ity of the anterior roots is depressed after section of the pos-
terior, other observers (v. Bezold, Uspensky, G. Heidenhain,
and others) have denied the statement with equal confidence.
But even if the fact were proved, it does not possess the great
importance claimed for it in pathology.
A tonus of the vascular muscles seems proved. The vaso-
motor nerves are its conducting paths; they are kept in con-
stant slight excitement by the centres demonstrated in the
medulla oblongata and the spinal cord, and, after these are
removed, by peripheral ganglionic apparatuses, which also have
the power of keeping up the tone of the vessels.
The tone of the sphincters of the bladder and rectum is cer-
tainly of a reflex character, and principally depends on the
lumbar cord.
60 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The application of physiological data to pathology is cer-
tainly of the greatest importance; it is the source of the only
light that has been cast on a great number of pathological pro-
cesses and their connection. It must be admitted, however, that
physiology is far from explaining everything, and that many
points can only be made clear by pathological observations and
experiments.
Physiological experiments very often produce a pathological
state (section, compression, irritation, etc.); similar states are
occasionally produced in man by a great variety of agencies,
including disease; and these are the cases in which a direct appli-
cation of physiological laws to pathology will prove most fruit-
ful of results.
But the states produced in physiological experiments are far
from being so various and general, and are seldom so exactly
localized, as are pathological conditions. From the nature of
the case they must be very limited in extent; the usual lesions
consist of severance of continuity, very small, and with hardly
any extension in the direction of the long axis of the cord.
Simple sections have hitherto formed almost our entire founda-
tion for the experimental pathology of the cord; and it is time
that the method of Nothnagel and Fournié, applied with such
success to the brain, were extended to the spinal cord.
A brief consideration shows that the experiments of physi-
ology and pathology can imitate neither those anomalies which
are widely distributed along the length of the cord, yet localized
in particular spots ; nor the slowly progressive conditions of irri-
tation and paralysis; nor the moderate and gradually increasing
and varying degrees of pressure; nor the various finer disturb-
ances of nutrition in fibres and cells.
In particular, it must be noted that possibly, even probably,
the properties of irritability inherent in the cord may be essen-
tially changed by pathological processes, so that, for instance,
the kinesodic substance becomes motor, the sesthesodic sensitive.
Thus conclusions, drawn from the healthy cord, cannot be trans-
ferred to the same organ in a morbid state, without certain
reserves.
These reasons may justify the objections which have been
PHYSIOLOGICAL INTRODUCTION. 61
made to a direct transference of physiological principles (in
many respects poorly founded) to the pathology of the cord.
Nevertheless, we think it not unsuitable to collect in this place
some of the principles deduced from physiological and patho-
logical experience, so far as they seem applicable to practical
needs, as a sort of clew to the interpretation and recognition of
complicated pathological processes.’
1. Section or limited affection of the posterior columns de-
stroys the sense of touch in parts situated behind the point of
injury, but leaves the sense of pain.
2. Disturbance of the conductive power of the gray substance
for a limited longitudinal extent suspends the sense of pain, but
leaves that of touch (analgesia).
3. Disease or destruction of the entering posterior root-fibres
(or of the network of fibres directly formed by them) must impair
the sense of touch equally with that of pain and the other classes
of sensation.
4, Injury or disease of the posterior columns at the level of the
lumbar cord leads to a diminution of the sense of touch at the
anus, perineum, etc., while the sensibility and motility of the
lower extremities remain unimpaired; the same lesions in the
lateral columns of the lumbar cord have the same effect upon the
lower extremities as those of the posterior columns in the dorsal
and cervical medulla.
5. When the gray substance is partially destroyed in the
transverse direction, and the posterior columns are also affected,
the conduction of sensory impressions is retarded, in a degree
proportional to the smallness of the transverse piece of gray mat-
ter that remains. But if the conductive power of the posterior
columns is retained, this retardation appears to extend only to
the sensation of pain, while the conduction of the sensation of
touch takes places with normal rapidity.
6. Destruction of the entire extent of the posterior columns
(inclusive of the sensitive root-fibres passing through them) must
be followed by anzesthesia of a corresponding extent.
1 Compare the ‘‘Corollarien fiir die Pathologie,” given by Schiff’ (Physiologie, p.
292), and Brown-Séquard’s statements in his Course of Lectures on the Physiology and
Pathology of the Central Nervous System. 1860. ™
62 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
7. Limited destruction of the entire transverse extent of the
posterior columns and of the gray substance is followed by com-
plete anzesthesia of the portions of the body lying poston
and weakness of motion or partial paralysis.
8. An irritation affecting a limited longitudinal extent of the
posterior columns (inflammation, hyperemia, etc.), produces a
spontaneous pain in only those roots which traverse the diseased
spot (girdle-pain); subjective sensations of touch (formication,
prickling, numbness, sensation of heat and cold) and some de-
gree of hypereesthesia occur in the parts situated posteriorly.
9. A lesion producing paralysis, affecting the posterior
columns in the same way, gives rise to a girdle of complete
insensibility, corresponding to the district supplied by the para-
lyzed nerve-roots; below this girdle the so-called sensations of
touch are absent, or greatly impaired; the sensation of pain is
retained, but is badly localized.
10. If an affection which at first irritates, and afterwards
paralyzes, progresses upwards, the painful girdle travels up-
wards, and leaves behind it a girdle of anzesthesia which gradu-
ally increases in width; in the parts situated behind this the
sense of touch is gone, but subjective impressions of touch (for-
mication, numbness, etc.) may be present.
11. When the power of movement is unimpaired, and a girdle
of pain without aberration of the sense of touch is present, then
only the nerve-roots, within or without the cord, are affected.
12. In diseases of the posterior columns and the gray sub-
stance, the parts behind the diseased portion may experience
only changes in the sense of touch, without any excentric pains. (?)
If the latter occur, they point to an implication of those nerve-
roots which are situated further back.
13. Disorganization of an anterior and a lateral column and
of the greatest part of the gray substance produces paralysis of
the same side.
14. Destruction of the anterior (and lateral) columns in their
entire transverse section (inclusive of the motor nerve-roots pass-
ing through them) is followed by a paralysis of corresponding
extent.
15. Limited destruction of the entire transverse section of the
PHYSIOLOGICAL INTRODUCTION. 63
anterior (and lateral) columns and of the gray substance is fol-
lowed by complete paralysis, also analgesia, but retention of the
sense of touch.
16. Disease of the antero-lateral columns and the kinesodic
substance alone produces paralysis without lesion of sensibility.
17. Disease of the motor ganglia, into which the motor roots
first enter, produces paralysis in the region of the related nerves,
without disturbance of sensibility, but with trophic disturbances.
18. Affections of the antero-lateral columns and the corre-
sponding gray substance produce contracture or convulsions only
in the muscles immediately dependent on the diseased spot and
its motor roots; but contractures of muscles supplied by the
roots given off behind the affected spot are not produced (?).
19. Slight pressure on the cord may bring on paralysis of the
extensors and secondary contractures in flexion, but this is never
severe.
20. Contractures and convulsions of the lower extremities
also occur in affections of the segments of the cord above the
lumbar region ; they are then a consequence of an implication of
the posterior columns, and arise reflexly. In the same way, in
diseases of the posterior columns, spasmodic symptoms occur in
the parts situated nearer the head.
21. Disorganization of the entire gray substance to a consider-
able distance must be followed by anesthesia and paralysis in
the posterior part of the body; if the lesion is limited to one
place, the sensory and motor paralysis may be partial.
22. If the movements of respiration are entirely intact in an
affection of the cervical cord which paralyzes the extremities and
trunk, then the lateral columns are not involved.
23. Conditions of irritation in the cervical medulla will pro-
duce dilatation of the pupil; paralytic conditions, contraction.
24, Unilateral lesion of the cord is followed by almost total
paralysis and increased sensory excitability on the injured side,
with very slight disturbances of motion and loss of sensibility on
the opposite side.
25. Complete compression or divisign of the spinal cord ex- .
ageerates the reflex acts in the region lying posteriorly to the
lesion.
64 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
26. In limited destruction of the dorsal medulla, the reflex
acts which are performed through the lumbar cord (evacuation
of urine and feces, vascular tonus, etc.) go on with very little
alteration ; only they can no longer be modified by the will.
27. The nutrition of peripheral parts (muscles, nerves, bones,
joints, skin, etc.) remains intact in the various diseases of the
spinal cord, in proportion as the gray substance remains normal.
The doctrine of the functional reparation (Ausgleichung) of
partial lesions of the cord, stated by Schiff, is of great import-
ance in pathology; the fact, namely, that while these lesions are
not anatomically made good, an apparently complete restoration
of function follows. Schiff’ affirms that in injury of almost any
part of the cord, the consequent functional disturbances may be
compensated for by an intact portion of the cord assuming the
function of the injured portion; the lesion of the posterior
columns alone leads to a permanent loss of the sense of touch,
which cannot be repaired.
The chief element in this functional restoration is of course a
vicarious assumption of the processes of conduction by intact
portions of the cord. This fact is not of itself strange, for we
can observe in the fine network of nerves what seems to be the
anatomical provision for such exigencies.
It is not yet settled how far such a vicarious substitution
may go in human pathology; but it is clear how wide must be
its significance in relation to the prognosis and cure of partial
lesions of the cord.
It will be proper to introduce here a few remarks on the ana-
tomical restoration of partial lesions of the cord. Daily expe-
rience shows that this happens very often, and may be quite
considerable in amount; it is not rare for apparently very severe —
injuries of the cord to recover. But the exact histological pro-
cesses are not known; it is not yet well ascertained how a chronic
inflammation, or the various degenerative processes, scleroses,
1 Centralbl. f. d. med. Wiss. 1872. No 49.
.
i
PHYSIOLOGICAL INTRODUCTION, 65
softening, hemorrhage, etc., are repaired, nor to what extent this
takes place.
Experimentally, this question has been very little examined,
although the physiologists have had material enough. <A few
positive facts were ascertained by Flourens, Brown-Séquard, H.
Mueller; but in recent years Masius and Vanlair * have been the
‘ first to institute thorough experiments upon frogs, showing after
a lapse of at least six months a great progress in restoration of
excised segments of the spinal cord. Motility and sensibility
were restored, and nerve-cells and fibres were found in the cica-
trix. In the higher order of animals, especially the mammalia,
the restoration seems to be less easy and perfect. The same
result appears from the latest experiments of Eichhorst and
Naunyn* upon very young dogs. After section or crushing of
the lower dorsal cord, the first occurrence is a complete degene-
ration and fluidification of the parts directly attacked ; after-
wards an intermediate substance, composed of a tissue like
neuroglia, rich in cells, is developed, which incloses a central
cavity. Subsequently the double-contoured nerve-fibres are re-
generated, and a limited number are seen to traverse the inter-
mediate substance. Regeneration of the ganglion cells was never
observed. Corresponding with these conditions, a partial res-
toration of function appears after many weeks (eight or ten, at
least); voluntary, but incomplete and ‘‘atactic,’ movements are
the first to appear, and sensibility returns later. But the ani-
mals die subsequently, probably in consequence of a secondary
hydromyelus.
On the other hand, Goltz and Freusberg have never seen a
regeneration and restoration of function in their numerous ex-
periments upon dogs, although some were kept living for an
extremely long time. For this reason Freusberg cannot avoid
expressing a suspicion of the correctness of the results, as re-
gards restoration of function, obtained by Naunyn and LEich-
horst.*
1 Centralbl. f. d. med. Wiss. 1869. No. 89; and Arch. de Physiol. norm, et path.
IV. p. 268. >
2 Arch. f. experim. Pathol. und Pharmacol. Bd. II. p. 225. 1874,
’ Pflueger’s Arch. Bd. IX. p. 390.
VOL, XIIL—5
66 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
It certainly follows from these experiments that in the higher
animals, and probably in man also, the regeneration of the spi-
nal cord, when once completely destroyed, will always remain
very imperfect, even if it takes place to any extent.
III. General Pathology of the Spinal Cord.
In this section we design to give a short account of the facts
and observations, but only as far as they seem to possess a pres-
ent interest and importance in relation to practice. We shall
lay the chief weight upon general symptomatology and thera-
peutics, and shall take leave to pass over the general patholo-
gical anatomy, which at present is not in a condition to be made
useful to the practitioner. General etiology and diagnosis will
be but briefly touched, in view of their present condition.
A. General Symptoms of Diseases of the Spinal Cord.
This involves a systematic enumeration of the several dis- —
turbances which occur in diseases of the cord, partly in order to
explain their significance and names, partly to reduce them to
their immediate causes and develop their pathology, partly to
point out somewhat in anticipation the more usual groupings
of symptoms. We shall thus be enabled to save many repeti-
tions and details in the special part.
1. Disturbances of Sensibility.
These are very frequent, and their form and grouping is often
very characteristic. They are very important in diagnosticating
and estimating diseased processes in the cord; for these reasons
they must be stated with great fulness.
In examining sensory disturbances, the several qualities of sensation must be
strictly distinguished. Let the sensations of touch, temperature, and tickling, of
pressure, of space, and of pain be tested. As regards the best methods of doing
eS ee
. GENERAL SYMPTOMATOLOGY. 67
this, compare Vol. XI. of this Cyclopedia, p. 212 [American ed.]. The qualities of
perception which are classed together under the name of muscular sensation, or
_ sense, should also be tested. Besides the methods given in the same volume, p.
234, there is a good method given by Leyden! for the exact testing of the sensation
of passive motions. No extensive apparatus is required for this; the same exact
results are obtained when the leg is suspended in a broad cloth, and by means of the
cloth is made to move in various directions, upwards, downwards, outwards, or
inwards——its position being either extended (for testing the hip-joint) or semi-flexed
(for the knee-joint). The patient is required to state the extent and direction of
the movements. In testing the passive movements of the ankle-joint, the front
part of the foot is grasped carefully with the hand, and is moved passively. This
method is quite sufficient, as the cutaneous sensibility of the patient is usually
impaired.
a. Diminution of Sensory Action—Anesthesia.
All the sensations which originate in the skin, the muscles,
and other more deeply-seated parts may be diminished in dis-
eases of the spinal cord; and the diminution may increase, even
to the extent of total loss of sensation. They may be extin-
guished all at once, or some may be lost and the rest retained.
The disturbance of sensibility usually appears first in the
lower extremities, ascending by degrees until it reaches the
upper extremities. But often the latter are the first attacked,
and the anzesthesia extends downwards.
Anesthesia is very commonly attended by various subjective
sensations, as the furry sensation (Pelzigsein) or numbness, un-
certainty in feeling the ground, sensation of walking on cotton
wadding, or on a bladder full of water, etc.
In general, the occurrence of anesthesia permits us to infer
an implication of the posterior half of the cord.
A widely diffused, total paralysis of sensation (total = af-
fecting all the qualities) occurs only when the entire transverse
section of the posterior columns and the gray substance is de-
stroyed ; that is, chiefly in affections which are diffused over the
entire section, extending to a variable distance in the longitudi-
nal direction. It also accompanies a complete severance, crush-
ing, or compression of the cord at any point; in which case the
1 Ueber Muskelsinn und Ataxie, Virch. Arch. Bd. 47. 1869.
i ay aaa
63 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
anzesthesia occupies all portions of the body which derive their
nerve-supply from behind the point of lesion.
Total paralysis of sensation, of a more limited extent, may
occur in various ways, viz.:
As unilateral anesthesia, localized in one leg, or a leg and
the corresponding half of the trunk, or finally, in these parts and
the corresponding arm. This occurs in traumatic or spontaneous
unilateral lesion of the cord, and the loss of sensation takes place
on the side of the body opposite to the spinal lesion, owing to the
decussation of the sensory paths in the cord. The muscular
sense, however, usually remains unimpaired, because the fibres
for it cross at a higher point. |
As anesthesia in the form of a girdle—a zone of varying
width, deprived of sensation, which surrounds at various levels
the pelvis, the abdomen, the thorax, or even the region of the
shoulder or neck on one or both sides. It is due to a local dis-
ease of the posterior roots within or without the medulla, which
extends over but a limited length of the cord ; or to a cireum-
scribed affection of the gray posterior cornua, embracing the net-
work of nerve-fibre which is formed by the entering root-fibres,
and the paths which traverse the gray substance before re-enter-
ing the posterior columns.
Finally, as circumscript anesthesia, limited to certain ex-
tremities or parts of extremities, or to the district supplied by
certain nerve-trunks. The most frequent cause of this lies prob-
ably in affections of single bundles of roots ; it may be produced
by local affections, limited to portions of the transverse section
of the spinal cord, and affecting only certain of the longitudinal
fibres, but this lesion would be more likely to produce a partial
paralysis of sensation. It is probable that the sensitive paths
for the upper and lower extremities, the anterior and posterior
surfaces of the body, etc., have a distinct arrangement in the
spinal cord; and it may easily be imagined how many forms
may be taken by such circumscript anzesthesia, according to the
horizontal or vertical distribution of the morbid change.
Partial paralyses of sensation, however (limited to certain
of the qualities of sensation), also occur, and nowhere more fre-
quently than in diseases of the cord ; the history of tabes dorsa-
= <a ge R ieee
——e -
—
GENERAL SYMPTOMATOLOGY. 69
lis gives the most numerous examples of this. They occur in
all possible combinations, as indicated in Vol. XL. p. 201. The
form most likely to attract notice, and perhaps the most fre-
quent, is analgesia ; but, as remarked, the greatest variety of
cases of partial anzsthesia occur. Each sort of sensation may
alone be lost or weakened; and, on the other hand, several may
suffer the same change, while only a single one exists in partial
or complete integrity.
In view of these facts, we can hardly avoid the conclusion
that the various sensations traverse distinct paths of conduction
in the cord, and that, according to the local distribution of the
morbid change in transverse section, sometimes one and some-
times another path is specially affected. Nothing exact is known,
however, in respect to this. It seems probable that the sense of
pain is conducted by the gray substance only, and impressions of
touch by the posterior columns only (Schiff). In opposition to
this view Brown-Séquard asserts that all sensations are chiefly
conveyed through the gray substance, and he even names distinct
regions of the latter, which are supposed to contain the respec-
tive groups of fibres. The result, therefore, will differ in each
case, according to the manner in which the disease is distributed
over the various parts of the transverse section of the cord.
But little of practical value can be drawn from these scanty
and uncertain facts. If disturbances of sensation are present,
the physician will have to put to himself the questions—whether
there is an affection of the posterior roots within or without the
cord, or whether there is an impediment to conduction within
the gray substance, or whether certain sensory paths have been
injured at a higher point, after leaving the gray substance. The
data which are given here and in the physiological introduction
_ will show the points which aid us in making these distinctions ;
but they will also show how few and unsatisfactory these points
are.
What is true of cutaneous sensation may be likewise affirmed
of the so-called muscular sensation ; both the muscular sense
and that which is called the muscular sensibility’ may be reduced
———
1 Compare Volume XI. p. 233.
70 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
or suspended in spinal diseases. The patients lose the sensation
of pain in the muscles, produced by various external agencies ;
they lose the sense of fatigue; they are not certain of the posi-
tion of their limbs in the dark, or when their eyes are closed ;
they have lost the feeling of passive movement of the limbs,
their ability to retain their equilibrium is diminished, ete.
Regarding the position of the routes which transmit these im-
pressions in the spinal cord, we know very little. According to
Brown-Séquard, at least a part of them remain on the same side
of the cord, and do not decussate till they reach the medulla ob-
longata. The application to pathology is evident.
A symptom which is not very rare under physiological con-
ditions is the retardation of the conduction of sensory impres-
sions. This remarkable fact was first mentioned by Cruveilhier’*
without accounts of special cases; since then, although often
observed, it has never been closely studied until very lately, and
even now the investigation is far from complete.
This retardation is very noticeable and measurable. While
in ordinary circumstances sensation follows directly upon the
application of the stimulus, in cases like this it is separated from
the latter by a noticeable interval of time, which is frequently a
fractional part of a second, but not rarely amounts to one or
several seconds; cases have even been observed where the sensa-
tion came from fifteen to twenty seconds later than the stimula- |
tion (Cruveilhier), thirty seconds (Topinard), and even several
minutes. In such cases the phenomenon is of course very easily
observed ; in less marked casés the existence and the degree of
retardation can be determined by exact measurements, such as
have been made by Leyden and Goltz.* The more powerful the
stimulus, the shorter the interval.
It has been repeatedly observed, and very recently established
with exactness, that this retardation relates only to a few of the
qualities of sensation, chiefly to that of pain. E. Remak® has
published a case in which pricking with a needle provoked in
every instance an immediate sensation of touch, which was fol-
1 Anatom, pathol. Livrais. XXXVIII. p. 9.
? Leyden, Klinik der Riickenmarkskrankheiten. I. p. 146.
3 Arch. f. Psych. u. Nervenkr, Bd. IV. p. 763. 1874.
GENERAL SYMPTOMATOLOGY. 71
lowed in three seconds by the retarded perception of pain. In
such cases every powerful impression gives rise to a double sen-
sation, first, one of touch, perceived with normal quickness, and
then a retarded sensation of pain. The case published by Nau-
nyn in the same journal’ seems on some accounts to belong here;
it included retardation of the sensation of pain, associated with
hypereesthesia, while the sensation of touch remained normal.
Vulpian? observed a similar state in a case of tabes ending in
apoplexy ; the prick of a pin was rapidly followed by a slight
reflex action, and two or three seconds later by a very full and
continued movement of defence. I have under my observation
at present a tabetic patient, in whom I have been able to demon-
strate this double sensation, not only as regards needle-pricks
and pinching, but also under the painful faradic current.
EK. Remak has treated very thoroughly of the question,
whether this retardation of conduction is always limited to the
sense of pain, and never affects that of touch. The observations
hitherto made seem almost to show that such is the case; but
the question needs further careful study, and it is hard to givea
reason why the sense of touch should not in some cases be
affected. The cases commonly tested are those of tabes dorsalis,
in which the sense of touch is more or less weakened, while that
of pain is retained; if both are retained, the double sensation
may occur. Topinard also states that the retardation affects
chiefly the senses of pain and of temperature.®
It has been made known through the physiological researches
of Schiff, that a transverse narrowing of the gray substance
(whether the posterior columns are cut or no) produces a corres-
ponding retardation of the conduction of sensation, which is
marked in inverse proportion to the amount of gray matter re-
maining.* Schiff has even been enabled by his experience to
1 Archiv f. Psych. u. Nrevenkr. Bd. IV. p. 760.
* Arch. de Physiol. norm. et path. I. p. 405. .
® Hertzberg (Beitr. zur Kenntniss der Sensibilitiitsst6rungen bei Tabes. Diss. Jena.
_1875) has lately demonstrated, in some very carefully examined cases, that the most
frequent occurrence is that of retardation of the sense of pain alone, but that the sen-
sations of touch and temperature also are not rarely retarded, though to a less degree.
4 See Schiff’s Physiologie. p. 245.
>
72 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
predict the existence of double sensation in man, which has
lately been confirmed by the beautiful observation of E. Remak;
he looks for the appearance of this symptom in every case where
the transverse dimensions of the gray substance have been di-
minished by pathological processes, while the posterior columns
have remained intact.’
It may be assumed, on the strength of these facts, that wher-
ever retarded sensation exists, there is an alteration of the gray
substance ;.and it would be entirely consistent with this assump-
tion, if it should be found that the retardation always affects the
sensation of pain only, and never that of touch. It would then,
according to Schiff, depend on the condition of the posterior
columns, whether the sensation of touch is absolutely wanting,
or appears in reduced amount, but with the normal rapidity. =
The investigations of Burckhardt,’ who has tried to measure _
the sensory conduction of the cord in an isolated form, are of
ereat interest. He found that the cord conducts impressions of
pain decidedly more slowly than those of touch, and suspects for
this reason that the gray substance in general conducts more
slowly than the white. The retardation of tactile conduction | |
under pathological circumstances is referred by him directly to
a loss of white substance (degeneration of the posterior columns) ; |
the more the gray substance is called upon to perform the func-
tion of conduction, the more slowly is the function performed.
He thinks, also, that every narrowing of the gray substance— —
which is naturally a slow conductor—must still further retard
the conduction ; the examination with the second-hand of awatch
will not bring out the fact of retardation until such narrowing ~
has taken place. As long as the gray substance is intact, the
retardation can only be demonstrated by the aid of fine physio-
logical apparatus for measurement. 7
The retardation of the conduction of sensation is perhaps con-
nected with another phenomenon, usually observed in the same
patients—namely, the inability to count correctly several inupres-
sions of sensation which follow rapidly (e. g., pricks of a needle).
1 See Physiol. p. 294. Coroll. 3. ¢.
* Physiolog. Diagnostik der Nervenkrankheiten. Leipzig. 1875.
GENERAL SYMPTOMATOLOGY. 73
Persons in health are able to state without fail the number of
pricks (from two to six), even when they come very close togeth-
er, while patients cannot do this unless the individual impres-
sions follow at considerable intervals. These intervals are sup-
posed to bear a direct ratio to the degree of retardation of the
conduction of sensation. This symptom would therefore seem
to be also dependent on a change in the gray substance. Nor is
it easy to see why the impressions are not perceived as separate,
since each impression must have precisely the same obstacles to
surmount.
It is more probable that this phenomenon is connected with
another disturbance, which commonly accompanies it—namely,
remarkably persistent after-sensations, following impressions of
pain. The patients, when their skin is pinched or pierced with a
needle, give expression to a much longer and severer pain than
is usually felt by well persons. Rapidly succeeding impressions
of sensation run together into one, therefore, because the new
sensation coincides with the after-sensation of the one before it.
‘The change in the cord upon which this depends cannot at pres-
ent be stated with certainty. We may suppose that there are
coincident changes in the posterior columns and the gray sub-
Stance.
b. Exaggeration of Sensory Action.
This is one of the commonest symptoms in diseases of the
cord, and may appear in various forms, viz. :
1. As simple hyperesthesia ; more or less increase of sensi-
tiveness to-all possible kinds of sensory impressions, which di-
rectly increase to pain. This hypereesthesia not seldom resembles
anzesthesia in its manner of appearance and distribution—in fact,
it often precedes anzesthesia ; thus, a hypereesthesia in the form
_ of a girdle may be observed above or below an anesthetic zone,
and may gradually move its position on the body, in company
_ with the latter. Hyperesthesia may also be confined to single
_ denominations of sensibility (pain, senge of temperature, espe-
cially sense of cold), and may occur in connection with partial
paralysis of sensation.
74 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
It is known from physiological experiments that section of
the posterior columns is followed by a hyperesthesia of the pos-
terior half of the body, which at first increases rapidly and con-
siderably, and afterwards very gradually diminishes and disap-
pears ;* and that when only one posterior column is cut, the
hypereesthesia remains confined to the same side. The hyperas-
thesia increases, if the cut is carried into the lateral columns,
and a part of the gray substance (Brown-Séquard) ; it is much
less marked when the lateral or anterior columns are cut, and the
posterior are left intact.
It is hard to give a decided interpretation of these facts.
Tuerck and Schiff think them due to a state of irritation of the
cut parts and the adjoining regions, especially the posterior col-
umns. But the finer mechanism of the process is still uncertain,
and the conducting paths are unknown. May it not be that the
narrowing of the sensory conductors, produced by the section,
has something to do with this result, by increasing the excite-
ment of such conductors as remain intact ?
At all events, Schiff's assumption of an irritative condition in
the posterior columns is in satisfactory agreement with the fact
that these hypereesthesiz are by far the most common in such
forms of disease as we have been accustomed to ascribe to de-
generation of the posterior columns. Nevertheless, it is not
unlikely that there are other processes capable of occasioning
hypereesthesia, e. g., implications of the nerve-roots in meningi-
tis, etc.
2. As paresthesia. Nothing is commoner than to hear pa-
tients with disease of the cord complain of abnormal sensations,
which are best called subjective sensations of touch. Thus the
feeling of furriness (Pelzigsein), numbness, crawling, tingling,
etc. These sensations are referred by Schiff to a moderate
excitation of the paths for the sensation of touch, lying in the
posterior columns—an hypothesis which seems a little bold, in
view of the fact that the posterior columns, with the exception of
the root-fibres crossing them, are stated to be inexcitable. The
hypothesis would have to be supported by the further one, that
1 See Schiff, Physiol. p. 274.
GENERAL SYMPTOMATOLOGY. 75
pathological processes are able so to change the excitability of
the posterior columns that pathological stimuli will arouse sensa-
tions.
It is certainly possible that excitation of the posterior roots
at their entrance may assist in producing such changes in the
sensation of touch; and that a part of these modifications may
depend simply upon a dulling of the sensibility (as regards
touch), produced by various diseases of the cord.
Subjective sensations of temperature also occur, a feeling of
burning or cold that may become very intense. These sensations
are in part referred by Brown-Séquard to direct excitation of the
fibres in the gray matter which conduct the sensations of tem-
perature. Schiff, however, believes that changes in the amount
of blood circulating in the skin, due to vaso-motor disturbances,
may so act upon parts which are already hyperesthetic as to
produce a sensation of increase or diminution in the warmth of
the skin. But this explanation can hardly suffice for all cases.
This is the place to speak of the girdle-sensation, that pecu-
liar modification of subjective perception which produces the
impression of having a girdle or a broad bandage tied about the
trunk or limbs. This feeling, when situated at the upper part of
the thorax, may be accompanied with a severe sense of pressure,
and is always very troublesome to the patient. Cruveilhier
described it. It may occupy various levels on the trunk, but
may also attack various parts of the lower extremities, particu-
larly in the region of the ankle and knee of one or both sides.
This sensation is probably produced by a slight excitation of
the entering posterior roots in cases where the spinal affection is
limited in its longitudinal extension. It usually accompanies
inflammatory or other irritative conditions of the cord, and origi-
nates with the root-fibres which occupy the upper limit of the
disease. But any sort of local disease of the cord and its neigh-
boring parts, which irritates the posterior roots to a moderate
extent, may produce the symptom.
3. As pain. This is seldom quite absent in diseases of the
cord ; it varies extremely in form and distribution. —
Among the most characteristic are The so-called lancinating
or neuralgiform pains, which are almost pathognomonic of the
76 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
early stage of tabes dorsalis. These pains are usually very se-
vere; they are either continuous, or appear periodically and
under certain provocations (especially change of weather, rain,
storm, snow-squalls), and are localized in a certain nerve or
certain fibres of it, or certain regions of skin; they rage for a
time in one place, and then leap suddenly to another, seldom
remaining long in one spot. They are described as tearing,
shooting, or going through like lightning ; the patient feels as if
a knife or a red-hot wire were thrust into his flesh, or as if cer-
tain portions of his limbs were screwed up in a vice; often the
pains are localized in deep parts, as the bones, but they often
invade the skin, where they are frequently connected with cir-
cumscribed hyperesthesia. They prefer the night, and are not
rarely connected with circumscript vaso-motor disturbances, or
even with reflex muscular jerkings. They may occur in any
nerve-region whatever, though they are certainly most common
in the lower limbs and the trunk, where they often simulate
intercostal neuralgia very closely ; they may appear in the upper
extremities, and even in the region of the trigeminus.
The origin of these pains is almost universally referred to irri-
tation of the posterior root-fibres ; their extent and location de-
pend on the extent to which the latter are implicated. The
eases of which they form a symptom are almost exclusively
those of degeneration and sclerosis of the posterior columns, and,
according to Charcot, of the so-called external bands. solely,
which contain the inner root-fibres. It is, however, also possible
that irritation of the longitudinal fibres of the posterior columns,
or of the gray substance, may lead to such excentric’ pains;
under pathological conditions ; though usually the gray sub-
stance is only zsthesodic.
The localization of these and similar pains in the dorsal nerves
and a part of the lumbar nerves produces the girdle-pain. This
is a neuralgic pain, which may take the form of a bilateral neu-
ralgia of the intercostal or lumbo-abdominal nerves, at various
levels on the trunk, but is often confined to one side. It oc-
curs in cases of limited irritation of the dorsal cord, and still
14%, ¢,, originating in a central organ.
GENERAL SYMPTOMATOLOGY. 77
oftener in diseases which directly irritate the sensitive roots, as
especially in inflammation, caries, carcinoma of the vertebrae, etc.;
it is a valuable sign of the presence of the latter, and often be-
trays at a very early period the beginning and the location of a
severe disease, which by degrees leads to compression of the
cord.
Generalized pains are not infrequently met with in the
lower extremities, and in the portions of the trunk situated below
the point of disease. These pains may differ greatly in degree,
and are described by the patient as a more or less extensive sen-
sation of pain, hard to describe, but exceedingly unpleasant,
which is usually continuous, but from time to time undergoes
exacerbations. In some the feet and lower half of the legs are
the chief seat of these pains; others complain more of the back,
the loins, or the thigh ; very often the pains are excited or in-
ereased by spontaneous or reflex twitchings and spasms in the
lower (paralyzed) extremities, or by efforts to walk. They occur
in all sorts of diffuse, transverse myelitis, in compression of the
cord followed by myelitis, in acute and chronic spinal meningitis,
etc.
The source of these pains is not yet fully clear. The original
explanation referred them to a direct irritation of the root-fibres
within or without the cord; but it is probable that an irritation
of the ssthesodic paths in the cord may have the same effect.
Schiff, however, denies the possibility of this, believing that, in
such cases, the disease always extends to the root-fibres. Many
facts render it probable that pathological conditions may con-
siderably alter the excitability of the zsthesodic substance, and
it is possible that pathological irritations act differently from
our coarse mechanical or electrical stimulations. Hyperzesthesia,
when-present, may also assist in the production of such pains.
Special notice is due to the pain in the back, so common in
diseases of the spinal cord. It accompanies a great number of
spinal diseases, assumes a great variety of forms, and is referable
to a variety of causes. Thus rhewmatic or rheumatoid pains,
which are most frequent; they are localized in single, distinct
muscles, are excited by certain movements, respiration, or pres-
sure, and are almost always referable to the influence of cold.
78 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Although they occur at times in well persons, they are very
especially common in spinal patients, who, as a class, are very
sensitive to cold, and in the latter may be excited in similar
ways by a variety of influences which weaken or irritate the spi-
nal cord, as excesses in the use of alcoholic drink or in sexual
indulgence.
fyperesthetic pains in the back also occur, consisting of
burning, tearing, or duller sensations in the skin of the back,
especially between the shoulder-blades, or at certain spinous
processes, which, in these cases, become extremely sensitive (spi-
nal irritation). This pain indicates abnormal conditions of irrita-
tion and hypereesthesia in the posterior roots and columns, and
may be more or less diffuse, according to the extension of these
processes. The excentric neuralgiform pains, which have been
already mentioned, may of course also occur in the back. They
are very violent, tearing, boring, localized in various spots, ac-
cording to the seat of lesion, but preferring the region of the
nape or the loins. Inflammations, hemorrhages, tumors, degen-
erations of the cord, etc., produce these pains, and they probably
point, in most cases, to pathological irritation of the root-fibres.
The pain is often of much significance in affections of the verte-
bre ; it is localized in one or several spinous processes, is espe-
cially felt when pressure is made upon them, or when the spine
is moved, is usually associated with excentric girdle-pains, and
with a very rigid position of the spine; but the latter cireum-
stance occurs in some other kinds of spinal pain, without lesion
of the vertebree.’
Pains localized in the vertebral column are best examined by
pressure on the spinous processes, or by tapping them with the
percussion hammer or fist, or by vigorous flexion of the spinal
column, a forcible push of the head or the shoulders, ete.; ; the
hyperesthetic portions may also be very well ascertained by
passing over them a sponge dipped in cold or hot water, or by
electrical examination.
A brief notice of headache is necessary, which, not including
accidental complications (fever, cerebral disease), is not a rare
' Compare also A. Mayer, Die Bedeutung des Riickenschmerzes bei Erkrankungen
des Riickenmarks und der umgebenden Theile. Arch. der Heilk. I. p. 349. 1860.
GENERAL SYMPTOMATOLOGY. 79
accompaniment of spinal diseases. A direct involvement of the
Sensitive fibres of the cervical plexus in the lesion of the cord
_ May give rise to (occipital) pain; in like manner the trigeminus,
which receives an ascending root from the cervical cord, may
sympathize ; finally, headaches are not seldom observed, which
_ resemble hemicrania, and are perhaps referable to an implication
of the conductors which lie in the cervical sympathetic and
originate in the cervical medulla. It follows that any sort of
continued and violent pain of the head is generally to be as-
cribed to an affection of the cervical medulla. Such pains occur
in tabes, in local sclerosis, in bulbar paralysis, tumors of the
_ cervical medulla, etc. (7. ¢., in cases of disease of the cord).
2. Disturbances of Motility.
These are the most common, and in many cases the predomi-
nant and most troublesome symptoms of spinal cord diseases,
They deserve a most attentive study in all cases.
The proper methods for examining the motor apparatus have been fully explained
by me in Vol. XI. of this Cyclopedia, p. 267, and I would refer to the statement
there made. It cannot too often be repeated, that the examination of these points
should be as thorough and general as possible in all cases; in many cases of diffi-
cult diagnosis this furnishes the only possible means of attaining an exact idea of
the disease, and it is only by this path that we can ever hope to reach a clearer
definition of diseases than we now possess.
a. Diminution of Motility— Weakness and Paralysis.
All degrees of “ palsy,’’ from the slightest paresis to complete
paralysis, occur in diseases of the cord; and as to the situation
any part may be affected, though by no means with equal fre-
‘quency.
Inthe earlier stages the patients complain of being quickly
fatigued, of diminished power of performance and endurance in
their limbs, then of a slight weakness and incertitude in execut-
ing certain movements, perceived only™by themselves, and at
last a slight dragging of the legs is observed. In these early
‘ iJ
. 4
)
a)
‘
he
ee |
80 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
stages it is often especially striking to observe the inability to
stand still for any long time.
By degrees the symptoms of weakness become plainer; it
becomes harder and harder for patients to mount on a chair or
ascend stairs; every little impediment in their way annoys them
and detains them ; their powers grow continually weaker, short
distances exhaust them completely, they have to stop or sit down
at every other step.
Thus it goes on till palsy is complete, with absolute inability
to move the muscles ; it may be weeks, months, and years before
this point is reached.
But, on the other hand, the paralysis may occur almost sud-
denly, becoming complete in a few minutes or hours ; bed-ridden
patients often observe, at the moment when they wish to make
use of their limbs, that they are more or less completely para-
lyzed, so stealthily and rapidly may the palsy develop itself.
This point depends on the nature of the disease of the cord
which causes the paralysis. |
Our observations upon this matter are defective enough ; but
as far as they go, they allow us to associate spinal paralytic
symptoms in the first place with affections of the anterior half of
the cord ; it seems from pathological observation that the worst
disturbances of voluntary motion originate in the lateral columns
and the anterior cornua. We are not yet certain as to the part
played in man by the anterior columns proper. It is clear that
the causal lesion of paralysis may have various locations; in the
anterior roots, within or without the cord, in the large (motor)
ganglion cells of the anterior cornua and their immediate off-
shoots, or finally, in the paths which lead up in the antero-
lateral columns to the brain. The lesion may, further, be cir-
cumscript, or may extend over a great part of the length of the
cord. |
The nature and the distribution of the palsy are not very
characteristic by themselves, but their combinations with other —
symptoms give many points which assist in an accurate localiza-
tion. Thus the presence or absence of reflex actions, secondary
muscular atrophy, muscular tension and contracture, changes in
electrical excitability, etc., furnish very important landmarks of
GENERAL SYMPTOMATOLOGY. 81
the seat of disease, and it will be proper here to mention briefly
some of these points.
Paralysis rapidly followed iy a marked degree of atrophy
and by the reaction characteristic of degeneration (Entartungs-
teaction)' points to disease of the anterior roots (rarely), or of
the gray anterior cornua (more frequently). In this case all
‘reflex actions are absent. :
Paralysis with tension and contracture of muscles, without
‘atrophy, is very probably due to an affection of the lateral
columns.
Paralysis without loss of reflex function and without atsbphiy
points to an affection of the paths which ascend to the brain,
outside of the gray substance, or at least outside of the ganglia
of the anterior cornua. Such are mostly cases of circumscript
disturbances of conduction, the end of the cord below the lesion
remaining intact.
Paralysis with trophic disturbances gives room for suspecting
an affection of the gray substance, since primary affections of the
roots are very rare.
Very extensive palsy with much atrophy, the reaction of
degeneration, absence of reflex acts, points to a ewidely diffused
lesion of the anterior gray substance.
Paralysis in the districts of certain pairs of roots (e. g., in
those of the upper extremities alone, or both crural nerves, etc.),
_ points to a strictly localized affection of roots or lesion of the
_ gray anterior cornua.
Of course these statements are not by any means exhaustive,
and give only general assistance ; the difficulty of making the
_ distinctions is at present very great ; in many cases a variety of
_ other circumstances (spasms, aneesthesia, pains, palsy of the
bladder, etc.) may assist the judgment, but in other cases they
_ only add to the difficulty. Such combinations are very common,
and are extremely various, especially in the different forms of
- myelitis.
The conclusions which are formed regarding the nature of
the lesion in the cord are far less certain than those relating to
>
Volume XI. p. 426.
VOL. XIII.—6
$2 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
its place. The diagnosis is commonly established by a considera-
tion of the symptoms as a total.
In respect to the extension of the Deeno, 6 dow ae
remain to be made.
By far the commonest case is that in which the lower extrem-
ities, usually both together or nearly so, are attacked by the
paresis or paralysis, which gradually ascends, reaching succes-
sively the trunk and the upper limbs. In fact, paraplegia is so
characteristic a form of spinal palsy, that when it occurs we
always think first of a spinal affection. (A paresis occurring
‘In this form may be designated as paraparesis:) Paralysis of
both lower extremities and the trunk to various heights, accom-
panied by disturbances of sensibility, palsy of the bladder and
rectum, and bed-sores—such is the usual form; but the latter —
symptoms may be entirely wanting.
The most frequent causes of paraplegia are affections which
involve the thickness of the cord, or complete compression from
vertebral caries, tumors, etc. ; but paraplegia occurs also in affec-
tions which are strictly localized in the motor apparatus, such
as spinal palsy of children, hemorrhage in the gray anterior cor-
hua, etc.
If the upper extremities, and finally the muscles of respira-
tion, are also invaded, the affection takes the form of wniversal
spinal paralysis, which is observed in various spinal affections,
described in the special part of this work. :
If only the two upper extremities are attacked by palsy, the
legs remaining free, we have paraplegia brachialis or cervicalis ;
a rather rare form. It occurs in connection with processes which
affect in an isolated manner the anterior roots of the cervical
enlargement, or in strictly circumscribed lesions of the anterior
‘cornua in the cervical enlargement (as in spinal palsy of children,
progressive muscular atrophy, perhaps also lead palsy[?}). In
disease of the white columns it is rare that an isolated affection
of the paths for the upper extremities occurs. r
Hemiplegia spinalis (Brown-Séquard) is the name given to
palsy of an arm and a leg of the same side, originating in a spi-
nal affection; the face is not attacked. It occurs in unilateral
disease or injury of the cord, in which case the motor palsy is on
a
—@ »
tS, See ee Ae ee -*
oan tl
GENERAL SYMPTOMATOLOGY. 83
the same side as the lesion of the cord, while sensory palsy exists
on the other side. If this palsy is confined to one lower extrem-
ity, it is called hemiparaplegia spinalis. For further remarks
see below, in the section upon Unilateral Lesion of the Cord.
Finally, partial paralyses of spinal origin are frequent.
They may be limited to a single extremity, single groups of
muscles and nerve-territories, or even single muscles; this de-
pends entirely on the nature and distribution of the lesion in the
cord. Such partial palsies are usually due to quite circum-
scribed local lesions, which show little tendency to spread ; small
hemorrhages in the medulla, circumscribed myelitic foci in the
gray substance, little islands of sclerosis, etc. It is often hard,
or even impossible, to distinguish these from circumscript affec-
tions of the roots or other peripheral palsies.
6. Imperfect Co-ordination of Movements—Atazia.
This peculiar and frequent disturbance of movement has been
made the subject of numerous debates within the past ten or
twenty years, since Duchenne introduced the term ‘‘ ataxie loco-
motrice’’ into nosology.
Ataxia is characterized by inability to make combined or com-
plicated movements with certainty and exactitude, or even (in
advanced cases) to make them at all, while the simple individual
motions and the gross force of the muscles are normal, or but lit-
tle impaired.
This disturbance is most marked in standing and walking.
A patient who presents the characteristic signs cannot perform
these acts with security ; in walking, he brings his foot down
with a stamp, the motions of his legs are exaggerated, wild, jerk-
ing, the movements are various, impulsive, often made in the
wrong direction and with an unsuitable degree of force.
It soon becomes necessary to exercise an increased control
with the eyes over the movements. The patient has to keep his
eyes on his feet and on the ground while walking ; in the dark,
or with closed eyes, his uncertainty increases considerably, espe-
cially when there exists an impairmertt of the sensibility of the
legs. It soon becomes impossible to walk without the aid of a
$4 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
cane, or a pair of sticks; finally this also, and even standing, is
beyond his power. |
While lying down, all the simple movements are at first per-
formed with ease and certainty, and even with normal force; but
a distinct failure of force, and, still more, of endurance, is usu-
ally seen at an early stage. All complicated movements, on the
contrary (describing a circle or other figure with the tip of the
toes, touching objects with the toes, etc.), are more or less inter-
fered with, even in the lying posture, by the zigzag movements
of the leg. This at last extends to the simple movements; the
leg is jerked hither and thither, away from the intended line of
action, or it falls back upon the bed in a spot different from that
intended.
In the severest forms of ataxia, every attempt at innervation
puts a great number of muscles in action; the limbs are thrown
about irregularly, and perform clonic shaking motions which
are beyond the control of the will. These motions may ex-
tend from one to the other leg, and in severe cases even to the
trunk and arms; they cease as soon as voluntary acts are not
attempted. :
In the arms and hands we observe the same order of progress ;
-all the finer complicated movements become uncertain, clumsy,
sprawling, and at last quite beyond the power of the patient to
execute. When he tries to seize an object, he passes by it,
‘spreads his fingers at the moment when he should grasp, moves
his hand forwards in irregular zig-zags, and reaches his object
with difficulty and after many efforts. He cannot carry his food
to his mouth, spills the contents of his spoon and glass, thrusts
these objects into his face, etc. Buttoning the clothes, sewing,
writing, playing the piano, soon become impossible from the
interference of the involuntary motions ; in severe cases a shak-
ing and sprawling accompany every attempt to move, and put the
patient in a condition of complete helplessness.
But the gross force is very often retained to a great extent
and for a long time in the arms, the simple movements of exten-
sion and flexion being performed quite well; if a hand is offered, —
the patient presses it powerfully, and is able to make very ener-
getic resistance to passive movements.
GENERAL SYMPTOMATOLOGY. 85
In rare cases the same disturbance of movement seems to
extend to the speech, and even to the motions of the eyes.
_ If the phenomenon is closely examined, it is at once evident
that the motor disturbance is of a peculiar kind. The simple
motor conduction is not disturbed ; it is entirely possible to per-
form any simple motion; the force of the muscles is often re-
tained for a long time, or only a little diminished ; the case can-
not, therefore, be one of real palsy, however helpless the patient
may often be made by these disturbances. There is rather a
deficient harmony among the impulses to motion which are requi-
site for every combined and associated movement. We may
therefore give the following definition: Ataxia is the disturb-
ance of movement, produced by defective co-ordination of the
latter. Wherever a co-ordination of several muscles is requisite
to the production of a certain movement, this symptom appears,
and is distinct in proportion as the desired movement is compli-
cated.
The manner in which ataxia may be produced appears from
that which has already been stated (see p. 39 et seq.) concerning
the co-ordination of movements—namely,
a. By abnormal extension of the motor innervation to too
many or too few muscles, so that in some cases more, in others
fewer than are normally required, are put in use for the attain-
ment of a definite object of motion.
b. By abnormal strength of the innervation sent to each
muscle in the case of a complicated movement.
A division of these disturbances into ataxia proper (cases under a) and disturb-
ances of innervation (under b), as proposed by Cyon,! is impracticable. The effect
of both disturbances upon the visible movement is plainly the same. And since,
at any rate, the two functions—the choice of the muscles to be innervated, and the
strength of the single innervations—are simultaneously executed by the same
apparatus (that for co-ordination), the disturbances of this apparatus will always
affect both functions more or less.
Exactly how these disturbances come to passis hard to say ;
irritative and inflammatory processes in the apparatus for co-
ordination may sometimes be the cause.
1 Zur Lehre von der Tabes dorsualis. Berlin. 1867.
86 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
It has been stated above, that the-proper centres of co-ordina-
tion do not lie in the spinal cord ; that at all events they are by
no means to be demonstrated in it.
By this one fact, the hypothesis of Brown-Séquard, Jaccoud, Cyon, and others
is rendered very improbable; these authors believe that in spinal affections ataxia
originates in a disturbance of the reflex function, because, under normal circum-
stances, co-ordination is effected reflexly within the cord, in the gray substance.
Although there are a few motor acts, such as standing and walking, in which it is
impossible entirely to deny the co-operation of reflex processes; although, more-
over, the absence of the tendon-reflex in tabes (recently discovered by Westphal,
and confirmed by myself) might be employed to assist this position, yet a closer
consideration shows that it is entirely untenable. The subject cannot be further
discussed here.
In ataxias originating in spinal disease only those conductors
can be disturbed whose assistance is required in producing co-
ordination. Such paths are either
Sensory paths (for the cutaneous or muscular sensation, etc.),
which are of use in superintending the movements and in main-
taining the equilibrium of the body ; or
Those motor paths which convey the impulses from the cen-
tres of co-ordination to the motor roots; these paths are prob-
ably distinct from the simple paths for motor conduction, which
furnish a direct connection between the voluntary centres and
the muscles ; they form a sort of side-channel.
Ataxia in diseases of the spinal cord must therefore be either
sensory (caused by disturbance of the centripetal paths) or
motor (caused by disturbance of the centrifugal paths’).
The existence of these two forms, and the evidences for sup-
posing their existence in various spinal diseases, form the
nucleus for the recent theoretic dispute about the existence of
spinal ataxia of movement.
A very exquisite ataxia is found in various spinal diseases,
-as sclérose en plaques, and more especially in tabes dorsalis
(ataxie locomotrice progressive, gray degeneration of the pos-
terior columns). The strife is very hot upon the latter point.
While authors like Friedreich, Spaeth, Niemeyer, Topinard,
1 Central ataxia, caused by disease of the centres of co-ordination, may be placed in
a class distinct from these forms.
Ea CIO Eee
r
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GENERAL SYMPTOMATOLOGY. 87
Finkelnburg, and others, have supported the theory of motor
ataxia, others, as Axenfeld, Landry, Leyden, Ruehle, Clifford
Allbutt, have tried to base ataxia upon sensory disturbances.
The view of Leyden is at first very plausible ; it has been thor-
oughly stated in several works,’ and has gained a very large
number of supporters. We will briefly inquire whether the rea-
sons brought forward in support of this view are sufficient or
not. : |
Leyden’s theory of ataxia may be stated as follows: Co-
ordination of movements is rendered possible, and is effected
through sensibility ; suspension of the sensibility (of the skin,
joints, muscles, etc.) suspends co-ordination ; gray degeneration
of the posterior columns is accompanied by disturbance of sensi-
bility, along with the ataxia ; we are acquainted with no other
than sensory functions in the posterior columns; consequently,
ataxia is a result of disturbance of sensibility.
First, we cannot consider the experimental proof of this the-
ory as very fortunate ; we do not wish to endorse Cyon’s violent
criticism, but we are forced with him to draw from Leyden’s first
series of experiments the conclusion, ‘‘that the disturbance in
muscular function which follows section of the posterior roots
has nothing in common with what we are accustomed to call
disturbance of co-ordination.’? And the second series of experi-
ments on frogs,* with section of the posterior regions of the cord,
cannot prove anything in regard to the present question, not to
speak of the great complication of the circumstances ; it proves
at most that when certain portions of the cord are cut, disturb-
ances of sensibility and of co-ordination appear simultaneously.
It is impossible to draw from these experiments a conclusion as
to the dependence of the latter upon the former.
The demonstration from pathological cases is based on the
fact that in not a few cases of ataxia there exist various degrees
of disturbance of sensibility, and especially disturbance of the
so-called muscular sense. This also proves nothing of itself ; it
1 Die graue Degeneration der Hinterstriinge des R.-M. 1863.—Zur grauen Degenera-
tion der hinteren Riickenmarksstriinge. Virch. Arch. sBd. 40, 1867.—Ueber Muskelsinn
und Ataxie. Virch. Arch. Bd. 47. p. 321. 1869.
® Virchow’s Arch. Bd. 40. p. 198.
88 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
shows, at the most, that in gray degeneration of the posterior
columns sensory and co-ordinatory paths are attacked together. |
A positive argument against this view is, however, found in
the disproportion between the intensity of the sensory disturb-
ance and the ataxia; there are cases of severe ataxia with slight
disturbance of sensibility, and of severe disturbance of sensibility
with slight ataxia; they are not rare in any considerable series
of cases.
Again, the existence of ataxia in a high degree without any
disturbance of sensibility militates against this view. Fried-
reich’ has published such cases. Leyden does not fully admit
their existence. I myself, however, have very recently examined
two cases of this sort most carefully in regard to this point, and
have found severe ataxia associated with a sensibility completely
intact in every point (touch, temperature, pressure, pain, sense of
tickling, muscular feeling, feeling of position of limbs, of passive
movements, etc.), so that the existence of such cases is proved to
my mind beyond the possibility of doubt.
Again, the occurrence of severe anesthesia without ataxia
does not harmonize with such a view. Literature is not want-
ing in cases in which there was anesthesia of the legs, without
ataxia, from one or another cause. In the printed accounts
of cases of unilateral lesion, moreover, I have found that ataxia
has never been observed in the anesthetic leg. These cases,
however, may be met with the statement that only cutaneous
anesthesia was present, while the muscular sense was intact.
The only decisive case would be that of complete spinal anes-
thesia (involving the skin, joints, muscles, etc.) without ataxia.
Such a case exists. It was repeatedly examined by various
trustworthy observers, with special regard to the question in
hand; an autopsy was had, and the state of the cord was
given with great accuracy. This is the case of Remigius Leins,
first published in Spaeth’s work;* the autopsy was fully de-
scribed by Schueppel.* Its importance obliges us to give a brief
account of it.
- 1 Virchow’s Arch. Bd. 26 and 27. 1863.
? Beitr. zur Lehre von der Tabes dorsualis. Tiibingen. 1864.
3 Ueber einen Fall von allgemeiner Anisthesie. Arch. d. Heilk. XV. 1874. p. 44,
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GENERAL SYMPTOMATOLOGY. 89
Remigius Leins, aged forty-two, in the year 1862, has suffered for twenty years
with anesthesia of the hands and arms, which rapidly became severe ; for six years
similar troubles have existed in the lower extremities. Present condition: upper
extremities wholly anesthetic ; on the soles of the feet the sensations of touch, pres-
sure, and pain are entirely extinct, and in the legs considerably diminished. He
falls when his eyes are closed. In the dark, when in bed, he feels as if floating in
the air, as the anesthesia extends to the trunk.
March, 1864.—Sense of pressure in the upper extremity, and the sense of force,
entirely extinct. Sense of position of the upper extremity and of passive movements
of the latter completely extinct. Movements of the upper extremities powerful and per-
Sectly correct ; the patient eats alone, dresses himself, etc., as far as he can direct
his acts with his sight. When the eyes are closed the arms are moved nearly like
those of a blind man. In the lower extremity, besides the cutaneous anesthesia,
there is complete loss of the sense of passive movements and of the position of limbs.
In spite of this the patient can walk without support, quite fast and securely, for a
good distance. If he is asked to raise his foot to a given height while his eyes are shut,
he accomplishes the act by a perfectly quiet and suitable motion.
June, 1872.—Sensibility continues the same. When the eyes are shut he has no
idea at all of the position of his limbs, and, if standing, falls. He can still walk,
clumsily, but not atactically. He can perform all desired actions with his arms, as
long as he can see them.
Death, May, 1873.
Autopsy.—A cavity in the entire length of the cord, from the level of the first
cervical nerve to the first lumbar. Posterior columns in the lower half of the cer-
vical medulla wholly destroyed and gone; above, gray degeneration ; in the dorsal
part slight atrophy and increase of connective tissue; the lumbar part normal.
Anterior columns everywhere quite uninjured and normal, Anterior commissure,
from the second cervical to the twelfth dorsal nerve, completely destroyed. Lat-
eral columns in the same regions sclerotic in the neighborhood of the posterior
cornua. Gray substance mostly implicated in the cavity; gray commissure and
posterior cornua almost wholly destroyed in the entire cervical and dorsal medulla;
anterior cornua almost entire, and only in the cervical region reduced to a small
size; a lateral strip of gray substance is also retained everywhere. Anterior roots
normal. Posterior roots, from the third to the eighth cervical nerves, in a state
of complete connective-tissue degeneration,’ and, to the end of the dorsal medulla,
more or less atrophied. Lumbar part, with its roots, normal; etc.
This case is perfectly clear and convincing ; in my opinion it
entirely overthrows Leyden’s theory. If the maintenance of
sensibility were a necessary condition of co-ordination of move-
ments, the extreme of ataxia ought to have accompanied this
absolute anesthesia ; but there was no ace of ataxia.
1 This fact is also very decisive against the reflex theory of Brown-Séquard and Cyon,
90 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
It results without question from this, that the retention of
sensibility is not necessary, in order that co-ordinate movements
shall be performed ; it may be necessary in acquiring the faculty
of doing them, and without doubt it is of great importance in
maintaining equilibrium, but it is not indispensable in perform-
ing co-ordinate movements which have been learnt. Loss of sen-
sibility, therefore, can in no way interfere with these movements, .
when once acquired by practice.
It seems to us, therefore, quite unjustifiable, upon scientific
grounds, to make a disturbance of sensibility responsible for
ataxia, when both occur together. It must rather be believed,
that there exist special co-ordinatory paths in the cord, which are
attacked in tabes dorsalis and cognate affections, when the symp-
toms of ataxia appear.
In the present state of our knowledge, therefore, we + ae 20
right to assume any other than a motor ataxia in tabes.
In examining the question whether a motor ataxia can be
objectively distinguished from the sensory form, this will become
still plainer; it will also be seen whether, and how far, the
assumption of a sensory ataxia is justified.
A purely motor form of ataxia is to be assumed when the sen-
sory apparatus is entirely normal (sensibility, muscular sensa-
tion, vision). If sensibility (in its widest sense) is perfect, and
the movements are still atactic, it must be that the cause lies
only in the apparatus for co-ordination, and not in the accessory
sensory apparatus. We have above shown that such cases exist
beyond a doubt. |
We know further, from two series of observations, mutually
confirmatory, that the retention of a single sensory control-
apparatus is sufficient to render possible a perfect co-ordination
of movements, if only the apparatus for co-ordination is itself
normal. For (1) blind persons, or well persons with shut eyes,
show no trace of ataxia, and (2) anesthetic patients, even when
the cutaneous and the muscular sensibility, etc., are completely
extinct, show no trace of ataxia as long as their eyes are open
and they can control their movements by vision; this is an in-
controvertible inference from the Spaeth-Schueppel case.
Hence we may conclude that a case of ataxia, even when only
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GENERAL SYMPTOMATOLOGY. 91
one sensory control-apparatus remains in activity, must be of a
purely motor nature. This is the case when an anesthetic patient
makes atactic movements with open eyes, or when, with normal
sensibility, the eyes being blind or shut, ataxia is present. Such
cases are indeed not wanting; they form the great majority of
tabetic diseases; they must, heeled be instances of motor
fF) 6 ataxia.
It is harder to characterize sensory ataxia; and it is ques-
tionable whether that which is commonly called ataxia ever origi-
nates in disturbance of the sensory control.
If, in spinal affections, all voluntary, complex movements,
such as are acquired by practice, are well performed, and if no
disturbances occur until movements are attempted, for which a
sensory control is indispensable (e. g., maintaining equilibrium,
standing upright, etc.), then there will be a certain propriety in
speaking of sensory ataxia. It will be recognized by observing
that disturbances of motion are absent, so long as even one sen-
sory control-apparatus is in action, but make their appearance
when, one apparatus being already impaired, the other (intact)
apparatus is excluded ; thus, when a blind man becomes anzes-
thetic, or—to choose a more likely example—when an anzesthetic
patient closes his eyes. In these cases, considerable disturbances
of motion will inevitably occur. It seems to us, however, ex-
tremely questionable whether these disturbances show an agree-
ment with or even a resemblance to that which we call ataxia.
When a patient whose hands are anesthetic shuts his eyes,
he can no longer hold firmly a needle, a button, or similar ob-
jects ; he cannot fasten his clothes, etc. ; the things fall from his
hand, he does not complete the motions, he performs them falsely
—but he does not become atactic. The movements are correctly
willed, and probably also correctly executed ; but the patient is
no longer able to judge whether the end is attained ; the move-
ments are therefore often carried beyond the point desired, or
they fail to reach it—but they do not become properly atactic.
It is the same as when an object is held before a blindfolded per-
son, and he is asked to seize it; he will make the most unsuita-
ble movements, but they will not be atactic,
If the feet are anesthetic, and the patient shuts his eyes while
92 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
standing, he will fall immediately, because he has no oversight
(** Controle’’) as to whether the voluntary efforts for the purpose
of retaining the equilibrium are sufficient or insufficient. In
lesser degrees of anzesthesia, tottering, at least, will occur, because
an adequately strong sensory impression is not made by any
minute deflection of the body. Walking with closed eyes be-
comes uncertain, tottering, even impossible ; but it is not. at all
necessary that a proper ataxia should exist. This also results
from the case of Spaeth and Schueppel.
The intentions of the will may be formed and executed quite
properly, but they are incorrect with respect to the desired ob-
ject, being too great or too small, because the patient is deprived
of a standard by which to measure them. Jn this case, there-
Sore, the purposes of the will and the voluntary impulses to
movement are false, but they are correctly carried out, while in
ataxia proper the purposes of the will are correct, but are falsely
carried out.
The notion of sensory ataxia is, therefore, only admissible in
case the motor impulses which maintain the equilibrium are pro-
duced quite involuntarily by the action of centripetal excitement
on motor paths (in the thalamus opticus, the corpora quadrige-
mina, or the cerebellum), that is, in apparatus which is usually
called co-ordinatory. : But the symptoms of such cases are cer-
tainly essentially different from those of motor ataxia.
It seems to me, however, much more desirable fo separate the
processes which serve to maintain the equilibrium and position
in space from the processes of co-ordination proper of the (volun-
tary) movements ; this will certainly conduce to clearness in the
question of ataxia. The discovery by Goltz of the different cen-
tres for equilibrium (lobi optici) and for locomotion of the body.
(cerebellum ) is a weighty argument for this separation. Of
course, the processes of movement which contribute to the main-
tenance of equilibrium, etc., equally require the apparatus of
co-ordination in order to act normally, and this is put in action
by impulses from the centres for equilibrium, as it is by the
centres of volition in voluntary actions. The centres of equi-
librium, therefore, and those of volition may be considered as
standing in a similar relation to the apparatus for co-ordination.
GENERAL SYMPTOMATOLOGY, 93
It follows directly that a disturbance of the centres of equilib-
rium does not at all necessitate a disturbance of co-ordination
of voluntary movements; also that a disturbance of the sensory
excitations which put the centre of equilibrium in action is not
necessarily followed by a disturbance of co-ordination, but that,
on the other hand, every disturbance of the apparatus of co-ordi-
nation will more or less impair the performance of the move-
ments necessary for equilibrium. It will be well in future to
apply the test separately in both directions in these cases of spi-
nal disease.
This brings before us the consideration of another motor
symptom, which is usually placed in the most intimate connec-
tion with ataxia, namely, tottering and falling when the eyes are
shut, a symptom to which, under the name of the Brach-Rom-
berg symptom, too much importance has certainly been at-
tached. |
lt is easy to prove that many patients with disease of the cord
(especially tabetic patients, with a more or less marked ataxia and
disturbance of sensibility), who are still able to walk and stand
quite tolerably with open eyes, begin immediately to totter as
soon as their eyes are shut; the tottering becomes worse and
worse, and in severe cases the patient presently falls. This tot-
tering is most plain when the eyes are closed, and the patient is
made to stand with his feet together. ‘The intensity of this dis-
turbance usually seems to be directly proportionate to the de-
gree of ataxia, but this is only apparently true.
This phenomenon is evidently due to a disturbance of equilib-
rium and of the power of maintaining position in space. We
have already shown that these cannot be maintained without a
| continued sensory control (principally furnished by the sensory
impressions in the lower limbs and by the sense of sight). If one
part of this sensory control be taken away by shutting the eyes,
the maintenance of equilibrium and position in space will be dif-
ficult, in proportion as the other factor is already impaired, that
is, corresponding with the existing disturbance of sensibility.
In fact, this symptom also is found chiefly or exclusively in
cases of marked disturbance of sensibilify of the lower limbs; in
complete anesthesia the patients fall quickly when their eyes
94 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES
are closed. This phenomenon, therefore, is simply an indica-
tion that the sensory control exercised by the soles of the feet,
the joints, and the muscles is insufficient. This is in harmony
with Benedikt’s statement, that in a great many instances of
difficulty in standing with closed eyes, he has never seen one
where there was not a disturbance of the muscular conscious-
ness. But, on the other hand, there are some quite severe cases
of ataxy (as I have seen most clearly demonstrated), in which
the tottering with closed eyes is absent or scarcely exists, when
the sensory control from the skin, the muscles, etc., is perfectly
intact, 7. e., when there is no disturbance of sensibility. It is
well, however, to remember that in atactic persons this symptom
must be more marked, since the movements which serve to main-
tain equilibrium are inco-ordinate, so that they usually totter
very perceptibly, even when their eyes are open.
It should here be added, that in many atactic patients the
want of co-ordination increases decidedly, the movements become
much more excessive and ungovernable, when the eyes are shut.
This proves no more than that the control by the eyes may fur-
nish a means of partially compensating for the disturbance of
co-ordination, so that, as in the process of learning how to co-
ordinate, a continuous influence upon the centres for this fune-
tion may be exercised; if this influence ceases (when the eyes
are shut) the disturbance of co-ordination returns in its full force.
This may be the reason why atactic patients, without disturb-
ance of sensibility, occasionally totter a little when their eyes
are shut, because the muscular actions that are called into use
in supporting the equilibrium, already atactic, are no longer
under the direction and control of the sense of sight.
These symptoms, however, are always much more marked in
cases where there is impairment of the sensibility, especially of
the so-called muscular sense ; in this case the movements become
excessive and entirely irregular, because when the eyes are closed
the sensory control entirely ceases, and to the existent disturb-
ance of co-ordination there is added an uncertainty respecting
the extent of the voluntary impulse required, the standard for
estimating which has been lost. In such cases the ataxia in-
creases considerably when the eyes are shut, while in atactic per-
GENERAL SYMPTOMATOLOGY. 95
sons who retain their sensibility perfectly no increase of ataxia
worth mentioning occurs, the sensory control afforded by the
skin and muscles being complete and adequate.
This entire series of symptoms is only a proof that the dis-
turbance of co-ordination may be partially made good by sen-
sory control exercised through the vision.
We have to add, finally, that in a few cases it has been ob-
served that atactic persons who were completely blind, but were
able to stand, also experienced a distinct increase of tottering
when they shut their eyes. It is clear that this cannot be due to
any further diminution of the sensory control of the eyes; but
it is hard to find any explanation for this singular phenomenon.
The most obvious conclusion is, that the phenomenon is a psy-
chical one. Might a sudden calling off of the attention cause
an increase of uncertainty in the legs? Or may it be that a new
act of motor innervation can send impulses to the co-ordinatory
apparatus, which increase the existent disturbances in the lat-
ter? At present we do not know. |
The preceding appears to furnish a sufficient demonstration
of the fact that the chief form of ataxia in spinal affections is of
a motor nature. There must, therefore, exist in the spinal cord
special centrifugal fibres, employed for co-ordination (Spaeth),
and ataxia in a spinal affection occurs only when these fibres are
attacked. Their site is entirely unknown.
Most observers place them in the white posterior columns,
because the autopsy of atactic patients usually shows gray degen-
eration of the posterior columns. If it were proved to a cer-
tainty that in such patients the posterior columns were exclu-
sively attacked, we might regard this as demonstrated. But
this is not yet proved; it is even probable that in such patients
there is a more or less considerable implication of the gray sub-
stance and the lateral columns, as a rule.
Further, the case of Spaeth and Schueppel is rather decisive
against the localization of the co-ordinatory paths in the pos-
terior columns, although the duration of the case was such that
a compensatory conduction might be thought possible.
Where, then, are we to look for th®se co-ordinatory paths?
In the gray substance? In the antero-lateral columns? The
96 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
experiments of Brown-Séquard, who was enabled to produce
ataxia in birds by lesion of the gray substance of the ventriculus
lumbalis, point rather to the gray substance. On the other hand,
according to the experiments of W oroschiloff, the co-ordinatory
paths lie (in rabbits) in the lateral columns, in their innermost
part, in the sinus between the anterior and posterior columns,
At present the question is not settled in the case of man; further
exact investigations are necessary to bring it to a solution; per-
haps we may gradually approach a conclusion by careful com-
parisons of suitable cases of spinal sclerosis in patches. Till
then, our first thought in ataxia will be of a disease of the pos-
terior columns, and especially (as would appear from Charcot’s
latest statements’) the lateral portions of these columns, adja-
cent to the gray substance, called the ‘‘région des bandelettes
externes,” region of the inner bundles of root-fibres.
ce. Various Characteristic Gaits in Spinal Disease.
The form of the lesion may often be recognized by the
patient’s characteristic gait, as soon as he enters the room. I
believe that for practical purposes it is sufficient to distinguish
the following leading varieties, which may be distinctly sepa-
rated : |
1. The paretic and paralytic gait—caused by a more or less
extensive palsy of the lower extremities. The gait is shuffling,
the tip of the foot drags on the ground, the fore-part of the
foot hangs down, the sole is planted awkwardly, usually with
the outer edge first; the knee is raised high, or is drawn after
the patient in an extended position ; a certain stiffness of the legs
is often remarked. The patient walks with one or two canes, or
is supported by crutches or guides; he totters but little, stands
quietly and securely, and when left alone simply sinks to the
ground, in most cases. The manner of walking differs some-
what, according to the distribution of the palsy among the
groups of muscles ; if the whole leg is palsied, it is different from
1 Charcot, Lecons sur les maladies du systéme nerveux. II, Série. 1. fasc. Paris.
1878, « | S.
——— I a a
_ —_,
ae oN ee ee ee oe
“a * 1 a, y" a
GENERAL SYMPTOMATOLOGY, 97
what it is in palsy of the lower half of the leg ; in the latter case
it is waddling, and especially characteristic.
2. The atactic walk—caused by disturbance of co-ordination
in the legs. It is characterized by irregular hurling movements ;
the point of the foot is thrown forward and outward with force; _
the heel is brought down with a stamp, the leg stiff at the knee.
The patient’s eyes are continually on the ground. The gait is
tottering, staggering, or even reeling from side to side; the move-
ments are hasty, spasmodic, quite unequal; in turning about,
especially, there is great uncertainty, and danger of falling. In
severe cases the patient falls after a few steps.
3. The stiff, spastic walk—caused by reflex muscular contrac-
tions or tension associated with paresis of the leg. This gives
rise to a very peculiar and characteristic walk; the legs are
somewhat dragged, the feet seem to cleave to the ground, the
tips of the feet find an obstacle in every inequality of the
ground ; every step is accompanied by a peculiar hopping eleva-
tion of the whole body, dependent on a reflex contraction of
the calf; the patient immediately gets upon his toes, and slips
forward on them, showing a tendency to fall forward. The legs
are close together, held stiffly, the knees somewhat depressed
forward, the upper part of the body slightly bent forward.
There is no throwing about of the feet. This gait depends on
muscular tension and reflex contractions in the various groups
of muscles, which are set in activity during the process of walk-
ing.
These forms may be more or less distinct ; there occur transi-
tional forms of a mixed character; but not every patient with
spinal cord disease has a characteristic gait.
ad. Increase of Motility—Spasm.
Motor symptoms of irritation are among the commonest of
spinal symptoms; they occur in a great variety of forms.
The simplest form is without doubt the so-called muscular
tension. In this case the muscles (which are usually in a con-
dition of greater or less paresis) are in a state of moderate tension
or contracture, which makes the execution of passive movements
VOL. XIII.—7
98 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
quite difficult. This tension often occurs at the moment when
a passive movement is being performed, especially if it is done
rather quickly ; there then follows a jerking, impulsive resist-
ance, which enables us to recognize with ease the slighter forms
of the disturbance. The voluntary movements, also, are more or
less obstructed and clumsy, are performed as if the patient were
in a semi-fluid medium, and require the expenditure of an ab-
normal amount of force.
It is easy to show that these tensions in passive motion occur
chiefly in the muscles which are stretched and pulled on by the
movement ; thus, in passive extension, the flexors, and vice versa.
The tension seems here to be reflex in character, and is probably
connected with the abnormal tendon-reflex action, to be men-
tioned later.
In severer cases the movements grow more and more stiff,
the resistances greater, and a condition may finally exist which
resembles the flexibilitas cerea of catalepsy. The contraction is
not always equally distributed through the entire muscle; in
some muscles it may be only partial, forming knots or lumps.
A simple exaggeration of this state doubtless constitutes what
is called stiffness of the muscles, rigor. The muscles are stiff
and stark, much swollen, and firmly resistant to the touch; on
pressure, they are usually very painful; both active and pas-
sive movements are extremely difficult. The extensor muscles
are usually the principal ones affected ; very often also the mus-
cles of the nape and back (torticollis).
In the worst cases, decided contractures occur, which may be
limited to a few muscles or groups of muscles, but often attack
many in a variety of places. Sometimes the flexors, and some-
times the extensors are more affected, hence the difference of
posture in the different cases.
I do not now refer to the so-called paralytic contractures,’
which are certainly nothing uncommon, even in spinal diseases,
but exclusively to neuropathic contractures, which owe their
origin to abnormal states of irritation in the cord. The muscles
are much shortened, their tendons quite prominent, and passive
'Vol. XI. p. 379.
GENERAL SYMPTOMATOLOGY. 99
movements are entirely impracticable. If energetic attempts to
perform them are made, vigorous clonic contractions of the
muscles manipulated are often produced, or the contracture is
increased, leading to a momentary tetanic stiffness of the whole
limb.
It would be very difficult, at the present time, to refer all
these conditions of irritation to pathological changes in certain
portions of the cord. But there is no doubt that there are two
ways in which muscular tension and contractures may come to
pass; first, a reflex origin may be conceived, which is doubtless
the chief element in cases where sensory phenomena are promi-
nent, in diseases of the meninges, the posterior roots, the poste-
rior columns, the reflective gray matter, etc.; such reflex mus-
cular contractions are said to attack by preference the flexors.
On the other hand, these symptoms may originate through
direct irritation of the motor parts of the cord. The seat and
the character of this irritation are hardly known; a direct irrita-
tion of the anterior roots is possible ; according to Charcot’s later
observations, sclerosis of the lateral columns is a very common
cause of such motor symptoms of irritation ; it is not at all
known how far the gray substance might produce them. In
such cases of direct irritation, at least in the lower extremities,
the extensors are said to be principally affected.
In respect to the exact pathogenesis of these motor symptoms
of irritation, we know only this, that they chiefly occur in acute
or chronic inflammatory conditions of the cord and its mem-
branes, in the various forms of meningitis and myelitis, in many
cases of multiple sclerosis, paraplegia after acute sickness, etc.
We know still less about one of the severest forms of spinal
spasm, namely, tetanus, and its pathogenesis. This is a power-
ful tonic spasm of almost the entire muscular system; the spasm
occurs in paroxysms, which are brought on, or increased, by reflex
action, but continues in the intervals in the form of a moderate
degree of rigidity. Tetanus is probably caused by an (inflam-
matory or toxic) affection of the gray substance, which enor-
mously increases the reflex excitability. A like condition exists
in meningitis spinalis.’
1 See Volume XII.
100 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The attacks of so-called tetany have a remote resemblance to
tetanus. By this we understand attacks of tonic spasms, oceur- »
ring in regular paroxysms, and affecting the extremities chiefly.
It is probably of spinal origin.’
Among the forms of clonic spasm, in spinal disease, tremor,
in the first place, is not rare; either permanent or transitory,
accompanying certain movements, following exhaustion, etc. Its
manner of origin is as yet quite unknown; one is naturally in-
clined to refer it to the gray substance.
A higher degree of tremor is present in shaking, which accom-
panies and disturbs all voluntary movements in multiple spinal
sclerosis; a sort of greater tremor, which begins whenever a
voluntary innervation occurs, and may perhaps be regarded as a
very severe degree of ataxia, although, as it appears, it is essen-
tially distinct from the latter. We have not yet succeeded in
forming an exact pathogenesis of this symptom ; and we may
say the same of that characteristic form of tremor, most marked
during repose, which is the essential feature of paralysis agitans.
Few of the other clonic spasms can be referred with probabil-
ity to the cord; those of single muscles, or groups of muscles,
have seldom been derived from the cord, and general convul-
sions, as occurring in epilepsy, eclampsia, urzemia, etc., have
commonly been ascribed to the medulla oblongata.
A few special cases remain to be described. Among these is
a peculiar form of clonic spasm in the lower extremity, which
appears in various lesions of the cord, and runs an extremely
characteristic course. In its lightest form, it consists of that
clonus of the foot and lower leg which appears when the attempt
is made to bring the foot quickly into dorsal flexion by pressure
upon the sole; a rhythmic, clonic jerking of the foot begins, which
ceases as soon as the foot is let go and brought back into plantar
flexion. I have demonstrated that this symptom, described by
Brown-Séquard” and Charcot, most probably originates in the
reflex manner, through irritation of the tendo Achillis.* In se-
1 Volume XI. p. 368.
2 Journ. de la Physiol. de "homme et des anim. I. 1858. p. 472.
3 Uebér Sehnenreflexe bei Gesunden und Riickenmarkskranken. Arch. f. Psych. u.
Nervenkr. V. Heft 3. p. 792.
“a
4
GENERAL SYMPTOMATOLOGY. 101
verer cases a very slight pressure on the sole or the toes suffices
to produce the phenomenon; for which reason it seems often to
arise spontaneously. Then the spasm extends to other parts;
the whole leg falls to trembling convulsively, and the other leg
soon does the like. When the evil is at its worst, any irritation
whatsoever, originating in the skin or the intestines, and acting
reflexly, is followed by a tetanic stiffness, together with convul-
sive tremor, of one or both legs, lasting several minutes. This
severest degree of reflex convulsion, which is hardly found
except in entirely palsied, paraplegic limbs, is what Brown-
Séquard (loc. cit.), and after him Charcot,’ have rather unsuita-
bly termed tonic spinal epilepsy. This phenomenon is especially
observed in cases of compression of the cord, or circumscript
affections of its entire transverse dimensions, if the reflex excita-
bility is also much increased by an accompanying state of irrita-
tion. The slighter degrees of this phenomenon seem also to
occur in sclerosis of the lateral columns,* while in severer cases
we should always think of an implication of the gray substance.
The so-called saltatory spasms, recently described by Bamberger, Guttmann, and
Frey, would seem to belong to this category, and to present a specially marked
modification of these reflex cramps.
It is evident at a glance that this phenomenon has nothing
whatever to do with epilepsy proper. But doubtless there are
certain relations between epilepsy and spinal disease, which we
must briefly speak of in this place.
Brown-Séquard * made the remarkable discovery, and studied
it with the greatest thoroughness, that in guinea-pigs and other
mammalia epilepsy appears in four or five weeks after uni-
lateral section of the lumbar or dorsal cord; an attack may .be
produced at any moment by irritating an epileptogenic zone,
1 Clinical Lectures on Diseases of the Nervous System. 1872-3. p. 216.
* Hrb, Ueber einen wenig bekannten spinalen Symptomencomplex. Berl. kin.
Wochenschr. 1875. No. 26.
® Compt. rend. de la Soc. de Biolog. 1850. Vol. II.; Arch. de Médic. Févr. 1856;
Researches on Epilepsy. Boston, 1856-57; Lecturesyn the Physiol. and Pathol. of the
Central Nervous System. Phila. 1860. p. 178; Arch. de Physiol. norm. et path. I. 1868.
p. 317; Il. 1869. pp. 211, 422, 496; IV. 1872. p. 116.
102 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
comprising portions of the region of distribution of the trigemi-
nus and the two or three upper cervical nerves. We need not
give all the details of Brown-Séquard’s experiments, though
they are extremely interesting ; they have, at all events, demon-
strated a fact which has since received contirmation from other
sources, namely, that, after unilateral injury of the cord, a dis-
eased condition develops in a few weeks, which presents an un-
mistakable likeness to epilepsy. We are, however, still in uncer-
tainty regarding the interior relations and mechanism of these
processes. Brown-Séquard found also that section of one sciatic
nerve produces, after a few weeks, exactly the same epileptiform
accidents as the section of the cord. Finally, Westphal’ found
that simple tapping on the heads of guinea-pigs would give rise
to an exactly identical form of epilepsy with epileptogenic zone,
etc.; he found, in every instance, small hemorrhages, irregularly
distributed, in the medulla oblongata and the upper part of the
cervical cord, and very often further down, even in the dorsal
cord. Westphal is inclined to regard the hemorrhages in the
cord as furnishing the case for the subsequent development of
epilepsy.
It therefore appears to be proved with sufficient certainty
that, in animals at least, certain injuries of the cord—as small
hemorrhages, and probably other lesions—are capable of giving
rise to epilepsy in a manner hitherto unknown. But the ques-
tion whether such a thing occurs in the human subject is not yet
decided with certainty. It is true there are several cases in
which epilepsy appeared after lesion of the sciatic nerve, just as
in animals; and Leyden? has published a case in which epilepsy
occurred after an injury of the head, and which seems to resem-
ble Westphal’s experiments; but in the case of diseases or inju-
ries of the cord the demonstration of secondary epilepsy has
been much less clear. Brown-Séquard quotes some cases from
older accounts, which he believes establish this point. Charcot*
mentions periodic epileptic attacks among the symptoms of com-
1 Ueber kiinstl. Erregung von Epilepsie bei Meerschweinchen. Berl. klin. Wochen-
schr. 1871. No. 38.
? Virchow’s Archiv. Bd. 55.
* Legons sur les malad. du syst. nery. II. Sér. 2, fase. p. 137,
- a
GENERAL SYMPTOMATOLOGY. 103
pression of the spinal cord, and cites a series of cases in proof of
it; a case by Duménil' seems especially convincing; and Oppler?
has quite lately published the case of a young, powerful soldier
who had never suffered from epileptic spasms, but had several
attacks during the convalescence from a traumatic spinal menin-
gitis. In spite of this, it would be desirable to have more obser-
vations upon the human subject.
Considering the very great frequency of lesions of the cord,
the occurrence of epilepsy as caused by such lesions is extremely
rare, and therefore of little practical consequence. It would be
of great interest, if cases should be observed, to demonstrate the
existence of an epileptogenous zone.
A less common series of spinal symptoms is furnished by the associated move-
ments, by which we mean involuntary, often spasmodic actions, which, making
their appearance when any voluntary movements are to be executed, complicate
and disturb them, The region of their origin seems to be usually the brain, and
especially the centres of co-ordination in the brain. No doubt many symptoms in
diseases of the cord belong to this class; thus we cannot altogether refuse to regard
the atactic movements, the shaking in local sclerosis, etc., as associated movements,
although they are decidedly of spinal origin. In the same class are the movements
of antagonists, which accompany the effort to innervate palsied or paretic muscles;
these, however, are not a true spinal symptom, but simply express the fact that a
large number of muscles receive a commen co-ordinated innervation, some of which
have become insufficient to perform their functions, thereby permitting the action
of their antagonists to appear more distinctly ; this occurs in all palsies. It is not
certain to our mind whether the spasmodic and wholly uncontrolled movements
which often occur in paraplegic extremities when a powerful act of the will is
directed to them, are to be considered as belonging to this class. They seem to
depend rather on an abnormal diffusion of the process of excitation among the
motor paths, when pathologically irritated—a diffusion which might be explained
by reference to the structure of the nervous network in the inflamed gray substance,
and by supposing an interruption of the chief paths to have taken place.
Probably, however, a part is owing to the presence of reflex aetions, the stimu-
lus to which originates in the skin of the palsied parts, under the influence of the
motions of the trunk and arms; this symptom is almost always associated with an
excessive increasé of reflex excitability. It is quite certain that the reflex process is
concerned in those tonic or clonic contractions of paraplegic legs, which are often
1 Gaz. des hépit. 1862. p. 470.
* Riickenmarksepilepsie ? Archiv fiir Psychiatrie u. Nervenkrankheiten. Bd. IV. p.
784,
104 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
associated with the act of evacuating the urine or feces. The same have been
observed by Freusberg in dogs whose spinal cord had been cut.
It is hardly necessary to repeat, that in all the above symp-
toms of motor irritation our first thought should be of an affec-
tion of the gray substance and the antero-lateral columns. We
are at present unable, or at best are able in but a few cases, to
define the point where the implication of either terminates, or
the general pathogenesis of the spasms. It should not be for-
gotten that an affection of the sensory portions of the cord may
give rise to reflex symptoms of spasm.
e. Alterations in the Velocity of the Motor Conduction.
Recent observations have made us aware that this class of
alterations is by no means infrequent; but at present they have
been little observed. Retardation of the motor conduction, long
known by physiologists, was first observed under pathological
conditions by Leyden and von Wittich,’ who made careful esti-
mates of its extent. Their three cases, however, are probably not
affections of the spinal cord proper, but of the pons and medulla
oblongata. The rate of conduction was reduced to one-third of
the normal speed, and in correspondence with this, the move-
ments of locomotion, speech, and so forth, were greatly retarded,
and the patients were unable to execute the same movement
several times in rapid succession.
The principal attention was directed to measuring the motor
conduction as a whole. Burckhardt’ has lately undertaken to
measure the spinal motor conduction alone, by the aid of a vari-
ety of physiological methods, and has reached very remarkable
results. He found that under normal circumstances the spinal
motor conduction takes place from two to three times as slowly
as the peripheral, and he suspects that the reason lies in the in-
tercalation of ganglion cells in the motor conductive path. But
under pathological conditions he found sometimes an accelera-
tion of spinal conduction (as in writers’ cramp, in spinal palsy of
? Virch. Arch. Bd. 46. p. 476, and Bd. 55. p. 1.
2 Die physiol. Diagnostik der Nervenkrankheiten. Leipzig. 1875.
encase
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Sa ee YC. eh, ee o ey
GENERAL SYMPTOMATOLOGY. 105
children, in central myelitis, in some cases of tabes, etc.), and
sometimes a more or less considerable retardation (as in myelitis
of the white substance, in diffuse sclerosis of the cord, in certain
cases of tabes, etc.). He concludes that the anatomical basis of
central retardation probably lies in the white substance, and that
of central acceleration in the gray. Retardation of motor con-
duction in the cord gives ground, therefore, for inferring a dis-
ease of the white substance, and acceleration for inferring disease
of the gray.
It scarcely need be said that these theories are greatly in
need of more exact establishment and elaboration.
J. Electric Reaction of the Motor Apparatus.
The labors of Marshall Hall, Todd, Duchenne, and others gave
rise to great expectations of improvement in the diagnosis of
spinal diseases through the use of electricity ; but these expec-
tations have not been fulfilled.
In fact, the electrical examination seldom gives decisive evi-
dence, to enable us to place the seat of a disease in the cord, or
brain, or peripheral nerves ; this can be done only under special
conditions. In many cases, however, valuable information is
given as to the state of.nutrition of the nerves and muscles, and
thereby indirectly as to the nature and probable location of the
disease. (Compare the full statements of this matter made in
Vol. XI., p. 423 et seq.)
A practically useful general statement of the changes in elec-
trical excitability which occur in diseases of the cord cannot be
given at present; the investigations hitherto made are few, and
not free from objections. The most frequent, and probably the
most important, forms of alteration—namely, the slight quantita-
tive changes in electrical excitability—suffer from a serious want
of observations; the results have in almost all cases been ren-
dered untrustworthy by defective methods of investigation. I
have shown! the method which should be observed in seeking
>.
_~ 1 Brbd, Zur Lehre von der Tetanie, nebst Bemerkungen iiber die Priifung der elektr.
Erregbarkeit motorischer Nerven. Arch. f. Psych. und Nervenkr. IV. p. 271.
106 - ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
(particularly in spinal diseases) for certain and exact results. I
give here a few points briefly.
In diseases of the spinal cord the electrical reaction of the
nerves and muscles, under the faradic and galvanic currents, may
be increased or diminished ; the degree of alteration is usually
slight. The diminution may.amount to a complete extinction of
electrical excitability, but this is usually preceded by the change
denominated the reaction of degeneration (Entartungsreaction).
Distinct pathological conclusions cannot be drawn at present
from the slighter degrees of quantitative change.
The reaction of degeneration * is by no means rare; it is more
frequent than has been supposed. It is not yet known whether
it takes the same strongly-marked course as in traumatic lesions
of peripheral nerves; from certain observations, which, however,
are not conclusive, it seems to me that the increase in the suscep-
tibility to galvanic currents is not quite so marked as in peri-
pheral palsies, or perhaps that it passes off more quickly. It is,
however, certain that the qualitative change of galvanic excita-
bility occurs in a perfectly characteristic form, with a contrac-
tion at anodic-closure which is stronger than that at cathodic-
closure (AnSZ >KaSZ), and with a sluggish and protracted con-
traction.
The inferences we are permitted to make in respect to the
histological changes in nerves and muscles, which exhibit such
reactions, are the same that may be made in peripheral palsies.
They are of a good deal of importance, and the changes they
indicate are of the most striking character. By patient care a
great number of facts have been collected, of which mention will
be made further on, and in the special portion of this work (see
‘Trophic Disturbances’’ and the chapter on ‘‘ Spinal Paralysis
of Children’’); we have learnt that identical histological changes
may originate from direct lesions of the gray substance of the
anterior cornua (spinal origin), and from an impediment to con-
duction between that gray substance and the peripheral parts
(peripheral origin). When, therefore, in a disease which can be
demonstrated to be of spinal origin, we find the reaction of degen-
1 See Volume XI. p. 427.
GENERAL SYMPTOMATOLOGY, 107
eration, we may infer a lesion of certain parts (anterior cornua)
of the gray matter, provided, however, that a peripheral origin
can be disproved. On the other hand, when the electrical exci-
tability is retained in its normal form in a spinal disease, it is
allowable to infer that these portions of the anterior gray sub-
stance are not involved in the lesion.’
As avery general rule, it may be stated that the results of
electrical examination cannot safely be applied to the diagnosis
of spinal disease, except in the closest connection with the other
symptoms.
We shall give a more detailed presentation of the known
facts in connection with the respective diseases.
3. Disturbances of Reflex Activity.
It is of the greatest importance to test the reflex activity in
spinal diseases ; the most valuable information in respect to the
disease may often be thus had.
Diminution or suspension of the reflex actions is usually
recognized with ease ; it is shown by the partial or complete fail-
ure of the ordinary means of stimulation, as applied to the skin
or to the tendons and other parts from which we expect reflex
results. It is necessary to remember that many persons have
normally a very slight reflex reaction; but this will be easily
recognized, as a pathological diminution is usually limited toa
portion of the body.
It may be produced—
a. By disease (arrest of conduction) of the entering sensory
rootjibres ; in which case there must be more or less anzesthesia
in the regions supplied by these root-fibres.
b. By disease (arrest of conduction) ef the departing motor
root-jibres ; in which case there must be a more or less complete
paralysis of corresponding extent.
c. By disease of the gray substance of the reflex apparatus
itself, when both sensibility and motility may be present, or
_,
—_
! Compare the observations of Burckhardt in Physiolog. Diagnostik der Nerven-
krankheiten. pp. 264 and 270.
108 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
one or both of them may be altered to a greater or less extent,
according to the extension of the disease in the gray substance.
Examples of all these forms are furnished by pathology.
d. Finally, it is permissible to entertain the case of reflex
arrest, in accordance with known physiological facts (see above,
p. 51); but we have at present no pathological facts.
The decision between these various possibilities will be facili-
tated by an exact estimation of the weight of each element in the
problem.
A retardation of reflex actions has been found in pathological cases under the
same circumstances as retardation of sensory conduction. We have mentioned this
fact previously (p. 70).
A more frequent and interesting circumstance is the increase
of reflex actions. .
It makes its first and its most conspicuous appearance in the
. voluntary muscles. They twitch at the lightest irritation; often
the movements are slight and imperfect, but more often they are
very powerful, complete, or violent ; the legs and arms are thrown
about forcibly in all directions, twitch frequently, or enter into
a clonic tremor or a fully developed tetanus; the motions are
almost always unsuitable and disorderly; flexion and extension
of the joints alternate, giving rise to irregular sprawling move-
ments; the patient’s leg can often be placed at will in reflex
extension or flexion by a definite localization and intensity of
irritation ;+ orderly and fitting movements are rarer; thus Mc-
Donnel’* reports that a patient, who suffered with compression
of the cervical cord, continually moved his paralyzed left hand
to his genitals during catheterization.
Such reflex acts are usually produced with most ease by ir-
ritating the skin ; tickling, pricking and pinching, or stroking
the skin, especially that of the soles, the inner surface of the
thighs, the toes and fingers, and the palm, produce them ; Pflue-
ger’s law of extension of reflex phenomena can often be con-
firmed in such patients. Reflex acts are also excited from the
intestines ; in certain spinal affections nothing is more common
1 Virchow, Gesammte Abhandl. p. 683.
2 See Virchow-Hirsch’s Jahresber. 1871. Bd. II. p. 7,
mip ha se Oe a ee ee ree ee a ee ee
een Pe:
"
A oe
I Tah
\
TL) SEC ORTON EL TA ay nde ere eed Eee ann are ant
fe ayer, of ie —
=
GENERAL SYMPTOMATOLOGY. 109
than to find full, powerful, and very troublesome reflex actions
taking place in the legs during evacuation of feeces or urine, in
consequence of colic pains, or during catheterization ; they often
continue for a considerable time in a semi-rhythmic manner. The
reflex actions which originate in tendons, fascie, and articular
ligaments are also very important. We have given above (see p.
48 et seq.) a brief account of their physiological occurrence ; in
pathological cases they often increase to such a degree that the
lightest tapping on the tendons leads to the most vigorous jerk-
ing; in this case the phenomenon can be produced from many
more tendons than usual; thus, I have seen them originate from
the ligamentum patelle, the tendo Achillis, the tendons of the
adductors, gracilis, biceps femoris, tibialis anticus and posticus ;
in the arm, from those of the triceps, supinator longus, radial ex-
tensors, flexors of the fingers, biceps, flexor radialis, etc. Their
relation to the reflex actions of the skin is very variable ; some-
times both are present and are exaggerated, sometimes those of
the tendons are absent while those of the skin are present, and
sometimes those of the tendons are enormously increased while
those of the skin are normal or diminished. These circumstances
are probably of great importance in a diagnostic point of view,
but this requires further observation.
The class of tendon-reflexions ought, in our opinion, to in-
clude a reflex phenomenon which has long ago been described
by French authors (Brown-Séquard, Charcot, Vulpian, Dubois,
and others)—namely, the reflex clonuws which appears in the foot
and lower leg when the foot is rapidly brought into dorsal flexion
by another person. If the fore-part of the sole is vigorously
pressed up with the flat of the hand, the rhythmic reflex con-
tractions of the calf produce a clonic tremor of the foot, which
continues as long as the pressure on the sole lasts, and ceases
immediately when the pressure is withdrawn or when the foot is
brought energetically into plantar flexion. When the reflex
excitability is greatly increased, the slightest pressure on the
sole is sufficient to set in motion the clonus; the action may
extend to the whole leg, and even to the other leg; in its most
violent forms, tetanic rigidity of the legs alternates with convul-
sive shaking, and we have the phenomenon described by Brown-
110 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Séequard and Charcot as spinal epilepsy (see p. 101). In my arti-
cle on Tendinous Reflex Actions’ I have attempted to prove that
this reflex clonus is nothing but a tendinous reflexion, produced
by the sudden tension of the tendo Achillis, and maintained in a
very simple way by the continued pressure against the foot. I
have recently succeeded more than once in producing just the
same phenomenon from the tendo patelle, and have observed it
in the biceps femoris. It also occurs in the foot, when the skin is
irritated, if the excitability is very much exalted. I have ex-
plained (p. 50) the mechanism of this. It cannot be denied that
the phenomenon may possibly be produced directly from the
skin in many cases; but we require more convincing proof than
Joffroy* has brought forward.
The increase in reflex activity may manifest itself in the 77-
testines and the vaso-motor apparatus ; but this has been little
studied in the human subject. For example, I have observed
in paraplegic patients that a sudden discharge of urine can be
produced by external pressure upon the bladder, or by introduc-
ing the finger into the rectum; I have also seen a mucous fluid
evacuation of the bowels occur regularly upon the occasion of
dressing and cleansing a large bed-sore ; I also have seen erections
produced by irritation of the skin of the penis or perineum, or
by introduction of a catheter, etc. It is probable that a closer
inspection will frequently discover a reflex action upon the cuta-
neous vessels, etc.
This excess of reflex action is explained, first by a separation
of the reflex apparatus from the brain, which puts a stop to the
action of the centres of inhibition. In fact, the highest degree of
excess is found in all those affections of the spinal cord which
put a complete stop to the transmission of impressions in the
cord; in separation or compression, in circumscribed transverse
myelitis or softening, in tumors or cavities of the cord, ete. It
must be considered an indispensable condition for the production
of the reflexions, that the gray substance situated below the
point of lesion should be intact ; and it is not strange that parts
1 Arch. f. Psych. u. Nervenkr. Bd. V. p. 792.
® Gaz. méd. de Paris. 1875. Nos. 33, 35.
GENERAL SYMPTOMATOLOGY. 111
which have retained their reflex excitability usually possess also
their electrical excitability, because the gray substance is the
essential factor in the conservation of the nutrition of nerves and
muscles.
The second cause of increased reflex action is the increased ex-
citability of the gray substance—a condition which may certainly
be produced by inflammatory and other irritative conditions, by
many sorts of disturbance of nutrition, and by certain poisons,
as strychnia, opium, belladonna, etc. The greatest increase will
be found when both these causes act together, as in the case of
myelitis from compression, or when strychnia is acting on the
paraplegic parts ; this is confirmed by daily experience.
Whether an increase of the excitability of the sensory con-
ductors (hyperzsthesia), or of the motor conductors (convulsi-
bility) is capable by itself of producing an increase of reflex ac-
tivity, is a point which requires closer examination, but is not
improbable a priori,
4. Vaso-motor Disturbances.
These are very frequent. They consist of the two conditions
of spasm and palsy of the vessels, with the consequences. In
view of the complicated mechanism for innervation possessed by
the vessels, explained on page 42, it is extremely difficult to inter-
pret these phenomena, especially as there are many others to be
taken into consideration along with them.
The following appear to constitute the principal facts :
In many cases local hyperemia and fluxion, increased rea-
ness, and elevation of temperature occur in the parts affected
(usually paralyzed); thus, for example, in complete severance or
compression of the cord, of acute origin ; and most distinctly of
all, in unilateral lesions, where the difference between the dis-
_ eased and the well side is very striking. If the lesion is entirely
local, and the vaso-motor centres situated within the cord are
left nearly intact, the normal condition returns after a short time.
_ In such cases the symptoms of vascular paralysis are mostly
temporary, and the normal condition returns after some weeks
or months; while at a later time paleness, diminution of tempera-
112 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
ture with subjective feeling of cold, and even cyanosis, are very
often observed.
In other cases, especially in the early stages of tabes or mye-
litis, before any symptoms of palsy appear, there is a striking
coldness, great paleness, and anemia of the lower extremities,
a tendency to goose-skin, the subjective feeling of icy coldness of
the feet and inability to warm them even in bed, a small pulse,
excessive sensitiveness to the impressions of cold, ete. It can-
not be doubted that these phenomena are due to conditions of
abnormal excitability of the vascular nerves, with increased con-
traction and excitability of the vessels.
Finally, in very severe or old cases (usually of spinal palsy)
we observe, in connection with the subjective and objective cold-
ness of the parts, a marked lividity, a cyanotic tinge of the skin,
puffiness, swollen veins and capillaries, slow and poor circula-
tion ; in this case there evidently exists a state of great vascular
atony, and a more or less distinct venous stagnation; the arterial
pressure is lessened, the venous increased, the circulation re-
tarded.
These three groups of vaso-motor disturbances may be natu-
rally interpreted by what we know of the laws of vascular inner-
vation.
In the first group— paralytic hypereemia—we should recall
the hundreds of experiments that have been made upon section
of the cord; every such section produces paralytic hypereemia in
the parts situated behind it. Goltz has shown how, when the
_ spinal centres recover themselves, the circulation may return to
nearly its normal point; only when the destruction of these
centres is quite extensive (as in spinal apoplexy, hematomyeli-
tis, etc.) will the fluxion and elevation of temperature be more
permanent, and finally result in atony of the vessels.
For the second group —ischemic pallor and coldness —ab-
normal excitement of the vaso-motor centres and conductors is
doubtless responsible ; they are most frequently caused by chro- —
nic inflammatory conditions of the cord, and may be produced
either directly or reflexly. |
In the third group —atonic hyperemia by stagnation —it is
commonly supposed that the absence of muscular action in the
LES ID ag AG ELA AO ALOIS ae,
GENERAL SYMPTOMATOLOGY. 113
palsied limbs produces disturbances of the venous circulation,
and thence gives rise to the other symptoms. It may, however,
be easily seen that this cyanosis occurs in parts which are not
at all palsied, and may be absent in completely palsied regions.
The assigned explanation, therefore, is at least insufficient ; the
absence of muscular contraction may favor the production of
atonic hyperzemia, but cannot by itself produce it. It seems to
us that, in order to produce such results, a more or less general
palsy of the vaso-motor nerves is required, such as is produced
either by destruction of the vaso-motor centres in the gray sub-
stance, or by interruption of the vaso-motor conduction in the
lateral columns or the anterior roots. The longer this paralysis
exists, and the more complete it becomes, the more marked will
be the vascular atony. Spinal palsy of children (destruction of
the vaso-motor centres in the gray substance) is a good example
of the former case ; in disease of the lateral columns the question
has not been fully studied, but in one case of probable sclerosis
of the lateral columns I have observed an exquisite development
of the atonic hyperemia of stagnation.
Conditions of great vascular irritability in the skin are oc-
casionally observed ; sudden blushing or paling of certain por-
tions of skin, erythema fugax, etc. They appear most frequent
in association with meningitic conditions.
It therefore appears plainly that vaso-motor disturbances
may afford us some information respecting the nature of the
disturbances in the cord, but enable us to draw no certain con-
clusions respecting its exact locality.
5. Trophic Disturbances.
These constitute one of the most interesting, and also one of
the obscurest symptoms of spinal disease, and there is still a
great deal of controversy in regard to their interpretation. We
must necessarily speak of the different tissues separately, in our
enumeration of these symptoms.
The trophic disturbances of nerves afd muscles have received
great attention, especially in spinal diseases; it has very lately
VOL. XIII.—8
114 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
been discovered that they may occur apart from palsy, becoming
a subsequent cause of palsy, as in the typical form of progres-
sive muscular atrophy.
But it is not all the forms of spinal paralysis that are accom-
panied by considerable trophic disturbances of nerves and mus-
cles. In many cases the nutrition and the electrical excitability
of these parts suffer not the slightest change; such cases are
always due to circumscribed disease of the entire transverse sec-
tion of the cord, or a disease of the white substance, which may
be of great extent. The affection of these parts seems, therefore,
to have nothing to do with the nutrition of the nerves and mus-
cles ; an inference which is certainly correct in regard to the
entire posterior columns and the posterior section of the lateral
columns, but is still doubtful in respect to the portions of the
anterior columns which are traversed by the anterior roots. It
seems certain, however, that in all cases of paraplegia without
atrophy the gray substance—at least that of the anterior columns
—is not altered to any considerable extent.
There are also cases in which a simple atrophy of the muscles
occurs, which may make great progress, and may even emaciate
the legs to the condition of a skeleton ; the histological condition
of the muscles remaining for the most part intact, with only a
diminution of the breadth of the fibres, and in places a certain
increase of interstitial fatty tissue, but without a trace of pro-
liferation of interstitial connective tissue, of multiplication of the
nuclei in the muscles, etc. In correspondence with this condi-
tion, the electrical excitability remains entirely intact, with, at
the most, a slight quantitative diminution, and the reflex actions
are mostly present. .
This form of atrophy occurs in the later stages of tabes, in
many cases of chronic myelitis, in paralyses due to compression
from vertebral caries, etc.; it appears most frequently to attack
persons who are debilitated or weakly. This simple atrophy is |
commonly referred to the palsy, the long-continued disuse of
the parts, but we are not content with this explanation in all —
cases. We cannot but think that certain distinct changes in the —
spinal cord must exist before this form of atrophy can come to
pass. At all events, this question is still in great need of inves-
GENERAL SYMPTOMATOLOGY. 115
tigation, both in its histological and its pathogenetic relaticns.
Our present knowledge of it is extremely small.
The same is true to a certain point of the most important
form of disease of nutrition in nerve and muscle, the degenera-
tive atrophy. In certain spinal affections, this is developed very
quickly and in a strongly-marked form. Although the histologi-
cal account of this disease is in many respects defective, espe-
cially in the earlier stages, yet our present knowledge, in connec-
tion with the results of electrical examination (which invariably
gives the ‘‘reaction of degeneration’’) points with tolerable cer-
tainty to the conclusion that the essential histological changes
are the same as those which so invariably follow severe traumatic
lesions of peripheral nerves—fatty degeneration and atrophy of
the nerve-fibres, simultaneously with proliferation of cells and
hyperplasia in the neurilemma; atrophy with increase of nuclei
and chemical changes in the muscular fibres, simultaneously with
proliferation of the interstitial connective tissue ; and in the last
stages excessive loss of muscular substance and transformation
into connective tissue with secondary deposition of fat. We
would refer the reader to the full description of degenerative
atrophy of the nerves and muscles given in Volume XL., p. 411.
We are convinced that the changes are essentially the same ; it
remains, however, to be decided by more careful examination
whether the process in spinal diseases runs its course with the
same rapidity and intensity as in traumatic palsies, and whether
there are not certain differences in degree, which require further
statement.
This degenerative atrophy occurs regularly in the so-called
spinal palsy of children and the analogous affection of adults ; it
is regularly found in the typical form of progressive muscular
atrophy (atrophie muscul. progress. protopathique of Charcot) ;
it appears to occur also in the sclérose latérale amyotrophique
_ described by Charcot,' and in many other spinal affections, when-
ever they implicate the gray substance of the anterior cornua.
The past few years have given us a series of discoveries in
relation to the spinal palsy of children and progressive muscular
=
’ Lecons sur les maladies du systéme nerveux. II. Sér. 3. fascic. p, 213 et seq. 1874.
116 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
atrophy (which we may regard as types of the spinal affections here
considered), which indicate a great improvement in our knowledge
of the trophic functions of the spinal cord. It has been shown
that these diseases are uniformly associated witk an affection of
the anterior cornua, in the former case acute, in the latter chronic,
which regularly and in quite a peculiar way involves the great
motor ganglion cells. The most recent observations, without ex-
ception, state this point, which was formerly almost always
overlooked, owing to defective methods of examination. It
would lead us too far, if we were to undertake to enumerate and
criticise all these observations. "We would refer to the memoirs,
chiefly published in the Archives de physiol. norm. et pathol., by
Charcot, Joffroy, Hayem, Duchenne, Vulpian, Pierret, Gombault,
Troisier, and others, and the experiments of Voisin and Hanot,
Lockhart Clarke, Roger and Damaschino, Roth, and others,
which are thoroughly convincing. These observations contain in
addition a series of facts which decidedly refute the view that the
affection is due to an inflammation conducted from the primary
focus in the cord to the nerves and muscles; but further special
observations on this point are desirable. Observers are not
agreed as to whether the change of the ganglion cells is primary,
or whether it is the consequence of an interstitial myelitis. That,
however, is a subordinate question, as concerning the object of
our study. It appears to be certain, at any rate, that functional
injury or destruction of these great ganglion cells of the anterior
columns is most closely related to degenerative atrophy of the
nerves and muscles.
It certainly can hardly be doubted any longer that the trophic
centres for the motor nerves and muscles are situated within the
gray substance of the cord, very close to the point where the
anterior roots of the nerves concerned enter. While this is ren-
dered exceedingly probable by the above facts of local destruc-
tion of the anterior cornua, it is on the other hand strongly sup-
ported by the fact that the degenerative atrophy is absent, even
in cases of the severest spinal paraplegia, when the correspond-
ing sections of the gray substance are intact. Compare upon this
point two cases given by Burckhardt.’
) Physiol. Diagnostik der Nervenkiaakh. p. 264. Beob. 45 und 46.
GENERAL SYMPTOMATOLOGY. 117
Of the nature of the connection between these trophic centres
and the peripheral parts, of the manner in which, and the chan-
nels through which their influence is distributed from the one to
the other, we are ignorant ; and the boldest hypotheses are allow-
able. Anatomy and physiology are not informed of the exist-
ence of proper trophic nerve-paths ; but of those who write upon
the subject, one party regards them as a physiological postulate,
while the other refers the transmission of trophic influences to
the motor and sensory fibres. I have attempted to show,* by the
comparison of a series of mutually corroborative cases, that the
trophic paths cannot be fully identical with the motor. Those
facts certainly show that the motor and the trophic paths must
be distinct at some points, as they are capable of being diseased
_ independently of each other. Such separation certainly exists in
_ the central organ ; but it is as yet doubtful how far outwards it
_ extends—whether motor and trophic fibres run separately as far
_ as the periphery, or whether the motor fibres are also capable of
. conducting the excitation from the trophic centres. Burck-
’ hardt’* is of the latter opinion, and claims for the great ganglion
- ¢ells of the anterior cornua the function of centres of nutrition
for the motor fibres which pass from them, and for the muscles.
In fact, the recent investigations into the structure of the gan-
glion cells furnish a ready and plausible form for conceiving of
the double or manifold functions of these great ganglion cells.
_ If the plan which Max Schultze’ gives of the fibrillary structure
of the ganglion cells is correct in the case of the human subject
-—and that can hardly be doubted —it can easily be conceived
how such a cell may form the point of union of fibrils of the
‘greatest variety of physiological rank (motor, co-ordinatory,
_reflectory, etc.), which unite, in part, in the nerve-process, and
enter the anterior roots. While thus the cell serves as the point
; of union for these various fibres, it is also capable of acting as a
‘trophic centre for them, and of sending from its own substance
_ trophic fibrils to the anterior root-fibres. The well-known fibril-
'Bin Fall von Bleilihmung. Arch. f. Psych. u. Nervenkrankh. Bd. V. 1879.
_ p. 445. >
. ? Loc. cit. p. 271.
® Stricker’s Handb, der Gewebelehre. p. 130.
“7
118 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
lary composition of the axis-cylinder would even permit us to
dispense with the hypothesis of trophic nerve-fibres, as the axis-
cylinder of the motor nerve may easily be supposed to contain
fibrils of: very various physiological functions. We will not,
however, enter too far into the field of purely hypothetical con-
siderations.
One last question is still awaiting a decision—the question
whether the processes of degenerative atrophy should be referred
to an irritation or a palsy of the trophic central apparatus.
_ Charcot’ is of the former opinion, thinking that irritation of the
trophic ganglion cells and the trophic fibres produces degenera-
tive atrophy, while simple paralysis, or separation of the cells
from the peripheral parts, leaves the nutrition of the latter intact.
He bases his opinion chiefly upon the supposed fact that crush-
ing, inflammation, and similar injuries of the peripheral nerves
act in a different way from simple section ; in the latter case the
characteristic histological changes being supposed not to occur.
The incorrectness of this position is sufficiently proved.* The
processes of infantile spinal paralysis also render this assump-
tion quite impossible; for, firstly, the initial phenomena, the
complete palsy, etc., make an increase of the activity of the
ganglion cells very improbable; and secondly, the complete dis-
appearance of the cells, which is demonstrated in the later stages
of all such cases, would necessarily (upon Charcot’s theory) re-
sult in repair of the disturbances of nutrition, so that the nerves
and muscles would return to their normal state — which is the
contrary of what we know to be the case. We are, therefore,
at present of the opinion that a paralysis or destruction of the
central trophic apparatus, or a separation from the peripheral
parts, produces the symptoms of degenerative atrophy. ‘This
may make the matter harder to understand, but we are obliged
to take the facts as they are.
Upon the whole, we are justified by the present state of our
knowledge in assuming a disease of the anterior cornua when the
electrical examination shows the existence of the reaction of de-
1 Lecons sur les maladies du systéme nerveux. 1872-3. pp. 19, 23, and ch. 2.
2 rb, Zur Pathol. und pathol. Anat. peripherer Paralyse. Deutsch. Arch. f. klin,
Med, Bd. V. p. 58.
SE Sa eaghee Oe Cary St eae ee eye
ae ee .
-% 6h] ;
WET CORE Pye RR Pe “se i
GENERAL SYMPTOMATOLOGY. 119
generation, and consequently of degenerative atrophy of nerves
and muscles, provided the disease is clearly of spinal origin.
It is well known that an increased deposit of fat in the interstitial connective
tissue of the atrophied muscles is not rare in the later stages. I have very recently
seen a case of palsy from spinal apoplexy, in which the muscles of the calf, at first
atrophied, became by degrees excessive in size, probably from deposition of fat,
the paralysis continuing.’ This is a kind of pseudo-hypertrophy of the muscle. But
it is still a controverted point whether the peculiar disease known by this name
(also atrophia musculorum lipomatosa, paralysie musculaire pseudohypertrophique,
etc.) is of spinal origin; Charcot, Eulenburg, and Cohnheim are opposed to this
view; L. Clarke, O. Barth, and others, are in favor of it; Friedreich considers the
disease as a mere progressive muscular atrophy modified by certain peculiarities of
infancy; and W. Mueller likewise considers the lipomatosis as a more or less acci-
dental complication of the atrophy. At all events, we must wait for further investi-
gation of the matter.
The same must be said of those cases of true muscular hypertrophy—rare at pres-
ent—which have been found sometimes alone (Auerbach, Berger), and sometimes
_ accompanied by progressive muscular atrophy (Friedreich*). The neurotic origin
of these cases cannot at present be established. They should not be confounded
_ with the hypertrophy from use, which occurs here and there in muscles which have
had to do double duty on behalf of paralyzed ones. A good instance of this is
presented by the left sartorius, in the case described by me, as above mentioned.*
4 Trophic disturbances in the structures of the skin are very
- common in spinal disorders. Those of the epidermoid structures
are of subordinate importance, although their theoretic interest
- is considerable. For instance, in some cases of spinal palsy an
abnormal growth of hair* has been observed. Closely associated
with other disturbances of the skin, with atrophy of the muscles,
etc., occur decided alterations of the nails, deformity, increased
curvature, and furrowing, clubbed swelling, yellowish or brown-
ish discoloration, and the like. The changes of the skin itself
are more important.* First, and not infrequently, erythematous
SS
1 Arch. f. Psych. u. Nervenkrankh. Bd. V. Heft 3. p. 782.
2 Ueber progress. Muskelatrophie, ueber wahre und falsche Muskelhypertrophie.
Berlin. 1873. Cap. VI.
8 Loc. cit. Bd. V. p. 780.
4 Jelly, Brit. Med. Jour. 1873. June 14. >.
5 Compare in particular the beautiful account given by Charcot in his Clinical Lec-
tures,
120 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
spots and eruptions, which may appear almost anywhere, and
usually are very transient; then lichenoid or papulous erup-
tions, extending over greater or smaller portions of the skin,
often restricted to the district of a single nerve or to a single
limb; not infrequently wheals of wrticaria, of greater or less
size and extent, usually accompanied by violent itching; or
herpes zoster, in its characteristic mode of appearance; and
finally, in rare cases, pustule-formation, related to pemphigus
and ecthyma, and usually leading to ill-looking and badly-heal-
ing ulcerations.
Besides these alterations, which remind us of the appearances
of well-known and typical diseases of the skin, there occur others
of a more diffuse sort; uniform thinning of the skin, abnormal
smoothness and shining look of the epidermis, connected with
more or less livid redness (‘‘ glossy skin’’)—changes of which
we have spoken in Vol. XL, p. 409, under Paralyses; on the
other hand, there are often abnormal thickening and swelling of
the skin and subcutaneous cellular tissue, not seldom connected
with cedema, or gradually developed from it.
Our knowledge of the theory of all these phenomena and
their special connection with the spinal cord and with the dis-
eases of certain sections of it, is still very defective. The idea
that they may be of neurotic origin is hardly yet familiar, but
from what parts they may originate, and how, is still a matter for
guesses merely. In some cases they are usually associated with
violent sensory phenomena (the lancinating pains of tabes, etc.) ;
hence it has been inferred that they might depend on an irrita-
tion of trophic fibres—a position which is strongly supported by
the manner in which herpes zoster occurs in neuralgia and after
neuritis ; on the other hand, it is not to be denied that another
group of these phenomena occurs only under circumstances
which almost conclusively point to paralysis of the trophic paths.
At present it cannot be decided with certainty what special part
the irritation or paralysis of trophic fibres takes in the produc-
tion of cutaneous changes. .
The peripheral channels through which the trophic influence
passes to the skin and its adnexa appear beyond a doubt to lie
in the sensitive nerves ; this is supported by a large number of
OO ae
GENERAL SYMPTOMATOLOGY. 121
unquestionable facts. But it is still doubtful where the centres
for the nutrition of the cutaneous structures are situated. They
appear, at all events, not to be in the anterior cornua; this fol-
lows from our experience in regard to the spinal paralysis of
children. And, as the gray substance is the only probable
region, there remain only the posterior cornua, or the spinal
ganglia; the latter site has been rendered probable by many facts,
and is accepted by several authors. We must leave it for the
future to establish the influence of these structures upon the
nutrition of the skin.
By far the most important trophic disturbance which the skin
experiences in spinal disease is gangrene from pressure or bed-
sore. Its occurrence is a sign of the greatest danger, and is often
decisive of the prognosis. In practice it is well to distinguish
two forms: the one is acute, is caused by slight irritation or brief
pressure, is preceded by an inflammatory eruption, appears a
few days after the beginning of the central lesion and leads
rapidly to gangrenous destruction (decubitus acutus of Samuel) ;
the other, more chronic in its origin, accompanies the later course
of spinal diseases, is chiefly dependent on prolonged pressure,
and takes the form of simple gangrenous death of the skin and
the subcutaneous tissue (decubitus chronicus).
Decubitus acutus, of which Charcot (l. ¢.) has given a very
vivid picture, usually begins a few days after any severe spinal
lesion or after a severe exacerbation of a spinal disease, and is
characterized by a very rapid development. Upon a portion of
skin which has been exposed to pressure or to any irritation
{and often when no such circumstance has occurred), erythema-
tous spots appear, which are soon covered with vesicles, the con-
tents of which, at first clear, become rapidly brownish or reddish ;
under favorable circumstances these vesicles may dry up, and
the spot recovers without further change; but this is not com-
monly the case; the vesicles burst and leave ill-looking ulcera-
tions, the basis of which is composed of the skin, infiltrated with
blood, and usually in a state of phlegmonous inflammation. The
base of the ulcer perishes by gangrene, the neighboring skin is
infiltrated with blood, and inflamed to" greater and greater ex-
tent, the gangrenous destruction goes deeper and deeper, laying
122 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
bare and including in its destructive operations tendons, fascia,
ligaments, and bones.
This entire cycle of processes is complete in a few days, and
cannot be avoided by any care or cleanliness; at the same time,
cystitis and hematuria are sometimes observed, or the muscles
become the prey of a rapid atrophy.
The consequences of such extensive gangrene soon appear;
violent fever with severe chills and great variations of tempera-
ture, a septiceemic condition, purulent infection, gangrenous
thrombosis and embolism occur, and the fatal result is preceded
by a general marasmus; or the gangrene extends still further
into the interior of the vertebral canal, when a purulent or icho-
rous meningitis, rapidly ascending to the cranium, soon closes
the painful scene.
Simple chronic decubitus usually originates in a somewhat
different way. In chronic diseases of the spinal cord, in para-
plegias, there is seen a diffuse dark redness of the portions which
are most pressed upon in sitting or lying; often mingled with
superficial ulcerations. Some day there appears upon this red-
dened portion of skin a black spot, which rapidly enlarges if the
pressure is continued. The skin dries to a black leathery mass,
around which a bounding line of inflammation soon appears,
which under proper treatment leads to a throwing off of the gan-
grenous layer, and cleaning up of its base, with the formation of
eranulations. But if the pressure is continued, the ulcerated
surface assumes a bad, unwholesome color from infiltration with
blood, the inflammation assumes an appearance more like that
of a phlegmon, and the gangrene may spread rapidly, deeply, and
cause horrible destruction. And then the symptoms above
named as characteristic of acute decubitus appear and soon put
an end to the patient’s life.
This form of gangrene may occur at any place which is
exposed to a continued pressure, but is far the most common on
the coccyx and buttocks, next over the trochanters and ischiatic
protuberances, heels, and knees, the spinous processes of the
vertebree, the shoulder-blades, elbows, etc. In severe cases of
this sort, the patient, with his numerous large sores, presents the
very picture of wretchedness. Nor is the end of this misery
—e ol oe,
GENERAL SYMPTOMATOLOGY. 123
always speedy ; if attention and care be given, the sores often
clean up, good granulations appear; but the tendency to heal is
very slight, and it is a desperate while before cicatrization occurs.
I have seen a patient, who had nine large bed-sores and several
small ones, linger along for over a year under faithful care.
Though some places may cicatrize, a new sore will appear here
or there; the occurrence of bed-sores, therefore, unless they
improve rapidly and considerably, must always be considered a
very bad omen for the patient. The occurrence of acute decubi-
tus renders the prognosis extremely bad in all cases.
Very various accounts are given of the way in which bed-sores
originate. :
Continuous pressure is commonly thought to be the chief
cause of the bed-sore ; its action is supposed to be considerably
favored by the complete immobility of paralyzed patients, by the
absence of sensation in some others, by the filth from the bladder
and rectum which is liable to accumulate; the more of these
causes are present, the more confidently is the occurrence of bed-
sores expected.
In fact, we may count with certainty on the appearance of
bed-sores when all these causes coincide. But this by no means
proves that the sores are due to such causes. In acute myelitis
of the anterior columns (spinal paralysis of children, etc.), in
many forms of hysterical palsy, in fractures of the thigh, and
similar cases, we find abundant proof that long-continued pres-
sure, palsy, etc., are not by themselves adequate to produce bed-
sores. Charcot has seen decubitus acutus occur, even when all
pressure and all befouling of the person was avoided.
It seems therefore absolutely necessary to seek for another
explanation. The vaso-motor paralysis, which is commonly
present, and the anesthesia, have been thought of ; but it is easy
to prove that this view is incorrect, and that both these circum-
stances act only as facilitating the action of pressure, which itself
is not the essential element in the production of bed-sores.
- It is manifest that there must be some very special changes in
the nervous system, special influences added or subtracted, in
order to produce such fearful gangrenous destruction in patients
whose general health is good, and the action of their hearts
124 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
vigorous. Such influences may most properly be called trophic.
In chronic decubitus we may assume that the trophic disturb-
ances cause a diminished power of resistance, a lessened vital
turgor, on the part of the skin, which, in connection with the
weakness of the circulation caused by the vaso-motor paralysis,
probably explains the gangrene of pressure ; as to acute decubi-
tus, Charcot believes that he has proved that it is caused by a
‘‘violent irritation of a more or less extensive district of the
spinal cord.”’
Acute decubitus is found associated chiefly with severe trau-
matic lesions of the cord (compression and destruction en masse
by fractures of the vertebre, etc.),in acute myelitis, hematomy-
elia, and the like; it has also been observed in unilateral trau-
matic lesions of the cord, upon the anesthetic side only, not on
the paralyzed side. Chronic decubitus is found in chronic myeli-
tis transversa (affecting the cord diametrally), in the last stages
of tabes, in paraplegiz of slow origin, and similarly also in peri-
pheral palsies in the district of the cauda equina. If the latter
originate acutely, ¢. g., by fracture of the sacrum, they may
themselves be followed by acute decubitus.
It seems to us that the one element which the above affections
share in common is rather the destruction and paralysis of cer-
tain parts than their irritation, and we think it most probable
that the chief cause of the decubitus in spinal affections is the
paralysis of certain trophic centres in the cord, or their severance
from the peripheral parts; in certain cases of acute decubitus,
however, it is not yet proved that the disease does not originate
in irritation.
The exact location of these trophic centres is as little known
to us as is the way in which they exercise their trophic influence
upon the skin. Many things render it probable that they are to
be found in the gray substance, especially in the central portions
and the posterior cornua, and that the paths which begin in
these parts are situated in the posterior roots. Observations of
unilateral lesion of the cord have also made it probable that the
trophic fibres for the skin decussate in the cord like the sensory
fibres. The relations of the spinal ganglia to these processes are
not clear.
:
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;
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GENERAL SYMPTOMATOLOGY. 125
The conclusions in regard to the seat and nature of the spinal
affection, which are to be drawn from the occurrence of bed-
sores, are obvious.
The dones often undergo trophic disturbances in spinal dis-
ease. One of the commonest symptoms in the spinal paralysis
of children is arrest of growth of bones. The bones of the ex-
tremities remain short and small, the limbs are shortened, the
pelvis displaced, and the spinal cord in consequence curved. If
a series of cases be compared, it will plainly appear that this
impairment of growth is not always proportional to the muscular
atrophy or the degree of palsy ; it is to a certain extent indepen-
dent of these circumstances, and in such cases the paralysis and
muscular atrophy may be the chief feature in one limb, and the
atrophy of the bone in the other.
In other cases, on the contrary, a swelling, thickening, hy-
pertrophy of the bones is observed ; they become heavier, and are
often greatly enlarged, especially at the joints. This condition
may coexist with pseudo-hypertrophy of the muscles, or with
degenerative atrophy. A closer examination, however, shows
that in all such cases the essential element is a hyperplasia of
connective substance, both in the bone-tissue and in the muscles.
An abnormal brittleness of the bones has been observed in
very rare cases.
There can be no doubt that the majority of these changes
depend on disturbances of the nervous system. The facts of
infantile spinal paralysis render it almost certain that the trophic
centres for bones are in the anterior cornua, but that they are
‘certainly not identical with those for the muscles. Further
exact study of these conditions is needed.
Especial attention has been lately given to the trophic dis-
turbances of the joints, which occur in many spinal diseases, and
are very interesting.
It is very common, both in spinal and peripheral palsies, to
find slight swelling, stiffness, a little pain, and a moderate
amount of ankylosis of the joints. This is probably due in part
to long disuse, and occurs in like manner after the long wearing
of a plaster of-Paris bandage, but it ig partly, no doubt, of ner-
vous origin.
126 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Charcot’s admirable researches’ have very recently placed
before us an extremely characteristic affection of the joints, of
manifestly nervous origin, chiefly associated with tabes ; its char-
acteristic symptoms are an abundant serous discharge, wasting
of the cartilages and bones, subluxations, and the like. This is
the so-called spinal arthropathy of tabes.
This affection of the joints is very strikingly different front
the ordinary spontaneous inflammations of a rheumatic or trau-
matic origin. It much prefers the knee-joint ; after that, in
diminishing frequency, the shoulder, elbow, hip, and wrist joints.
It begins, usually suddenly and unexpectedly, without any ex-
ternal cause, and its first symptom is a large diffuse swelling of
the joint, caused by an abundant exudation of serous fluid in
its cavity ; fever, redness, and pain are usually altogether want-
ing. The adjoining parts are always considerably swollen, which
often extends to nearly the entire extremity. This swelling is
partly cedematous, and partly of a harder nature. It usually
disappears in a few days and the articular effusion likewise,
after which the ends of the bones come in contact, are worn
away and their cartilages and ligaments destroyed; these
changes are indicated by a good deal of cracking and rubbing
noise in the joint. Deformities of the joints are the result—sub-
luxations, loose joints, and the like. This may continue for
months or years and then disappear, but usually the changes
which result are incurable.
These advanced stages, when examined anatomically, exhibit
the marks of arthritis sicca, but with this distinction: that the
erosion of the articular extremities is considerably greater than
the growth of new bone.
This arthropathy is most common in the early stages of tabes,
and chiefly in the preliminary period, before the atactic disturb-
ances of motion have appeared, and when the lancinating pains
constitute the chief feature of the complaint. It has, however,
been observed in the same, or nearly the same, form in compres-
1 Cf. Charcot, Arch. de Physiol. 1. 1868; II. 1869; III. 1870 (with Joffroy); and
Clinical Lectures on Diseases of the Nervous System. I. and II. series.— Ball, Gaz. des
Hop. 1868 and 1869.—Buzzard, Lancet. 1874. Aug. 22.— Weir Mitchell, Amer. Journ.
Med. Sci. April. 1875. p. 8389.—See also below, section on Tabes Dorsalis.
GENERAL SYMPTOMATOLOGY. 127
sion of the cord from vertebral disease, in acute myelitis, progres-
sive muscular atrophy, traumatic unilateral lesion of the cord
(on the palsied side), etc.
It can hardly be doubted that this arthropathy depends on
disturbances of the nervous system. Charcot has supposed that
they were referable to a pathological irritation of central trophic
apparatus, and has, in fact, found in autopsies of tabetic patients
suffering from this arthropathy, an atrophy of corresponding
portions of the gray anterior pillars and disappearance of their
ganglion cells. But in a later case he has failed to find this
lesion, in spite of careful search, which discovered marked altera-
tions in the spinal ganglia. Further examination is therefore
needed to decide this difficult question. The rarity of the arthro-
pathy in spinal palsy of children, and its close connection with
tabes, certainly require of us great care in forming an opinion.
Of trophic disturbances of the intestines in spinal disease we
know little, and this little will be set down under the proper
heads hereafter.
The general nutrition, in most spinal diseases, suffers only in
very exceptional conditions, or when the duration is very pro-
tracted. It is not rare to see a spinal patient in the most hope-
less case—paraplegic, or excessively atactic—confined to his bed
or the wheeled chair, who nevertheless looks very well in com-
plexion, is muscular and plump, has a good appetite and diges-
tion, and for years and tens of years enjoys a tolerable existence.
In other cases the nutrition fails fast, the general health is much
impaired, the patient sinks rapidly into marasmus. The causes
of this loss of health are as follows: continued rest, want of
motion and fresh air, poor digestion, severe pain which takes away
sleep, fever, malignant new-formations, and, above all, cystitis
and bed-sores. We shall see in the course of this account that
these causes are very frequent, and accompany all sorts of spinal
disease.
The state of the general bodily temperature, and the fever of spinal diseases, may
here be mentioned. The local changes of temperature, limited to single extremities
or parts of bodies, are accounted for by the vaso-motor disturbances
128 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Inflammations of the cord are accompanied by fever, like those of the other
organs, Its type and course will be described under the several diseases of the
cord, as acute meningitis, acute myelitis, acute spinal paralysis, paralysis ascendens
acuta, etc, Fever also occurs in consequence of many complications of spinal dis-
ease, as in gangrenous bed-sore, etc. This is of subordinate importance at present.
On the other hand, the often enormous rise of temperature which accompanies
or closes many severe spinal diseases, and which is of great theoretic interest,
deserves a brief mention here. This phenomenon is commonly ascribed to the
“‘neuroparalytic agony,” and has been frequently observed and several times criti-
cally described in severe disease of the various parts of the nervous system, espe-
cially in severe lesions of the cord!
The chief interest for us lies in those cases where, after crushing and injury of
the cervical medulla, the bodily temperature continued to rise, and finally reached
an enormous height (42.9-44.0° C.=109° to 111.3° Fahr.), followed by death. The
first case of this kind was observed by Brodie; other similar ones are given by
Billroth, Simon, Quincke, Fischer, and others. Unusually high temperatures have
also been observed in the agony of tetanus (Wunderlich), of meningitis cerebro-
spinalis (Erb), etc. Very lately, J. W. Teale’ has published a case of spinal
disease, perhaps inflammatory, caused by an injury, in which the axillary temper-
ature several times reached the incredible height of over 50° C. (122° F.) ; the case
nevertheless recovered.
With a view to explaining the connection between this rise of temperature and
the spinal lesion, various experimental observations have been made which, how-
ever, have not yet furnished conclusive results. It has been found that section of
the dorsal cord produced a depression, while section of the cervical cord in the
neighborhood of the pons produced a considerable rise of temperature (Tscheschi-
chin); that crushing of the cervical cord uniformly raised the temperature, if pe-
ripheral cooling was prevented by suitable measures (Naunyn and Quincke); and
finally, that an injury of the cervical cord produces no rise of temperature, provided
the anterior columns are spared (Fischer),
It would lead us too far, to attempt to give the conclusions drawn from these ex-
periments in respect to the exciting and moderating influence of the spinal cord upon
the development of heat. In doing it we should have to enter upon the theory of
fever, which is confessedly one of the most difficult parts of general pathology.
1 For further information see the following: Wunderlich, Archiv der Heilkunde, II.
p. 547; and III. p. 175.—Brodie, Med. Chir. Trans. 1837. p. 416.—Billroth, Beo-
bachtungsstudien iiber Wundfieber. 1862. p. 158.—Hrb, Deutsches Archiv f. klin. Med.
I. p. 175. 1865.—Tscheschichin, Reichert und Du Bois’ Archiv. 1866. p. 170.—Naunyn
and Quincke, Reichert und Du Bois’ Archiv. 1869. pp. 174 and 521.—Quincke, Berl.
klin. Wochenschr. 1869. No. 29.—H. Fischer, Centralbl. f. d. med. Wissensch. 1869.
No. 17.—R. Heidenhain, Pflueger’s Archiv. 1870. p. 578.—Riegel, Ibid. Bd. V. 1872.
p. 629.—Naunyn and Dubczanski, Arch. f. exper. Path. u. Pharmak. I.
* Lancet, 1875, March 6, p. 840 (Clinical Society of London).
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GENERAL SYMPTOMATOLOGY. 129
For the present it seems to us most natural to assume, with Naunyn and Quincke,
that in these experimental lesions of the cervical cord, as well as in those of a
pathological nature, there is a paralysis of certain paths which serve to restrict the
production of heat. At the same time, however, an extensive vascular paralysis
takes place, whereby an increased amount of heat is given off, which more or less
compensates for the increased production. According to the preponderance of one
or the other factor, the rise of temperature will be more or less considerable, or may
be absent or even a minus quantity. Here much plainly depends on accidental
external circumstances (temperature of the air, covering of the body, proportion of
surface to weight of body, etc.). It is found, however, that an increase of the bodily
temperature is most prominent in lesions of the cervical cord. The whole question
deserves a fresh investigation, in view of the recent discoveries of Goltz respecting
the vaso-motor centres in the cord.
The experiments cited have shown that in cases of section of the cord a lowering
of temperature often occurs, especially where the effect of the vaso-motor paralysis
is chiefly directed to the loss of heat from the surface. A similar condition exists
in many diseases of the spinal cord; mechanical lesions (Fischer, }. c., Nieder '),
chronic myelitis, the closing stage of tabes, etc. The temperature falls to 35°, 32°,
30° C. (95°, 90°, 86° Fahr.), or even lower; the patients meanwhile often live on for
days and weeks, These are probably sometimes the temperatures characteristic of
collapse, but at other times they are doubtless due to excessive loss of heat from
vaso-motor paralysis.
6. Disturbances in the Urinary and Sexual Apparatus.
These are among the most important symptoms, for they
always inflict great discomfort, and often influence the prognosis
seriously. Our acquaintance with them, it must be admitted, is
in many points defective.
a. Disturbance of the Secretion of the Kidneys.
But little is known of this at present, in spinal affections.
In various spinal lesions, especially the more severe and acute
forms, considerable changes in the character of the urine rapidly
appear, but it is not yet clearly settled how far the kidneys and
their innervation are directly concerned in this. After crushing
of the cord by fracture of the vertebra, after knife-wounds of the
cord, after spinal apoplexy, in acute myelitis, etc., we often see
— ns
‘ Med. Times and Gazette. 1873. No. 1180.
VOL. XIIL—9
130 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
the urine becoming turbid and slimy in a few days after the
event, with blood and pus, with alkaline decomposition and its
inevitable results, triple phosphates, and a horrible smell. It is
generally thought that this change is caused in the first place
by retention and ammoniacal decomposition of urine in the blad-
der, the result of which is a cystitis and an inflammation of the
kidneys, secondary to the cystitis. Rosenstein! believes that he
has obtained certain proof of this. But Charcot,’ in view of the
very rapid appearance of change in the urine, and the ecchymo-
ses and foci of inflammation repeatedly found in the kidneys very
soon after the spinal lesion, is forced to the conclusion that the
spinal affection may be of itself the eause of the acute inflamma-
tion of the kidneys, and he lays special weight upon the element
of irritation in these spinal lesions. Whether the case is similar
in chronic disease, or whether in the latter the affection of the
kidney is always secondary to that of the bladder, is likewise
undecided at present.
Still less is known about anomalies of secretion, or extensive
anatomical changes. The increased excretion of phosphates,
observed in many chronic spinal cases, occurs in many other
neuroses.
In respect to the alteration in the guantity of wrine in spinal
diseases very little information is furnished by human pathol.
ogy. An analogy with the temporary suppression of this secre.
tion, observed by Eckhard after section of the cord, may proba-
bly be found in a case of laceration of the cervical cord, observed
by Brodie, in which the quantity of urine passed was extremely
small. <A considerable increase of the secretion sometimes occurs,
a literal diabetes insipidus, accompanying spinal diseases (Fried-
reich, in degenerative atrophy of the posterior columns) ; it may
be assumed with probability in these cases that the process has
extended to the medulla oblongata.
1 Pathol. u. Ther. der Nierenkrankheiten. 2. Aufl. p. 287.
* Lecons sur les maladies du systéme nerveux. 1872-3. p. 117.
GENERAL SYMPTOMATOLOGY. 131
b. Disturbances of the Bladder and Changes in the Charac-
ter of the Urine.
Spinal patients, without number, are attacked after a longer
or shorter time by such disturbances, the occurrence of which
always marks an unfavorable phase of the disease, owing to the
difficulty of giving relief and the fact that they very often form
the starting-point of the most serious complications.
These disturbances almost always begin with the paralysis of
the bladder, so common in spinal complaints, and the consequent
retention and stagnation of urine in the bladder.
In the chronic cases, which are the more frequent, and in
which there is often no other complication than an incomplete
and an infrequent evacuation of the bladder, decomposition of
the urine occurs with slight alkalescence and deposition of con-
cretions in the bladder; the consequence of this is a catarrhal
cystitis, with formation of. mucus and pus, abundant develop-
ment of vibriones (which increases the facility of decomposition),
an alkaline reaction, and a foul ammoniacal smell of the urine.
Examination of the turbid urine shows a muco-purulent deposit,
a few blood-corpuscles, numerous crystals of triple phosphate,
vibriones, etc. The mucous membrane, at first in a state of catar-
rhal inflammation, is covered by degrees with erosions, is thick-
ened and swelled, contains hemorrhages and pigment-deposits in
its substance ; the muscular coat of the bladder is hypertrophied,
the wall of the bladder is thickened and retracted, etc. Purulent
pyelitis and purulent disseminated nephritis very soon appear.
This is the usual condition at the close of chronic spinal diseases
(myelitis chronica, tabes dorsalis, etc.).
In quite acute cases the affection of the bladder not rarely
opens with hematuria, with which are associated acute purulent
or even ichorous cystitis, pyelo-nephritis, etc., very quickly lead-
ing to the most extensive decomposition of urine with all its con-
sequences, high fever, urzemia, etc.
It remains to be proved whether the stagnation of the urine,
produced by the vesical paralysis, is th® sole cause of all these
disturbances, or whether, as is extremely probable in acute cases,
182 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
and is certainly possible in chronic cases, the lesion of the cord
of itself constitutes a distinct cause of this inflammatory condi-
tion of the bladder and all its consequences. We know nothing
certainly in respect to the nervous paths and centres in the cord
which are concerned in these processes.
But it is certain that these conditions of the bladder may lead
to the severest disturbance of the whole system, by the fever, the
loss of fluids, and the retroaction upon the kidneys, which are
associated with them.
ec. Disturbances of the Function of Urination.
This very common and important class of symptoms compre-
hends many varieties, differing in their origin and course, as
might be expected in the case of such complicated mechanism. —
In the chronic cases, which are by far the most common, the —
first symptom is frequently a certain difficulty in passing water ;
the patient has to wait a longer time than usual, has to press
more strongly in order to set the process going, and when the
stream comes, it is small and slow, and at the close there is a
more or less prolonged dribbling. Later, this increases more and
more, and actual retention of wrine occurs, which compels the
regular use of the catheter, or may produce the ‘‘ischuria para-
doxa,’’ in which a distended bladder keeps up a constant drib-
bling. It is, however, possible that the retention may go on to
the production of actual incontinence.
But, on.the other hand, énmcontinence of the bladder may be
the first symptom ; the patient has to make haste the moment
he feels the inclination to pass water; soon the discharge occurs
at the same time with the inclination, and at the last it comes
unexpectedly and involuntarily, is often quite unnoticed, and
passes into the bed, the clothes, etc., at any time. The discharges
may be considerable in quantity, and take place at certain inter-
vals, or they may be frequent and small, or the urine may drib-
ble constantly. Any of these disturbances may be further com-
plicated by the appearance of cystitis.
In acute cases (sudden destruction or squeezing of the cord,
myelitis acutissima, spinal apoplexy, etc.) complete retention
- — a ET eS SST OS ee
GENERAL SYMPTOMATOLOGY. 133
usually exists from the outset, or within a few days. In many
cases, as in experimental section of the cord (Goltz), it is merely
the result of concussion of the entire cord, and depends on paral-
ysis of the centres in the lumbar cord. Soon, however, the spon-
taneous (though not the voluntary) discharge returns, and passes
directly into incontinence. The form which is assumed by the
incontinence then depends essentially upon the seat of the lesion
and the secondary changes in the cord. There either occurs,
from time to time, a full, regular discharge of the bladder against
the patient’s will, and often without his knowledge—a sign that
the reflex centre in the cord is in existence and the detrusor is
not palsied—or there is ischuria paradoxa, an excessive fulness
of the bladder with continual dribbling, in which case either the
reflex centre is paralyzed and destroyed, or else the peripheral
paths are interrupted. The detrusor is paralyzed together with
the sphincter. The bladder is at first excessively distended,
often reaching nearly to the navel; but subsequently, owing to
catarrh of the bladder and hypertrophy of its wall, its dimen-
sions diminish continually, though the incontinence continues
unchanged.
Subsequently the symptoms may alter as partial improve-
ment occurs in one or another of the nerve-paths; but the above
description will be recognized as giving the ordinary traits of spi-
nal paralysis of the bladder.
With our present knowledge of the mechanism of the evacua-
tion of the bladder (see p. 54), it is not difficult to understand
how the various forms of paralysis originate. It is, however, in
special cases, often extremely difficult to decide which nervous
apparatus is involved, as most of the symptoms may originate in
more ways than one.
The complexity of these conditions will best be shown by a
brief mention of the disturbances which may follow lesions of
different portions of the paths which convey the innervation to
the bladder. The evacuation of the bladder may be interfered
with: 1, by lesion of sensory and motor peripheral paths ; 2, by
lesion of the reflex centres in the lumbar cord ; and 3, by lesion
of the sensory or motor paths which lead to the brain above the
lumbar region.
134 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
If the peripheral sensory nerves of the bladder are alone par-
alyzed, the patient will probably perceive no further impulse to
urinate, but will be able, from time to time, to pass water volun-
tarily by the action of the brain upon the centres in the lumbar
cord ; in this case the patient does not feel the evacuation. If
the motor nerves of the bladder are peripherally palsied, the
consequence will be retention with incontinence (ischuria para-
doxa), in which voluntary urination is impossible. If both sen-
sory and motor paths are paralyzed, as in lesions of the cauda
equina, ischuria paradoxa, or at least absolute incontinence, will
be the unavoidable result. (It is not yet established, whether the
bladder, deprived of its spinal innervation, may continue to con-
tract independently by virtue of the influence of the ganglionic
apparatus situated in its walls.) All this holds good, of course,
of the sensory and motor paths within the spinal cord previous
to their connection with the reflex centres.
If these centres are paralyzed or destroyed, the necessary
consequence will be complete retention followed by incontinence
(ischuria paradoxa). The utmost that can be accomplished by
the patient in such cases will be an incomplete evacuation by
the aid of abdominal straining.
If the sensory paths on the other side of (7. e., above) the lum-
bar cord are alone paralyzed, while the centres in the cord are
uninjured, a regular discharge of the bladder will occur from
time to time when it has reached the proper fulness; but the
patient feels nothing of it, and therefore cannot prevent its occur-
rence. If only the motor paths above the lumbar cord are pal-
sied, the patient can neither discharge his urine voluntarily, nor
arrest, by voluntary contraction of the sphincter, an evacuation
which has begun or is threatening; but he feels the inclination to
urinate, which immediately excites a reflex evacuation of the
bladder, withdrawn as it is from voluntary control. If all the
paths above the lumbar cord are paralyzed, the periodical reflex
discharges of the bladder take place without the patient’s feeling
anything of them, and without any power on his part to influ-
ence them. In most of the cases of this group the action of ab-
dominal straining will not occur; but this does not much alter
the symptoms.
c
GENERAL SYMPTOMATOLOGY. 155
We see that all the symptoms that have been described can
be thus naturally explained, and it is necessary in each case to
examine every circumstance with care, in order to ascertain the
precise seat of the lesion. Such experience will soon convince
us that the various forms of vesical palsy are very characteristic-
ally distinct ; it will be easy in particular to decide whether the
centres in the cord are in action or not, by irritating the wall of
the bladder and producing reflex evacuation. Many cases, how-
ever, in which the disturbance is complicated and diffuse or ill-
defined, will present insurmountable obstacles to exact diagnosis.
The localization of which we have spoken relates rather to
ascertaining at what height in the spinal cord the nervous sup-
ply for the bladder is intercepted. We know, however, but
little of the course taken by the paths concerned within the cord,
and therefore are unable to say much about the location of a
disease, relatively to the ¢ransverse section. ‘The affections of
the reflex centres must always be located in the gray substance
of the lumbar cord ; yet it should be remembered that a lesion
of the root-fibres as they pass out may give rise to just the same
disturbances as a lesion of the centres. In the case of the paths
which lead to the brain, we must first think of the gray sub-
stance; in that of the motor paths, of the anterior columns also
(Budge). Further information-can only be given by special in-
vestigations.
The reflecting reader will find it easy to comprehend the
course and the complications of those cases in which the altera-
tions begin in a primary focus, and spreading from that gradu-
ally include other points in the conductive path; for example,
when crushing of the dorsal medulla gives rise to myelitis of the
gray substance, which extends downward to the lumbar cord and
there paralyzes the centres for the bladder. It will also be easy
to form a correct view of the processes of initial or slight dis-
turbances of the functions of the bladder.’
1In these statements we have intentionally avoided making a sharp distinction
between palsy of the sphincter and of the detrusor, because, although conceivable
theoretically, such a distinction hardly occurs in practice. We have reason to believe
that the paths leading to both muscular systems, ftom the brain as well as from the
centres in the lumbar cord, are close together, and therefore, as a rule, are affected
136 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
We have spoken only of spinal paralysis of the bladder; of
its spasmodic affections in spinal disease little is known. As
such, we ought perhaps to speak of numerous cases of excessive
desire to pass water, or a few cases of ischuria. Nothing precise
is known of these cases.
d. Disturbances of the Sexual Functions.
These have always been considered closely related to the
spinal cord, and especially in the causal relation. They form,
however, a very prominent portion of the symptoms of spinal
troubles, and are much more noticeable in the case of the male
sex, owing to the far closer dependence of the function upon the
_ integrity of the cord in this sex than in females.
The symptoms in men suffering from spinal disease are:
Increased sexual desire and increased sexual excitability ;
every lustful thought, the sight, or the merest touch of a woman,
causes erections. A state of weakness is usually associated with
this ; in coitus the ejaculation takes place too quickly ; the erec-
tions mentioned are often immediately followed by ejaculation ;
pollutions by day and spermatorrhceea make their appearance.
Whether there is really an increased potency, a power to prac-
tise coitus normally with unusual frequency, is questionable and
is hard to decide, as, even under physiological circumstances,
the sexual powers of performance differ extremely in individuals.
Far more common is the so-called irritable weakness of the
sexual organs, which is especially observed at the beginning of
spinal diseases and in functional debility of the cord. In this
condition erections easily occur, which are weak, insufficient, and
of short duration; the ejaculation during coitus takes place too
soon, occurring before or immediately after intromission of the
penis. The sexual sensations during coitus are diminished or
quite wanting ; the sexual appetite is lessened ; the performance
of the sexual act is followed by great exhaustion—a feeling of
weakness, sweating, pain in the back, sleeplessness for several
together. It will also be very easy to make out the cases of isolated palsy or weakness
of the sphincter, which, properly speaking, is directly subject to the will alone.
GENERAL SYMPTOMATOLOGY. 137
hours, etc., and a feeling of great exhaustion usually lasting
several days. Repetition of the act is impossible.
This condition is followed by diminution and complete loss
of potency. The erections become continually rarer and weaker,
are confined to the morning when the bladder is full, are usu-
ally absent when most wished for, and finally cease altogether.
The sexual appetite usually disappears, but pollutions may occur
with more or less frequency by day or night with or without
sexual feeling ; they may, however, be entirely absent.
Priapism is not rare, in the form of frequent and continuous
more or less complete erections. The power of copulation may
be retained, and the sexual desire increased. Those cases are of
more importance in which such pathological erections accom-
pany a more or less complete interruption of conduction in the
spinal cord; they may originate in apparently a spontaneous
manner, when the penis continues for a considerable time in a
semi-erected state, more rarely in complete erection; but more
usually such erections are reflex, depending on external irrita-
tion, introduction of the catheter, friction of the skin of the glans
or perineum or of the inner side of the thigh.
The investigations of Eckhard and Goltz furnish an easy
and plausible theory of the manner in which these various dis-
turbances originate under pathological circumstances, of the
way in which interruption of the peripheral sensory and motor
conduction, paralysis and irritation of the reflex centres in the
lumbar cord, or cutting off or irritating the paths which pass
from the lumbar cord to the brain, act upon the processes of
erection, ejaculation, and copulation. It is not necessary to ex-
plain these in detail.
It may be added that the present state of our knowledge per-
mits us to draw very few conclusions from disturbances of sexual
functions, as regards the exact seat and nature of the spinal lesion.
As respects the disturbances of sexual function in women
who suffer from disease of the cord, little is known. Ovulation,
pregnancy, parturition may take place normally, even during
severe spinal troubles.
In regard to the libido sexualis, and the act of copulation,
nothing satisfactory is known.
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138 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
7. Disturbances of Digestion and Defecation.
Of the chemistry of digestion, the preparation and secretion.
of the digestive fluid in diseases of the cord, almost nothing is
known, though disturbances certainly occur. The secretion of
the intestinal juices seems to be impaired in many cases, probably
owing to the great tendency to constipation which often exists.
The intestinal movements are usually much affected, either
in the way of increase or of diminution.
The former, of which the symptom is a frequent, watery-
slimy diarrhea, is the less common condition ; it is often capa-
ble of being produced reflexly; thus, in a patient with chronic
myelitis, I observed the regular evacuation of a mucous fluid
mass from the intestine as often as his bed-sores were cleansed,
and the like has been seen in dogs whose lumbar cord was cut.
Much more commonly there is habitual, often excessively
obstinate constipation, of which almost all chronic spinal pa-
tients complain. The stool is slowly discharged, dry, and hard,
and the evacuation occurs only at considerable intervals, and
on application of energetic remedies. Several causes doubtless
contribute to this—diminution of the intestinal secretion and of
the peristaltic action, and probably also the weakness of the
abdominal muscles of compression, which is often present. If
there is an extreme degree of weakness, meteorism and accumu-
lation of feeces occur, with their consequences.
We do not know exactly from what portions of the cord these
disturbances proceed.
French authors, as Charcot,! Delamare, Dubois, and others, have described, in
connection with tabes and other spinal affections, certain peculiar attacks, to which
they gave the name of “crises gastriques,” comprising violent pains, radiating from
the back to the epigastrium, with uncontrollable vomiting, nausea, vertigo, ete.
These attacks may last several hours or days; they recur periodically like the lanci-
nating pains in the limbs of tabetic patients, and have manifestly a close analogy
with such pains. They unquestionably depend upon transitory states of irritation
in certain portions of the cord. I myself have repeatedly seen them in tabes.
In like manner, there is occasionally observed (chiefly in tabetic patients) a violent
1 Lecons sur les maladies du syst. nerv. II. Sér. I. fase. p. 32.
GENERAL SYMPTOMATOLOGY. 189
and painful pressure in the rectum, conjoined with acute pains in the perineum, the
anus, and the sexual parts. These symptoms also have, probably, a neuralgic
character.
Of much more importance are the disturbances of evacuation,
which accompany many diseases of the cord, and are analogous
to a certain extent with the disturbances of the function of urina-
tion. These cases are chiefly caused by a paresis or paralysis
of the sphincter ani, the consequence of which is a more or less
severe incontinentia alvi.
In the mildest cases, the patients cannot retain their stool for
any length of time, but are forced to yield to the pressure as
soon as felt. This weakness may so increase that the discharge
occurs at all times, and without obeying the person’s will in the
least. There may also be present a disturbance of sensibility,
which makes the matter still worse ; the patient does not feel the
call, and even if he possesses some voluntary control, he is sur-
prised by the discharge, of which he feels nothing, and is only in-
formed of its occurrence by his nose or eye, or by the sensibility
of his legs. This, we hardly need say, is a shocking infliction.
This paralysis of the rectum may, in acute cases, attain very
rapidly to its fullest development, but in chronic cases it comes
on very gradually.
It is easy to explain the several disturbances in the func-
tion of defecation, and their origin, by reference to the data
of physiology (see above, p. 54). In brief, we would refer to
what has been said under disturbances of urination, and in this
place would only remark that our attention should be directed
partly to the peripheral sensory fibres of the rectum and anus,
partly to the motor fibres of the sphincter, and to the reflex cen-
tres in the lumbar cord, and the sensory and the motor paths
which ascend from them to the brain. The action of abdominal
pressure must also be thought of; and the ganglionic apparatus
situated in the intestinal wall. The complexity of these points
will increase the difficulty of an explanation, but in most cases
we shall succeed in obtaining a satisfactory account of the nature,
and probably also of the seat of the lesion. The remarks pre-
viously made in regard to disturbances of urination may be
repeated here.
140 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
8. Disturbances of Respiration and Circulation.
Our knowledge of this branch of the subject is confined to
isolated points, and is applicable only in a slight degree to the
uses of pathology.
Disturbances of respiration occur in but few diseases of the
cord, and almost exclusively in those of the cervical portion.
The cord contains only conductor paths for the respiratory move-
ments, situated probably for the most part in the lateral columns,
and leaving the cord at various levels. The centres for respira-
tion lie higher, in the medulla oblongata.
Lesions of the upper dorsal and of the cervical medulla, when
they involve the lateral columns, always give rise to a disturbance
of inspiration, which is severe in proportion to the height of the
lesion. As long as it is confined below the point of exit of the
phrenic, there is no danger, for only the intercostals and some
auxiliary muscles of respiration are deprived of their function,
while the diaphragm—the chief inspiratory muscle—keeps up
the process of breathing to a sufficient extent. But, if the lesion
seizes upon the roots of the phrenic nerve, the inspiration is
always gravely impaired, even if only one side is attacked, while
if both sides are affected, a fatal result from insufficiency of
aération is inevitable. Hence the rapidity with which death fol-
lows severe injuries of the uppermost part of the cervical cord,
as in fracture of the odontoid process of the axis, etc.
In strictly unilateral lesions, disturbances of breathing will
be seen, limited to the side of the injury in all cases.
It is much more usual to see disturbances of expiration in
spinal disease, caused by paralysis of the expiratory muscles (of
the abdomen and back). If the organs of respiration are sound,
this gives rise to no great inconvenience ; at the most, it becomes
somewhat difficult to utter loud tones. But if bronchial catarrh
and similar troubles exist, for which an energetic expectoration
is required, the greatest danger to life may arise from accumula-
tion of mucus in the bronchi. Hence the frequent fatal result of
bronchitis, pneumonia, etc., in myelitic patients.
It is plain what must be the location of the disturbance in
GENERAL SYMPTOMATOLOGY. 141
the spinal cord, in order to produce this difficulty in expira-
tion.
The disturbances of circulation which accompany spinal dis-
ease have been very little examined, with the exception of the
vaso-motor. They are confined to alterations in the action of
the heart, which are seldom very great, as the influence of the
spinal cord upon the heart is only subordinate. Nevertheless,
changes in the activity of the heart seem not to be rare in spinal
diseases, though little noticed. Charcot’ notes a permanent
acceleration of the pulse as a frequent symptom in ataxia ; he
also speaks of a permanent retardation * of the pulse asa note-
worthy symptom of compression of the cervical cord, and de-
scribes it carefully.
The rapidity of the pulse can be influenced to a considerable
extent, both by the sympathetic fibres which pass in the cervical
medulla and by vaso-motor spasm or paralysis. If we further
reflect that the root-fibres of the vagus and the spinal accessory
descend to a considerable distance in the cervical cord, it will be
clear that alterations of the rate of action of the heart are fre-
quent in diseases of the cervical cord. The precise pathogenesis
of these alterations must be ascertained in each individual case.
9. Disturbances of the Oculo-pupillary Fibres, the Various
Cerebral Nerves, and the Brain itself.
We will here enumerate briefly a series of disturbances, of
which only a part are directly referable to lesions of the cord,
the remainder being more or less accidental complications, the
connection of which with the spinal lesion is wholly unknown
to us, even if it exists. But all these points may acquire such
an importance in reference to the diagnosis of cases or varieties
of disease, that it is quite worth while to mention them here,
although we shall have to defer a minute examination to the
special part of this work.
The connection between certain oculo-pupillary symptoms
1 Lecons, etc. 2. Sér. 1. fase” p. 56,
* Loc. cit. 2. fasc. p. 137.
142 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
and spinal diseases is very clear. The fibres destined for the
dilatator pupille originate in a centre situated in the medulla
oblongata ; they descend in the cervical medulla without decussa-
tion, and at various levels make their exit, passing to the cervi-
cal sympathetic, and thus to the eye. Irritation of these fibres
produces dilatation of the pupil (mydriasis spastica), paralysis
of the fibres causes contraction of the pupil (myosis paralytica).
These phenomena may be unilateral or bilateral, according to
the extent of the lesion in the cervical cord; in unilateral lesion
the alteration occurs on the same side; the phenomenon is very
characteristic, especially in lesions of one-half the cervical cord.
-Vaso-motor irritation or paralysis in the corresponding half of
the face often accompanies the corresponding pupillary phenom-
ena. A combination of the two constitutes a valuable symptom
in diseases of the cervical cord. It should be added that, accord-
ing to Robertson, Knapp and Leber,’ the pupil in spinal myosis _
reacts to impulses of accommodation, but not to changes of light. _
The hypoglossus nerve is affected only in diseases of the cord
which extend to the medulla oblongata; the resulting symptoms
are paralysis of the tongue, disturbance of speech, and atrophy of
the tongue.
The vagus and the spinal accessory seem not to be often
affected ; the consequences are spasmodic cough, dyspnoea, and
aibuialiss of the action of the heart.
Still less is known of the affections of the glosso- pharyngeus; ;
the paralysis of swallowing which occurs in many spinal diseases,
especially in the later stages, is probably due to an extension of
the morbid process to the paths of the glosso-pharyngeus, which
lie in the medulla oblongata. ;
The auditory nerve is now and then attacked (e. g., in tabes) ;
the connection between the atrophy of the auditory nerve and —
the spinal disease is entirely obscure. Nervous deafness, or loss ©
of hearing for high or low notes, is then observed. a
The facial nerve is very rarely affected in spinal disease; the —
lower branches are more liable. The usual cause is extension of —
disease to the medulla oblongata. |
1 Virchow-Hirsch’s Jahresbericht fiir 1872. Il. p. 544.
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GENERAL SYMPTOMATOLOGY. 143
Symptoms from the ¢rigeminuws are much more common; the
sensory fibres are oftener attacked, the motor more rarely. The
symptoms are formication, anesthesia, pain ; for which the affec-
tion of the upper cervical cord is a sufficient explanation.
The involvement of the muscular nerves of the eye is very
common in spinal diseases, and very hard to explain. It is espe-
cially common, in the stage of precursory symptoms in tabes, to
observe paralysis of one of these nerves, either in one eye or in
both. The oculo-motorius is most often attacked, next the abdu-
cens, less frequently the trochlearis. We have at present no right
to speak of this disease as depending on the spinal lesion; we
know nothing of a trophic action of the spinal cord upon the
cerebral nerves; we are forced to assume that the degenerative
atrophy is localized simultaneously in several points of the cere-
bro-spinal axis.
The same is true of those extremely common affections of the
optic nerve, which, associated with tabes dorsalis, add horrors to
a disease already sad enough. These cases are always due to
progressive gray degeneration of the optic nerve, recognizable by
the increasing atrophy of the papilla. Amblyopia, color-blind-
ness, contraction of the ‘field of vision, are the first symptoms,
and lead with frightful rapidity to total amaurosis. Similar
affections of the optic nerve, not quite so hopeless as to progno-
sis, occur also in multiple sclerosis. The connection between this
disturbance and the spinal disease is wholly unexplained ; the
amaurosis often precedes by many years the first appearance of
the tabetic symptoms (lancinating pains, aneesthesia, ataxia).
Of affections of the olfactory nerve in spinal diseases, nothing
is known at present.
A good deal of research will be required in order to establish
upon an accurate basis the connection between these diseases of
cerebral nerves and spinal disease. If we refuse to localize the
disorder in several spots at once, we shall be most likely to as-
sume a propagation of the process to the nerve-nuclei in the
medulla oblongata, and perhaps a spreading of meningeal pro-
cesses at the base of the brain; probably other relations, as yet
unknown, will hereafter be discovered. ,
Concerning the disturbances of speech, which are not rare in
144 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
spinal affections, a few words will suffice. These are never psy-
chical (aphasia proper), but probably are solely peripheral and
motor in character, originating in the muscular apparatus of
speech (anarthria). This may be due to paralysis of the hypo-
glossus, which will injure the lingual sounds, or of the facialis,
which interferes with the labials, or of the velum palati, which
gives a nasal tone to the voice, or, finally, of the accessorius,
which interferes with the formation of the voice, and may pro-
duce aphonia. Not infrequently a sort of ataxia, an inco-ordi-
nation of the movements of speech, an irregular stuttering way
of speaking, is observed, as in many cases of tabes; and finally,
a slow, scanning speech is highly characteristic of multiple scle-
rosis. Many other disturbances of speech occur, of more or
less importance.
The brain itself may be involved in the spinal disease in a
great variety of ways and in very various degrees. It is charac-
teristic of many cases of spinal disease, that the brain remains
intact with its functions of intelligence, memory, capacity for
work, etc., and that the cerebral nerves are not in the least af-
fected. But in other cases, not less characteristic, we observe a
more or less general implication of the brain in the morbid dis-
turbance. This may occur in several ways, é. g.:
(az) The same process may be localized both in the brain and
in the cord, or it may extend from the latter to the former; thus,
in multiple sclerosis, there may be sclerotic patches in both brain
and cord ; in tabes, gray degeneration of the posterior columns
of the cord and of the optic or other cerebral nerves ; in dementia
paralytica, simultaneous degeneration of the cord ; the same is
true, in syphilis of the central nervous system, in meningitis
cerebro-spinalis, in meningitis tuberculosa, paralysis ascendens
acuta, secondary descending degeneration of the lateral columns
in consequence of cerebral affections, etc. In every case the cere-
bral symptoms here form important features in the ensemble.
(0) Cerebral symptoms may further be caused by the second-
ary effects of the spinal disease; as by ureemia due to cystitis
and nephritis, by pyzemia due to decubitus, etc.
(c) Finally, severe cerebral symptoms occur in a way not yet
understood in the final stages of many spinal disorders ; as delir-
GENERAL SYMPTOMATOLOGY. 145
ium, coma, excessive temperature, spasmodic conditions, with
which cases of tabes or chronic myelitis often terminate. It is
hard to say how these symptoms originate; usually the exces-
sive cachexia, due to the spinal disease, may be the proximate
cause; but may it not be supposed that vaso-motor actions
originating in the cervical medulla may change the circulation
and nutrition of the brain, and thus form an intermediate mem-
ber between the spinal disease and the cerebral symptoms ?
We have now enumerated nearly all the forms of disturbance
which occur in connection with the spinal cord, and have endeav-
ored to develop their pathogenesis, as far as possible, in order
to give the practical physician a scientific view of the connection
between apparent diseases and the fundamental lesions in the
cord.
The coalition and varied grouping of single symptoms consti-
tute the characteristic forms of disease which we meet in prac-
tice. Daily experience serves to show that the greatest variety
exists here; sometimes we meet with a combination of motor
and vaso-motor disturbances, and sometimes one of sensory and
motor disorders; to these are superadded in various instances
alterations of reflex function, or anomalies of the function of the
bladder and sexual organs; in other cases single cerebral nerves
are implicated in the disorder, or the trophic disturbances assume
a leading place, etc. This multiplicity of symptoms permits us
to divide them into certain groups, many of which are already
well-known forms of disease, while others stand in need of a
stricter definition.
The exact localization of the several disturbances is often
significant ; for example, when both the lower or only both
upper extremities are attacked by palsy, when anesthesia or
pain exists at a certain level in the trunk or limbs, when the
motor palsy is confined to one side, and the sensory to the other
side of the body, ete.
It is the object of clinical study to ascertain what is charac-
VOL. XIII.—10
146 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
teristic and common in all these symptoms; having done which,
we are to draw sharply-defined portraits of disease, and to refer
the latter to changes in the cord, strictly defined as to locality.
In the special part of this work we shall see how far the pathol-
ogy of the day has gone in solving this difficult problem.
B. General Etiology of Diseases of the Spinal Cord.
The etiology of diseases of the cord is not in a very satisfac-
tory condition. A great many isolated facts have been recorded,
not always sufficiently well founded, but the really scientific re-.
sults are small, few general points have been established, and the
pathogenesis of the forms of disease remains obscure in most
cases. }
We must therefore content ourselves with brief outlines, leav-
ing the fuller details to the special part. We will state here only
that which is in some degree certain, but the most part of our
remarks will relate to defects in our knowledge.
First, there is a series of causal agencies and injuries which
place the cord in a condition of increased susceptibility to dis-
ease; these may be designated as predisposing causes. They
are certainly very prominent in the pathogenesis of spinal dis-
eases, but we should not forget that the same injuries may under
certain circumstances produce not only the morbid tendency, but
also the disease itself; and that, therefore, they may in some
cases become direct causes. This depends partly on the intensity
with which they act, partly on the accidental combination of
favoring circumstances.
One of the most powerful predisposing agencies is doubtless
the so-called neuropathic disposition, that peculiar disturbance —
in the nutriticn of the nervous apparatus which lessens the re-
sistance of the latter to all possible injuries, and increases the
tendency to disease in a definite direction. It may exist in the
spinal cord, and predispose it to pathological reaction under all
kinds of irritation. Numerous spinal diseases are, without
doubt, referable to this condition.
This neuropathic condition is certainly congenital in most
GENERAL ETIOLOGY. 147
cases, and is transferred from parents to children. Whole fami-
lies, many generations, may be thus burdened with neuropathy,
and cursed with a feeble power to resist, on the part of the ner-
vous system. In many cases the effect is seen in a general neuro-
pathic disposition ; all possible neuroses (hysteria, tabes, epilep-
sy, psychoses, etc.) are at home with the members of a family,
and each one is affected in only that portion of his nervous appa-
ratus which is accidentally the subject of a special injury. It is
not at all necessary that the parents should have suffered from
the same disease; the children, in such cases, inherit merely a
general disposition of the nervous system to disease, which may
be manifested in very various ways, according to the nature of
the incidental causes.
In other cases a perfectly definite disposition is inherited by
the cord, so that children are attacked by the same affection as
their parents (direct inheritance), of which progressive muscular
atrophy furnishes the best examples; or it may happen that
several or all of the children of one couple suffer from the same
disease when neither parent has had it, as in the cases of degene-
rative atrophy of the posterior columns, published by Fried-
reich.’ |
The way in which this neuropathic disposition is propagated
from generation to generation, often with increasing intensity, is
entirely obscure; and we are quite ignorant of what the finer
changes in the nervous system, and especially in the cord, may
be.
The exaggerated susceptibility to disease on the part of the
nervous system, and especially of the cord, may also be acquired
by a variety of circumstances which must be reckoned among the
predisposing causes.
Of these, sexual excesses and irregularities occupy the first
place. Their effects were formerly often overestimated ; but at
the present time the tendency of opinion is so strongly in the
other direction that an author like Leyden makes no mention of
them in his general etiology.”
1'Virch. Arch. Vols. 26 and 27.
® Klinik der Riickenmarkskrankheiten, I. p. 170.
148 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
My own opinion, based upon observations which for some
time past have been specially directed to this point, is that these
causes are decidedly important in the production of numerous
Spinal diseases—a view which is represented in the writings of
many prominent authors (Romberg, Nasse, Hammond, Salomon,
M. Rosenthal, and others).
I believe we may say that any gratification of the sexual pas-
sion, whether natural or unnatural, indulged in to excess and
Jor a long time, forms for many men—not for all—a cirewm-
stance that powerfully depresses the spinal cord, and predis-
poses it to disease. }
The processes which accompany the sexual act, especially
ejaculation, are attended with a very violent exaltation and shock
of the entire nervous system; and the spinal cord seems to be the
organ which suffers most.’ Certainly this element seems to us of
far more importance than the comparatively trifling amount of
loss of material which occurs in the discharge of semen.
The facts may be analyzed as follows:
Lzcessive natural coitus, in many persons, certainly produces
symptoms which point to a weakness and a diminished functional
capacity on the part of the spinal cord ; weakness of the legs,
inability to stand for a long time, trembling when forcible move-
ments are made, pains in the back, shooting pains in the legs,
sleeplessness, etc. This may often be noticed in the newly-mar-
ried, or in persons who have indulged in great excess for a short
time. If the cause of these symptoms soon disappears, the in-
jury may in most cases be quickly repaired ; but if the excesses
are continued, further injury, or even positive disease, occurs.
Any external injury, exposure to cold, excessive walking, etc.,
may then bring on the worst results.
It is really hard to say at what point excess begins. No number can be given;
the disparity in the powers of different men is enormous. While for some men
Luther’s rule, ‘die Woche zwier ” (twice a week) denotes the limit of their capacity,
others can with impunity do four, six, or ten times as much. This seems to depend
on congenital differences in the sexual power, such as is found also in animals
(stallions, etc.). A slight degree of potency seems to me to be a common circum-
stance among numerous members of nervous families. Of course such a weakness
1 Wundt, Physiologie. 2d edition. p. 690.
GENERAL ETIOLOGY. 149
may be acquired by all sorts of influences which depress the nervous system. In
determining the question of excess we must, therefore, take pains to ascertain the
powers of the individual.
In very young people, not fully grown, and in elderly per-
sons, the evil effects of excess are more readily perceived than in
persons of the vigorous age. If coitus is begun at a very early
age, and practised with excessive frequency, its evil consequences
follow with more or less rapidity in the form of spinal weakness,
general nervousness, etc. Youth has immense power to repair
losses, but the consequences of early squandering of power often
appear later in life.
A specially injurious effect upon the spinal cord is ascribed
by many physicians to coitus practised in the erect posture ; it is
often given as an occasional cause of acute spinal disease.
The effects of unnatural gratification of the sexual appetite
—onanism—are exactly the same as those of the natural indul-
gence. The consequences are much exaggerated, but neverthe-
less they do exist, and are much more pronounced in the case of
certain individuals—weakly, irritable, nervous persons—than in
that of others. Onanism, commenced early, practised frequently,
and continued for years, must be most decidedly injurious. The
undue irritation of the nervous system which it causes, occurring
in the period of growth and development, is seldom without in-
jurious results, of which the most prominent consist in weakness
and irritability of the nervous system.
It is common to consider onanism much more dangerous than natural coitus.
‘This does not seem credible to us. The effect upon the nervous system of a man
must be the same, whether the friction of the glans is effected in the vagina of a
female or in some other way; the nervous shock of ejaculation is the same; it
might even be naturally supposed that the nervous excitation would be greater in
case of connection with a woman. But the frequent repetitions of excitement at an
early period of life, which are caused by self-abuse, are certainly very dangerous ;
and it is furthermore quite certain that the feeling of degradation—so commonly
felt, and so well grounded—the perpetual struggle between the powerful impulse
and the moral duty, must wear and exhaust the neryous system. These circum-
stances may increase the evil effects of onanism. But it is only the excess—that
which for the individual is excessive—which does harm; if practised to a moderate
extent, onanism is no more dangerous than natural coitus. There are not a few men
who are unable to obtain the natural indulgence owing to circumstances, or who are
4
150 ERB,—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
afraid of contagion, or who think onanism less degrading than contact with public
prostitutes—who, from time to time, practise onanism, certainly without injury to
their health. Of the moral effects of this vice this is not the place to speak.
A similar effect is produced by habitual pollutions, if fre-
quently repeated for years together. They are especially com-
mon in onanists, and are rather to be taken as evidence of an
existing disorder, than as liable to become the cause of such.
But even in such cases they often aggravate the difficulty.
Finally, in delicate and nervous persons, very destructive
effects upon the nervous system are produced by long-continued
sexual excitement without gratification, such as often occurs in
prolonged and very affectionate courtship. |
All this is applicable only to the male sex. In the female,
very little is known of this matter, and it is of course very diffi-
cult to obtain information. I have never found that public pros-
titutes exhibited any special tendency to spinal diseases.
The effects of sexual excesses find a parallel in all sorts of
influences which give rise to an wndue strain upon the nervous
system, and especially the spinal cord. They produce exhaus- 1
tion and over-stimulation more or less quickly, and thereby |
increase the danger of disease. Among such circumstances may __
be named excessive bodily efforts, marching, climbing of moun-
tains, riding, etc., especially when the supply of nourishmentis
deficient, and sleep is insufficient ; also protracted watching by |
night, deprivation of sleep, violent and continuous excitement of
passions, and, without doubt, also excessive mental efforts, espe- |
cially when combined with other injurious agencies, such as
severe bodily exertion or sexual excesses.
To the period of life only a slight predisposing influence upon
certain spinal diseases can be assigned; such diseases occur at
all ages. In a few, however, there exists a decided preference
for childhood, and in others for adult or advanced life. The ten-
dency to spinal diseases is certainly greater in adults, as will be
shown in the special part of this work.
Sex has still less predisposing influence than age. There cer-
tainly are diseases which occur much oftener in men than in
women, as tabes, but this may be explained by the fact that men
are much more exposed than women to certain forms of injury.
NT te 68 i. Bee. + oe
nak adit Oe, laa EG Gk. ts NA Ab sls
a sictealt Da
GENERAL ETIOLOGY. 151
To general disturbances of nutrition, on the other hand, of
the greatest variety of character, we may ascribe a decided pre-
disposing influence; all states of aneemia and cachexia depress
the nutrition of the cord, simultaneously with that of the gene-
ral system, and increase its susceptibility to morbific agencies.
Thus may be explained the effect of loss of blood, chronic dis-
turbances of digestion, severe and protracted acute diseases, long-
continued loss of fluids, ete.
Among the incidental causes of spinal disease, the simplest
and most direct are without doubt those of traumatic origin.
There are numberless ways in which this may take place direct-
ly; cases are known of gunshot, stabbing, incised, and other
wounds, crushing and destruction of substance by fractures or
dislocations of the vertebrze, shocks from severe falls or railway
collisions (railway spine of the English), and so forth. No
explanation is needed of their mode of action, or of their conse-
quences (inflammation, softening, necrosis, degeneration, etc.).
In close relation to these causes stands that of slow compres-
sion by pathological growths, by tumors, abscesses, new forma-
tions, exudations, curvature of the vertebrae, etc. Inflammation,
secondary degeneration, etc., are of frequent occurrence in these
cases. . |
Direct propagation of neighboring morbid processes forms
an equally evident source of spinal disease. Thus, inflammation
and suppuration of the vertebral bones or the adjacent soft parts
may extend to the membranes of the cord, or to the cord itself ;
new growths may intrude upon it, the gangrenous inflammation
of bed-sores may seize upon the contents of the spinal cord, ete.
But the effect of exposure to cold, evident as it is in fact, is
quite obscure in its nature. Nothing is more certain than that,
in a very great number of cases, a sudden or continued cooling
of the surface of the body is followed by spinal disease. This
has been seen after a fall into the water, after sleeping on the
damp ground, sudden drenching of the clothes or exposure to a
draft when the body is heated, bivouacking in snow or rain,
working in ice, in damp cellars, in cold water, etc. There are
several diseases which may be produced™in this way, spinal men-
ingitis, myelitis, tabes, spinal palsy of children, tetanus, etc.
152 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
Of the activity of this cause there cannot be the slightest doubt ;
its effects seem most decided in nervous, irritable persons with
predispositions to spinal disease, or in cases where other injuri-
ous agencies, as great bodily exertion, mental excitement, ete.
(as in military campaigns), have come into play.
But the manner in which these circumstances act is still
entirely unknown ; it is probable that the morbific influence con-
sists in a reflex action, originating in the skin. But we have only
hypotheses as regards the way in which this influence produces
inflammations and other disturbances of nutrition in the cord.
It is not yet certain whether a cooling of the blood has a share
in the result—the lower temperature of the blood being supposed
to act as a direct stimulus to the cord. It is hard to conceive
how the direct action of cold should affect in any other way an
organ.so deeply placed as the cord, although myelitis can be pro-
duced by the application of severe cold to the exposed cord.
We are still wholly in doubt as to the reason why the same
cause produces in one person tabes, in another myelitis of the
gray anterior cornua, and in a third, meningitis or tetanus.
Disturbances of circulation, of very various origin, may cause
sundry disturbances of the spinal cord ; hence the effect of sup-
pressed menses, of hemorrhoidal disease, of arterial fluxions and
venous congestions, of vaso-motor disturbances, of embolism and
thrombosis, atheroma of the spinal arteries, etc. .
A frequent cause of spinal disease consists in excessive exer-
tion of any sort, exhausting the cord. In this category are in-
cluded sexual excesses, when practised frequently and at short
intervals, walking, riding, swimming, or other muscular acts
which go beyond the natural powers. All these may become the
point of origin for severe spinal disorders, especially when they
affect predisposed individuals, or when other agencies coincide—
as that of cold; whence the frequency of these affections after
laborious campaigns, bivouacs in winter, etc.
Psychical influences are a less frequent agency in the produc-
tion of spinal disease. Fright, alarm, disgust, etc., seem to have
a pretty clear connection with the origin of retical and diffused —
neuroses (epilepsy, chorea, hysteria, and the like); but not to
the same extent with that of spinal diseases. But there are some
bil bee
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ea
oe"
GENERAL ETIOLOGY. 153
eases in which paralyses and other disturbances of a probably
spinal nature have been seen to arise from purely psychical
states, especially fright and terror. Thus, J. Russell Reynolds’
observed the occurrence of paraplegia in a young lady, arising
from a fear of the disease ; she was nursing her father, who was
paraplegic. Hine’ saw an acute and fatal myelitis in a pregnant
woman, caused by violent emotion. Leyden reports a ease of
paraplegia caused by fear at the breaking out of a conflagration,
and Kohts* tells of similar occurrences at the bombardment of
Strasburg. It is quite uncertain how we ought to interpret these
facts, and whether the psychical emotions act through the vaso-
motor paths,‘ or whether they may directly produce a disturb-
ance of the finer processes of nutrition in the central nervous
elements.
Certain intoxications present well-known spinal symptoms ;
such are poisoning with strychnia, arsenic, phosphorus, lead,
etc. Some of these poisons seem to have the power, when long
continued, to produce marked spinal diseases; for example,
lead.
The local development of various infectious diseases, acute or
chronic, is of great importance in etiology. Syphilis, by becom-
ing localized in the vertebral column, the membranes, or the cord
itself, may lead to spinal symptoms; tuberculosis not seldom
attacks the cord and its membranes ; and of the acute infectious
diseases there is one (meningitis cerebro-spinalis) of which the
chief seat is the pia mater cerebro-spinalis. To these must be
added the cases, not few in number, of spinal affections j/ollow-
ing acute diseases (typhoid, acute exanthemata, intermittent,
influenza, pneumonia, etc.), which, as a rule, must be regarded
not as a specialized localization of the original process, but rather
‘as somewhat accidental complications of the latter, dependent on
a local predisposition established by the acute disease.
A very frequent source of spinal disease is found, lastly, in
| Remarks on Paralysis, etc., Dependent on Idea, Brit. Med. Jour. No. 6. 1869.
‘p. 483.
* Med. Times. 1865. Aug. 5. .
® Berl. klin. Wochenschrift. 1873. Nos. 24-26.
“In the third case of Kohts the menses were instantly suppressed by fright.
154 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
irritation and disease of peripheral organs. Of this we have
already numerous proofs. Paraplegia has been seen with espe-
cial frequency following severe and obstinate dysenteries and
other intestinal diseases, and chronic affections of the kidneys —
and bladder ; in many cases the autopsy has shown myelitis to —
be the cause of the paraplegia. Such occurrences have been less
frequently observed in uterine disease, which is more commonly
followed by hysterical palsies—though the latter also, in some
cases, are certainly of spinal origin. Myelitis has also been ob-
served to follow peripheral lesions of nerves, diseases of joints,
and so forth; the tetanus which follows injuries of nerves and
peripheral lesions certainly belongs to this class. .
All these processes have long been studied with great zeal ;
they have, in fact, been made into a special class of reflex disor-
ders (usually termed reflex paralyses), because they have been
commonly supposed to originate in the reflex way from periphe-
ral irritation. But the theory of these reflex diseases is in dis-
pute to this day; and the number of works written upon them is
very large.’ We have discussed this point in another place ;*
the statements there made relate chiefly to reflex paraplegia and
the myelitis which causes it, and we may therefore refer to that
place, to avoid repetitions. The spinal disturbances which fol- —
low peripheral irritation or disease cannot, therefore, as a general
thing, be referred to a purely reflex disturbance of function ;
they must, for the most part, be dependent on coarser changes
of nutrition (inflammation, softening, exudation) in the cord.
Regarding the connection of the latter with the primary irrita-
tion, we are not yet fully in possession of the facts ; it is in part
effected by an ascending neuritis, of the existence of which there
1 For more minute information we refer the reader to the following: Leyden, Ueber
Reflexlihmung. Volkmann’s Sammlung klin. Vortr. No. 2. 1870.—Lewisson, Hemmung
der Thitigkeit der motorischen Nervencentren, etc. Reichert u. Du Bois’ Archiy. 1869. E
—Feinberg, Ueber Reflexlihmung. Berl. klin. Wochenschrift. 1871.—Tiéesler, Ueber —
Neuritis. Diss. Kénigsberg. 1869.—Brown-Séquard, Lectures on the Diagnosis and —
Treatment of the Principal Forms of Paralysis of the Lower Extremities. London,
1861.—Jaccoud, Les paraplégies et l’ataxie du mouvement. 1864.— W. Gull, Med.-chir.
Transact. Vol. 39. 1856. p. 195, .
2 See Vol, XI. p. 399.
GENERAL DIAGNOSIS. 155
is no doubt; but in other cases the inflammation is transmitted
to the cord in the reflex way.
A few attempts have lately been made to settle this question,
but without much success. The investigation by Roessingh '
threatens to set us back a step, as he has arrived at entirely nega-
tive conclusions in his repetition of the experiments of Lewisson
and Feinberg. :
- Klemm’s?’ laborious studies leave room for many questions
and doubts. They by no means prove that a direct propagation
of the inflammation takes place along the nerve to the central
organ: an extension dy leaps was all that was proved. In this
case, therefore, and especially where inflammation is transmitted
to the symmetrically situated nerve of the opposite side of the
body, without demonstrable affection of the central organs, the
only explanation is that which assumes a sort of reflex transmis-
sion. The process may be essentially like that in which ex-
posure of the skin to cold produces inflammation of the spinal
cord. In so-called ‘‘reflex paralysis,’ the irritation is of an-
other sort, and acts upon some other organ than the skin.
The question of reflex disease of the cord is certainly still in
doubt, and is in great need of further clinical and experimental
study.
C. General Diagnosis of Diseases of the Spinal Cord.
When we encounter a complicated nervous affection, the first
Step to be taken is a careful enumeration of the existing disturb-
ances. The first and most important point is, to test all the de-
partments of the nervous system, and thus to ascertain the
existence, the grouping, the succession, and the history of each
Symptom. The diagnosis is made from the total of all these.
The next question is always that of the location of the dis-
ease; the organ affected; in nervous diseases, the choice lies
3 1 Bijdrage tot de Theorie der Reflexparalyse. Nederl#Tijdschr. vor Geneesk. 1873.
| Bd. I. No. 53. See Virchow-Hirsch’s Jahresb. for 1873. Bd. II. p. 44.
| ? Ueber Neuritis migrans. Diss. Strassb. 1874.
156 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
between the brain, the medulla oblongata, the spinal cord, the
peripheral nerves, and the sympathetic,
The reply to this question, in the case of the spinal cord, often
involves great difficulties. We may, it is true, follow the good —
old rule, to place the point of lesion at a spot where all the affected
paths lie nearest together. But this rule often goes but little
way with the spinal cord, both because all the paths which it
contains pass into the peripheral nerves, and may be diseased in
them, and also because a plurality of seats of disease is possible,
and, in the case of the central nervous system, is very common.
There is no function, quite specifically peculiar to the cord, the
impairment of which would lead us at once to recognize an affec-
tion of the cord: this statement is true, even in regard to the
disturbances of reflex activity.
When, therefore, disturbances of the sensory and motor sys-
tem, of the vaso-motor and the reflex functions, of the trophic
conditions and of the genito-urinary functions, etc., coexist, and
in parts which directly depend on the cord for their innervation,
then there is a great probability that the cord is affected; but
certainty does not exist until we have excluded the affections of
the peripheral paths. This is certainly possible in many cases,
but not in all; there are, for instance, diseases of the cauda
equina, which cannot be distinguished with certainty from those
of the cord, and the same is true of extensive disease of the
nerve-roots, ete. J
In such dubious cases, various means may be employed to
confirm the diagnosis, such as the data of the history of the case,
or the causal factor, which often give us an 5h tee to infer
a definite seat of lesion.
By far the best aid is that furnished by experience, which
teaches us that certain well-characterized groups of symptoms
correspond to very definite lesions of the cord. We are in pos- —
session of a series of groups of this sort, which can without
hesitation be recognized as dependent on disease of the spinal
cord; thus, tabes dorsalis, the so-called acute spinal paralysis of
children and adults, sclerosis of the lateral columns, progressive —
muscular atrophy, tetanus, and many others.
Experience goes still further ; it often gives us notice by a few
GENERAL DIAGNOSIS. 157
symptoms, often by a single one, of a threatening or actually
present disease of the cord, because the constant or almost con-
stant, coincidence between the symptom and the disease has be-
come established through observation; thus, for instance, tabes
may often be recognized by a precursory atrophy of the optic
nerve, or by lancinating pains.
It therefore follows that in order to form a correct and sure
diagnosis of a spinal disease, we need not only a very careful and
comprehensive investigation, not only an accurate statement and
estimation of the etiological and other elements, but also an
intimate acquaintance with the whole of the pathology of the
cord, and a good bit of practical experience.
There remain, however, a few cases in which the diagnosis
may be difficult, and in which the spinal location of the disease
is not quite certain. It then becomes necessary to distinguish
the spinal from the peripheral disease, on the one hand, and
from the cerebral on the other—which is often very difficult.
We must, however, here confine ourselves to naming afew points
which will assist diagnosis in given cases.
In favor of a peripheral localization, the following circum-
stances may be mentioned: Limitation of the disturbances to
single nerves or branches of nerves; exact coincidence of the
motor, sensory, vaso-motor, and trophic disturbances with the
distribution of a peripheral nerve ; absence of retarded conduc-
tion of sensation ; absence of all reflex action; absence of weak-
ness of the bladder and the sexual functions, etc., in case the
sacral nerve itself is not the seat of disease; presence of great
disturbance of the trophic function ; certain results of electrical
examination ;' the existence of a known local cause of lesion.
In favor of a cerebral location we may have the following
(among others): hemiplegic distribution of the disturbances, with
the sensory and motor disturbances upon the same side; unequal
intensity of the sensory and the motor disturbances ; absence of
all trophic disturbance; entirely normal electric reaction; re-
tention or exaggeration of all spinal reflex acts; retention of
| associate movements and automatic movements, and of the rectal
- >
1 See Vol. XI. p. 445.
158 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
and vesical functions; presence of disturbance of the higher
senses, and of various cerebral nerves (except so far as well
known to be often involved in spinal disease), of disturbances
of speech and of the mental functions; finally, the presence of
headache, giddiness, and causeless vomiting. |
In favor of the spinal seat of disease, the following circum-
stances may be used in evidence: the usually paraplegic distri-
bution of symptoms; crossing of motor and sensory disturbances
in case of hemiplegic symptoms; sensation of a girdle at the
upper limit of the other disturbances ; change in a portion of the
spinal reflex acts (exaggeration or weakening) ; weakness of the
genito-urinary functions; paralysis of the rectum; trophic dis-
turbances, bed-sores, etc.; definite pareesthesize, retardation of
the conduction of sensory impressions; disturbance of certain
automatic movements ; the peculiar local limitation of spasms of
cerebral origin ; absence of psychical changes, and usually, of dis-
turbances of the higher organs of sense and the cerebral nerves.
It must also be noted that all these points possess by no
means an absolute, but only a very conditional value; that their
significance is very often not decisive, except in connection with
many other symptoms, so that they cannot be made useful for
diagnostic purposes except after a very careful estimation of all
circumstances.
When we have decided that the cord is the seat of disease, we
have to proceed to localize the lesion within the cord. In doing
this, the distribution of the symptoms, especially those of paraly-
sis, usually furnishes an excellent point: it is often possible to
decide within a hair’s breadth to what height in the cord a certain
affection extends, and the gradually upward progress may often
be followed in a very beautiful manner. While thus the upper
limit of a lesion is usually very easily recognized, the same is not
equally true of the lower limit, and it is often hard to decide
whether the lesion is diffuse or circumscribed as respects the
longitudinal section of the cord. Yet there are certain points
which indicate that the lower portions of the cord are intact; the
principal of these (see General Symptoms) are those relating to
the reflex function, that of the bladder and rectum, and the
nutrition of skin and muscles.
ee
GENERAL DIAGNOSIS. 159
This is the case when disease extends over the entire trans-
verse diameter of the cord, and to some extent, also, in the longi-
tudinal direction of the cord.
We are enabled by experience to recognize also diseases con-
fined to limited parts of the transverse section; such may also
extend to a greater or less distance in the longitudinal axis.
Thus we can distinguish the affections of the separate white col-
umns, the anterior and the central gray matter, etc. ; those of
the white posterior columns (probably only the outer divisions)
furnish the symptoms of tabes dorsalis (see the special part) ;
that of the white lateral columns, the symptoms of Charcot’s
lateral sclerosis (which see); that of the anterior gray cornua in
its acute form, the symptoms of infantile spinal paralysis; in its
chronic form, probably those of progressive muscular atrophy ;
disease of one lateral half of the cord, symptoms of Brown-
Séquard’s unilateral lesion ; disease of the central gray substance
gives rise to an equally characteristic group, and in general, the
implication of the gray substance may be recognized by the dis-
turbances of nutrition, of reflex action, of electrical reaction, etc.
Thus, in many cases, it is possible to decide very accurately
with regard to the seat and location of the lesions in relation to
the longitudinal and transverse sections of the cord ; it is certain
that the perfection of the methods of anatomical research, recently
applied to the diseased cord, will soon add much to our means
of diagnosis. And a good deal remains to. be done, for there are
considerable parts of the transverse section, the lesions of which
have never yet been brought into relation with any group of
symptoms. .
It remains for us to decide the nature of the lesion—whether
paralysis or irritation, inflammation or degeneration, softening
or atrophy and sclerosis, compression or bleeding or other lesions,
are present in the cord.
It is difficult to establish general diagnostic rules for this;
symptoms of irritation (spasm, pain, increased reflex action) will
incline us to infer a corresponding pathological state ; symptoms
of paralysis will point rather to degenerative processes, softening
or compression and destruction of the.cord ; but we must be cau-
tious in these inferences, since both sorts of symptoms and both
160 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
pathological conditions are very often combined, and the same
disease in its progress not seldom leads to a manifold alternation
of symptoms.
But, as a rule, more and better points can be derived from the
results of experience, from the development and order of succes-
sion of the symptoms, from the history of the case, the etiology,
the objective examination, etc.
It would lead us too far to attempt to give and analyze ex-
amples of even a portion of the possible cases here alluded to.
We shall find opportunity for doing this in the special part of
this work. Our present object is confined to indicating the points
for diagnosis, and the methods and instruments, the precautions
and the care, required in order to render the diagnosis exact.
As regards complications, we will only say, in brief, that they
must be ascertained and judged according to the usual diagnos-
tic rules,
IV. General Therapeutics of Diseases of the Spinal Cord.
This branch of our subject presents many weak sides. In
most diseases of the cord, our success in the use of remedies is
rather small. The general opinion regarding spinal diseases, that
they are nearly or quite incurable, is but too well founded.
It is true that we have recently had to modify this view
essentially. A great number of curable diseases have been re-
ferred to a spinal origin; and, on the other hand, the prognosis
in many chronic spinal diseases has been much improved by the
progress of therapeutics.
Yet much remains to be done. And above all, we must learn
how to recognize the diseases, before we can treat them ration-
ally ; we are still at the threshold of exact knowledge of the
pathology of the cord, and the scientific therapeutics of its dis-
eases is still in its first stage.
The attempt to state the general principles of treatment at this
day seems hazardous, so small is the material, and so uncritically
reported. The attempt will nevertheless be made to present the
°
GENERAL THERAPEUTICS. 161
remedies which are used in disease of the cord, and especially
those which we have reason to suppose exercise a decided in-
fluence over that organ. For the present, we must be content
with such a mere attempt.
The indications in spinal disease are very numerous, consist-
ing of, a, the removal of so-called functional disturbances (intan-
gible disturbances of nutrition), especially those of a chronic
sort; 5, alteration of disturbances of circulation (hyperzemia and
anzemia) ; c, the cure of acute anatomical changes (acute inflam-
mation, softening, hemorrhage, etc.) ; and, finally, d, the removal
of chronic anatomical changes (degeneration, atrophy, sclerosis,
induration, new formations, etc.).
All the usual methods of treatment are, of course, employed
for these objects, with suitable modifications to adapt them to
the seat of the disease ; the functional disturbances are remedied
by regulation of the function, by slight stimulation of the latter,
by alteration and improvement of the nutrition and sanguifica-
tion ; for disturbances of circulation, we have a variety of means
for acting on the vaso-motor system and the vessels; acute in-
flammatory processes are treated by antiphlogistics, derivation,
etc.; the chronic alterations are usually attacked by alterative,
exciting, and derivative procedures. In the cure of these chronic
cases nature has, of course, the.chief part to play ; we have only
to supply the most favorable conditions for repairing the disor-
ders, to excite the desired change in the general nutrition by cer-
tain remedies, by promoting the formation of blood and the pro-
cesses of nutrition, by stimulating the metamorphosis of tissue,
: by regulating the function of the diseased parts, and soon. For
more particular remarks the reader is referred to the special
part of this work.
We shall here give the remedies and methods in general,
which are adapted to the above indications, and shall attempt to
_ make their mode of action intelligible upon scientific principles.
This attempt is made rather in the hope of stimulating exact
study than as an exhaustive presentation ; such a presentation
would be forbidden by the limits of the present work.
We shall first devote 4 section to the very important group of
external or physical remedies, then speak of the very scanty list
: VOL. XIII.—11
162 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
of internal remedies ; in a third section a series of symptomatic
remedies and methods will be mentioned, which may be employed
according to occasion in any spinal disease; and in the fourth
section the general regimen and diet.
1. Physical Remédies.—EHaternal Remedies.
Cold,
The application of cold to living tissues first depresses their
température, and lessens the supply of blood by ischemia ; this
retards the processes of metamorphosis, and limits those of exu-
dation and emigration; at the same time the excitability and
conductibility of the nervous apparatus are depressed.
Hence are derived the leading indications for the use of cold
in inflammations, hypereemias, and exudations, and also in cases
where there is abnormal excitement in the nervous system, pains,
and spasm.
In accordance with the latest researches of Riegel ! and F.
Schultze,’ it can hardly be doubted that the cord can be reached
directly by the action of cold, although the thickness of the
parts overlying it is so great that a very powerful and continu-
ous application of ice along the line of the spine is necessary to
produce that effect. The effects of Chapman’s well-known vaso-
motor therapeutics are also in favor of the possibility of such an
action.
Chapman,’ by the application of ice or of warmth to the spine, produces a pow-
erful action upon the cord and its vessels. He states that the continuous applica-
tion of ice produces ischemia of the cord, lessening the retlex irritability and the
other functions; alternate application of ice and warmth increases the flow of
blood and the manifestation of energy upon the part of the cord; repeated brief
applications of ice at longer intervals produces similar but less marked effects ;
and, finally, by application of ice to the back we can increase the circulation in
those peripheral regions which receive their vaso-motor nerves from the portion of
the cord thus treated.
1 Virchow’s Archiv. Bd. 59. Heft 1.
® Locale Einwirkung des Eises auf den thier. Organismus. Deutsch. Arch. klin. Med.
XIII. p. 500. 1874.
3 Med. Times and Gaz. July 18, 1863.
GENERAL THERAPEUTICS. 163
Besides this direct action, a reflex influence may be exerted
by the cutaneous nerves, as excited or depressed by the stimulus
of cold; this has not yet been carefully studied.
The application of cold to the spinal cord may be made either
by a common ice-bag or by several, if required, or (better) by
- Chapman’s bags; the complicated apparatus of Koopman’ does
not seem to be required. Less energetic and more transitory ef-
fects can be obtained by cold irrigation or cold affusion of the
back.
Warmth.
The effects of warmth are in many respects the opposite to
those of cold; it raises the temperature of the tissues, increases
the flow of blood towards them, and increases the excitability of
nervous apparatus. We therefore expect from its action an in-
creased transformation of tissue, or stimulation of the processes
of nutrition, and a consequent repair of defects of nutrition,
removal of atrophy, degeneration, sclerosis, etc. It is believed
_ to be an excellent remedy for increasing the process of resorp-
_ tion of finid or solid material, and for repairing chronic processes
of inflammation. It furthermore often soothes pain and spasms.
The way in which warmth acts upon the cord has not been
much studied. It is even doubtful whether it penetrates directly
to the cord when applied externally—though it probably does
so. On the other hand, the reflex action, effected by means of
_ the cutaneous nerves, is certainly not to be underestimated.
| The results to be expected from its use are: dilatation of the
blood-vessels, an increase in the quantity of the current of blood
and the other fluids, and of the processes of tissue-change in the
Se a =
. =
cord, an increased facility and rapidity in the nervous processes,
and finally, a removal of excitements which often affect the cord,
originating in the cutaneous nerves.
It follows from this, in what morbid conditions of the cord
the application of warmth will be considered most desirable.
But let it not be forgotten that warmth is known to be easily
>
1 Berliner klin. Wochenschr. 1870. No. 48.
164 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
capable of producing over-excitement and exhaustion, leading
to congestive states of the cord, and that the use of warmth
is contra-indicated in all cases where such results are to be
dreaded. :
The methods of applying warmth are very simple: cataplasms,
hot sand-bags, Chapm4h’s caoutchouc bags filled with hot water
and laid along the spine ; hot-water fomentations, or (the mildest
form of all) Priessnitz’s wet wraps, which gradually warm them-
selves.
Baths.
Compare Braun, Balneotherapie. 3. Aufl. 1873.— Valentiner, Handb. der Balneo-
therapie. 1873.—Sceegen, Heilquellenlehre. 2. Aufl. 1862.—Helfft-Thilenius,
Handb, der Balneotherapie. 8. Aufl. 1874.—Durand-Fardel, De la valeur des
eaux minérales dans le traitement des paraplégies. Bull. de Thérap. Mai 30.
1857. — Gotth. Scholz, Ueber Riickenmarkslihmung und ihre Behandlung
durch Cudowa. Liegnitz. 1872.—Runge, Die Bedeutung der Wassercuren in
chronischen Krankheiten. Arch. f. klin. Med. XII. p. 207. 1873.—Fr. Rich-
ter, Ueber Temperatur und Mechanik der Badeformen bei Tabes und chron.
Myelitis. Deutsch. Zeitschr. f. prakt. Med. 1875.
Baths form a very important group.of remedies in complaints
of the spinal cord. Great results must be ascribed to them, in
most of the chronic forms. It is very difficult, however, to define
their mode of action and their indications, partly on account of
our defective knowledge of spinal pathology, partly because the
subject of balneotherapeutics has as yet received but little scien-
tific development. The diagnosis of spinal disease is certainly in
a very defective condition ; our ideas regarding the anatomical
changes, as existing in individual cases and at determined peri-
ods, are equally imperfect; hence the uncertainty in regard to
indications, and the wide room for empirical treatment, which
too often passes beyond the allowed limit of experiment.
We will here speak of the different forms of baths, and their
mode of action as taught by the science of balneotherapeutics,
and shall attempt to state which forms are most suitable for the
treatment of different spinal diseases or groups of symptoms.
PPS AE ED Bn SG aS
GENERAL THERAPEUTICS. 165
Warm Baths
have from time immemorial been a favorite method of treat-
ing diseases of the spinal cord—especially paralyses, which us-
ually form the chief part of such as come for balneological treat-
ment. This has been especially true of the indifferent or acrato-
therme ; but the weak brine baths, alkaline waters, sulphur-
baths, etc., containing unimportant amounts of salt and gas, are
quite similar to their mode of action. The same is true of steam-
baths, hot sand-baths, and the like.
The effect of warm baths is first seen upon the skin, in which
a great dilatation of the cutaneous vessels occurs, followed later
by a moderate contraction. Thereby the circulation in the skin
is hastened, and a great evaporation and sweating follows, which
is rendered easier by the removal of the upper layers of epider-
mis. At the same time, the organism receives an access of
warmth, or, at least, is enabled to lay up a part of its own store
of heat. Thus the processes of oxidation are furthered, and the
discharge of most of the functions of the body is facilitated,
which accounts for the refreshing effect of a warm bath when one
is greatly fatigued.
For our purpose, the effects may be summarized as follows:
The warm bath increases the facility of all the chemico-physical
processes in the system, leading to stimulation of the metamor-
phosis of tissue and freedom of function, without any subsequent
reaction from excessive stimulation. At the same time, by shel-
tering the body from the continual change of temperature of the
outer air, it acts asasedative. By the fluxion of blood to the skin
it changes the distribution of this fluid, and acts as a derivative
in congestions of internal organs; it acts as a resorbent by stim-
ulating the nerve-centres, by changing the course of the blood,
and by the production of sweat, and by washing out the system.
Warm baths are best borne by feeble individuals, whose
power of resistance and of making heat are weakened. Their
effect depends very greatly upon their temperature. If this be
indifferent (32°-36° C. [90° to 97° Fahr.]), they are believed to act
chiefly as sedatives ; warm and very warm baths (36°-42° C. [97°
to 108° Fahr.]) are more stimulating, produce strong excitement
166 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
of the blood-vessels, much sweating, increase of tissue-changes.
Lukewarm baths (28°-32° C. [83° to 90° Fahr.]) are believed to
have a special depriment effect in the case of nervous, irritable
persons.
As the temperature rises, therefore, the exciting qualities
become more prominent; as it sinks, the soothing.
The geographical site of the baths must be considered, together
with the temperature, especially in the case of indifferent therma,
for experience seems to show that the higher the site the higher
may be the temperature that is borne, and that, the more irri-
table the patient is, the more elevated may be the spot to which
he is sent for cure. This is an important point in practice.
The indications which follow from these principles are not
easy to state. Most of the circumstances are very complicated.
If we confine our attention to the most prominent symptoms, the
matter seems very easy ; when the symptoms of irritation pre-
ponderate, and irritability is very marked (spinal irritation), we
choose rather the soothing baths ; if symptoms of depression are
prominent (anesthesia, paralysis, etc.), the exciting baths at a
higher temperature.
But unless we consider that a decided degree of irritable
weakness not only may be, but usually is present in cases of
spinal paralytic affection, and that in such cases we usually
have to do with an extremely irritable and exhausted nervous
system ; unless we bear in mind that important disturbances of
circulation and nutrition are usually present in the most impor-
tant organs, which may possibly be affected injuriously by the
warm baths, it will be impossible to avoid false steps. Nor have
they been avoided, in fact; certain spinal diseases (tabes, mye-
litis, etc.) have often been made worse by too warm baths.
The degenerative and sclerotic forms of spinal disease seem to
require the greatest care in this respect, and we are yet in need,
before we can be quite safe in using them, of a more careful
study of the special action of thermee upon these disturbances of
nutrition. ,
Our remedy, therefore, has not merely a directly exciting or
composing influence upon the nervous system, but also one of far
greater consequence, namely, the alterative action which it exer-
GENERAL THERAPEUTICS. 167
cises (by virtue of increasing the metamorphosis of tissue and
changing the direction of the blood-current) upon coarse and fine
disturbances of nutrition. We shall not be able to define the
indications until the latter mode of action is better understood.
The warm springs are now used in exhaustion of the spinal
cord after typhoid and other severe diseases, or excesses of any
kind ; in spinal irritation (moderately warm baths) ; in paraplegia
from shock to the cord (energetic use of very warm baths) ; in
tabes (avoid very warm baths! select baths of indifferent temper-
ature); in myelitis and softening of the cord (slightly warm); in
meningitis exsudativa (all warm springs, especially those of higher
temperature), etc.
_ Fr. Richter believes that only baths of a moderate warmth or
moderate coolness ought to be used in chronic inflammatory or
atrophic affections of the cord. The warmer baths (from 32.5°
C. [90° Fahr.] upwards) are considered by him the best adapted
for chronic inflammatory states of the cord with preponderant
symptoms of irritation.
We give the following list of the most frequented warm
springs, with the height above the sea-level and the temperature
of the water: Schlangenbad (900’ ; 30-32.5° C. [86° to 90° Fahr.}) ;
Badenweiler (1,425’; 30-32.5°) ; Landeck (1,398’ ; 31.0-32.5° [88° to
90° Fahr.]); Wildbad (1,323’; 35.0° [95° Fahr.]); Ragatz (1,570’ ;
88.0° [100.5° Fahr.]); Pfeffers (2,115’; 38.0°); Romerbad (755’ ;
88.0°); Gastein (3,315’; 32.5-40.0° [90° to 104° Fahr.]); Warm-
brunn (1,100’; 40.5° [105° Fahr.]); Wiesbaden (323’ ; 34.0-40.0°
[94° to 104° Fahr.]); Teplitz (648’ ; 37.5-42.5° [99° to 108° Fahr.]) ;
Leuk (8,309’ ; 39.0-50.0° [102° to 122° Fahr.]); Baden-Baden (616';
46.0-68.0° [115° to 154° Fahr.]); Plombiéres (1,310’; 19.0-62.0°
[66° to 144° Fahr.]). A proper selection may be made by attend-
ing to the special indications, the individual conditions, ete.
Weak brine-baths (containing not more than one per cent. of
chlorides), most sulphur-baths, and the weak alkaline springs act
exactly like indifferent springs, and may, according to circum-
Stances, be used in their place.
Steam-baths, hot sand baths, hot air-baths are of a very high
temperature ; they produce powerful gtimulation and diaphore-
sis, and may be of use, especially from the latter peculiarity, in
168 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
very torpid cases of meningitis exsudativa. But it is always
necessary to exercise the greatest caution in employing them for
spinal complaints.
The so-called Scotch douche (alternation of hot and cold
water) produces a very exciting effect upon the skin and the ner-
vous system ; it has also been recommended in spinal paralysis ;
it requires to be used with great caution.
Brine-Baths
are very like warm baths in their effects; the action of tempera-
ture is the same in both cases, to which the effect of the salt
contained must be added. The most suitable proportion is be-
tween two and four per cent. The special effect of this ingredi-
ent appears in a powerful stimulus of the nutrition and circula-
tion of the skin, increase of the change of tissue, repair of
disturbed nutrition, increase of resorption. On account of the
exciting effect of the salt, their temperature may be somewhat
lower than that of the plain warm baths. Their indications in
spinal disease are the same as those for warm baths; and besides,
they are often prescribed for the causal indication, in treating
scrofula, vertebral disease, caries, ete.
The air of the salt-pans, which may be breathed in many places while the patient
is taking his bath, is cool, refreshing, ozonized, and in the case of many irritable
patients is much to be desired as an accessory.
The warm brine-baths containing gas are far more important
than the simple warm ones. This class is represented by Rehme*
Oeynhausen, Nauheim, the Schénbornsprudel in Kissingen, and
the Soolsprudel in Soden a. T. Their effect is due to their tem-
perature and the salt they contain, in the first place, and, next, to
the abundance of carbonic acid, which acts as a powerful excitant
of the skin and the nervous system. Its direct effect is a moder-
ate subtraction of heat, followed immediately by a reaction, dur-
ing which the withdrawal of heat continues, and at the same
time a continuous stimulation of the nervous centres. It is as it
were a combination of the stimulating and calming effects of the
cool and the warm bath. |
GENERAL THERAPEUTICS. 169
The result is a general improvement of nutrition and the or-
ganic functions ; hence, resorption and removal of pathological
products ; at the same time, excitement of the nervous system
may improve the nutrition of that department.
These baths are cool ; they must not exceed 32°C. [90° Fahr.];
they are usually taken without moving the water, but if we wish
to increase the effect, the water may be agitated.
They are indicated in weakness of the spinal cord following
difficult convalescence or other exhausting influences, in tabes,
in paralysis after meningitis, in myelitis, spinal paralysis of chil-
dren, spinal irritation, etc.
Chalybeate Baths,
so-called, are baths with a very slight amount of iron, a more or
less considerable amount of salt, and a very considerable quan-
tity of carbonic acid.
Their action is usually referred by halinectiontites to their tem-
perature and the carbonic acid they contain, while the amount
of iron is believed to be insignificant. The physicians continue
to swear by the springs, but they fail to make.a probable argu-
ment for the effects of the iron, except as used internally.
It is certain that these baths, owing to the presence of car-
bonic acid, are among the most powerful stimulants of all, if
warmed with precaution, so as to retain as much of the gas as
possible. |
They are indicated wherever the thermal brine baths with
ntuch gas are required ; they should be avoided in all conditions
- in which great excitation is to be feared; but they should be
applied wherever we have to do with a torpid, inexcitable state
of the nervous system, especially when anemia is likewise
present.
While in general the use of steel-baths abounding in Co, is
held unadvisable in diseases of the cord, and they are admitted
only in very special forms of functional disturbance, Scholz has re-
cently attempted to save the credit of the steel-baths, especially
those of Cudowa, in spinal cases, and has stated their indications
and results with exactness. He recommends them very highly
170 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
for chronic congestion of the cord, especially in anzeemic persons
and the subjects of nervous exhaustion ; only by exception in
spinal meningitis, limiting their use to torpid individuals, and
cases of a sluggish nature; also in the initial stages of chronic
myelitis, with hope of success proportional to the weakness and
aneemia of the individual and the sluggishness of the case; in the
‘‘primary’’ form of tabes, without inflammatory symptoms,
under the same conditions ; finally, in all cases, for the sequel
of spinal concussion, as soon as the stage of excitement is past.
The best results are obtained with mitigated baths (diluted with
fresh water).
Although Scholz’s presentation is not wholly convincing, ver
it is proved that steel-baths, if used with care, are capable of
doing good service in many even severe cases. They deserve to
be tried thoroughly.
Among waters of this class the following deserve mention:
Schwalbach (900’), Pyrmont (400’), St. Moritz (4500’), Brickenau
(915’), Driburg (633’), Franzensbad (1300’), Cudowa (1235’), the
Kniebisbider (1200-1900’), ete.
Moor-Baths and Mud-Baths,
so-called, form a separate class. Their action is as yet far from
being explained; it cannot yet be stated with definiteness. A
part of the effect is due to their quality as warm baths, but this
is accomplished in some entirely specific and not yet understood
way, since they are much less exciting than warm springs. They
seem indicated wherever the thermal treatment is desirable, but
its stimulant action is not likely to be well borne; especially,
therefore, in weakly, irritable, and anzemic constitutions. Espe-
cial benefit has been observed in spinal irritation and the so-
called tabes dolorosa, then in paraplegias and contractures conse-
quent upon myelitis, lateral sclerosis, compression of the spinal
cord, etc.
The temperature and duration must be regulated according to
individual peculiarities.
Good moor-baths are found in Franzensbad, Marienbad, Tep-
GENERAL THERAPEUTICS. 171
litz, Driburg, Briickenau, Meinberg, Elster, Kilsen, Nenndorf,
Liebwerda, Pyrmont, Reinerz, etc.
Pine-needle baths, which have been much used and praised, are only warm
baths, in which a powerful stimulus is applied to the skin, not by high tempera-
tures or by Coa, but by the ethereal oil and the extract of pine twigs. They may
be used wherever the more stimulating forms of thermal treatment are indicated.
Among the most important agencies that we possess are
the cold and cool baths, including the use of cold water in the
greatest variety of forms—what is commonly known as
The Cold-water Treatment.
This treatment, having of late years been administered in a
rational manner and closely studied, has much increased in
popularity. Its results in all possible forms of chronic nervous
troubles are extraordinarily good.
There is as yet no entire agreement in respect to the theory
and the mode of action of the cold-water treatment. The condi-
tions are very complicated, and it has naturally happened that
individual practitioners of the method have reached more or less
one-sided views ; some consider the exciting or depressing effects
upon the nervous system the principal thing, while the effect in
modifying the change of material is subordinate; others try to
refer all the effects to the vaso-motor action upon the skin, while
a third party sees an explanation of all the leading phenomena
in the alterative action upon the metamorphosis of tissue.
It is certain that in the cold-water treatment we observe on
the one hand an action upon the cutaneous nerves, and thence
transferred to the entire nervous system; also, effects upon the
cutaneous blood-vessels, and through them upon the distribution
of the blood throughout the circulation ; and finally, changes in
the circulation and the entire process of transformation of tissue,
to which must be ascribed a very special influence upon the cure
of severe chronic diseases. |
Our present knowledge of the subject amounts to about the following:
A direct action upon the nervous system, of anwaciting or a depressing nature, can
be produced by the application of cold water; the subtraction of warmth acts as a
172 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
depressant, the stimulus of the cold as an excitant. According to the form, the
temperature, the duration of the baths, we can make the one or the other effect
more prominent (Petri).
The soothing effect is always produced where the same portion of water remains
in constant contact with the skin, as in half, full, and sitz baths without motion;
in the wet pack, in wet rubbing without moving the cloth. .
The exciting effect is always produced when the layer of water in contact with
the body is continually changed, so that the stimulus of cold is constantly renewed ;
that is, in half, full, and sitz-baths with agitation, in rubbing down with a cloth
which is moved, in washing, affusion, shower-baths, douches, surf-baths, sea-
baths.
The lower the temperature of the water, the more quickly and forcibly do these
effects appear. The exciting action of the baths may be increased by previously
wrapping the patient in dry blankets, while at the same time an excessive loss of
heat is prevented, as the quantity lost in the bath is no greater than what has been
saved by the wraps; this method is therefore of special value for persons who need
to save their strength. A frequent repetition of these excitations increases the energy
of the nervous system.
In regard. to the circulation, the following effects are to be seen in the skin, due
for the most part to nervous influence: great ischemia, goose-flesh, shivering,
and soon (though at various intervals), dilatation of the vessels, increased amount
of blood, increased secretion from the skin and perspiration, increased development
of warmth. These are the symptoms of reaction, which occurs with different
degrees of facility in different persons, and is of very great importance in the cold-
water treatment. In order to its proper development, a certain measure of force, a
certain resistance is required; in badly nourished, weak, irritable, and anzemic per-
sons, or those with degenerative disease of important organs, it occurs much less
readily; for this reason these persons do not bear the cold-water treatment.
The reaction is lively and vigorous in proportion to the lowness of the tempera-
ture of the water and its degree of motion, that is, the force of the stimulus. It is
favored by rubbing the skin at the same time, and especially by energetic mechani-
cal dry-rubbing after the application of the cold.
A frequent repetition of these actions upon the skin increases the circulation and
nutrition of the skin permanently, thereby producing a change in the distribution of
the blood. A more important effect is its derivative action upon chronic congestions
of internal organs, especially the spinal cord. But this can only be obtained with
safety when at the same time all injurious irritation of the diseased organ is avoided.
The cold water may act more directly upon the circulation in internal organs, by
producing ischemia of these organs through reflex action; thus, Runge states that
quite cold baths, applied to the lower extremities, have a direct vaso-motor action
upon the cord, diminishing the quantity of blood contained in it. But in aiming at
this, it is important that the reaction in the skin should have developed before that
in the spinal vessels is commenced, in order that the secondary hyperemia may be
directed principally to the skin. For this purpose it is useful to apply water not
Eat ee Us ae 14
D5 gp OP ee ae AR ges Te ee el
GENERAL THERAPEUTICS. 173
merely to the whole surface, but especially to the parts which are related more
closely to the affected organ, that is, the skin of the lower extremities and the back.
In regard to the processes of nutrition and change of tissue, it is settled beyond
a doubt that every subtraction of warmth from the outer skin is followed by a con-
siderable increase in the production of warmth (this forms a portion of the phenom-
ena of reaction); that the secretions increase, the appetite is improved, etc. It is
further probable that the repeated excitation of the nervous system has directly an
influence upon the changes of tissue, increasing the formation and destruction of
most of the tissues; and that the nutrition of the portions of the central nervous
system which are affected by the stimulus is stimulated and improved. We are in-
clined to believe that this method will certainly cure slight disturbances of the
nutrition of the cord, and that, under some circumstances, even severe degrees of
change may be gradually repaired.
In brief, then, cold water acts as follows: It strengthens the
functions, improves the nutrition, increases the circulation of
blood, in the skin; it thus alters the distribution of the blood,
and the process of circulation in the system ; it relieves, at first
temporarily, afterwards permanently, hyperemia of internal
parts (F. Richter); it quiets or excites the nervous system in
various degrees; it tones the nervous system by the functional
excitement and by the improved nutrition; it accelerates the
process of change of tissue, and increases the total nutrition; it
promotes resorption and formation.
If we add to this the effects which may be had from certain
forms of baths, the increased sweating, the consequences of the
increased consumption of water, the muscular movements which
are necessarily increased, the effects of diet, climate, altitude in
the case of cold-water cures, it becomes evident that we possess
but few remedies which have so powerful and various an influ-
ence upon the nervous system.
In point of fact, the cold-water cure has been much and
advantageously employed in diseases of the cord. Thus, for
conditions of irritable weakness of the cord (chiefly by withdraw-
ing caloric and moderate stimulation—cold wraps kept on till
warm ; rubbing down with moderate friction), for passive hyper-
gemia of the cord (washing and affusion of the back, stimulant
sitz-baths, and long-continued moist cold wraps applied to the
body), for fluxionary hyperemia (sogthing friction, soothing
sitz-baths with cold compresses on the back, etc.), for tabes dor-
174 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
salis (chiefly mild treatment, according to circumstances more
stimulating or soothing), for chronic myelitis (the same).
The greatest attention must always be paid to the individual ;
it should not be forgotten that every powerful action of cold
produces a powerful reaction, to sustain which a certain amount
of force is needed ; for which reason, let none be subjected to the
treatment but those who possess a certain power of resistance.
Weakly, irritable, aneemic persons bear only the more soothing
or the very mildly exciting procedures, under certain precau-
tions. In all cases, it may be set down as a rule that the tem-
perature should not be below 20° C. [68° Fahr.], unless special
trial shows that lower temperatures are well borne.
The Sea-Bath
is a special and very important form of the cold-water treatment.
Its effects are very energetic, because several factors coincide, —
among which the sea-air is by far the most important. It is,
properly speaking, a climate cure associated with a very power-
fully stimulant form of the cold-water treatment (7. e., a full bath
in vigorous motion, at a very low temperature). The proportion
of salt in the water of the North Sea, the Mediterranean, and the
Atlantic is equivalent to that in a brine bath of medium strength,
and serves to increase the action upon the skin.
The result is a great increase in the change of tissue, increased
excretion and formation, increased need of nourishment, increase
of bodily weight, tonic action upon the nervous system.
But the sea-bath is adapted only to able-bodied persons,
whose appetite and digestion keep pace with the requirements
made upon the system. Weak persons with feeble appetites or
bad stomachs are not suited ; the most that can be done for them
is to cause them to enjoy the sea-air, or, in some cases, to add
thereto the benefits of bathing in warmed sea-water. |
The very powerful stimulant and refrigerant effects of sea-
baths make them unfit for most cases of spinal disease. They
are useful in spinal irritation and spinal weakness, but only in
able-bodied persons; in tabes and similar diseases, only in the
lightest form and at the very beginning, or as a concluding treat-
Pr eae Ee -
GENERAL THERAPEUTICS. 175
ment after cure is nearly complete—but only when the organs of
assimilation are in a fairly good condition. In any case, the
baths must be used with great care, and the chief value ascribed
to the breathing of sea-air, to the climate cure.
Climate Cures
There exist no spinal climate cures for disease of the spinal
cord. But it is known that a very favorable influence is exer-
_cised upon many severe neuroses, including those of spinal origin,
- especially when of a functional nature, by certain climates and
regions.
The sea-air, of which we have spoken, is an example of this.
Very much the same is true of the mountain air; it has the same
power of stimulating the changes of tissue and the appetite, it
_ aids the performance of sensory and motor functions ; the bodily
exercise taken in the mountains has an especially enlivening
effect upon the nervous system. The higher and drier the site,
the more marked are these tonic effects—as, for example, in the
Ober-Engadin.
Beneke’ has made comparative examinations of the action of
sea and mountain air, and has reached the conclusion that the
‘increase of metamorphosis of tissue is decidedly greater at the
sea-shore than on mountain-summits (3,000’-6,000’), because the
subtraction of heat is quicker and greater. Irritable, nervous
people, who cannot bear great alteration of tissue, had better
choose a residence in the mountains. Experience confirms this
in a satisfactory manner.
Every one knows the beneficial effects of a continued resi-
dence in various elevated places in Switzerland, the Tyrol, etc.,
upon so many nervous patients, those with spinal irritation,
Spinal weakness, impotence, and so forth. And in the more
severe cases, the same may be recommended as after-treatment.
The choice among suitable places is extremely large: it
should be made with careful regard to all individual peculi-
arities.
1 Zur Lehre von der Differenz der Wirkung dét Seeluft und der Gebirgsluft.
Deutsch, Arch. f. klin. Med. XIII. p. 80. 1874.
176 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
After thus enumerating the different forms of baths and their
modes of action, let us formulate briefly the indications, giving
some theoretical deductions, which may be of use to the begin-
ner as a clew to treatment, though they require much further
confirmation by practice.
a. Purely functional disturbances of the cord, fine changes
in nutrition without demonstrable alterations—as in spinal irri-
tation, spinal weakness, concussion without coarse lesion, ete.
For the treatment of these we may take into consideration warm
springs, thermal brine baths abounding in gas, steel-baths abound-
ing in gas, the cold-water cure, sea-bathing, and mountain cli-
mates. The selection must depend, firstly, upon the individual-
ity off the patient ; for irritable, weak persons without much en-
durance, let the acrato-therme be chosen; the more irritable the
subject, the higher should be the location. Or at most, a mild
cold-water cure with moderate temperatures. For more vigor-
ous persons with good digestion, the cold-water treatment and
the sea-bath, or the thermal brine baths, may be considered. For
very torpid persons, the same baths and the steel springs. The
choice must further depend on the morbid symptoms and their
personal variation ; with violent symptoms of irritation in very
irritable patients, the cooler acrato-therme, the more soothing
forms of the cold-water method, sea-air, a mountain climate ;
with preponderant symptoms of debility in torpid persons, the
warm springs, the stimulant forms of the cold-water treatment,
the thermal brine springs, steel-baths, and sea-baths.
b. Hyperemic states of the cord and its membranes. For
passive hyperemia (so-called hemorrhoidal tabes, etc.) the
stimulant methods of cold-water treatment, steel-baths, and
thermal brine baths are the best. The therme are contra-indi-
cated. For active hyperemia, select the more soothing forms of
the cold-water treatment, combined with derivation to the skin
(soothing frictions and sitz-baths with cold compresses to the
back, etc.). Thermal brine baths and steel-baths require great
precaution. Warm springs and sea-baths will usually do harm.
c. Chronic inflammation of the spinal membranes, especially
if associated with fluid exudation. Here warm springs, thermal
brine baths, a powerful cold-water treatment will be useful; in
.
GENERAL THERAPEUTICS. (Wee
short, anything that promotes resorption and vigorously stimu-
lates the processes of metamorphosis of tissue—but always sub-
ject to the distinctions and contra-indications already stated
under a.
d. Chronic textural changes in the cord itself : inflammation,
degeneration, softening, atrophy, sclerosis, etc. Little is to be
expected except in the earlier stages of these complaints, and in
slight cases. The object is, to stimulate moderately the trans-
mutation of tissue, and the cord, so as to remove the disturbance
of nutrition ; and for this purpose warm springs, thermal brine
baths, steel-baths, moor-baths, and cold-water treatment are use-
ful. But we must always be extremely prudent. We should
remember that our patients are almost always irritable and weak
persons, suffering from a serious organic lesion, incapable of
enduring any severe shocks ; and that any increase of the hyper-
gemia of the cord may prove dangerous to them. Therefore, use
only warm springs of an indifferent or Inkewarm temperature ;
mild cold-water cures; mitigated steel-baths; well-regulated
thermal brine baths. Consider that the effect, at best, must be
slow and gradual, and that the cure cannot be completed by a
stay of four or six weeks at the baths.
The selection among the different baths should be made
according to the peculiarities of_the individual ; that of the spe-
cial method, according to the character of the case, the leading
symptoms, concomitant hyperzemia, etc. In general, avoid in-
dulging too much hope in these cases !
Such are the general principles for the balneo-therapeutic
treatment of disease of the cord. In the special part we shall
see how far they may be applicable to the different classes of
disease. Progressive experience will, without doubt, greatly
modify them.
A great deal might be added under this important head, but
we have not the space. It must be constantly remembered that
attention to individuals is of the first importance. An exact
diagnosis and a thorough estimate of the individual must go
hand in hand in forming plans for treatment. And complica-
tions, causes, external conditions often have to be considered, so
that the selection is extremely difficult.” The physician’s practi-
VOL, XIII.—12
178 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
cal tact and skill have here a wide field for displaying them-
selves.
Electricity.
Remak, Galvanotherapie. 1858. p. 448 et seq. Application du courant constant au
traitement des névroses. Paris. 1865.—Ranke, Ueber krampfstillende Wirkung
des constanten elektrischen Stroms. Zeitschrift f. Biologie. II. 1866.—Fies,
Galvanotherap. Mittheilungen. Deutsche Klinik. 1868.—2Hrd, Galvanotherap.
Mittheilungen. Arch. f. klin. Med. IIL 1867.—The Same, Anwendung der
Elektricitit in der innern Medicin. Volkmann’s Sammlung klin. Vortr. No. 46.
1872.—Brenner, Untersuchungen und Beobachtungen auf dem Gebiete der
Elektrotherapie. Bd. IL. 1869. p. 81.—Uspensky, Einfluss des const. Stroms auf
das R.-M. Centralbl. f. d. med. Wiss. 1869. No. 37.—Burckhardt, Ueber die
polare Methode. Arch. f. klin. Med. VIII. p. 100. 1870.—Ziemssen, Elektrici-
tit in der Medicin. 4. Aufl. 1872. pp. 24, 37, and 143.—Also the text-books of
electro-therapeutics by M. Meyer, Duchenne, Benedikt, M. Rosenthal, Beard and
Rockwell, and others.
No other remedy has, within a recent period, gained so much
ground as electricity in the treatment of spinal disease. But few
can be compared with it for activity. It is among the numer-
ous services rendered by Remak that he brought spinal disease
within the sphere of scientific galvano-therapeutics, and obtained
many striking successes with that treatment.
At first, great obstacles stood in the way of a general accept-
ance of his views ; first, the doubt as to the possibility of reach-
ing the cord with the electric current, which was expressed by no
less an authority than Ziemssen; and then a scepticism in re-
spect to the genuineness of his successes, which was in part justi-
fied by the excessive claims of the specialists, and in part was
supported by the failures which unavoidably occurred in old,
severe, and absolutely incurable cases.
These obstacles are now overcome; no one now doubts the
possibility of reaching the spinal cord with the electric current,
and the numerous and unanimous experience of almost all elec-
tro-therapeutists no longer allows us the right to doubt that elec-
tricity has accomplished many, in some cases very remarkable,
cures in diseases of the cord, and that it has essentially improved
the hopeless prognosis of many spinal diseases.
py
GENERAL THERAPEUTICS. 179
We must therefore pay especial attention to this remedy.
In this place we have only to speak of the direct treatment of
the lesion of the cord. For in most diseases of this sort there are
two things to be distinguished: the electrical treatment of the
cord itself and its affection, and the treatment of separate symp-
toms of the affection. Each of these two may be attended to
separately, or they may be combined. As to the second point,
we refer to the proper section in Volume XI. of this Cyclopedia,
in which the electrical treatment of paralyses, anesthesia, neu-
ralgias, spasms, etc., is given in full.
Here we encounter at once the question of the mode of action
wpon the cord and its diseases. Upon this point little is known,
and the material in our possession is more than scanty.
Physiology furnishes us with almost no facts to the purpose. The experiments
on stimulation of the cord have produced few results of consequence; it is still a
debated question whether the substance of the cord is excitable or not, and whether
all the phenomena of excitation may not be referred to irritation of the roots. The
question, however, seems to have been answered in the affirmative by the studies of
Fick, Engelken, and Dittmar, showing that at all events the white columns of the
cord are excitable. Some facts, also, discovered by physiologists (Nobili, Mat-
teucci, Ranke), in relation to the power of the galvanic current to quiet spasm—
facts discovered during the treatment of toxic tetanus by strong galvanic currents
sent lengthwise of the cord—are perhaps useful, but they require a fresh revision, in
view of the more recently discovered facts of the action of powerful currents in
arresting reflex actions. The primitive researches of Uspensky, which have shown
that the cord acts as a peripheral nerve (!), both for conduction and for reflex
actions—that it assumes the conditions of anelectrotonus and catelectrotonus—are
quite useless for our purpose. Of the action of electrical currents upon the nutri-
tion of the cord, nothing is known by physiology.
Almost all our knowledge is drawn from pathological and therapeutical experi-
ence, and consists chiefly of purely empirical facts, which are usually far from being
understood.
Our positive knowledge is really limited to this: that a number of diseases of the
cord, especially chronic forms, are relieved or cured during the use of electricity, em-
ployed in various ways. The precise connection between the therapeutic results and
the methods used is, however, usually obscure, especially as, in many cases, we are
unable to form any clear idea of what diseased condition exists in the cord and its
membranes, or what it is that we are removing by electricity.
We know, further, that individual symptoms of spinal disease may be removed
by electrical treatment of the cord, as tetanic spasms, contractures, tremor, lanci-
nating pains, anesthesia, paralysis, etc. But these facts are not always beyond a
180 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
doubt; for example, the results obtained by Mendel in tetanus with galvanic cur-
rents may be referred to a simultaneous action upon the peripheral nerves. In the
interesting observations by Dr. Rabow, communicated by Leyden,! the hypothesis
of a simultaneous action upon the periphery is almost always admissible; and the
explanation of the facts there described is at the present time impossible.
We possess, therefore, only inferences and hypotheses regard-
ing the possible action of electricity in the various categories of
disease.
Thus, in the so-called fwnetional disturbances of the cord,
we may first consider the exciting and modifying agency of
electric currents; probably, however, the so-called catalytic
action (comprising effects produced upon the blood-vessels, upon
resorption, osmosis, change of tissue, etc.) is of importance, as
relieving the minute disturbances of nutrition.
In disturbances of circulation (hyperemia, stasis, exuda-
tion) the explanation may be deduced from the powerful action
of electricity upon the vessels and the vaso-motor nerves, upon
the circulation of fluids, resorption and the like.
In marked anatomical changes (chronic inflammation, degen-
eration, atrophy, etc.) we must again refer to the ‘‘ catalytic”
action of the current, which can alone explain the fact and the
rationale of the cure of these diseases.
It follows that the so-called catalytic action of the electric
current probably constitutes the chief point in the treatment of
most diseases of the cord. It is a pity that this action is so
obscure, and so little susceptible of an explanation. We do not
care to present hypotheses.
The catalytic action is probably quite independent of the
direction of the current. The special action of the two poles
is also very obscure in this respect, although the attempt has
been made to define it. The simple passage of the current, in
sufficient strength and for a sufficient time, through the diseased
region, seems to be the essential thing. All details of application
must be discovered by empirical methods.
From these principles, the chief rules for the electrical treat-
ment of the cord naturally follow.
1 Klinik der Riickenmarkskrankheiten. I. p. 185.
——
_
wh Pe
GENERAL THERAPEUTICS, 181
The first point to be deduced is that the galvanic current
should be used almost exclusively in these affections ; first, on
| account of its physical properties, it being able to penetrate more
; easily and surely to the depth required than the faradic current ;'
and second, on account of its preponderant catalytic action,
i which is possessed in but a slight degree by the faradic current.
; Experience has fully confirmed this position; even the most
obstinate adherents of the faradic current claim for it little or no
success in organic diseases of the cord. We shall see further on,
however, that they are possible to a cevtain extent.
As regards the special methods of applying the galvanic cur-
rent* in diseases of the cord, we have first to settle the question,
whether the cord can be reached at all.
The possibility of this is proved by my experiments upon the
dead subject, and by numerous facts, discovered by myself and
other observers in the case of the living human subject ; not to
mention numerous therapeutic successes. No one now doubts
the possibility of reaching the spinal cord with the galvanic
current.
The principal object, in most cases, is to produce as general
and as powerful a passage of the current through the spinal ~
cord as is possible, especially in its diseased portions.
The cord is a deep-seated organ, and we must employ quite
powerful currents in order to reach it. And this can be suitably
accomplished without hurting the patient, only by using very
large electrodes, applied not too near together.
Too many offences are committed against this rule, which is a
simple inference from Ohm’s laws. If small electrodes are used,
f the strength of current required to affect the cord sufficiently
_ __-will produce intolerable pain.
EROS
I have often seen persons with sores on their backs, produced by the very pain-
ful application of Stéhrer carbon electrodes (quite unfit for this purpose) ; but
who have not seemed to me to have derived the least benefit from the treatment. I
always use, for galvanization of the cord, electrodes of at least ten centimetres (4 in.)
long and five (2 in.) broad. '
1 Helmholtz, Verhandl. des naturhistor. med. Vereins zu Heidelberg. Bd. V. p. 14.
1869.
* The same principles apply for the most part to the use of faradism.
182 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The greatest density of current is found immediately under
the electrodes; the portions of tissue lying between them are
not reached by any great quantity of the current, probably not
enough to have any therapeutic effect ; hence it follows that the
diseased regions should be brought in contact with the poles
throughout their whole extent. According to circumstances,
inclination, or theoretic views, the operator will prefer for the
purpose the one or the other pole. As the action of the poles
upon the cord is unknown, and as probably both poles are use-
ful in producing the catalytic action, it is perhaps desirable in
many cases to let both act, one after the other.
The relative position of the two electrodes will be determined
by the seat and the extent of the lesion in the cord.
If the disease is chiefly distributed in the longitudinal direc-
tion—and this is the most usual case—it is probably best to
place both poles on the vertebral column, one in the lumbar re-
gion, the other at the nucha. One pole, say the lower, being
fixed, the other may be moved quite slowly down over the back,
and thus brought in contact with a great part of the cord; and
likewise, the upper being fixed, the lower may gradually be car-
ried over the most part of the cord. Thus the “stabile” effect
may be made to preponderate, as is desirable in producing cata-
lytic actions, while the point of application is gradually changed.
In diseases of a more circumscribed locality (apoplectic foci,
spinal paralysis of children, circumscript myelitis, etc.), we shall
do best to cover the diseased spot entirely with the pole which is
intended to produce its effect, and to put the other pole upon
the anterior surface of the body, the abdomen or sternum; this
is the surest way of causing a direct passage of the current
through the cord; or if desired, we may cause both poles to act,
one after the other. Here, also, the electrodes should be made
as large as possible.
In all these applications, interruption or reversal is to be
avoided as. far as possible, unless there exist special indications
for their employment.
The direction of the current seems to be nearly indifferent, in
respect to results. In general—probably from some undefined
impression—the ascending current is preferred. The chief point
GENERAL THERAPEUTICS. 183
will always be tc secure the action of the single poles upon the
entire extent of the cord. |
In selecting the poles there are certain rules observed which
require to be confirmed by accumulated experience. Thus, we
may be decided to prefer the anode in case symptoms of irritation
are prominent, in excitable and sensitive persons, in recent, active
processes, and when we fear evil results from secondary hyper-
emia. The action of the cathode will be preferred in disease of
a more torpid nature, in persons but slightly irritable, in old
processes, associated with thickening and increased dryness of
the tissues (atrophies, scleroses, etce.). Generally, however, both
poles will be used with advantage.
| The cord may also be influenced indirectly by the electric
current.
It may be reached by the so-called’ indirect catalysis. of
Remak, through the sympathetic. This process is said to ena-
ble us to exercise a regulative influence upon the processes of
nutrition in the cord, by galvanization of the cervical sympa-
thetic, by excitation of the vaso-motor (and trophic) paths which
pass through it. The influence is a possible one, and even prob-
able, but is not proved. Flies has made further observations
upon this point, The possibility of this action has induced me
in many cases to apply my treatment in such a way that the
sympathetic may be included in the action. The cathode is fixed
over the ganglion superius on one side of the neck, and the
anode upon the opposite side of the spinal column (quite close
to the spinous processes), first between the shoulder-blades, then
moving downward very slowly (avoiding labile treatment) till
the conus terminalis is reached ; and then the same is repeated
upon the other side. To this is usually added direct treatment
through the vertebral column, anode below and cathode above,
slowly changing their positions. I believe that I have seen excel-
lent results from this treatment; perhaps, however, this depends
merely upon the more favorable way in which the cord is reached
by the current.
The cord may also be influenced from the skin. <A reflex
stimulation, transferred from the sensory nerves to the cord, may
very well act like a direct stimulation. Certainly a great part
184 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
of the effects of the cold-water treatment, or of carbonic acid in
baths, and the like, depends on this circumstance. We have
nothing precise upon this point; it seems probable, however, to
me, that a part of the results which are obtained in spinal dis-
eases by peripheral electrization of the skin and the muscles, is
referable to this cause. For this purpose cutaneous faradization
and faradization of the muscles may be employed, as well as gal-
vanization. These are the cases which give faradization a just
title to comparison with galvanism.
Thus, in M. Meyer (8. Aufl. p. 336), there is a case of spinal disease, which was
cured by faradization of the skin with a wire brush.
The remarkable centripetal action of the galvanic current, produced by irrita-
tion of peripheral nerves, discovered by Remak,' was thought by him to promise
great results in practice; but the matter has remained in obscurity, not having been
further looked into. |
The ‘‘ general faradization and galvanization,” recommended by Beard and
Rockwell,’ probably acts like peripheral faradization. It consists of a stimulation
of the skin and the muscles, extending over the whole body.
Beard * has also recommended a method of “ central galvanization” as especially
efficacious in all sorts of central lesions, especially in conditions of spinal exhaus-
tion. It may be useful in many cases. The cathode is placed upon the epigas-
trium, while the anode is applied successively to the vertex, the vertebral column,
the cervical sympathetic, in the labile manner.
Ranke (loc. cit.) believes that an improvement of the condition of the ‘muscle
and the consequent increase in the strength of the normal ascending current of the
spinal cord, will act favorably upon spinal nervous weakness, etc.
Finally, M. Meyer‘ has very recently pointed out that galvanic treatment of the
points of the spinal column, which are painful under pressure (found in many
affections of the cord, especially tabes), often succeeds wonderfully. He applies a
current of medium strength for five or ten minutes, placing the anode (unmoved)
upon the sensitive points.
The duration of single applications may be quite brief—from
a minute and a half to five minutes. This is usually enough.
Too long applications easily produce disagreeable excitement.
The sessions are given daily or less frequently. The duration of
the entire treatment is very undetermined; it depends upon the
1 Allg. med. Centralzeitung. 1860. No. 69.
? Med. and Surg. Uses of Electricity. 1871. p. 186, ete.
3 See Virchow-Hirsch’s Jahresbericht fiir 1871. I. p. 376, and 1872, I. p. 404.
4 Berl. klin. Wochenschr. 1875. No. 51.
GENERAL THERAPEUTICS. 185
character of the disease and the success obtained. It is often
well, after an electric treatment of several weeks, to interpose a
considerable period of rest, which may properly be filled up by a
visit to spas, a change of climate, or some similar alternative.
The diseases are usually very tedious in their course.
It is well not to make too light of the administration of elec-
tricity ; it is not for every one to undertake. It requires much
practice and experience. Manual skill, great technical experi-
ence, attention to a great variety of points, careful attention to
the individual symptoms are absolute requisites.
With the direct treatment of spinal diseases we often have to
associate a treatment of the symptoms—as paralysis and anes-
thesia, spasm and neuralgia, weakness of the genito-urinary
organs, paralysis of sphincters or of the muscles of the eye, atro-
phy of the optic and auditory nerves, ete. All this must be
done in accordance with the general rules of electro-therapeuties,
with special regard to the individual and to the seat of lesion.
Blood-Letting
may be indicated, under certain circumstances, just as in dis-
eases of other organs ; thus, in severe acute inflammations, hy-
pereemias and stases, with the consequent irritation or paralysis.
General blood-letting is seldom indicated, and is to be gov-
erned entirely by general therapeutic principles.
Local blood-letting is best practised on the back, at both
sides of the vertebral column, owing to the connection between
the inner and the outer plexus of vertebral veins; wet cups or
leeches may be applied there. For many cases of abdominal
plethora, hemorrhoidal affections, etc., blood-letting at the anus
is very useful.
Derivatives.
These formerly played a very prominent part; scarcely a
patient with disease of the cord escaped, even from the severest
of them all. The back of a chronic spinal patient was usually
covered with the scars of blisters, issues, moxa, and the hot iron.
In our day we are much less disposed to tise these remedies, and
perhaps make too little use of them.
186 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Their application and their modes of action are very manifold,
comprising derivative influence upon states of sensory excite-
ment, change in the molecular condition of the nervous system,
arrest of reflex actions, withdrawal of blood by the action upon
the circulation, derivation of inflammation and exudation by
establishing an exudative or purulent inflammation of the skin.
All this may also act upon the spinal cord, and probably does
act upon it directly, for the cord is undoubtedly the first of the
central organs to receive this class of impressions. But, unfortu-
nately, we know no more regarding it. The statements of Busch *
in respect to the application of the hot iron in various neuroses,
especially spinal diseases, are very interesting. He found at the
autopsy of one such a case that the iron, applied to the back of
the neck, acts to a great depth; in the deepest layers of muscle
in that region there were found portions suffused with blood, and
even the meninges under the burnt places were found reddened
with hyperemia. Busch is in the habit of burning on both sides
of the vertebral spines, in longitudinal strips; he considers this
a very powerful derivant in affections of the cord.
If it is allowable to transfer to the pia mater of the cord the
facts observed by Schueller in the pia of the brain — and there
can be no doubt of its propriety — then the effect of very large
Sinapisms, or, more properly, vesicants, would be a temporary
dilatation, followed by a very marked and continued contraction
of the vessels of the pia.
We may employ as derivatives cutaneous taradinaion sina-
pisms, vesicants, pustulating ointments, issues, moxe, and heated
iron. The place for application will almost always be the back, —
opposite to the diseased spot.
External Frictions.
These are much used and highly esteemed among the non-
medical public, but are usually rejected by physicians. In this
respect medical scepticism often goes too far.
! Berl. klin. Wochenschr. 1873. Nos. 37-39. Session of the niederrhein. Gesellsch.
at Bonn,
GENERAL THERAPEUTICS. 187
It is certainly conceivable that the irritation produced by
friction with spirituous or other substances upon the skin may
act like the stimulation of baths or electricity, exciting and enliv-
ening the action of the spinal cord and bringing to pass a better
functional condition and nutrition in it, or else, that the quieting,
soothing effect upon the peripheral cutaneous nerves produced
by inunction with warm oil or narcotic salves, or fomentations
and wraps of a similar nature, has a soothing action upon the
central nervous system, and thus contributes to the removal of
diseased conditions. I believe that I have in a few cases, quite
accidentally, proved to myself the efficacy of such procedures,
and am therefore unwilling to see them quite abandoned.
No great results will be reached, it is true, but the external
applications may be used as subsidiary remedies, and to sus-
tain the patient’s courage.
According to circumstances, we have the choice between the
more soothing frictions (with warm oil, infused oil of hyoscya-
mus, opium or belladonna ointment, etc.), and the more stimu-
lating and invigorating frictions (with French brandy, spirit of
ants, of wild thyme or of camphor, liniment of ammonia or of
camphor, etc.).
2. Chemical Remedies—Internal Remedies.
Cf. Nothnagel, Handbuch der Arzneimittellehre. 1870.—Husemann, Handbuch der
gesammten Arzneimittellehre. II. 1875.—Schueller, Ueber die Einwirkung eini-
ger Arzneimittel auf die Hirngefiisse. Berl. klin. Wochenschrift. 1874. Nos.
25 and 26.—Brown-Séquard, Lect. on the Diagnosis and Treatment of the Prin-
cipal Forms of Paralysis of the Lower Extremities. London, 1861. p. 110.
We have entered upon a region which is still very obscure,
and in need of thorough study. Of its contents, we know next
to nothing; the little that we have learnt from therapeutic
experience is neither sufficiently established by facts nor based
upon intelligible scientific principles.
We are acquainted with the specific action of some few reme-
dies upon certain functions of the cord, but these actions are
seldom required. We are still quite ignorant in regard to most
of the remedies we employ, How they act upon the cord and its
188 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
nutrition — although we are especially fond of using them in
organic diseases of this organ.
We therefore limit ourselves to as brief an enumeration as
possible of the internal remedies, leaving the most of what is to
be said to the special part of this work.
A leading remedy in disease of the spinal cord is certainly
strychnia, with the preparations of nux vomica. Its physi-
ological action consists in a very great augmentation of the
spinal reflex action, probably due to a direct irritation of the
central ganglion cells by the poison. It also stimulates the vaso-
motor centres very powerfully. Upon the motor nerves it seems
to have no influence, but upon the sensory apparatus it acts by |
increasing their capacity for excitement. Finally, it is said to
increase considerably the flow of blood to the spinal cord.
Strychnia has been applied in many ways to the treatment of
spinal diseases. But in most cases it is totally useless, for the
increase of reflex excitability can be of little use to the patient
so long as the disturbance of nutrition exists, which causes the
paralysis. It then does nothing but produce energetic reflex
jerkings in the paralyzed parts, without aiding the restoration of
tissues (Gull). In very irritable and easily exhausted patients, in
irritative processes in the cord (tabes, myelitis, spinal irritation,
etc.) it seems to do positive harm, and its use has been of late
almost abandoned. Even such fortunate cases as those lately
published by Acker,' are hardly to be considered in comparison
with the numerous cases of failure. 7
The use of strychnia is, however, only allowable in old cases
of palsy, or when the principal lesion has been repaired without
a full recovery of function. (Nevertheless, in the most of such
cases electricity will be a much surer and more harmless agent.)
It ought also to be tried in purely functional weakness of a torpid
nature, in order to add to our knowledge of the subject. In such
cases it seems to act in moderate doses as a nerve-tonic. In cases
of spinal anemia producing disturbance of nutrition, it may be
used. Finally, it seems to act well in paralysis of sphincters, in
weakness of the genito-urinary organs, in enuresis nocturna, per-
1 Arch, £. klin. Med. XIII. p. 488,
is OG ow ttt phan
GENERAL THERAPEUTICS. 189
haps when these disturbances depend on anomalies of the reflex
centres in the lumbar cord.
The watery extract of nux vomica is given in the dose of
from one-half to three grains (0.03-0.20); the alcoholic extract,
in the dose of from one-sixth to one grain (0.01-0.06) ; the tinc-
ture of nux vomica, from five to fifteen drops; and nitrate of
strychnia, from one twenty-second to one-sixth of a grain (0.003-
0.01), best by subcutaneous injection in the same doses.
Coniine acts in some respects in the opposite way. It directly
paralyzes the motor nerves, but seems also to have a specific
action upon the spinal cord, as it powerfully depresses the reflex
excitability. It is therefore available for the relief of spasmodic
conditions, especially those of a reflex character. (Dose of the
conium herb, from three-quarters to four and a half grains
(0.05-0.30) ; coniine, from one-sixtieth to one twenty-second of a
grain (0.001-0.003), dissolved in water.)
Curare has a very similar action, directly paralyzing the
motor nerves and diminishing the reflex action of the cord. It
is a very uncertain remedy, and may be dispensed with.
Calabar bean lessens and destroys the excitability of the
ganglia of the cord, especially in the gray anterior columns, giv-
ing rise to paralysis, loss of reflex excitability, and of the sense
of pain. This remedy is therefore to be used in cases of exagge-
rated reflex action (in tetanus, the intoxication of strychnia,
reflex contractures). Dose of extract, from one-twelfth to one-
third of a grain (0.005-0.02), in solution or pills.
Ergotin (or ergot) has a powerful effect upon the vessels, and
according to Brown-Séquard, a special tendency to the vessels
_ of the spinal cord. It is said to produce at the same time a dimi-
nution of reflex excitability. It affects all the smooth muscular
fibres, especially those of the bladder.
It is employed in fluxionary hyperzemia and paraplegia; in
the latter disease it is especially useful (according to Brown-
Séquard) when there is hyperemia or chronic inflammation of
the cord and its membranes, while it is contra-indicated in the
absence of symptoms of irritation or hyperemia. (Dose of
aqueous extract of ergot, from one and a half to seven and a
half grains (0.1-0.5) internally, from ong-sixth to one and a half
190 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
grains (0.01-0.10) subcutaneously ; of tincture of ergot, from ten
to thirty drops.
Atropine (or belladonna) has also a powerful action upon the
vessels, and in large doses, according to Brown-Séquard, it spe-
cially contracts the vessels of the cord. It further depresses the
excitability of the motor and sensory nerves and muscles; its.
action upon the cord itself is unknown. Brown-Séquard recom-
mends it in the same affections as ergot. (Dose of extract of
belladonna, from one-sixth to one and a half grains (0.01-0.10),
of sulphate of atropia, from one one-hundred and twentieth to
one-thirtieth of a grain (0.0005—0.001—0.002).
Nitrate of silver. This remedy was first recommended by
Wunderlich‘ in progressive spinal paralysis, and since then has
been much used in tabes and other forms of sclerosis of the cord.
It is undeniable that in many cases it has produced most decided
effects: that it removes the pain, lessens the anzesthesia, improves
the ataxia and the paralysis, and in many cases brings about a
complete cure. But its precise mode of action and its special
indications are as yet entirely unknown. Injurious effects are
reported by many physicians. Dose from one-sixth to one-third
of a grain (0.01-0.02), three times a day, best given in the form of
pills ; to be continued for a long period.
Lodide of potassium has been much used in diseases of the
cord, as in so many other neuroses; and not rarely with success.
Its mode of action and the special indications for its use are quite
as obscure as those of nitrate of silver. Its well-known action
upon a variety of pathological products, various forms of inflam-
mation, exudation, etc., furnishes so tempting an excuse, that
it is tried over and over again. It is prescribed a good deal in
exudative inflammations of the meninges, especially in the chro-
nic stage; in chronic inflammations of the cord itself, especially
when they can be ascribed to a rheumatic origin; in new forma-
tions, sclerosis, etc. Its chief employment is found, of course,
in cases where syphilitic action is suspected. Let the dose not
be too small; from fifteen to forty-five grains (1.0 to 3.0) each
day. Nearly the same is true of the mercurial preparations, so
frequently used.
’ Arch, der Heilkunde, II. 1861. p. 193, and IV. 1863. p. 43.
GENERAL THERAPEUTICS. 191
Bromide of potassium, among other effects, lessens the reflex
activity of the cord, and afterwards paralyzes the peripheral
nerves. It contracts the vessels of the brain, and is believed to
act thus as an hypnotic. It therefore appears indicated in cases
of increased reflex excitability, and in reflex contractures ; it
further appears useful in pain, neuralgia of centric origin, sleep-
lessness, and conditions of sexual irritation. The dose given is
from fifteen to thirty grains (1.0-2.0); or from one and a half to
two and a half drachms (6.0-10.0 .grammes) a day.
A portion of the toxic effects of arsenic are produced upon
the spinal cord; but we do not know them very precisely.
Probably the chief part is due to the effect upon the general
nutrition and the tonic action upon the nervous system; it is
highly recommended by Isnard, and is given in the usual
manner.
Phosphorus has been repeatedly recommended for various
neuroses, and in tabes, paraplegia, etc. It has not yet obtained
a general recognition ; it seems to be very dangerous, and not
specially efficacious.
Of the physiological action of zine and its preparations upon
the cord and upon spinal symptoms, we know almost nothing.
It is much used empirically as anervine, and may perhaps be of
value in conditions of functional weakness. It is most employed
in the form of the oxide and valerianate.
Quinia is held by many physicians, both old and young, to
be useful to the spinal cord. Physiological researches give us
few grounds for this belief. Its use in practice has been confined
almost exclusively to its anti-febrile and anti-zymotic effects ;
it has also an invigorant action. It cannot be doubted that
quinia has a powerful action upon the central nervous system,
but the manner of its action, and the parts affected, are quite
unknown.
It is employed in spinal nervous weakness, in excentric pains,
in fever, in spinal complaints which depend on malaria. The
dose is graduated according to the effect sought ; small doses are
the favorite ones for the strengthening ¢ffect.
The sodio-chloride of gold has been repeatedly recommended
as a remedy in spinal complaints; its claim to the title is still
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192 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
doubtful. The dose is from one-sixth (0.01) to three-quarters of
a grain (0.05).
We might prolong this enumeration at pleasure, but the
reader doubtless has enough ; further explorations of this dark —
and doubtful region will prove of little advantage.
We would add a few words upon the diet cures, which are
believed to act like courses of internal drug medication. They are
not of much importance in diseases of the cord. But milk cures, 4
whey and grape cures, and the like, may produce a desirable }
effect upon the general nutrition, and thus upon that of the |
spinal cord. :
The same is true of cowrses ef mineral water, taken inwardly. ‘
Nothing is known of any specific action upon the spinal cord
and its affections. Nevertheless, such courses may be required —
by certain causal or symptomatic indications, and may then ~
have a most excellent effect. | :
3. Symptomatic Remedies and Methods,
We are very often compelled to give sedatives in spinal dis-
eases ; especially for the relief of the frequent excentric pains,
pains in the back, painful reflex contractions and spasms, etc.
In addition to the ordinary narcotics we possess a number of
remedies, discovered empirically. |
The best of anodynes—opium with its preparations—increases
the reflex excitability of the cord, and does not depress it except
in large doses. It must, therefore, be avoided in cases of reflex
spasm, but is of very great value as a simple antidote to pain.
‘This is especially true of subcutaneous injections of morphia.
But the patient must not be allowed to form a habit of relying —
upon it, as that always exercises an unfavorable influence upon ~
the general progress of the disease, and the habit is extremely
hard to break up. |
It is recommended to make trial of the remedies above named
—coniine, atropia, calabar, etc. It has been found empirically A
that in many cases bromide of potassium, quinia, etc., have a
specially quieting influence.
‘
GENERAL THERAPEUTICS. 193
Electricity also often has a very good effect; the relief to
_lancinating pains, especially by local faradization or galvaniza-
tion, is often quite magical—though usually but temporary.
For painful priapism, or great sexual excitement, use bromide
_of potassium, lupulin, camphor, ete.
For obstinate sleeplessness, the ordinary hypnotics are used ;
they often fail, and their continued employment is not without
danger. We must then have recourse to all auxiliary methods.
The cold-water treatment (cold washing of the feet, Priessnitz’s
packing of the calves) is very advisable. |
In other cases we shall make more use of irritants, as in
, 4 paralysis, anesthesia, weakness of the bladder, etc. Here elec-
tricity is the chief remedy. After it, strychnia, ergot, etc.
Tonics are often indicated, as the preparations of iron, the
chalybeate springs ; also quinia, various bitters and tonics, ac-
cording to general principles.
_ In many diseases of the cord, the treatment of cystitis forms
a specially important point, as this often constitutes the first
serious danger to life.
_ The observance of suitable prophylactic rules will be of the
first importance in this complaint ; and of these the chief one is
—never to allow the urine to stagnate in the bladder. The evacu-
_ ation ought, therefore, to be aided by pressure upon the bladder,
or by exciting reflex action by kneading and pressing the wall of
_ that organ ; or by raising the patient in order to gain the mechan-
ical advantage. If necessary, catheterize regularly and from
the beginning, twice a day, hut with extreme precaution and
cleanliness. It is also advisable to assist and complete the evacua-
tion by the principle of the siphon, depressing the outer orifice
_ of the catheter below the level of the fundus vesicee. In all cases
we should see that the bladder is frequently evacuated, and
- should lessen. the tendency to decomposition in the urine by
making the patient drink copiously of common water, by the use
of the waters of Ems, Selters, or Wildung, by exhibition of sali-
cylic or benzoic acid.
If there is incontinence of the bladder, the best means for
keeping the patient in a state of tolerable cleanliness consists in
a regular artificial evacuation. Frequ@nt washing, the use of
194 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
portable urinals, or (in the case of women) placing sponges in
front, are also necessary.
When catarrh of the bladder has appeared, it may be arrested
in its further progress, or even cured, by preventing the process
of decomposition, and checking the tendency of the urine to be-
come alkaline. For this purpose salicylic acid is found a most
excellent remedy, according to the experience of Fuerbringer,’
which my own in part confirms. From thirty to sixty grains
are given daily in watery solution or emulsion by the mouth,
and injections into the bladder (1 part to 500) may be added. It
brings back the acid reaction, removes the foul odor, and clears
up the urine. Benzoic acid is said by Gosselin and Robin’ to act
similarly, and is claimed to be the best agent for restoring the
acid reaction to ammoniacal urine, and relieving the catarrh
which depends upon this condition. (Dose from thirty to ninety
grains daily in emulsion or powders.) ‘The use of lime-water,
Wildung water, and various alkaline waters (Ems, Vichy, Selters,
etc.), seems to have a good effect in light cases. Clemens * recom-
mends ergotin for the same purpose.
As a direct remedy for catarrhal inflammation of the bladder,
the usual astringents are given—uva ursi, tannic and gallic acid,
copaiba, oil of turpentine, tar-water, etc.
But in all severe cases, accompanied with abundant formation
of pus and mucus, a good deal of ammoniacal decomposition,
ulceration, etc., it will be indispensable to wash out the bladder,
regularly and with great precaution. Injections for this purpose
are composed of lukewarm water, which may gradually be made
colder, of salt water, weak solutions of tannin, nitrate of silver,
salicylic acid (1 : 500), etc. They may be made either with a sim-
ple syringe or with the irrigator, but the catheter d double cou-
rant is the most suitable.
In all such cases it is advantageous, while pursuing the above
plan, to attack the palsy and anzesthesia of the bladder with elec-
tricity.
’ Berl. klin. Wochenschr. 1875. No. 19. Zur Wirkung der Salicylsiiure. Jena, 1875.
p. 62.
* Traitem. de la cystite ammoniac, par l’acide benzoique. Arch, gén. Nov. 1874.
* Deutsche Klinik. 1865. No. 27.
GENERAL THERAPEUTICS. 195
A careful regulation of the diet is very important. Patients
with decided catarrh of the bladder must use the blandest and
most digestible articles of diet, avoiding all acid and highly
spiced articles; the use of beer and strong sweet wine is unad-
visable ; but a light semi-acid white wine, or a good red wine,
diluted with water, is allowable.
Of almost more importance than the treatment of cystitis is
that of ded-sores. These form one of the most horrible complica-
tions, infinitely increasing the patient’s sufferings, and must be
avoided by all possible means, as it is extremely hard to heal
them when once fully developed.
The chief remedies are of the prophylactic sort, and the princi-
pal point to observe is the avoidance of all continued pressure
on the skin. This can be attained by frequent change of pos-
ture, by air-pillows, water-cushions, lying on bags of millet, on
buckskin, ete. All filth and irritation of the skin where pres-
sure is borne must be avoided as far as possible ; removal of
feeces and urine, frequent washing, anointing with grease and oil
are the chief precautions. And finally, a slight stimulation of
the tone of the cutaneous vessels may assist in preventing bed-
sores, for which purpose frequent washing in cold water, or in
spirit, or the alternate application of ice and poultices (Brown-
Séquard), or moderate cutaneous faradization may be used.
If a bed-sore appears in a light form (superficial ulceration,
furuncles, etc.), it may often be healed by simple treatment,
though slowly. Great cleanliness, frequent washing, dressing
with zinc ointment, or mildly irritant salves, chamomile water, or
aromatic wine will be sufficient in connection with the prophy-
lactic rules.
The matter is less simple in the case of the true gangrenous
sore, which often reaches an enormous size, and extends without
cessation downwards and at its borders. The first object in this
case consists in assisting the throwing off of gangrenous portions,
and developing the reactive inflammation ; according to Brown-
Séquard, the alternation of ice (for ten minutes) with poultices
(for one or two hours) is an excellent means to thisend. The
dead tissues, separated by the line of demarcation, should be got
rid of as soon as possible, and an antiseptic dressing applied.
196 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Carbolic acid has great advantages over the remedies formerly
used (camphor wine, aromatic wine, “‘unguentum contra decubi-
tus,’’ etc.). It should be applied in a watery or oily solution, by
preference upon good surgical wadding. Under this treatment I
have seen the wounds take on the most healthy granulations, and
even very advanced bed-sores heal.’
It is often very hard to find a suitable position for the pa-
tient, especially when there are bed-sores on the sacrum, the
ischiatic protuberances, trochanters, heels, etc. Much care and
observation must be directed to the prevention of new sores.
Water-pillows and air-pillows must be used in their various
forms. In the worst cases I have found it useful to swing the
lower leg on a pillow, placing the knee-joint and hip-joint in the
position of rectangular flexion; this may, to some extent, also
free the sacrum from pressure.
4. General Observations—Method of Life.
The general care of patients with spinal disease, their diet and
manner of life, must be governed strictly in accordance with the
requirements of the disease. Many mistakes and negligences are
committed in these matters, which neutralize the success of the
other treatment.
The rules must differ widely, of course, in different cases.
In the acute, inflammatory, and similar forms, the proper
diet, rest in bed, avoidance of all excitement and effort must be
ordered.
But in the chronic forms also, in functional as well as organic
disturbances, the patient must in general be very careful, and
must observe the following general rules (with suitable adapta-
tion to his case), with a strictness proportionate to the weakness
and irritability of the patient’s nervous system, to the amount
' Hammond (Diseases of the Nervous System, 3d edition. 1873), following Crussel
and Spencer Wells, recommends a simple galvanic element as an excellent means of
curing bed-sores, A thin silver plate is laid on the sore, a similar plate of zinc, with a
piece of moist cloth underneath, upon a distant part of the skin, and the two are con-
nected by a wire. After a day or two the beneficial effects are seen. I have no per-
sonal experience of this, :
GENERAL THERAPEUTICS. 197
of symptoms of irritation present, to the readiness with which
he suffers from the effects of external circumstances.
The dieé must be corroborating and tonic in most cases, with-
out being in any way exciting. Milk, meat, eggs, light vegeta-
bles, puddings, and fruits are allowed and required; an abun-
dant supply of fatty nutriment (butter, cream, oil, cod-liver oil)
is perhaps useful in a good many cases; strong seasoning, and
very complicated and heavy dishes must always be avoided. A
glass of wine or beer at table is usually allowable, but their ex-
cessive use is to be strictly forbidden. Strong tea and coffee
must be avoided in most cases, Smoking within moderate
bounds is allowed.
In regard to the general regulation of the life, the allowable
amount of work and rest, of bodily and mental activity, we must
be governed chiefly by the state of the patient’s strength, It is
but rarely that chronic cases can be condemned to continuous
confinement in bed ; yet there may be many decided indications
for it. Brown-Séquard directs the avoidance of lying on the
back, as far as possible, in conditions of inflammation and hyper-
gemia.
It is usual and desirable to allow a moderate amount of active
bodily exercise when practicable, but let the patient be warned
against every excess of exertion! Great injury is thus often
done; for instance, by too long walks; the patient must be espe-
cially cautious about this while taking a course at a medicinal
spring.
Mental effort, the practice of a profession, cannot always be
forbidden on account of circumstances; and the disease is usually
so tedious that such a measure would be excessively irksome.
Let this, therefore, be allowed within judicious limits, every ex-
cess of effort being forbidden, especially night-work, which is
especially injurious.
The same is true of sexual indulgence; between different
persons and cases there is a very great difference of power. The
permission must be determined by the patient’s condition ; in all
cases it is well to limit the indulgente as much as possible, and
in many to forbid it wholly ; in a small number, moderate indul-
gence is permissible.
198 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
In most cases the need of sleep is among the things to be first
attended to, and in connection with this, all exciting and fati-
guing society must be forbidden. The patient must also avoid
taking cold, and clothe himself accordingly. He may by degrees
harden himself by using cold ablutions, and so on.
A great deal of fresh air will almost always be beneficial to
patients ; let them sit or drive in the open air, especially on the
mountain and in the forest. This is the principal reason for
ordering many patients to pass the winter in the south, especially
‘ when their home is in a rough northern climate, which keeps
them in-doors the whole winter. Such patients will find a winter
in South-western Germany a great pleasure; others will like the
banks of the Lake of Geneva, the Riviera, Meran, Venice, etc.,
where they may spend several hours every day in the air. All,
however, will depend on individual circumstances.
Il.
SPECIAL DISEHASKHS.
1. Diseases of the Membranes of the Spinal Cord.
1. Hyperamia of the Meninges of the Cord, and of the Cord
itself.
J. P. Frank, De vertebralis columne in morbis dignitate. Select. opuscul. med.
Ticin. 1792. p. 1.—Ollivier, Traité des malad. de la moélle épin. ITI. éd. 1837.
Tom. II. pp. 1-137.--Hasse, Krankh. des Nervensystems. 1855; 2. Aufl. 1869.
p. 656.—Brown-Séquard, Diagnosis and Treatment of the Principal Forms of
Paralysis of the Lower Extremities. London, 1861.—Hammond, A Treatise on
the Diseases of the Nervous System. 8d ed. 1873. — Leyden, Klinik der
Riickenmarkskrankheiten. I. 1874. p. 362.—M. Rosenthal, Klinik der Nerven-
krankheiten. 2, Aufl. 1875. p. 270.—G@auné, Epidémie de congestion rhachid.
Arch. gén. Janv. 1858. p. 1.—A. Mayer, Die Bedeutung des Riickenschmerzes
u. s. w. Arch, d. Heilk. I. 1860. p. 373.—Zeudet, Arch. génér. Mars. 1863.
p. 257.—Desnos, Observat. de congestion méningo-spinale, etc. Gaz. méd. de
Paris. 1870. No. 14. p. 187.—Steiner, Fall von Riickenmarkshyperimie. Arch.
der Heilk. XI. 1870. p. 233.
It is impossible to treat of hyperemia of the spinal meninges
without including that of the spinal cord. And it is hardly con-
ceivable that any considerable hyperemia of the meninges should
exist without a similar condition existing in the cord also, as the
vascular supply of both is the same. The symptoms of menin-
geal and spinal hyperzemia coincide ; their etiology and treat-
ment are the same. Defective as is our knowledge of both forms
of disturbance, we must therefore consider them together.
Definition.—By hyperzemia of the cord and its membranes
we understand an increased supply of blood in the tissues con-
tained within the vertebral canal, the spinal cord, its membranes,
and the extra-meningeal cellular tissue. This excess of blood
2900 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
may be due either to an increased flow of blood, when it is usu-
ally of an arterial character (active, arterial hyperemia, fluxton),
or to arrest of the return current of blood, when it is usually rs
a venous character (passive hyperemia, venous stasis).
practice, these two sorts cannot always be clearly separated.
The frequency and importance of spinal hyperemia have certainly been over-
estimated hitherto. This results chiefly from the fact, that in many fatal cases
those who examined the body have been content with the mere macroscopic ap-
pearance of hyperemia of the cord, without reflecting that a cord which looks
quite normal to the naked eye is by no means necessarily so in its finer anatomy.
Ollivier, in especial, has gone much too far in this, and has thrown together under
the title of ‘“‘Congestions spinales” a variety of things which are certainly of a
much more serious character. The spinal and meningeal hypereemias certainly need
a fresh and more discriminating study.
Etiology and Pathogenesis.
Little is known as to the existence of any special predisposi-
tion to spinal hypereemia. On the contrary, it deserves special
attention, that the arrangement of the vessels of the cord pro-
tects it in a peculiar manner from mechanical disturbances of
circulation, as is shown by Hayem’s* luminous observations
upon the distribution of the arterial and venous vessels within
the spinal canal. The many anastomosing arteries, coming from
all sides, and the enormous venous plexuses, which carry off
the blood from the spinal canal both above and below the dia-
phragm, are the cause of this. The diseases of the vessels of
the cord have not yet been accurately studied. ,
In respect to the occasional causes, we must attempt to dis-
tinguish the two principal forms of hyperemia.
Active hyperemia has certainly some relations to hyperzemia
of the brain ; this follows from the fact that the spinal arteries
originate from the vertebrals. But hyperemia of the cord usu-
ally recedes into the background, as compared with hyperemia
of the brain, if the latter is present.
Hypereemia of the cord and its membranes is produced—
a. By functional stimulation of the cord. In this case, as
Des hémorrhagies intrarhachidiennes. Paris. 1872. pp. 7-20.
HYPERZMIA OF THE SPINAL MENINGES, 201
everywhere, the activity of the organ is accompanied by an in-
creased flow of blood towards it; and in case of excessive exer-
tion the flow may continue and form a pathological state, as in
overwork of body, severe marching, violent sexual excitement,
excess of coitus, spinal spasm, and so on. The absolute proof
of the agency of either of these circumstances remains to be
brought.
b. By nutritive stimulation. Active hypereemia accompanies
a number of disturbances of the nutrition of the cord and its
membranes, is never absent in acute inflammations of the organ,
and in the first stages of the latter is often the only macroscopic
appearance.
c. By toxic stimulation. Poisoning with strychnia, nitrite
of amyl, carbonic oxide, chronic poisoning with alcohol or ab-
sinthe, etc., produce spinal hyperzemia.
d. By collateral fluxion, as in sudden suppression of the
menses, in dysmenorrheea, in the turgor of hemorrhoids or men-
struation, in suppression of hemorrhoidal bleeding, in sup-
pressed perspiration of the feet or when the feet are always cold,
etc. In most of these cases, nothing but the assumption of a
lessened resistance on the part of the spinal vascular system can
explain why this particular region should become the seat of
hyperzemia.
e. By the effects of cold. This is thought by Hammond to be
the most common cause of spinal hyperzemia; a wetting to the
skin, when one is making too great bodily exertions, is thought
especially dangerous. Cold produces its effects both by collate-
ral fluxion, through interference with the circulation in the skin,
and also by a reflex action from the cutaneous nerves upon the
spinal vessels, which are dilated.
J. By trawmatie causes, as shock to the cord, a fall on the
back or seat, etc. (Leudet); the mechanism of this action is still
obscure.
g. Finally, severe febrile diseases (typhoid, acute exanthe-
mata, malarial infection, etc.) have been observed to be accom-
panied by spinal hyperzemia, and thé latter has appeared epi-
demically in a girls’ boarding-school (Gauné).
Of passive hyperemia, the most prominent cause is to be
902 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
sought in general venous congestion or stasis, such as is pro-
duced by diseases of the heart and lungs, or accompanies severe
spasmodic affections (tetanus, eclampsia, etc.), and occurs dur-
ing the death-agony ; also, in local venous stasis, especially such
as is produced by obstructions in the portal system, or in the
pelvic veins, in the case of hemorrhoids, abdominal plethora,
affections of the liver, tumors in the pelvis or by the side of the
spine pressing on the venous trunks and plexuses.
Pathological Anatomy.
The anatomical evidence bearing upon hypereemia in the spi-
nal canal is as uncertain and ambiguous as possible. Compara-
tively very few spinal canals are opened at autopsies, which
makes it hard to estimate the relative proportion of normal and
of pathological conditions. The post-mortem changes add a
great deal to the difficulty of establishing the fact of hypere-
mia; the arteries are emptied, the veins over-filled; we may
find, on the one hand, a deceptive disappearance of hyperzemia,
which existed during life, and, on the other, a deceptive appear-
ance of hyperemia, having its origin during the death-struggle
or after death, without having existed during life. Add to this
the imbibition of the coloring-matter of the blood, and the gravi-
tation of blood to dependent parts—all of them circumstances
which may confuse the judgment and obscure the facts. |
Nevertheless, the existence of hyperemia, in marked cases,
can generally be detected with certainty.
Active hyperemia is betrayed by a rose-color or scarlet fod:
ness of the cord and its envelopes, by injection of the minute
vessels, by tortuosity of the arteries and veins; the white sub-
stance of the cord appears of a rose-color; the gray is darkened,
reddish-gray, brownish ; under the microscope the finer arteries
and capillaries are seen crowded with blood. In the more
marked cases punctiform extravasations and ecchymoses are
seen dotted over the membranes and in the substance of the
cord, and often larger extravasations. The spinal fluid is usu-
ally increased, is muddy, and of a reddish color.
HYPERAMIA OF THE SPINAL MENINGES. 203
In passive hyperemia the extra-meningeal plexuses of veins
are especially crowded with blood, all their veins are enlarged
and tortuous, and the coloration approaches a cyanotic hue.
Ecchymoses may be present here also; the spinal fluid is almost
always increased to some extent.
In a few cases something is seen which lies between the condi-
tion of congestion and that of inflammation.
In chronic or often-repeated hyperemia the pia and arach-
noid are thickened and opaque, and highly pigmented.
These hypereemias do not always extend over the entire spi-
nal canal, but often are confined to the cervical, or lumbar, or
other portions.
The cerebral hyperzemia, and the diseases of other organs
which cause spinal hyperzemia, need not here be described.
Symptoms.
In spite of the great certainty with which congestions and
stases of the cord are spoken of, their symptoms are still ex-
tremely obscure, and the diagnosis is surrounded by many diffi-
culties and doubts. We may therefore sum up the subject very
briefly, leaving to the future a more thorough elaboration of this
branch of spinal pathology.
The most prominent symptoms are those of sensory irrita-
tion ; the patient complains of pain in the loins and along the
spine; the pain is dull, oppressive, not very severe, and is not
always increased by pressure upon the spinous processes. The
additional symptoms of paresthesia (tingling, formication, etc.)
and fearing pain in the extremities (especially the lower) are
soon perceived. A slight hyperesthesia of the skin is usually
associated with a moderate increase of reflex activity. The girdle
sensation is often felt (Hammond). Symptoms of motor irrita-
tion are more rare; as slight transitory jerking of the muscles,
trembling of the limbs, etc. The electrical excitability is said to
be often increased (M. Rosenthal). *
All these symptoms can be derived without difficulty from
the increased flow of blood, and the consequent stimulation of
904 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
the nervous apparatus, and doubtless belong principally to the
condition of active hyperemia; but they may also, in part, be
explained by the mechanical irritation and the violence done to
the tissues by the dilated vessels,
Distinct symptoms of depression are also seen, and usually
make their appearance at the beginning with those of irritation.
A sensation of numbness and heaviness is perceived in the lower
extremities ; slight anesthesia is also demonstrable, but seldom
ina severe form. Motor weakness is never absent, though usu-
ally quite moderate in amount (slight fatigue, heaviness of the
limbs), and it is rarely—perhaps in simple hyperemia never—
the case that complete paraplegia occurs. Symptoms of weak-
ness or palsy of the bladder seem rare, but are occasionally de-
scribed. Hammond says that he has often observed erection of
the penis.
It is not easy to explain the paretic symptoms. We may
take into account the pressure of dilated vessels upon the ner-
vous elements of the cord and the nerve-roots, the pressure ex-
erted by an increased quantity of spinal fluid, and finally, per-
haps, the defective nutrition of the nervous apparatus, dependent
on the biocking of the cireulation.
The symptoms of spinal hyperemia are, almost without ex-
ception, bilateral, and are usually limited to the lower half of
the body, or at least they begin in the lower extremities; they
seldom ascend to the upper, and if they do the extension is usu-
ally rapid ; the respiration, in such cases, is said to have been
disturbed, with short, dyspnoic breathing, and even paralysis of
both facial nerves (Steiner).
Usually the symptoms exhibit a certain transitoriness, which
is quite characteristic ; they change their seat and degree of se-
verity quickly, and even grave symptoms may completely dis-
_ appear with striking rapidity.
Brown-Séquard says that he has observed all the symptoms
of hyperemia aggravated by lying on the back, with the head
and legs raised, while they were relieved by lying on the face, or
by standing and walking, owing to the effect of gravitation upon
the circulation in the spinal canal. For this reason such patients
are said to feel worse in the morning while in bed. Others say
HYPERZMIA OF THE SPINAL MENINGES, 205
that standing and sitting make the symptoms worse, especially
those of paresis, and refer this to the gravitation of the increased
quantity of spinal fluid ; such patients are better in the horizon-
tal posture.
There is no fever in simple hyperzemia of the cord. The pulse
may be accelerated, or retarded, if the hyperemia extends to
the spinal centres of cardiac innervation. The general health is
more or less interfered with.
Distinct groups of symptoms belonging respectively to active
and passive hyperemia have not yet been made out. But con-
clusions drawn from the preponderant nature of the symptoms
will in most cases be correct. If those of an irritative character
prevail, we shall think rather of active hyperzemia ; if symptoms
of depression, of a passive form. But we should remember that
most of the symptoms may occur in either form, though in vari-
ous degrees of intensity.
Course.—The development of hypereemia of the cord is either
sudden, so that the entire series of symptoms is soon completed,
or it is slow, and gradually increases in intensity ; this is the
more usual case. Having been developed, they continue with
various degrees of fluctuation for days, for weeks, or months.
The disease usually ends in recovery; this is often brought
about rapidly, by critical hemorrhages (menstruation, hemor-
rhoidal bleeding) or therapeutic measures. Relapses are not
rare; and the cure is often accomplished by a very gradual dis-
appearance of all the symptoms.
In many patients (those with piles, ete.), we find hyperemia
of the cord becoming habitual, returning regularly and fre-
quently. This may lead by degrees to severer disturbances, by
the development of chronic inflammations and proliferation.
Death, as resulting from hyperemia solely, is rare ; it is con-
ceivable that it might follow an extension of the affection to the
important centres in the medulla oblongata and cervical medulla.
But, as a rule, the danger to life depends on hemorrhage, soften-
ing, and other changes of the spinal cord.
206 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
Diagnosis.
A demonstration of the fact that hypersemia can exist in the
spinal cord and can be recognized by its symptoms is not re-
quired. Although its existence is often very hard to demonstrate
in the dead body, or quite impossible, yet is its existence in the
highest degree probable, besides being proved by a number of
clinical observations which are hardly susceptible of any other
interpretation.
Not all, nor nearly all, the cases known in literature by this
name are to be considered as deserving it; few of the uncompli-
cated cases which end in death can be reckoned as hyperemia ;
and if nothing is discovered af the autopsy of such patients, the
cause, doubtless, lies in defective methods of observation. It
certainly seems to us improper to interpret as simple hyperemia
the large class of cases with severe and threatening symptoms
(e. g., the case of Desnos, numerous cases in Ollivier, etc.) ; and
the fact that nothing besides hyperemia has been discovered in
many instances of so-called acute ascending paralysis, after care-
ful microscopical examination, is far from proving that the fatal
result was due to hypersemia.
The diagnosis of hyperemia of the structures within the
spinal canal is chiefly based upon the slightness of the sensory
and motor disturbances, which very rarely become severe ; upon
the frequent and rapid changes in symptoms, especially as
regards their location; upon their non-febrile, wsually short
_ and favorable course, and upon the success of treatment suited
to relieve hyperzemia.
It is obvious how uncertain these signs are, and how hard it
is to separate them from those of slight inflammation or func-
tional weakness. It is the duty of the future to throw light
upon the matter. For the present, the following hints must suf-
fice for the differential diagnosis. Spinal hyperemia is distin-
guished from
Concussion of the spinal cord, by its comparative slowness of
access, mildness, and rapid disappearance ;
Spinal meningitis, by the absence of spasm of the back and
neck, fever, and pains on moving the limbs ;
HYPERZMIA OF THE SPINAL MENINGES. 207
Acute myelitis, by the absence of fever; severe symptoms of
paralysis, contractures, paralysis of the bladder, and bed-sores ;
Spinal apoplexy, by the comparatively slow development,
slightness of the paralytic symptoms, and rapid termination in
recovery ; '
Spinal anemia, chiefly by the fact that lying on the back
gives relief to the symptoms of the latter.
Thus, by exclusion and by observation of the course of the
disease, we shall in many cases attain a tolerably certain diag-
nosis.
The prognosis of spinal hyperemia must be regarded as fa-
vorable upon the whole. Serious complications may, of course,
render it gloomy. In habitual, frequent hyperemia, if the cause
continues to exist, if the walls of the blood-vessels possess little
power of resistance (involving the danger of hemorrhage), the
prognosis will, of course, be serious.
Treatment.
Everything must first be tried, to fulfil the cawsal indication
—in regard to which, detailed directions will not be required.
The most favorable cases are those where we can ascertain that a
discharge has been interfered with, or venous congestion exists,
or exposure to cold has occurred; the remedies for these are
obvious.
As a direct measure against the hyperemia, the patient should
be made to take a switable position, avoiding the back, and
preferring the side or face, with the extremities as low as possi-
ble. Next in order, blood-letting is the remedy most recom-
mended. Venesection will be practised only when the symptoms
are very violent—in plethoric, robust persons; a much better
plan is to draw blood from the region of the spinal column,
or from the anus, vagina, cervix uteri, etc., according to the
nature of the case. From ten to twelve moist cups along the
vertebral column, or a corresponding number of leeches, repeated
according to circumstances at fixed ingervals, will be most useful.
The attempt has also been made to treat spinal hyperemia
by derivation to the skin. A great variety of remedies may be
208 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
used ; the physician may select according to his patient’s special
case, but the indications are, unfortunately, very unsettled. The
cold-water treatment has certainly a considerable sphere. For
active hypereemias, the hydro-therapeutists recommend milder
procedures, as cool affusion and wraps to the back, - soothing
frictions, and sitz-baths; for the passive form, a more energetic
course, including cold affusions and douches, exciting sitz-baths,
energetic cold. packing, and sea-baths ; for such cases the gaseous
thermal brine-baths (Rehme and Nauheim) seem especially suited.
A direct derivation of the blood to the skin is obtained by
hot foot-baths with mustard and the like, by the warm douche
applied several times a day to the back, by washing with a cold
and a hot sponge alternately, by moderately warm full baths.
Sinapisms, blisters, etc., may also be of use in some cases.
A direct action upon the vessels of the cord has been attempted —
by applying Chapman’s ice-bags to the back, and by the galvanic
current. The indications for these measures are not precise, and
it will be necessary in each case to be governed by the success
that seems to be obtained.
Derivation to the intestine is also much favored in the form
of saline purgatives, or, in more chronic cases, of the saline medi-
cinal springs (Homburg, Kissingen, Marienbad, Karlsbad, etc.).
Among internal remedies, ergotin and belladonna should be
tried by preference; the former must be given in large doses
(Hammond). ,
Diet and regimen must be governed by personal circum-
stances ; everything which might increase the hyperemia (espe-
cially coitus) must be avoided.
2. Hemorrhages of the Membranes of the Cord—Hemator-
rhachis—Meningeal Apoplexy.
Ollivier, 1. c. 8° 6d. I. p, 465; IL. pp. 90-1387.—Hasse, 1. c. 2. Aufl. p. 664.—
Hammond, 1. c. 3d edition. p. 440.—Leyden, Klinik der Riickenmarkskrank-
heiten. I. p. 867.—M. Rosenthal, 1. c. 2. Aufl. p. 274.
Fallot, Hémorrhag. méningée spinale sousarachn. Arch. gén. 1880. T. XXIV. p.
438.—Boscredon, De l’apoplexie méningée spinale. These. Paris, 1855.—Ch.
Bernard, Observ. d’hémorrh. rhachid; Union méd. 1856. No. 62.—Jaccoud,
Les paraplégies et l’ataxie. Paris, 1864. p. 282.—Levier, Beitriige zur Path-
2S ae ge pa
MENINGEAL HEMORRHAGE. 209
ologie der Riickenmarksapoplexie. Diss. Bern. 1864. (Contains a copious list
of authorities).—Rob. Jackson, Case of Spinal Apoplexy. Lancet. July 3. 1869.
—Hayem, Des hémorrhag. intrarhachidiennes. These. Paris, 1872.—Rabdouw,
Fall von Meningealapoplexie in Folge von iibermiissiger Kérperanstrengung.
Berliner klin. Wochens. 1874. No. 52.
Dejinition.—Hematorrhachis implies any effusion of blood
in, about, or between the spinal meninges. It occurs rarely, but
in quite a characteristic manner. The vertebral canal does not
present favorable conditions for the production of hemorrhage,
as has been reasonably explained by Hasse.
Ktiology and Pathogenesis.
Little is known regarding the individual predisposition to
meningeal hemorrhage. Most of the cases are observed in men.
Of diseases of the vessels of the meninges (fatty degeneration,
‘atheroma), we are mainly ignorant. The relation of hypertrophy
of the heart to these hemorrhages has not been examined.
Among the occasional causes, the first to be mentioned are
surgical injuries of the vertebral column, with or without direct
lesion of the membranes. Such hemorrhages have been observed
to occur in consequence of stabs with swords and knives, frac-
tures, contusions, and shocks of the column, a fall on the feet
and seat, or upon the arms and back of the neck, in new-born
children after severe labor, etc.
Inflammatory and carious processes in the vertebra have in
some cases led to lesion of the membranes and to bleeding from
them. Congestions of the vertebral canal and its contents (the
causes of which have been enumerated in the previous section),
especially those due to suppression of the menses or of a hemor-
rhoidal discharge, are considered especially important causes of
meningeal apoplexy. Mental emotions may act in a like manner
by increasing the action of the heart.
Excessive bodily exertions are a frequent cause of meningeal
bleedings, probably through disturbances in the circulation:
such are the lifting of a heavy weight (Rabow), sudden violent
movement, etc. Among these should be included the meningeal
VOL, XIII.—14
910 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES
apoplexies which so often occur during the violent spasms of
epilepsy, eclampsia, tetanus, trismus neonatorum, etc.
The bursting of blood-vessels or aneurisms into the vertebral
canal has been repeatedly observed (Laénnec, A. Cooper, Pfeufer,
Traube, and others).
Blood effused in the brain or cerebral membranes often passes
down and fills the cavity of the spinal canal.
Of the occurrence of these bleedings in the various hemor-
rhagic and infectious diseases (scurvy, morbus maculosus,
hemorrhagic small-pox, typhoid, etc.) little is known, except
from a few reports of autopsies (see Hayem).
Pathological Anatomy.
It is necessary here to distinguish the various forms according
to the position, distribution, and extent of the bleeding. We
pass over those small ecchymoses and suggillations which so
often accompany hyperemia and inflammation within the verte-
bral canal.
Bleeding between the dura mater and the vertebral canal (in
the extra-meningeal cellular tissue) is probably the most frequent
cause. A dark, usually coagulated extravasation covers the
outer surface of the dura to a varying depth, and infiltrates the
cellular tissue between it and the vertebral canal, especially at its
posterior wall. This extravasation may enclose the entire dura,
but more usually it embraces it only partially ; not rarely there
are several separate foci. The dura is suffused with blood to a
greater or less extent, and often covered with ecchymoses. The
extravasation must be very considerable in order to produce a
visible compression or change in the cord. It often extends
around the nerve-trunks passing out of the vertebral canal.
Bleeding between the dura and the arachnoid (in the so-
called arachnoid sac) is usually diffuse, very movable, partly
fluid and partly coagulated, and usually consists of blood ef-
fused in the brain, though it may proceed from the bursting of
vessels in the spinal meninges.
Of the hemorrhage accompanying many forms of internal pachymeningitis, pro-
MENINGEAL HEMORRHAGE. 211
ducing hematoma of the dura mater, and situated likewise between the dura and
the arachnoid, we will speak under Inflammations of the Dura Mater.
Bleeding in the arachnoid and pia (so-called subarachnoidal
bleeding) is rare. It usually occurs in the subarachnoid cellular
tissue, as the dense tissue of the pia seems little suited to extra-
vasations. A more or less thick layer of dark-red, coagulated
blood, infiltrated into the tissue of the soft membranes, sur-
rounds the cord like a sheath, partly or completely, but in most
cases it is limited in longitudinal extent, being confined to the
length of one or two vertebre. It may be found at various
levels, and in all cases it inflicts severe injury upon the cord.
In all these forms of bleeding, the meninges usually exhibit
but slight signs of reactive inflammation.
The cord itself may be more or less compressed, stained with.
red, softened, and (in the neighborhood of the seat of hemor-
rhage) hyperemic. The same is true of the nerve-roots. The
spinal fluid is turbid and of the color of blood.
Little is known regarding the other changes associated with
extravasations. But it is hardly doubtful that in the spinal
canal the color soon disappears, and the extravasation is partly
reabsorbed and organized. Adhesion of the membranes, prolifer-
ation of connective tissue, and strong pigmentation of the mem-
branes, are considered as the final changes.
Symptoms.
The disease usually begins suddenly and violently—often in
the manner of apoplexy. The patient suddenly falls, with vio-
lent pains, almost always without serious disturbances of con-
sciousness and sense. This mode of attack may be more or less
complicated by the causes, by the nature of the injury, ete.
A slow development of the symptoms is rarer; with warnings
of various kinds, symptoms of spinal congestion, lumbar pain,
headache, for a longer or shorter time before the attack. Pare-
sis then slowly appears, often unaccompanied by pain. The se-
verity of the symptoms may increase after a few hours or days.
The characteristic symptoms are first those of excitement,
caused by physical irritation of the meninges with their abun-
912 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
dant nerves, the nerve-roots, and the cord itself, next those of
paralysis, dependent on the pressure of the extravasation upon
the cord and nerve-roots. According to the seat of the extrava-
sation, it may press more upon the sensory or the motor por-
tions.
The phenomena of excitement are the most prominent at the
first, and chiefly consist of a violent pain, localized at a spot
answering to the seat of the bleeding, and radiating in various
directions, usually corresponding to the distribution of the nerve-
roots first attacked. With this are conjoined excentric sensa-
tions, pain, formication, burning, tingling, etc., in the same re-
gions ; hypereesthesia is also occasionally mentioned, but this
seems rather to belong to the period of reactive inflammation.
Symptoms of motor excitement appear at the same time,
which seem to be of characteristic importance. Spasmodic jerk-
ing of the muscles, occasionally increasing to complete convul-
sions, trembling of the extremities, tonic tension and contracture
of various groups of muscles, are the chief of these. They may
become so active and so prominent that a special form of ‘‘con-
vulsive’’? meningeal apoplexy has been distinguished. These
Spasms are partly deducible from direct irritation of the motor
roots, and partly from reflex excitement.
The vertebral column is stiff and painful at this stage, mak-
ing it very hard, or quite impossible, to rise in bed, sit, or bend.
Great excitement and loss of sleep are caused by these pains and
the muscular contractions.
The remarkable observation by Jackson proves that these symptoms of irritation
are not necessarily always present ; in the case given by him they were entirely want-
ing.
It is not long; especially if the quantity of blood effused is
considerable, before paralytic symptoms appear in the lower
half of the body, but seldom reaching a great development, or
amounting to complete paraplegia. Asa rule, the patient has a
furry feeling, numbness, sensations of swelling and heaviness in
the limbs and trunk, with more or less distinct anesthesia in the —
same parts. A feeling of very great muscular weakness and ex-
haustion indicates the same disturbances in the motor sphere; a
MENINGEAL HEMORRHAGE. 213
more or less severe paresis is more frequent, and complete paral-
ysis is rare. The distribution depends on the seat of extravasa-
tion.
Reflex excitability has been found depressed in a few cases,
but this probably occurs only in the regions supplied by the
nerve-roots directly affected, though it might be exaggerated in
the regions posterior to such roots.
Weakness of the bladder and rectum is rarely mentioned,
but is usually present in severe cases. _
fever is absent, at least at the beginning of the disease ; it
may appear during the irritative reaction which sets in on the
second or third day, but never becomes excessive.
According to the various levels occupied by the extravasa-
tion in the cord, the symptoms differ a little. The following
symptoms indicate that the cervical region is affected :
The attack begins with pain in the arms and shoulders, with
stiff neck and pain in the occiput; anesthesia and paralysis
most marked in the upper extremities ; oculo-pupillary symp-
toms; difficulty of breathing and swallowing ; violent dyspnea ;
retarded and weak pulse.
The dorsal region is indicated when there is pain in the back
and abdomen and pain in the-form of a girdle, stiffness of the
dorsal part of the spine, paralysis of the legs and the abdominal
muscles ; retained reflex power in the legs.
The lwmbar region is indicated when there is pain in the
loins, tearing pains in the lower extremities, the loins, perineum,
bladder, and genitals ; stiffness of the loins; well-marked paral-
ysis of the lower extremities, with loss of reflex activity ; paraly-
sis of bladder and rectum.
Course and Termination.—After a sudden or gradual begin-
ning, the symptoms usually remain stationary for a certain time,
and sooner or later take a turn for the better. The symptoms of
reactive inflammation are seldom prominent, or they disappear
among the other symptoms. Slight fever appearing on the second
or third day, with renewed pains, more distinct hypereesthesia,
etc., should be referred to the same ;,after two or three weeks
these symptoms usually disappear.
In the majority of cases the disease runs a favorable course,
914 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
unless the nature of the cause or the complications prevent it.
A gradual improvement in the symptoms occurs, the paralysis
disappears, but partial anesthesia and paralysis often remain
for a long time. The whole course is usually run in a limited
time; in a few weeks or months a tolerably satisfactory cure —
may be completed.
Death is not rare—often occurring in a few hours or days ;
as when the extravasation is at a high level, and produces dis-
turbance of the heart and respiration, or when blood effused
extends upward to the brain, or when the central nervous system
suffers a sudden severe impression (shock). If the extravasations
are considerable, the severity of the compression may lead to
complete paraplegia, cystitis, bed-sores, etc., and death may
occur at a late stage.
Diagnosis.
The diagnosis of a meningeal hemorrhage is not always pos-
sible. If other severe diseases of the nervous system are present
(hemorrhage of the brain, tetanus, convulsions, injury of the
cord), it will not be in our power to recognize the complicating
element of meningeal apoplexy, except under very peculiar cir-
cumstances. In such cases it will usually fail to be recognized,
but that is seldom of much consequence.
The diagnosis of idiopathic and uncomplicated meningeal
apoplexy can, however, be established in many cases. |
It is chiefly based upon the swdden occurrence of the symp-
toms, upon the peculiar combination of symptoms of meningeal
irritation and spinal paralysis, upon the absence of severe
cerebral symptoms, the paraplegic character of the symptoms at
the outset, the speedy improvement in the more severe symp-
toms, and the usually favorable termination. If we know the
cause, that knowledge will often assist the diagnosis.
There is a series of spinal troubles, which closely resemble
meningeal apoplexy in their symptoms, and are hard to distin-
guish from it; such are:
Commotio medulla spinalis (shock), in which the symptoms
of spasm are wanting, and the paralysis reaches its highest point
MENINGEAL HEMORRHAGE, 215
at the onset. It should be remembered that commotio and menin-
geal apoplexy may occur together.
Bleeding in the substance of the cord (spinal apoplexy) is
usually followed by severe palsy, including especially a high
degree of anesthesia; the pain and tendency to spasm are less
marked; the latter is said by Brown-Séquard to be always ab-
sent in hematomyelia. This lesion usually causes rapid death, or
incurable paralysis.
Meningitis and myelitis can usually be distinguished with
readiness ; they do not develop so rapidly, or if they do, they
are always accompanied by fever. But the central myelitis
which begins with fulminant symptoms (see below, under Mye-
litis) may give rise to confusion. In the latter, however, severe
anesthesia is never wanting, and the paralysis, also, is usually
complete from the beginning.
For the diagnosis of the seat of the hemorrhage, the points
given above may suffice ; it may be ascertained from the distribu-
tion of the symptoms of palsy or irritation.
The prognosis is always dubious ; but if the causal injury be
not especially severe, and the extent of the hemorrhage not very
great, it may be considered as comparatively favorable. We
may say that if the first few days are passed in safety, the prog-
nosis will become more favorable.
It is an unfavorable circumstance when the bleeding is very
considerable, or is seated in the cervical region, or when marked
reactive symptoms occur, or severe paraplegic symptoms, cysti-
tis, bed-sores, etc.
If the bleeding is of small extent and the symptoms corre-
spondingly mild, if the reaction is moderate and the patient
young, all these circumstances are in the patient’s favor.
Confinement to the bed of one or two months’ duration, fol-
lowed by a convalescence of several months, may be predicted.
Treatment.
Much can be done by way of prevgntion; by treating hyper-
zemia of the cord, or spasms, by regulating the menses, the hem-
orrhoidal bleeding, etc.
916 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
When the symptoms of meningeal bleeding have occurred,
the first thing to be prescribed is absolute rest in a proper post-
tion (upon the side or face). Then the bleeding must be pre-
vented from extending ; the usual remedies consist of the ener-
getic application of ice to the vertebral column, repeated powerful
purges, and full local bloodletting (on the spine or anus). The
effect of these may be aided by hot applications to the extremi-
ties, and by the internal or subcutaneous exhibition of large
doses of ergotin. The diet must of course be properly regulated.
Venesection can only be justified by very special circumstances
(great plethora, violent action of the heart).
If symptoms of inflammatory reaction appear, the local blood-
letting along the spine may be repeated, and as Leyden recom-
mends, small portions of mercurial ointment may be rubbed in,
and calomel given in subdivided doses.
The period of resorption demands special attention; it may
be hastened by the internal and external use of iodine, by luke-
warm baths, by a proper cold-water treatment, by the galvanic
current. In later stages, the patient's strength may be supported
and restored by tonics (quinia) and nux vomica.
In many cases a symptomatic treatment is demanded ; thus,
in the beginning, for. the relief of pain and spasm (narcotics, etc.) ;
later, for anzesthesia and paralysis (electricity) ; for cystitis, bed-
sores, etc
3. Inflammation of the Spinal Dura Mater—Pachymeningitis
Spinalis—Perimeningitis.
Ollivier, 1. c. II. pp. 272, 280. 3d ed.—Hasse, 1. c. 2. Aufl, p. 689.—Leyden, 1. ¢.
pp. 885-406.—M. Rosenthal, 1. c. 2. Aufl. p. 279.
H. Koehler, Monographie der Meningitis spin. 1861.—Ruehle, Klin. Mittheilungen.
I. Bd. Zur Compress. des R.-M. Greifsw. med. Beitr. I. p- 5. 1863.—TZraube,
Deutsche Klinik. 1863. No. 20; Gesamm. Abhandl. Il.—Mannkopf, Berlin.
klin. Wochenschr. 1864. Nos. 4—7.—A. Meyer, De pachymeningitide cerebro-
spin. interna. Diss. Bonn. 1861.—7wh. Simon, Ueber den Zustand des R.-M.
in der Dementia paralytica. Archiv f. Psych. u. Nervenkrankh. II. 1869. p.
137, 148, 347.—R. H. Mueller, Ueber Peripachymeningitis. Diss. K6nigsberg.
1868.—H. Wagner, Arch. der Heilkunde. XI. 1870. p. 322.—Charcot, Pachy-
méningite cervicale hypertrophique. Soc. de Biol. 1871. p. 35; Gaz. méd. de
INFLAMMATION OF THE SPINAL DURA MATER. 217
Paris, 1872. No. 9; Lecons, etc. 2° série. 3° fase. p. 246. 1874.—Joffroy, De la
pachymén. cervic. hypertroph. Paris, 1873.
The inflammations of the spinal dura mater, though known
for a long time, have not been closely studied till quite lately.
The significance of the disease has been better recognized, and
a sharper line of separation from the other forms of spinal men-
ingitis has been drawn, since it has been observed to occur iso-
lated and spontaneously.
It is true that there exist but very few good observations ; for
this reason, the symptoms and diagnosis are very imperfectly
made out. But we may properly make a distinction of two
forms, according as the outer surface of the dura is preferred,
and the morbid products are deposited between the dura and the
vertebral column (external pachymeningitis), involving the loose
cellular tissue, or as the inner surface is attacked, and becomes
the seat of deposits (internal pachymeningitis).
a. Pachymeningitis Spinalis Eaterna—Peripachymeningitis.
Definition.—This disease consists of inflammation of the
outer surface and layers of the dura and of the cellular tissue
surrounding it. The morbid-products, exudation, pus, connec-
tive tissue, are deposited between the dura and the vertebral
column. This form of meningitis has been studied in but very
few cases, and is in much need of further examination.
The chief cause of this form of inflammation consists in the
presence of inflammation of the vicinity, which extends to the
dura and the cellular tissue outside of the meninges. This is
quite certainly the case in vertebral caries, and in deeply ulcer-
ated bed-sores, which, especially when seated on the sacrum,
easily provoke irritation of the structures within the cord. A
similar thing, however—extension of the purulent and phlegmo-
nous process of inflammation into the canal—has been observed
in purulent inflammation of the dorsal muscles and the psoas
(Traube), in inflammation in the connective tissue of the neck
(Mannkopf), in the subpleural cellular tissue (H. Mueller), and
all possible forms of chronic inflammation of the abdomen and
218 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
thorax, especially peripleuritis, and also neuritis migrans, have
been named as possible causes of peripachymeningitis.
It seems to us that this view of the secondary nature of the disease is carried
quite too far. The observations which are quoted in proof certainly leave much
room for doubt. Traube’s cases are explained by him upon the supposition that
the pachymeningitis externa was the primary complaint, the suppuration extending
thence into the muscles of the back. This is quite in harmony with the clinical
course and the results of autopsies. It is more natural and probable, a priori, that
pus should force its way out through orifices in the narrow vertebral canal, with its
rigid walls, and should afterwards spread in this direction or that, than that sup-
puration of several muscles should find its way simultaneously into the vertebral
canal. There is a case in the Medical Times for January 6, 1855, p. 19, unfortunately
reported very incompletely, which seems to confirm this view. An observation by
Ollivier ' seems to us of still more importance. In Mannkopf’s case the secondary
nature of the peripachymeningitic lesion could only be made extremely probable.
‘R. H. Mueller’s case cannot prove anything, as the connection between the peri-
‘pleuritic membranes and those of the peripachymeningitis was in no way proved,
and there were also found similar membranes, quite isolated, on the outer surface
of the cerebral dura mater. The case reported by Leyden? lacks the confirmation
of an autopsy.
We are therefore probably justified in claiming the possibility
of the spontaneous and primary origin of pachymeningitis ex-
terna, especially as there is no solid objection to it.
We must await the result of further observations, for infor-
mation as to whether surgical injuries, exposure to cold, syphilis
and other causes may not originate this disease.
Pathological Anatomy.
More or less of the spinal dura mater is thickened ; its outer
layers are separated by inflammatory exudations, infiltration
with cells, etc. This alteration is usually confined to short por-
tions of the cord, the level of a few vertebrae, but it may extend
over the greater part of the dura.
On the outer surface there is found a more or less abundant
exudation of varying thickness; it has been found as much as
half an inch thick (Ruehle). This consists either of pus, either
‘IT, p. 260. 3d ed. * Loc. cit. p. 391.
INFLAMMATION OF THE SPINAL DURA MATER. 219
fluid, or dry and caseous, enclosed in thickened connective tis-
sue, and with the extrameningeal cellular tissue infiltrated ; or
of a soft, plastic, reddish gray young connective tissue, very vas-
cular, sometimes covered with pus and full of small abscesses,
sometimes undergoing cheesy degeneration. The last is the usual
case in pachymeningitis resulting from vertebral caries (Mi-
chaud); there is a fungoid growth, originating from the outer
surface of the dura, which is stimulated to produce the growth
by the presence of carious pus.
The essential disease is, therefore, an inflammation of the
outer layers of the dura and the surrounding cellular tissue,
with exudation of a purulent, plastic, tuberculous, or other
material.
The inner surface of the dura is also often thickened and
opaque, often covered with a delicate fibrinous deposit. The
pia and arachnoid seldom participate, but they have been seen
adherent to the dura, opaque, and infiltrated with pus.
The cord itself is more or less compressed, flattened, pale,
anemic; often softened, full of microscopic fat-granules and
granular corpuscles, and presenting, more frequently than is
supposed, the signs of transverse myelitis. In the neighborhood
of the place compressed, red softening and hyperemia are found ;
in more chronic cases, ascending and descending secondary de-
generation of the white columns (upwards in the posterior col-
umns, downwards in the lateral).
The nerve-roots which pass out at the seat of pachymeningitis
are compressed, atrophied, inflamed, and soft.
Add to these the anatomy of those processes which have acted
as causes of pachymeningitis, or have accompanied it (vertebral
caries, peripleuritis, muscular abscesses, phlegmons, etc.).
Symptoms.
The usual character of the disease is like that which will pres-
ently be described under Leptomeningitis, a more common affec-
tion. We therefore shall give but a short account of the chief
symptoms in this place. The most important are as follows:
Pain in the back, various in seat and extent, according to the
220 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
location of the disease. Stiffness of the vertebral column, which
renders it difficult and painful to sit up. TZension and jerking
in various groups of muscles. Hacentric pains, in the form of
a girdle or shooting into the extremities ; sensation of a cord tied
around ; formication and slight hyperesthesia of the skin.
To these are added, sooner or later, the symptoms of com-
pression of the cord, gradually increasing ; paralysis of various
degrees, sometimes more marked in the motor, sometimes in the
sensory sphere, sometimes in both at once; muscular tension,
increased reflex action, especially those connected with tendons ;
paralysis of the sphincters, and bed-sores. These symptoms are
due, partly to compression, partly to the myelitis which com-
plicates it.
According to the nature of the original disease and the com-
plications and secondary changes, disturbances of the general
health, fever, and many derangements of internal organs may
occur. |
The symptoms of pachymeningitis may develop in an acute
or a chronic way ; in the acute (purulent) forms the symptoms
-of irritation are the more prominent, while in the chronic (plas-
tic) forms these recede into the background, and the symptoms
of compression of the cord dominate.
Of the course of pachymeningitis externa nothing can be said
with definiteness, in the present state of our knowledge. The
unfavorable cases which come to an autopsy cannot indicate the
average event, for it is impossible to estimate how many have
run a favorable course without being recognized in our present
uncertainty regarding the diagnosis. We certainly know that
the form in which it so frequently accompanies caries of the
vertebre is quite frequently arrested and partially recovered
from, since the paralytic symptoms caused by it disappear. We
have learnt only thus much: that in the severer cases the course
may be various, but usually is protracted, and does not termi-
nate unfavorably nor lead to a slow convalescence, until after
the lapse of a considerable number of weeks.
The diagnosis is founded chiefly on the causal agencies we
may be able to discover, and the associated, slowly increasing
symptoms of meningeal irritation and of compression of the
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INFLAMMATION OF THE SPINAL DURA MATER. 221
cora. The most difficult thing will always be to distinguish it
from the other forms of meningitis. There is a diagnostic point
—though of very doubtful value—which consists in the fact
that external pachymeningitis but rarely ascends as high as the
upper cervical region, and is therefore seldom accompanied by
stiffness of the neck. . In most cases, however, it will be impos-
sible to decide whether the dura alone is affected, or whether the
other meninges of the cord are also inflamed.
The prognosis follows from what has been said regarding the
course of the disease. In forming it we shall be obliged to pay
especial attention to the causal element.
In the treatment we ought principally to aim at a removal of
the original lesion ; if we succeed in curing this, we greatly im-
prove the chances of curing the pachymeningitis. The special
directions for this purpose need not be given here. |
For the relief of pachymeningitis we proceed as is directed in
the section on Leptomeningitis. It is of special importance to
procure such relief in vertebral disease, where the improvement
of the paraplegia depends upon the removal of the meningeal
affection. In addition to treatment directed against the verte-
bral disease, the measures regarded with most confidence are
the energetic use of brine-baths (bathing and drinking), the use
of iodide of potassium and iodide of iron, pencilling the back
with iodine, frictions with mercurial ointment, and the like.
The white-hot iron, a very old remedy, has recently been warmly
recommended for obstinate cases by Charcot.
b. Pachymeningitis Interna (Hypertrophica et Hemorrhagica).
Definition.—Inflammation, chiefly of the inner surface of
the dura ; deposition of morbid products (exudations, extrava-
sations, proliferation of connective tissue) on its inner surface,
between dura and arachnoid. Frequent implication of the arach-
noid and pia.
Two principal forms of this disease are known, possessing to
a certain extent clinical characteristics; a simply hypertrophic
form, leading to thickening of the dura (and usually of the finer
membranes also) with connective tisshe ; and a pseudo-membra-
992 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
nous, hemorrhagic form, characterized by a more or less abun-
dant extravasation of blood. But few observations have been
made as yet upon either.
Etiology.
The causes usually assigned are exposure to cold, and damp-
ness of the dwelling (Charcot, Joffroy). Excessive use of alcoho)
seems to have some effect.
As to the hemorrhagic form, it seems to be established that
it usually accompanies the affection of the same name in the
cerebral dura mater, hematoma dure matris, and therefore owns
the same causes. The disease has not infrequently been found
with psychical disorders, especially dementia paralytica (Simon,
A. Meyer); also as a consequence of continued abuse of alco-
hol, of which Magnus Huss, Magnan, and Bouchereau have
cases. Finally, Leyden describes a traumatic form; but the
case adduced to illustrate it is not above doubt, as the patient
was a drinker, and had suffered from symptoms of disease before
the fall which caused the fracture of his skull; it is, therefore,
not quite certain whether the fissure was the cause of the internal
hemorrhagic pachymeningitis. A. Meyer says that both his
cases occurred in cavalry soldiers, a class which is exposed to
frequent falls and shocks.
Pathological Anatomy.
In the hypertrophic form we find a great thickening of the
dura, chiefly caused by a considerable proliferation of its inner
layers, which change into a hard cicatricial mass of connective
tissue, with usually a distinct concentric arrangement of layers.
Usually there is an intimate adhesion to the soft membranes,
which are also thickened and proliferated, and form one continu-
ous mass with the thickened dura mater; often, however, they
are comparatively unchanged.
Thus there is formed a more or less extensive deposition,
which compresses the spinal cord from one side or the other (usu-
ally from the rear), or which embraces it like a ring for a greater
INFLAMMATION OF THE SPINAL DURA MATER. 223
or less distance. The cord is sometimes simply compressed, pale,
and soft, but more usually it presents all the marks of transverse
myelitis of various extent, with secondary degeneration, forma-
tion of cavities, etc. The nerve-roots which are involved in the
disease are wrapt up, compressed, and often in a state of ad-
vanced atrophy. The muscles which belong to them possess the
microscopic characteristics of the usual degenerative atrophy.
In the hemorrhagic form the dura is covered to a greater or
less extent with a mass of exudation, soft, rusty-brown in color,
composed of fibrin and connective tissue, which is strewn with
numerous extravasations of blood, and not seldom contains one
or several large sacculated masses of blood. These masses con-
tain dirty-brown, decomposed blood, numerous blood-crystals,
pigment, detritus, etc. The enveloping mass of exudation is, in
many places, yellowish, easily broken or torn, is disposed in
layers, is attached but slightly to the dura or the arachnoid, and
possesses an abundance of vessels.
These sacs of blood may vary in size and number. The hem-
orrhagic false membrane often extends over a great part of the
cord, entirely enveloping it.
The process is exactly the same as that of hematoma of the
cerebral dura mater ; it is probable that the fibrinous inflamma-
tion is the primary element, and the bleeding only secondary.
Yet it is not impossible that a primary bleeding may give rise to’
a subsequent inflammation.
The condition of the cord is as in the other form. The pia is
usually tinged with blood, and so is the abundant spinal fluid.
Symptoms.
The hypertrophic form is at present thoroughly understood
only as occurring in the cervical region, which seems to be its
favorite seat ; when situated there it has a somewhat character-
istic course, and is described by Charcot as ‘‘ pachyméningite
cervicale hypertrophique.”’
He makes a first stage of the symptoms of irritation, which
lasts two or three months, and is chiefly characterized by pains.
These are very violent in the back of the neck and head, the
-
994 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
shoulders, and arms ; are continuous, and from time to time ex-
perience exacerbations ; are often connected with a painful sen-
sation of being bound with a cord in the upper part of the chest.
The neck is stiff, but the spinous processes are not specially sen-
sitive to pressure. ormication and numbness, and sometimes
also slight weakness of the upper extremities, appear at this
stage. Trophic disturbances of the skin are not infrequent—
eruptions of herpes, development of vesicles on the upper ex-
tremities. Nausea and vomiting are but rarely observed.
The transition to the second stage, chiefly characterized by
paralysis and atrophy, is very gradual. The upper extremities
are more or less completely paralyzed, especially the district of
the median and ulnar nerves, while in all cases hitherto observed
the radial region has remained comparatively free. The result
of this is the formation of a peculiar position of the hand in ex-
tension, the fingers being held like claws. This paralysis is con-
joined with severe and quite uniform atrophy, so that the gen:
eral aspect of the case reminds one of progressive muscular
atrophy. The faradic excitability of the muscles is diminished
or suspended. Contractures of the muscles appear, and single
spots of anesthesia of greater or less extent.
All this is doubtless mainly the result of the affection of the
nerve-roots.
Ata later period, paralysis and contracture of the lower ex-
tremities occur. Atrophy, however, is not associated with the
affection in these parts, or not until a very late period. In severe
cases complete paraplegia with marked anesthesia, paralysis of
the bladder, bed-sores, etc., may arise, and bring on the fatal ter-
mination.
These severe symptoms are doubtless to be referred to trans-
verse myelitis at the spot compressed, and descending degenera-
tion of the lateral columns, originating at that point. But the
course is not always so bad ; there are cases in which’ the symp-
toms cease to make progress, or even are distinctly improved ;
but the disease is always chronic.
The symptoms of hemorrhagic pachymeningitis interna are
still very obscure, and in most cases are complicated by those of —
the coexistent cerebral affection. The usual symptoms of a slow
a
INFLAMMATION OF THE SPINAL DURA MATER. 225
meningitis, with periods of exacerbation, pain in the loins and
back, tearing pains in the extremities, stiffness of the vertebree
and of the nucha, increasing weakness of muscles, sometimes ris-
ing to complete palsy and paraplegia, moderate contractures,
hyperesthesia and anesthesia of the skin in various degrees,
weakness of the bladder, etc., are sufficient, in case certain
causes are present (as drunkenness, paralysis, heematoma of the
cerebral dura mater), to arouse a suspicion of disease of the spi-
nal dura, and, at least in many cases, to lead to a probable diag-
nosis. ;
We have yet to learn whether this disease, like the cerebral
form, is marked by aggravation of the symptoms from time to
time, and whether this fact can be made useful in diagnosis.
The disease, in this form, will usually take an unfavorable
course.
The diagnosis may be inferred from the previous brief sketch
of the two forms. Pachyméningite cervicale hypertrophique has
a certain resemblance to progressive muscular atrophy, atrophic
lateral sclerosis (Charcot), etc. The most important points of
distinction are the stage of pains, the partial anzesthesias, para-
plegia without atrophy, etc. It will not be always possible to
distinguish it from meningeal tumors. |
The hemorrhagic form is in need of a more exact diagnostic
boundary.
The prognosis requires no remarks.
The ¢reatment will resemble that of meningitis in general (see
next section). In more acute cases antiphlogistics of all sorts
will be of use.
In later stages and chronic forms we may have recourse to
derivatives, preparations of iodine, galvanism, and the use of
baths or the cold-water treatment. Prominent symptoms, as
pain, paralysis, atrophy, etc., require a special symptomatic
treatment.
VOL. XIIL—15
996 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
4. Inflammations of the Pia Mater and Spinal Arachnoid—
Leptomeningitis Spinalis—Perimyelitis and Arachnitis.
P. Frank, 1. c. 1792.—Ollivier, 1. c. 3d ed. II. p. 232.—Hasse, 1. c. 2. Aufl. p. 690.—
Hammond, 1. ¢. 8d ed. p. 444.—Leyden,'l. c. pp. 406-443.—M. Rosenthal, 1. c.
2. Aufl. p. 283.—Koehler, Monographie der Meningitis spinalis. Leipzig. 1861.
(Contains a great deal of valuable matter and very full references.)
Klohss, Diss. de myelitide. Halis. 1820. Hufeland’s Journ. XVI. 1823.—Funk,
Die Riickenmarksentziindung. Bamberg. 1825.—Henoch, Schmidt's Jahrb. Bd.
28. 1846.—Hvans Reeves, Diseases of the Spinal Cord and its Membranes.
Monthly Journ. of Med. 1855. p. 506; Edinb. Med. Journ. 1855-56. pp. 120
and 302.— Noetel, De meningitide spinali. Diss. Berlin. 1861.— Beaumetz,
Méning. spinale, suivie de roideur des extrém. infér. Gaz. des H6p. 1861. No.
129.—Brown-Séquard, Lectures on the Principal Forms of Paralysis of the
Lower Extremities. London. 1861. p. 66, etc.—Camerer, Ueber Meningitis
spin. chron. und deren Differentialdiagnose. Wirtemb. Correspondenzblatt.
XXXII. 1862.—Jaccoud, Lecons de clinique médicale. 1867. pp. 372-420.—
Vulpian, Note sur un cas de méning. spinale et de sclérose corticale annulaire
de la moélle ép. Arch. de Physiol. II. p. 279. 1869.—Liouville, Etude anato-
mo-pathologique de la méningite cérébro-spin. tubercul. Arch. d. Physiol. III. —
p. 490. 1870.—<Stokes, Chronic Inflammation of the Spinal Cord and its Mem-
branes. Dubl. Journ. of Med. Science. Vol. LVI. p. 62. 1873.—Bruberger, Fall
von Meningitis syphil., ete. Virch. Arch. 1874. Bd. 60.
Compare also von Ziemssen, Meningit. cerebrospin. epidemica, in Vol. IL of this
Cyclopedia, and the full references there given,
Inflammation of the soft membranes of the spinal cord is the
most important and the most frequent of spinal meningeal affec-
tions ; and this is what is intended when spinal meningitis with-
out further designation is spoken of. All treatises by the earlier
authors relate to this. But a great deal has been thrown under
this title which must certainly be separated from meningitis, or
which occurs simultaneously with it. It is reserved for future
investigations to show more clearly than has been done the line
of demarcation between meningitis and myelitis ; for this pur-
pose accurate histological examination of the cord by the latest
methods in cases of meningitis is absolutely needed. We have, ©
however, very little positive information upon this point.
It would seem hardly probable that any considerable inflam-
mation of the pia mater could exist without involving the cord
to some extent. The pia distributes the vessels to the entire
INFLAMMATION OF THE SPINAL PIA MATER, 227
cord ; from it pass out the processes of connective tissue which
compose the framework of the latter; so that any inflammatory
irritation affecting the vascular district of the pia must be felt
more or less in the vessels of the cord, and when once a morbid
process is established in the connective tissue of the pia, it is
hard to see why it should not spread to some extent in the cord.
A certain degree of independence on the part of the two vas-
cular districts of the pia and the cord must be admitted, as each
may be affected singly ; this fact is certainly established in rela-
tion to the cord, and suggests to us that the nervous elements
themselves possess some influence upon the disease, and that
they may be primarily attacked, or, at least, may bear a promi-
nent part in the production and localization of diseases of the
connective substance.
It is in diseases of the pia mater that we shall be obliged to
pay special attention to the possibility of an implication of the
cord. This has been done far too seldom, in my opinion ; patho-
logical anatomy has devoted too little attention to the point. The
most that has been done has been to demonstrate an implication
of the nerve-roots that pass through the diseased membrane;
or an affection of the cord in very severe cases. Few observa-
tions have been made systematically and with the aid of delicate
methods. Mannkopf, in epidemic cerebro-spinal meningitis, has
seen abundant cell-infiltration following the course of the vessels
even into the cord. Fronmueller has seen the central canal full
of pus-cells in the same disease; Liouville, in tubercular menin-
gitis, has seen tubercles in the processes of the pia, in the fis-
sures of the cord, and Vulpian has demonstrated in one case of
inflammatory thickening of the pia an annular sclerosis of the
cord, extending to some depth, especially in the posterior columns,
the dependence of which upon meningitis is, however, at the
least doubtful. , 7
This deficiency has been made good by the investigations of
Dr. F. Schultze,’ relating to three cases of leptomeningitis spina-
1 Berl. klin. Wochenschrift. 1876. No.1. Dr. Schultze has permitted me to view
his microscopical preparations bearing on this point, and it is my agreeable duty to
acknowledge gratefully the various assistance which the free use of his numerous and
excellent preparations has rendered to me,
998 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
lis which show a very considerable implication of the nerve-roots
and the cord itself. The principal results of these investigations
is the following ; for some further details the reader is referred
to the pathological anatomy of acute meningitis. ?
The nerve-roots are in a state of marked inflammation (infil-
tration with cells, especially in the neighborhood of the vessels,
the nerve-fibres swollen, granular, beginning to break down,
the axis-cylinders swollen and granular); the bundles of root-
fibres which enter the cord are more or less considerably swollen.
In the cord itself, there is found a peripheral interstitial myelitis
(infiltration of the neuroglia with cells and nuclei) penetrating to
a greater or less depth, or actual parenchymatous myelitis in
large and small foci (enormously swollen axis-cylinders, cloudi-
ness and granular decay of the medullary sheath, axis-cylinders
breaking down, etc.). In the gray substance there were found
signs of oedematous swelling in the ganglion-cells, but no other
distinct changes. Only the central canal appeared closely packed
with round cells, and its vicinity also infiltrated to a considerable
distance with the same elements.
It certainly follows from these facts that we shall have to
take a somewhat different point of view from what has previously
been customary in explaining the origin of the symptoms of
spinal leptomeningitis. It is quite clear that the inflammation
of the pia can produce no very marked symptoms by itself; the
principal would be that of pain and the consequent reflex phe-
nomena, owing to its abundant supply of nerves. But the most
important and essential symptoms must arise from an affection
of the nerve-roots and the cord itself; and for this reason it will
be very desirable to distinguish between purely meningeal and
purely spinal symptoms, as well as those referable to the roots.
A delicate clinical analysis will be required to distinguish
these groups of symptoms.
I have premised these remarks in order to facilitate the under-
standing of the symptoms of meningitis, and to indicate the de-
fects in our knowledge.
As for distinguishing the inflammation of the pia, the so-
called perimyelitis, from arachnitis, I consider it impossible, both
upon pathologico-anatomical and practical grounds.
INFLAMMATION OF THE SPINAL PIA MATER. 229
Finally, the best division that we can make in practice—in
spite of the great variety of form which spinal leptomeningitis
may take—seems to me to be that which recognizes but two chief
forms, the acute and the chronic.
a. Leptomeningitis Spinalis Acuta.
By this title we understand a febrile inflammation of the soft
membranes (pia and arachnoid) of the cord, beginning with vio-
lent symptoms and characterized chiefly by an exudation of a
purulent-fibrinous, more rarely a sero-fibrinous nature. It occurs
most frequently in an epidemic form, and in association with the
corresponding affection of the cerebral membranes, as cerebro-
spinal meningitis. But it also occurs sporadically; and this
form is that which will occupy most of our attention.
Etiology and Pathogenesis.
The predisposition to acute spinal meningitis is quite general,
although the causes upon which it depends are not yet ade-
quately known. It attacks by preference children and young
persons, and the male sex ; it is more frequent when there is ten-
dency to scrofulosis and tuberculosis; all sorts of weakening
influences (bad dwellings, poor food, sexual and other excesses,
etc.) increase the tendency. As regards the way in which these
causes act upon the spinal membranes, we know nothing precisely.
Among the immediate causes, exposure to cold certainly
plays a very important part. It has often enough been observed
that sleeping on damp ground or snow, or the action of a cold
wind striking upon the back while sweating, or an unexpected
fall into the water, and other similar occurrences, have led to an
attack of acute leptomeningitis. But in this case, as in most in-
flammations of internal organs caused by cold, we know nothing
with certainty of the delicate mechanism of the entire process.
The action of the sun’s heat, insolation, upon the back is a
very questionable source of acute spinal meningitis.
Surgical lesions, however, constitufe an unquestionable and
very frequent cause. The disease has been observed after simple
930 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
concussion of the spine, as in falling down stairs ; after cutting,
stabbing, and gunshot wounds of the spinal column and its con-
tents; after luxation and fracture of the vertebre ; after the
operation for spina bifida, etc.
Inflammations and other affections of neighboring parts are
often propagated to the spinal meninges and arouse inflamma-
tion in them; thus caries of the vertebree, acute inflammation of
the dura spinalis and the extra-meningeal cellular tissue, deep
bed-sores reaching to the cavity of the sacrum ; bursting of cavi-
ties in the lungs into the vertebral sac ; carcinoma of the vertebree ;
and finally, acute inflammations of the cord itself, which extend
to the pia. The most frequent cause among this class is the
acute inflammation of the cerebral pia mater, which is usually
complicated with that of the spine. The spreading is usually
effected through the open communication between the cerebral
and the spinal cavities, through the anatomical continuity of the
meninges, the current of the cerebro-spinal fluid, the gravitation
of the inflammatory products, extravasations, etc., into the spinal
cavity, and theresetting upaninflammatory irritation ; and finally,
it is doubtless due to other causes acting upon both the cerebral
and spinal meninges at once. Thus it is easily understood how
the inflammation of the cerebral pia mater so often extends
downwards to the spinal pia mater.
Of tubercular basilar meningitis, according to recent observa-
tions, a tubercular spinal meningitis is a quite regular accom-
paniment. Hence the appearance of spinal symptoms in this
disease.
The publications of Weber! and Bierbaum? are of comparatively little force as
evidence. The most important cases are three by Koehler,? which demonstrate the
coexistence of tubercle in the pia mater of the brain and of the cord. Also two
cases presented by the same author in his monograph.‘ Liouville has recently
stated that the occurrence is a very regular one, and that among numerous cases, he
has seen it in every one. In F. Schultze’s three cases, above mentioned, the spinal
pia participated each time in the cerebral inflammation. Leyden,® also, gives a
case of this kind, without making any exact statements regarding the frequency
of its occurrence. It is certainly much more frequent than has been supposed.
Deutsche Klinik. 1852. No. 34. p. 380.
: Journ. f. Kinderkrankh. Bd. 26. p. 355. 1856. 4 Loc. cit. p. 127.
* Ibidem, Bd. 32. 1859. p. 409. * Loc. cit. p. 488.
INFLAMMATION OF THE SPINAL PIA MATER. 231
Among the somewhat doubtful causes of acute spinal menin-
gitis may be mentioned dentition, suppressed perspiration of the
Jeet, suppression of the menses and of hemorrhoidal bleeding,
disappearance of acute exanthemata, etc., although instances
of all these are given in the older literature.
The disease also occurs now and then in company with, or
during convalescence from febrile diseases (pneumonia, acute
articular rheumatism, etc.), or infectious diseases (acute exan-
themata, cholera, typhoid, etc.). But this seems to apply chiefly
to the epidemic variety. In child-birth, Koehler has repeatedly
observed acute spinal meningitis.
Finally, we must speak of epidemic and infectious influences.
The form of spinal meningitis which originates in company with
cerebral meningitis under the action of some as yet unknown
infectious material, and has repeatedly during the present cen-
tury assumed the dimensions of a wide-spread epidemic, is by
far the commonest and the most important. We can only refer
to von Ziemssen’s admirable delineation of the disease, in Vol. II.
of this Cyclopeedia.
Gauné' reports the occurrence, in a girl’s boarding-school, of a light epidemic
of favorable termination, not going beyond the symptoms of hyperemia of the
cord in some cases. The immediate cause was unknown.
Pathological Anatomy.
The morbid changes found in acute spinal meningitis differ
according to the stage of the disease. In general, three periods
may be distinguished, which of course pass imperceptibly into
one another: 1. A stage of hyperemia and commencing exuda-
tion. 2. A stage of serous or purulent fibrinous exudation, and
3. A stage of resorption or termination in some other way. The
one most commonly observed is the second ; the first much more
rarely, especially in the fulminant attack of epidemic cerebro-
spinal meningitis.
In the first stage, the pia contains a great deal of blood, is
colored from a rosy to a dark red tint, is full like velvet, and in
_,
=
1 Arch, gén. 1858,
932 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
places is dotted with blood, or with ecchymoses of various size,
while the blood-vessels are very full. The tissue is succulent,
swollen, imbibed with serum, and the cerebro-spinal fluid is
slightly turbid. The arachnoid shares in these characters to a
greater or less extent ; the hypereemia usually extends also to
parts of the dura of various extent, and is also to be seen in the
substance of the cord itself.
The second stage comes on by degrees ; the watery contents
of the tissues increase, the spinal fluid becomes more and more
turbid, fibrinous flocks and plates are formed in the subarachnoid
tissue, or adhere to the surface of the dura ; the pia is more and
more opaque, the subarachnoid tissues swell to a gelatinous mass
which more and more conceals the former redness. The purulent
character of the exudation becomes more and more distinct ; the
opacity increases, the tint alters to a whitish yellow, or green-
yellow, and at last the whole pia and subarachnoid tissue are
infiltrated uniformly with pus. The spinal fluid, growing more
turbid, assumes a sero-purulent appearance and contains numer-
ous flocks of fibrin, some floating and some covering the free
surfaces of the meninges. In some cases there is to be seen, in
addition to the exudation, a variable number of small miliary
nodules, gray or whitish yellow, chiefly distributed in the course
of the vessels, in the pia, and arachnoid, but not infrequently
strewn over the surface of the dura in considerable numbers
(tuberculous meningitis). In this form the exudation is usually
of a rather gelatinous consistency, serous, yellowish in color, and
rarely constitutes a strictly purulent infiltration.
The distribution of the exudation varies greatly. Sometimes
it is spread over a larger, sometimes over a smaller space, but it
usually covers the greater part or the entire length of the cord ;
the posterior surface is apt to have more of it than the anterior,
owing doubtless to the patient’s lying on his back. It is evident
from what has been said, that the exudation frequently extends
to the membranes of the brain, though in very various amount.
In such case a direct connection between the masses in the brain
and cord can always be shown to exist along the base of the
brain, although the quantity deposited on the medulla oblon-
gata is often remarkably small. 3
INFLAMMATION OF THE SPINAL PIA MATER. 233
The arachnoid is almost regularly involved in the inflamma-
tory exudation. It is opaque and thickened, infiltrated with
serum or pus, and often abounds with gray miliary tubercles ;
in such cases the subarachnoid connective tissue is always infil-
trated similarly, and in its swollen condition forms a layer of
exudation, surrounding the cord like a sheath. The dura spi-
nalis is less frequently mentioned as involved, yet it is often
hyperzemic, often opaque to a considerable extent, and covered
with thin, fibrino-purulent exudation. In afew cases peripachy-
meningitic hemorrhages have also been seen.
The xerve-roots are always more or less involved in the in-
flammatory changes; they are enveloped in thick masses of exu-
dation, swollen, softened, their fibrillation is indistinct, their
consistency diminished. |
Of the condition of the cord itself in acute meningitis our
information is quite scanty ; it has been found pale and cedema-
tous, at other times more hyperemic, but usually softened; the
softening may be somewhat uniform, or it may be disseminated
and limited to certain spots; in a few cases a purulent infiltra-
tion of the cord, of variable extent, could be distinctly seen with
the naked eye. |
Microscopical examination discovers in the soft membranes of the cord all the
signs of exudative inflammation—abundant cell-infiltration, especially along the
vessels, great fulness of the capillaries, swelling and spreading of the bundles of
connective tissue, etc. Such tubercular nodules as may be present show the char-
acteristic histological marks, and are chiefly found along the vessels. F. Schultze
found abundant infiltration with cells in the walls of the vessels which run in the
anterior and posterior nerve-roots ; the infiltration extended to the neuroglia, Some
of the nerve-fibres of the roots appeared altered, their medullary sheath being cloudy
and granular, the axis-cylinders decidedly swollen and in a state of granular
degeneration. The bundles of roots which passed into the cord seemed, therefore,
to be thickened at many points, and could be followed for a short distance into the
cord, where they resumed their normal dimensions and appearance in the neigh-
borhood of the gray substance.
In the cord, F. Schultze distinguished two sorts of affection. Either there was
infiltration with cells and nuclei, affecting chiefly the neuroglia, without direct im-
plication of the nerve-fibres, and limited to the peripheral layers of medulla (peri-
pheral interstitial myelitis), or the nerve-fibres were principally involved in the
inflammatory processes (parenchymatous myelitis), so that distinct myelitic foci of
various extent and position could be recognized. Thus there were found in the
934 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
transverse section (especially in the lateral columns) narrow wedge-shaped regions
of inflammation, with the point directed towards the centre, of which the longi-
tudinal extent varied. Single nerve-fibres in the condition of inflammatory swell-
ing were found at all parts of the transverse section. In the vessels of the cord no 3
essential changes were found; in the gray substance not much that was abnormal
could be seen, except an apparently cedematous swelling of many of the ganglion-
cells; the central canal, however, was regularly obliterated, plugged with roundish
cells, and its vicinity also infiltrated with similar round cells.
The second stage is that in which death usually occurs;
hence its anatomical changes are the best known. In cases not
terminating in death a third stage must be admitted, in which a
complete restoration to the normal state occurs with complete
resorption—a process which can only be observed by fortunate
accident—or various permanent changes occur, residua and con-
sequences of the acute process of very various significance, and
not rarely developing in a chronic way. The most frequently —
seen are opacity and thickening of the soft membranes; adhe-
sions of these membranes to one another and to the dura are not
rare; large accumulations of fluid in the arachnoid space (hy-
drorrhachis) ; more rarely chronic processes develop in the cord
which continue to increase—sclerosis and atrophy of the cord,
either affecting single columns, or distributed in the form of
islands of disease, or diffused through the whole medulla. We
have, therefore, after acute spinal meningitis, either the perni-
cious changes, progressive chronic meningitis or myelitis, or else
those comparatively harmless processes (opacity, thickening, eal-
careous plates, etc.), which are so often found in the body with-
out having given rise to special symptoms during life.
The anatomical changes of the other organs during acute
spinal meningitis require no special description here. They dif-
fer, according to the course of the disease and the manner of
death, but do not present anything especial. The most impor-
tant of them have been sufficiently described in Vol. IT. Se
Cerebro-Spinal Meningitis.
Symptoms.
Characteristic as are the features of acute spinal meningitis,
it is yet rarely found pure and isolated ; ; 1t is especially common
INFLAMMATION OF THE SPINAL PIA MATER. 235
to find the cerebral pia mater affected at the same time, which
complicates the picture and hinders the precise interpretation of
the symptoms. Yet with some attention and experience the
characteristic features of spinal meningitis can be deduced from
the symptoms as a whole.
General Description.—Acute spinal meningitis usually be-
gins suddenly ; often with fulminant symptoms. Distinct and
marked precursory symptoms are observed in only a minority of
the cases ; general heaviness and depression, slight chill, and a
little gastric disturbance, fleeting pains in the head and back,
restlessness and sleeplessness, preceding for a time the outbreak
of more serious symptoms. .
The proper commencement of the disease is marked by a more
or less severe chill, directly followed by violent febrile symp-
toms ; the temperature is raised, without any regularity of curve,
the pulse is full, hard, rapid, very rarely retarded at the outset.
Vomiting and severe cerebral symptoms are observed only in the
cerebro-spinal form.
The painful symptoms very soon become the most prominent ;
the chief one consists of an intense, deep-seated, boring pain in
the back, which is much complained of. According to the local-
ization of the inflammation, the pain may occupy various places
(loins, back, or nape of the neck), and have a various extent, but
is increased less by pressure on the spinous processes than by
movement of the vertebral column and the extremities; it is
usually very violent, but remitting ; and from the place where it
is seated, pains shoot out around the trunk in a ring, or extend
‘to the extremities, piercing them in all directions. Thus all
movements are rendered extremely painful.
The pain in the back is regularly and characteristically asso-
ciated with a severe rigidity of the spine, most marked at the
height of the disease. The best-known variety is that which
attacks the nucha, and is so constant in epidemics ; if the disease
is situated lower down, the lumbar spine may be the chief seat
of the painful stiffness, and when the disease is diffuse, the rigid-
ity, produced by muscular tension and contracture, may extend
to the entire column, and produce a*very close resemblance to
tetanic spasm.
936 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Quite analogous phenomena are observed in the muscles of
the extremities; painful tension and stiffness, not rarely in-
creased to the point of extreme contractures, producing rigid
immobility of the limbs; in some places spasmodic twitchings
occur, which give the patient extreme pain, and somewhat re-
semble tetanic spasms, but seldom amount to general convul-
sions. Such twitchings, in single muscles, are apt to be produced
by attempts to use them.
The skin of the extremities and the trunk, as far as its sensi-.
tive nerves originate from roots which are involved in the inflam-
mation, is in a state of marked hyperesthesia, so that every
touch, every movement of the patient, calls out expressions of
pain, even in cases where the consciousness is quite impaired.
Hyperesthesia of the muscles seems to be equally demonstrable
in many cases. |
The reflex activity is usually increased at the beginning, but
diminishes during the course of the disease. |
With these sensory and motor symptoms, disturbances of the
evacuation of urine and feces are early allied ; these functions
are performed with difficulty, owing, as is usually supposed, to
a@ spasmodic condition of the sphincters; artificial means are
often required in order to regulate them.
Disturbances of the thoracic viscera do not occur unless the
cervical part of the cord is involved in the inflammation. In this
case difficulty of breathing appears, due to the rigidity and
painfulness of the muscles of respiration; in the advanced
stages, serious symptoms of dyspnoea occur, which may increase
to complete asphyxia. Disturbances of the action of the heart
(great retardation or acceleration) may be added.
Cerebral symptoms, as vertigo, violent headache, delirium,
unconsciousness, coma, etc., are not rare; when they occur, it is
usually in cases in which some degree of implication of the cere-
bral pia mater is present. They may appear at an early period,
or later in the course of the disease, and when fully developed,
often indicate the probability of a fatal event.
As the disease progresses, the symptoms of itritation may
become less and less prominent, and give place to more distinct
symptoms of paralysis ; but both classes of symptoms may be
INFLAMMATION OF THE SPINAL PIA MATER, 237
intermingled in various ways. Pareses and paralyses occur; the
immobility of the limbs is no longer owing to muscular tension,
but to motor weakness ; symptoms of vesical paralysis occur ;
the cutaneous sensibility is lessened, and even high degrees of
anesthesia may appear; at last, paralysis of the respiratory ap-
paratus may lead to very threatening symptoms.
When the disease has reached this height, everything may
rapidly go from bad to worse, and death may soon occur; the
immediate cause of death is usually a progressive paralysis of
respiration and circulation, associated with deep coma, and not
rarely with a great rise of temperature during the agony.
At other times the course is more protracted ; the severity of
the symptoms lessens, deceitful signs of temporary improvement
appear, while the disease, as a whole, continues to make prog-
ress; severe paralysis, bed-sores, etc., appear, and death follows
after long suffering. A secondary implication of the cord is
always to be supposed in such cases.
Improvement may really occur; in slight cases this is often
wonderfully speedy, with a short convalescence, while in severe
cases it is more gradual, and has many fluctuations. The conva-
lescence is then tedious, the forces recover themselves but slowly,
the abnormal irritability disappears very gradually, and the
patient needs care for a very long time. Incurable injuries are
often left behind; paralysis and atrophy of single muscles and
groups of muscles, or of whole extremities, contractures, anes-
thesia, etc. Signs of degeneration and sclerosis of single columns
of the cord may continue after the disease is over.
Interpretation of the symptoms.—Among the most constant
and important, is, without doubt, the pain in the back. It is
usually very severe, deep-seated, boring, and tensive, of various
extent, but hardly ever absent. It is a special characteristic, that
it is very much increased by every movement of the trunk or
limbs, so that the patient is often compelled to maintain absolute
repose from this circumstance alone. The movements connected
with evacuation of urine and feces also naturally increase the
pain in the back. Pressure on the vertebral column does not
always increase it. .
This dorsal pain doubtless owes its existence to inflammatory
988 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
irritation of the nerves of the pia and dura, to inflammation of
the posterior roots, and the consequent hy pereesthesia, but hardly
to an inflammatory implication of the cord itself.
Pains in the extremities, of a tearing or boring character, and
increased by every movement, are seldom wanting, and have
doubtless the same origin. They correspond in their location and
extent with the inflamed portion of the cord.
To similar processes of irritation in the motor apparatus may
be referred the equally frequent and important symptoms of
muscular tension, contractures, spasms, stiffness of the spine or
neck, etc. The most characteristic of all is the stiffness of the
spine and neck, with the head drawn backwards, the back-
stretched, often in the position of opisthotonus, and stiff and
hard, especially when active or passive movements are made. In
the. extremities, the extensors are most affected, but often the
flexors; the limbs in this condition are often of the hardness of
stone, and immovable. This tension relaxes a little at times,
is especially increased by attempts at moving, but is usually not
much increased by reflex irritation.
The pathogenesis of these motor symptoms is not yet settled.
It is commonly believed that they originate in the reflex way,
owing to the abnormal irritation of the posterior roots, and might
be regarded as reflex contractures. This may be true to some
extent and in some cases. It is, however, quite certain that
the muscular tension is half voluntary in character, or is in-
creased by a voluntary act, which has for its object the preven-
tion of movement when all movements are so painful. The chief
weight, however, should be laid upon direct irritation of the
motor apparatus. | i
Such a condition may depend in part on inflammatory irrita-
tion of the anterior roots, in part on irritation of the motor paths
in the lateral columns by secondary points of myelitis (as F.
Schultze has shown). If the latter were the correct solution, it
would lead us to infer that the fibres for the trunk-muscles occu-
pied some exposed situation (possibly in the external periphery
of the lateral columns), inorder to explain the great amount of
rigidity in these muscles and in those of the nucha. The assump-
tion of a direct irritation of the motor apparatus is confirmed in
INFLAMMATION OF THE SPINAL PIA MATER, 239
an interesting manner by two cases in which Leyden! saw the
muscles of the back of the neck paralyzed in the latter part of
the disease. And, in fine, the clonic muscular twitchings which
occur spontaneously, or during efforts to move, may best be ex-
plained by direct irritation of the motor paths.
It is hard to say how the hyperesthesia, which is almost
always present in a high degree, is to be explained. It is most
marked in the skin, but extends also to the deeper parts, the
joints, muscles, etc. It may be so severe that the slightest touch
. or change of position calls forth the strongest expressions of
pain; even unconscious patients may shrink and make motions
of defence, when taken hold of. All voluntary movements of the
hyperesthetic parts cause severe pain. The hyperesthesia is
usually most marked in the lower extremities and the lower half
of the trunk, while it is less marked and more rare in the upper
limbs.
We are not yet in a position to assign any cause for this hy per-
eesthesia except the inflammatory irritation of the posterior roots,
and perhaps also an implication of the white columns of the
cord. It must be admitted that this explanation is very inade-
quate.
The anesthesia and paralysis which appear at a later stage
are more intelligible. They vary much in form and distribution ;
there may be a paralysis of single muscles or groups of muscles,
with or without atrophy ; paralysis of an entire lower extremity,
or paraplegia ; the upper extremities are reached, or are the ex-
clusive seat of paralysis, in few cases. In complications with
cerebral meningitis, paralysis of some cerebral nerves, disturb-
ances of the senses, etc., are frequent. These paralyses often dis-
appear quickly as the disease improves, while at other times
they improve very slowly, or may be quite incurable; and from
these circumstances inferences may be drawn as to the nature of
the causal lesion.
We cannot be much mistaken if we ascribe the majority of
these sensory and motor paralyses to the demonstrably severe
affection of the posterior and anterior roots. It requires no ex-
eee >
1 Klinik, ete. I. p. 417.
240 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
planation to show that the swelling and opacity of the nerve-
fibres and axis-cylinders may very easily reach a point which is
incompatible with the further performance of their functions;
that plastic infiltration of the neurilemma may so compress the
root-fibres as to render them unfit for conduction ; and that the
embedding of the delicate bundles of root-fibres in a considerable
mass of fibrinous exudation will very easily destroy the function
of the roots. It is, however, also possible that the myelitie
points in the white columns of the cord, especially in the lateral
columns, may in the course of the disease become dangerous .
to various paths of conduction, and produce paralysis. And
finally, we may remember that the presence of a large fluid
exudation in the sac of the dura may compress the cord and —
the nerve-roots to such an extent as to produce paralysis, This
lesion will become probable only under special conditions, as
when the paralysis is diffuse and not very severe.
The symptoms on the part of the vegetative organs are less
constant, and often hard to interpret; their physiological con-
nection with the cord is well known to be undetermined in secs:
points. |
In the urinary apparatus, a frequent disposition tor pass
water, in connection with ischuria or complete retention of
sseiais has often been observed ; it has been usual to explain
these symptoms as the consequence of a direct or reflex spasm
of the sphincter of the bladder. At a later stage, well-marked
weakness and paralysis of the bladder often occur, usually
accompanied by paraplegia. For the explanation of this we
require the same facts which explain motor paralysis; the
mechanism of the various forms is that which has been stated
on page 79 et seq. i
The composition and quantity of the urine seem to depend
on the severity of the fever; it is at first saturated, dark, scanty,
clouded with urates, but later becomes abundant, light, and clear.
In a good many cases (especially of the epidemic form), an un-
usual excess in quantity has been observed, which is usually
ascribed to a direct nervous stimulation of the secretion, origi-
nating in the cord ; and in like manner the rarer affection, melli-
turia.
INFLAMMATION OF THE SPINAL PIA MATER, 241
In the digestive apparatus we observe the disturbances which
usually accompany febrile complaints, and in addition, most
frequently constipation, which is referred by Koehler to spasm
of the intestinal muscles, and consequent interference with peri-
staltic action, and to the spasmodic tension of the abdominal
muscles. This explanation may be correct in the first stages,
but at a later point, the sluggishness and weakness which are
so characteristic of intestinal movements in many spinal diseases
are more probably the cause. The abdomen is usually sunken
and tense ; swelling and meteorism are rare, and so is diarrhcea.
Vomiting, which often occurs, is probably always due to a local-
ization of the process at the basis of the brain, and therefore is
most frequent in cerebro-spinal meningitis.
The respiratory apparatus is remarkably affected in all
severe attacks of spinal meningitis, especially when located in
the cervical region. All the degrees of accelerated and difficult
breathing occur, up to the extreme of dyspnoea, and even as-
phyxia. The explanation is to be sought in the following cir-
cumstances: irritation of the cervical roots, and the consequent
spasmodic tension and immobility of the respiratory muscles, or,
at later periods, paralysis of the same apparatus; irritation or
paralysis of the respiratory paths in the lateral columns of the
cervical medulla ; and finally, the direct affection of the medulla
oblongata and the centres of respiration which it contains. Near
the fatal termination, the Cheyne-Stokes phenomenon of respira-
tion has been repeatedly observed, which probably always indi-
cates that the medulla oblongata has been reached by the inflam-
mation.’
The disturbances of the apparatus of circulation have been
but little studied, and owing to their complicated origin, they
are hard to interpret. They depend firstly and chiefly upon the
fever. Increased frequency of pulse is the rule; yet retardation
often occurs, especially in cerebral complications ; great irregu-
larity in rapidity and rhythm is often observed ; in fatal cases,
towards the close, as the temperature rises, the pulse often be-
comes too fast to count. It may be left to the reader to form
>
Of. Hrb, Arch. f. klin. Med. I. p. 185. 1865.—Leyden, Klinik, etc, I. p. 421.
VOL. XIII.-—16
242 BERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
for himself a suitable explanation of the disturbances in such
a case, by reference to the physiological principles governing the
innervation of the heart from the cord and medulla oblongata.
The reaction of the pupil has not been fully studied; and it
seldom gives us an unqualified indication. <A striking contrac-
tion may occur, as well as unilateral or bilateral dilatation. It
will, however, not always be easy to decide whether paralysis or
irritation of the oculo-pupillary fibres in the cervical cord is the
cause of these disturbances, and whether the oculomotorius is
not also involved.
The cerebral symptoms which occur at times during spinal
meningitis and regularly in the cerebro-spinal form—delirium,
coma, general convulsions, epileptiform attacks, trismus, grind-
ing of the teeth, disturbances of the organs of sense, spasm and
paralysis of single cerebral nerves, vomiting, sleeplessness, loss’
of speech, giddiness, etc.—are merely enumerated here, as they
have been fully described and explained under Epidemic Cere-
bro-spinal Meningitis (Vol. II.),and Cerebral Meningitis (Vol.
XII.). |
The fever of sporadic spinal meningitis has been but little
studied. The temperature seems to be very irregular; in the
beginning it is usually high, but at the later period considerable
variations occur, which may continue during early convalescence-
In fatal cases a rise of temperature is often observed during the’
agony. As regards the fever of the epidemic form, see the trea-
tise by von Ziemssen in the second volume of this work.
Pathological eruptions of the skin (herpes, roseola, petechia,
erythema, urticaria, erysipelas, etc.) seem not to be constant or
particularly significant, except in epidemics; we therefore refer
to the place where the latter are described.
The general nutrition usually suffers greatly ; the patient
emaciates quickly and to a great extent, owing to the severity —
and duration of the fever, the deficient supply of food, the great ’
physical suffering, and the loss of sleep. In severe and pro-
tracted cases, emaciation may become extreme.
As a matter of course, not all the cases of spinal meningitis
are accompanied by all the above symptoms. In given cases, -
the appearance of the disease may differ greatly. The lead-
INFLAMMATION OF THE SPINAL PIA MATER. 243
ing symptoms are more or less distinct in all cases, but the
accession of the other symptoms, which are not invariably found,
may give rise to many varieties of the disease, which cannot pos-
sibly be enumerated here. Let it suffice to state that age and
individual constitution may produce considerable differences in
the course of the symptoms, and that the nature of the cause
usually influences the form of the disease; that essential or acci-
dental complications with inflammation of the membranes of the
brain, inflammation and other diseases of the internal organs,
may greatly modify the character of the disease ; and that,
finally, the portion of the spinal cord which is attacked has a
great influence upon the symptoms.
It is with regard to this latter point that we would briefly
mention the chief signs for locating the disease in the lumbar,
dorsal, or cervical region.
If the Zwmbar region is the part chiefly attacked, we shall
find pain in the loins and sacrum, stiffness of the lower part of
the spine, pain radiating to the hypogastrium and the lower ex-
tremities, spasm and paralysis limited to these parts, severe uri-
nary difficulties, ete.
If the dorsal region is also involved, the pain reaches a higher
point of the trunk, pain and stiffness of the back go up as high
as the shoulder, disturbances of respiration, preecordial anxiety,
etc., are perceived, while the symptoms in the lower extremities
continue.
If the process extends to the cervical region, the characteris-
tic symptoms of stiffness of the back of the neck, excentric phe-
nomena [7%. é., pain, etc., of a central origin] extending to the
upper extremities, severe difficulty of breathing and swallowing,
anomalies of the cardiac action, pupillary symptoms, etc., are
observed.
Finally, if the inflammation extends to the medulla oblon-
gata and to the base of the cranium, then, in addition to the
chief spinal symptoms, those of a cerebral nature become more
and more prominent ; vomiting, headache, delirium, paralysis of
ocular muscles, trismus, disturbances of respiration and speech
are observed, and impart to the dise&’se a very characteristic
appearance.
244 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
Course, duration, termination.—In describing these, we must
make a division into groups.
In the severest cases death occurs early. In epidemics it has
occurred within a few hours (meningitis cerebro-spinalis side-
rans), but more usually is postponed for a few days; the vio-
lence of the symptoms increases from hour to hour, tetanic
spasms interrupt the constant rigidity of the muscles, severe dis-
turbances of respiration and circulation occur, comatose symp-
toms appear, and death follows amid profound collapse, often
preceded by a great rise of temperature, and, in the last hours, a
general relaxation of the muscles.
In less violent cases the duration may be two or three weeks ;
the severity of the symptoms fluctuates, but in general those
which import danger increase, the patient’s forces sink, and at
last the serious symptoms above enumerated appear, and lead to
death in like manner.
There are other cases which have a very protracted course.
The fever and the acute symptoms diminish, but there is no sign
of recovery ; the most important symptoms persist and increase,
giving rise to the chronic form of the disease. This form may
either take the ordinary course of chronic spinal meningitis, or
it may be aggravated by a deep affection of the cord, and the
patient dies with symptoms of chronic spinal paralysis, often
after many months. .
As to recovery, that is often hoped for in vain. In the most
favorable cases it may occur very soon; the threatening symp-
toms grow less so in a day or two, soon disappearing, or if re-
turning, it is in a milder form and for a short time. This rapid
convalescence is often introduced by critical symptoms—profuse
Sweating, bleeding from the nose, or hemorrhoidal or menstrual
bleeding, abundant discharge of urine, etc.; and cases have been
reported where patients have been able to go about their busi-
hess in a week or two. But the recovery usually lasts longer ;
the convalescence drags on for weeks and months, the pains and
paralytic symptoms disappear by degrees, the strength improves
slowly, the patient has first to use crutches, and often lingers for
months in an invalid condition, from which he finally recovers
completely after several courses of treatment. Such are the cases
INFLAMMATION OF THE SPINAL PIA MATER, 245
in which inflammatory products, exudations, adhesions, etc., re-
main to retard recovery.
There are, of course, a few cases in which incurable traces of
mischief remain, after the general health has been fully restored ;
this constitutes an imperfect recovery. The patient is well, with
the exception of some paresis or paralysis of certain groups of
muscles, partial atrophy, local anesthesia, permanent stiffness of
the back, etc. A marked tendency to relapses, of various de-
grees of severity, often persists for a time.
Diagnosis.
The symptoms, when fully developed, form a very character-
istic group, not easy to be mistaken. The chief diagnostic diffi-
culty arises when we have to separate this group from among
more complicated symptoms, or to distinguish it from related
diseases.
The general marks of the disease are fever, pain and stiffness
in the back, stiffness of the back of the neck, muscular spasms,
hyperesthesia and paresthesia of the skin, pains in the limbs,
retention of the feeces and urine, dyspnoea, and, in the later
stages, paralysis. Where all or most of these symptoms are
present, it will be quite easy to form a diagnosis.
We shall very often have to put the question whether an
existent cerebral meningitis is complicated with the spinal affec-
tion. In the cerebro-spinal form, the cerebral symptoms consti-
tute the most prominent feature, while the presence of spinal
inflammation is indicated by pain in the back and loins, stiffness
of the nucha (which doubtless depends on an implication of the
cervical medulla), stiffness of the back, hyperzesthesia and pain
in the extremities, particularly the inferior.
The diseases most readily confounded with spinal meningitis
are acute myelitis and tetanus. The diagnosis from acute myeli-
tis may be hard to make in many cases, especially as (in our
belief) the two diseases are very often united, and myelitic symp-
toms are often of more prominence than those of the other dis-
ease. But a little attention will enable us to decide the case on
one or the other side with very great probability. In acute
246 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
myelitis the pains in the back and limbs, especially the excentric
pains in the limbs, are very much in the background ; the stiff-
ness of the back and neck are absent ; hypereesthesia is by no
means prominent, and the limbs are not rendered immovable by
pain and muscular tension. But in myelitis actual paralysis is
very early a prominent symptom ; it occurs much more quickly
and completely than in meningitis, and in the sensory sphere it
is quite prominent in the form of early and severe anesthesia.
To this is soon added paralysis of the bladder and rectum, often
acute bed-sore, and much increase of reflex action. The fever is
not, however, so high. From these symptoms it will be easy to
recognize myelitis if present, either alone or as complicating
meningitis.
From tetanus, the anatomical basis of which was often sup-
posed to consist of acute meningitis, the latter can usually be
distinguished with ease and certainty. Apart from the causal
elements, which often much assist in making the diagnosis, the
following criteria must be taken into account, Tetanus is a non-
febrile affection—in the commencement, at least, it is always
such; it begins with trismus, with scarcely an exception, while
in meningitis this symptom is postponed to the later stages;
there are never any signs of cerebral implication ; the peculiar
expression due to rigidity of the facial muscles (Koehler, Koenig)
is especially characteristic, but does not belong to meningitis ;. in
tetanus hyperesthesia of the skin is absent, but the reflex excita-
bility is increased to a degree which very seldom occurs in men-
ingitis; the spasms are much more violent and severe in teta-
nus ; very severe dyspnoea and trouble in swallowing occur early,
while in meningitis they accompany only the affection of the cer-
vical region and the base of the brain, which is always denoted
by marked disturbances of the cerebral nerves, changes in the
pupils, etc., that do not occur in tetanus. ;
It will hardly be necessary to give the points of diagnosis
between spinal meningitis and acute febrile rheumatism of the
muscles of the back, which is characterized by its light and
favorable course, the local painfulness of the muscles, absence of
pain in the limbs, of hypereesthesia of the skin, paralyses, etc.
Diseases of internal organs, as, for instance, inflammation of
INFLAMMATION OF THE SPINAL PIA MATER. 247
the lungs and pleura, heart, cesophagus, abdominal viscera, etc.,
cannot possibly be confounded with spinal meningitis except in
persons with marked spinal irritation, in whom all febrile dis-
eases are associated with pain in the back, tenderness of the ver-
tebrae, etc. This confusion may easily be avoided by careful
attention and physical examination.
Among the forms of spinal meningitis, the tuberculous is the
only one deserving of careful attention, as its diagnosis is known
to involve grave consequences in respect to prognosis and treat-
ment. As it is probably always associated with tubercular basi-
lar meningitis, we may refer to Vol. XII., where are given the
points which need attention in distinguishing this form from the
other forms of cerebral meningitis. A bad constitution, scrofu-
losis, tuberculosis, slow development of the symptoms, moderate
and irregular fever, retarded pulse, the cerebral symptoms, etc.,
will guide the diagnosis. Ophthalmoscopic examination, by show-
ing tubercles in the choroid, will perhaps often decide the point.
Prognosis.
According to the form and causes of spinal meningitis, the
constitution of the person attacked, the complications, etc., the
prognosis will vary extremely. Only the strictest weighing of
the case can make clear the leading points, which can only be
given in outline in this place.
Cases which begin and continue with sudden violence (foudroy-
ant) are absolutely unfavorable. The tuberculous form is equally
so. Those caused by deep bed-sores or severe vertebral lesions are
very unfavorable. The rheumatic cases and those due to simple
traumatic lesion are more favorable, and so are many cases of
epidemic origin.
The progress is influenced for the worse by the following cir-
cumstances: a very youthful or very advanced age; bad consti-
tution, aneemia, the previous occurrence of severe disease, etc. ;
-by the height to which the disease ascends in the spine, towards
the brain; by early symptoms of paralysis, signs of general loss
of strength, high fever, continually rising temperature and in-
248 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
creasing frequency of pulse ; great difficulty in breathing, dys-
phagia, severe cerebral symptoms, etc.
The opposite of any of these conditions is Javorable for thie
‘patient. A moderate intensity of the chief symptoms and the
fever, in robust persons in middle life, will permit an especially
favorable prognosis.
But in all cases we should be cautious in making predictions.
Acute spinal meningitis is always a serious disease. Even in
what seem the lightest cases it should always be kept in mind
that the inflammation exists in the immediate neighborhood of a
vital and extremely delicate organ, and further, that when all
immediate danger to life is past, a transition to the chronic form
is but too easy, the prognosis of which is not at all favorable;
and finally, that unforeseen relapses may occur, which will sud-
denly alter the situation in a disastrous way. |
The prognosis in later stages, with regard to duration and
mode of termination, sequele, etc., should be made in accord-
ance with general rules, keeping in mind what has been pre-
viously said. We should be no less careful here ; for not rarely,
in spite of the apparent insignificance of the residual affection,
partial paralyses, atrophies, etc., will obstinately resist all treat-
ment, while at other times they certainly yield with surprising
quickness to rational treatment.
Treatment.
No effective prophylactic measures can be mentioned in spo-
radic spinal meningitis; the precautions to be taken in the epi-
demic form are given in Vol. II.
In so acute a disease, we can seldom speak of fulfilling the
causal indication. As a rule, we have little to hope from this;
but in some cases the removal of foreign bodies, the treatment of
fractures of the vertebrae, of suppuration in the neighborhood, of
more remote diseases, and the like, may be necessary; of the
manner of accomplishing this, we need not here speak. If the
cause is unquestionably of a rheumatic nature, energetic diapho-
resis may be tried.
We shall usually have the disease in its full development to
i
INFLAMMATION OF THE SPINAL PIA MATER. 249
treat. The severity and threatening nature of the symptoms
usually tempt to energetic measures; and, in fact, much has
always been done and many things recommended.
Let us keep in mind, above all, that the treatment should be
determined upon with careful regard to the individual circum-
stances, the amount of strength, the causes, the prominent symp-
toms, and that these ought to be our chief guide in choosing
remedies. t
We shall, in the first place, always find reason for energetic
antiphlogistic measures, among which bloodletting and cold are
the chief. General bleeding, venesection, will be used only in the
rarest cases, namely, in very robust, plethoric patients, and when
the initial symptoms are very intense. Local bloodletting will
generally suffice ; it must be free and frequent. Cups and leeches
on the vertebral column are the best, in number dependent on
the seat and extension of the disease, the patient’s age and con-
stitution. In many cases blood may also be drawn from the
anus and vagina.
The application of cold along the spinal column must in all
cases be attempted, and, if possible, carried out with great thor-
oughness. Unfortunately, it is often hard to fix the ice-bags on
the spine, on account of the patient’s restlessness, and yet cold
applications and wraps, irrigation and affusion of the back can-
not properly replace the bags.
To this add a vigorous derivation to the intestine or skin.
For the former purpose, drastic purges may be advised (the best
is calomel with jalap), or strong saline purges, ‘‘ aqua laxativa,”’
ete. ; of course with allowance for individual constitutions. For
derivation to thé skin, the best and most successful method con-
sists in the repeated application of large blisters along the spinal
column. In the milder cases, frictions with pustulating ointment
and painting with tincture of iodine along the vertebral column,
hot mustard foot-baths, sinapisms to the back and calves or
thighs, etc., are sufficient. The white-hot iron seems not to act
especially well ; it might at most be tried in desperate cases of
disease in the cervical region.
Mercury has always been recommended as an antiphlogistic
from the earliest times; the most usual methods are the rubbing
2950 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
in of mercurial ointment upon the back or extremities, in the
quantity of from one to four grammes (from fifteen grains to a
drachm] daily, and the internal exhibition of moderate doses of
calomel (0.15-0.25 [from two and a quarter to four grains], two
or three times a day); the usual precautions against salivation
being of course employed. We have no certain proof of the
efficacy of this method. Among the internal remedies, tartar
emetic was formerly much given, but is now for the most part
abandoned. It is for the future to determine whether ergotin
deserves the recommendation given by Hammond on account of
its action on the vessels.
The entire surroundings of the patient must be arranged in
conformity with the idea of antiphlogistic treatment ; a quiet,
airy, moderately warmed room; absolute rest in bed, best on the
side or face, avoiding the back as much as possible; prevention
of all noise and excitement ; avoidance of bodily movement and
exertion ; for nourishment, a fluid, easily digestible diet, at first
cooling, but soon to be made tonic and roborant; for drink,
water, lemonade, juices of fruit, mild acid drinks, but no spiritu-
ous drink, no coffee or tea—such are the chief things to be
attended to.
But this is far from exhausting our therapeutic aims, for
there remain very important symptomatic indications to be ful-
filled, which usually become imperative, owing to the severity of
the patient’s sufferings.
In the first place, sedatives are required, in order to relieve
pain, sleeplessness, hypereesthesia. The opiates are universally
recommended for this purpose above all other remedies, and they
have been sufficiently tested in the great epidemics of cerebro-
spinal meningitis ; large doses of opium, subcutaneous injection
of morphia. With this may be mentioned chloral hydrate, and
in some cases the inhalation of chloroform.
May not belladonna deserve the preference over opium in such cases? Bella-
donna is stated to contract the vessels of the cord, and it also possesses narcotic
virtues. Favorable sedative results are also te be expected with certainty from the
use of bromide of potassium. All these remedies seem especially efficacious when
given directly after bleeding.
Baths, especially lukewarm, protracted full baths, occupy
EEE
INFLAMMATION OF THE SPINAL PIA MATER. 251
the second place as sedatives. If such are used, we may dis-
pense with cold affusion of the head and back, unless the latter
be called for by special indications—violent cerebral symptoms,
delirium, collapse, etc. Moist packing of the whole body often
soothes and brings sleep.
For hyperesthesia and pain, muscular tension and spasm,
many trials of external remedies have been made; little is to be
expected of them; the most likely to succeed are frictions with
warm oil, chloroform liniment with infused oil of hyoscyamus,
and similar applications.
For the fever, we shall seldom have to take special measures ;
if necessary, we should employ the regular methods of large
doses of quinia and cool baths.
For weakness of the heart and threatened collapse, the usual
analeptics are to be used when required, just as in other inflam-
matory affections. For disturbances of respiration we can do
but little, unless we succeed in directly checking the inflamma-
tion in the cervical region.
If convalescence has begun quickly and favorably, no further
treatment is usually required, except care of the diet and the
usual precautions against overexertion. To provide against re-
lapses, the wearing for a long time of a vesicating plaster (of one-
half the usual strength) upon the-back has been recommended.
But if the affection has only assumed the chronic form, it is
needful, above all, to assist the resorption and withdrawal of the
exudation, for which purpose iodine seems most suitable; to be
used externally in the form of ointment, internally in large doses
of iodide of potassium, to be continued for a considerable time.
For the relief of this stage we must also take into account warm
baths, thermal and brine baths, suitable water-cures, etc., accord-
ing to the rules given in the following section on Chronic Menin-
gitis.
The residua and sequele (palsy, atrophy, anzesthesia, weak-
ness of the bladder, etc.) should be treated upon general prin-
ciples, mostly with baths and electricity. Compare the sections
on Chronic Meningitis and Myelitis.
252 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
b. Leptomeningitis Spinalis Chronica.
By this term we understand a non-febrile inflammation of
the soft membranes of the cord, slow in development and course,
or one which has become sluggish after having run an acute
course. The anatomical changes which characterize this form
are usually slight, rarely well-marked, The symptoms, at first
often very trifling, afterwards assume a more severe character, —
and may develop by degrees with very destructive effect. Chro-
nic spinal meningitis is often the point of origin for chronic in-
flammatory processes in the cord.
Etiology.
The causes of this disease are quite obscure in many respects ;
the disease is very often unrecognized or disregarded, as its
symptoms disappear amid the crowd of symptoms of severe com-
plicating processes.
The disease very often originates from the acute form, and
has, therefore, the same cause. All possible debilitating infiu-
ences, bad nourishment, abuse of tobacco, etc., are said to favor
the occurrence of this transformation, and, in general, to produce
a certain predisposition to chronic spinal meningitis.
In general, the same causes which produce the acute form
may give rise directly to the chronic, provided that they are less
intense, but perhaps more continuous or more frequently re-
peated.
Many cases are directly traceable to cold ; the occupancy of
damp dwellings, working in the wet and cold, bivouacking in
bad weather (hence rather common among officers in the field—
Braun), are those most usually spoken of.
Traumatic lesions of moderate severity often lead to chronic
meningitis. Especially, simple shocks, falls upon the seat or
back, contusion of the spine, slight railway accidents and the
like may by degrees lead to inflammation. |
Chronic inflammatory processes or neoplastic processes of
neighboring parts often pass to the spinal membranes; thus, in
INFLAMMATION OF THE SPINAL PIA MATER. 253
caries of the vertebree, chronic periostitis of the same, carcinoma,
and other new formations of the vertebre or the spinal mem-
branes, etc. This connection is especially important in most of
the chronic diseases of the cord ; in chronic myelitis, sclerosis,
atrophy, and gray degeneration of the cord nothing is more com-
mon than extension of the chronic inflammation to the soft mem-
branes of the spine. Here are to be included the syphilitic and
leprous affections which often occur in the vertebral canal, the
specific products of which are usually surrounded by more or
less extensive chronic myelitis. Bruberger once found an exqui-
site syphilitic spinal meningitis of the cervical part of the cord
in connection with syphilitic basilar meningitis.
How far suppressed excretions (e. g., suppression of the hem-
orrhoidal or menstrual discharge, or of perspiration of the feet,
the disappearance of chronic eruptions, etc.) may act as causes
of spinal meningitis, we dare not decide.
The misuse of alcohol, however, seems to be certainly a very
active cause (Huss). Hacess of bodily effort and sexual excesses
may be considered rather as predisposing than as direct causes.
Koehler lays stress upon chronic disease of the heart and
lungs, disease of the liver, and all sorts of circumstances which
may give rise to impediments in the vertebral veins, as regular
causes of chronic and slow inflammations of the coats of the
cord, but he seems not to have paid enough attention to distin-
guishing the simple hyperemia of blocked circulation, with
' transudation, from actual inflammation.
Pathological Anatomy.
The morbid appearances are in most cases quite constant,
showing, however, some differences in the intensity and extent
of the process.
Besides a more or less distinct hyperemia, the principal ana-
tomical characteristics of chronic meningitis spinalis consist in
opacity and thickening of the pia and arachnoid, close aggluti-
‘nation and adhesion between these and the dura, unusually firm
adherence of the pia to the cord, and an abundance of spinal
fluid. .
954 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
The hyperemia is mainly of a venous character; the small
veins and capillaries are dilated, the color is.rather a dark red, ©
more or less diffuse.
The thickening with connective tissue may be very great, so
that the soft membranes assume an opaque tendinous appear-
ance, and unite in forming one uniformly hard membrane. The
latter may be pigmented in spots, sprinkled with small extrava-
sations of blood and spots of pigment, and is often connected
with the dura by means of more or less extensive false mem-
branes. Jaccoud found in an interesting case great fibrous
plates in the arachnoid along the region of the nerve-roots,
almost continuous in the cervical and lumbar cord, affecting
chiefly the anterior, less the posterior roots, and leading to atro-
phy. It is more common to find a deposition of thin, small,
more or less numerous plates of lime upon the arachnoid, which,
especially in the lumbar region, are often found without any
other marked sign of inflammation.
An abundant secretion of spinal fluid is almost always found,
seemingly in much increased quantity. Many cases, formerly
described under the term hydrorrhachis, evidently come under
this class. The serum is often clear and of the usual consistency,
but is oftener turbid, flocky, tinged with blood, or mixed with an
abundant fibrinous exudation. Stokes found an abundant puru-
lent exudation in a case which had been unattended with fever.
The dura mater often shares in the inflammatory process to a
corresponding extent, being thickened, opaque, sometimes gran-
ular, covered with growths of connective tissue and adhesions
(cf. also what was said under Pachymeningitis Interna, pp. 221
and 222).
The cord itself is implicated (myelomeningitis) in most cases,
though in various degrees and to a various extent. Often only
the processes of the pia mater which enter the cord appear thick-
ened and swollen; but more frequently there is a more or less
extended sclerosis (so-called) of the cord, in various-forms. Such
a sclerosis is sometimes annular in shape, beneath the pia, some-
times if occurs as longitudinal bands in certain columns of the
cord, sometimes is disseminated in spots, and sometimes it is a
chronic myelitis, occupying the entire transverse section, and
INFLAMMATION OF THE SPINAL PIA MATER. 255
extending to a greater or less distance longitudinally. We often
_ see, originating in such seats of disease, degeneration ascending
_ in the posterior columns, and descending in the lateral columns,
and reaching to a great distance. The result of this process
_ may be a considerable atrophy and diminution of the diameter
_ of the entire cord.
The nerve-roots are usually atrophied, pale, gray, degenerated ;
they are lost to the eye amidst the thickened and opaque mem-
_ branes of the spinal cord, and suffer more or less radical changes,
_ proportionate to the intensity and duration of the disease.
The following additional affections of a secondary nature are
_ found: atrophy and degeneration of peripheral nerves and mus-
_ cles, bed-sores in all stages and situations, chronic cystitis, etc.,
and as accidental oma disease of any of the internal
pects.
Symptoms.
This subject is not quite clear. The disease has not been suffi-
ciently studied, and, besides, is almost always complicated with
some other affection.
- In general the symptoms must be the same as those of the
acute form, except that they are much slower and less violent in
_ development, are without fever, and often are not prominent for
a long time.
When the disease develops tim the acute form, the violent
symptoms abate, the fever disappears, but a portion of the symp-
F toms—of the pain and stiffness, the weakness and abnormal sen-
: sations—remains for a longer time, and, gradually developing,
leads to an unfortunate condition : it has become chronic menin-
gitis.
In many cases repeated attacks of the subacute form recur ;
_ thus the disease becomes firmly rooted, the intervals between the
attacks diminish, and the disease assumes a regular chronic form.
| In most cases, however, the disease first appears in the chronic
form ; the beginning is quite latent, being, at least, not observed
_ by the patient, or not considered of any special importance.
The commencement is marked by occasional abnormal sensa-
256 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
tions in the lower limbs, gradually increasing pain, and some
stiffness of the back. The pain of the back increases, but is usu-
ally not very severe, being often described as merely a sense of
drawing and pressure in the back, a feeling of weight; it is not
usually increased by pressure on the spinous processes or the
dorsal muscles, but usually is made worse by movements of the
vertebral column. <A certain stiffness of the nape of the neck is
not usual in the early stages.
The excentric symptoms in the trunk and limbs which follow
are striking and important. Corresponding with the seat of the
disease the annoying sensation of a girdle is often felt, and in
the same region shooting and boring pains may occur, especially
if provoked by movements. In the limbs a feeling of great
heaviness early appears; in the skin the patients speak of all
kinds of paresthesia, often of a very singular character—tin-
gling, cold, formication, and the like; these are very often ac-
companied by tearing or shooting pains, either confined to the
region of some nerve-trunk, or else changing from place to place.
These pains are exasperated by movement, and not seldom by
change of weather, dampness and fog, snow-fall, or a low ba-
rometer. Finally, various degrees of cutaneous hyperesthesia,
not so marked as in the acute form, have been observed not
infrequently.
All these excentric symptoms are confined to the distribution
of the nerves whose roots originate in the part chiefly affected.
They may, therefore, be most marked either in the upper or in
the lower extremities, but the latter is the more usual case.
Symptoms of motor irritation are of subordinate importance
in chronic meningitis, but are not usually absent. A degree of —
stiffness of the back, and sometimes of the neck, is almost an
invariable symptom, and may in some cases become severe.
Trembling of the extremities, twitching of certain muscles, sud-
den starting of the body, involuntary drawing up or extension
of the limbs are not rare.
At almost any period in the subsequent development of the
disease symptoms of increasing weakness, going on to full paral- |
ysis, become prominent. The heaviness and weakness of the
limbs become greater, the patient loses more and more of his
INFLAMMATION OF THE SPINAL PIA MATER. 257
control over the extremities, symptoms of sensory paresis, of
vesical weakness, of disturbed rectal function occur, and para-
plegia develops, by degrees increasing in degree and extent.
This paraplegia, though it varies much in different cases, is
seldom complete, but usually comprises only a very severe pare-
sis ; a certain fluctuation in the intensity of the paresis seems to
be rather characteristic; the patient can perform this or that
movement better on one day, worse on the next; it is thought
that this fluctuation is connected with variations in the amount
of fluid exudation in the spinal canal, or the fulness of the circu-
lation ; if the spinal fluid is excessive, the paralysis increases
when the patient stands, because the lower parts of the cord are
more compressed, while, on the contrary, passive congestion may
cause it to increase while the patient is lying on his back, and
when standing or walking he is better. These two factors, there-
fore, act in contrary directions.
Severe anesthesia is rare; there is usually only a slight dull-
ing of the sensations of the skin, limited to the soles, feet, and
lower part of the legs. These disturbances are always accom-
panied by marked pareesthesie, not seldom mixed with hyper-
esthesia; but the latter is usually not marked, though some
reported cases give the impression that it may become very
severe. ;
The associated paralysis of the sphincters increases, and in
severe cases there may also be a strongly marked atrophy of the
muscles, with loss of electrical excitability.
The disturbances of sensibility increase, the reflex function
becomes extinet, bed-sores and cystitis appear, and the scene is
closed by marasmus,
Disturbances of any of the internal organs (of respiration,
circulation, or digestion) are very common, and originate in the
same way as in the acute form, although different from it in
degree.
The pathogenesis of the symptoms is about the same as in the
acute form; perhaps the cord is still more likely to be affected
than in the latter. We can refer upon this point to what has
been said under Acute Spinal Meningitis.
Course, Duration, Result.—This disease is always slow and
VOL. XIIL.—17
2958 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
chronic, extending to months and years, often many years. The
symptoms often fluctuate considerably ; intercurrent, acute ex-
acerbations are not rare.
Some of the cases recover ; these are the lightest, and those
which have early been taken in hand. The return to health is
always very slow and gradual, often occurs by successive steps,
and is often interrupted by relapses; the sensory disturbances
are usually the first to disappear, and the motor remain the
longest. Even when recovery is complete the patient usually
remains feeble for a long time, with a tendency to relapse.
The cure is often incomplete. The improvement reaches a
certain point, all symptoms of the active inflammatory process
disappear, but residua and sequel remain, doubtless due to the
relics of exudations, compression of the roots by adhesions and
thickening, cicatricial sclerosis in the cord, etc. In this category
may be included partial or complete paralysis of single mus-
cles or extremities, with or without atrophy, circumscribed anes-
thesia, weakness of the bladder, etc.
The cure is often interrupted by repeated relapses.
In a great proportion of the cases chronic meningitis leads
directly to death. The processes and occurrences which may
bring this to pass are many; they usually include the symp-
toms of grave spinal paralysis—paraplegia, vesical palsy, cys-
titis, bed-sores, with consecutive anzemia and hydremia, and, at
last, general marasmus. In other cases, the sad termination is
brought about by the extension of the process to the cervical
region, causing progressive difficulty in breathing and degluti-
tion, secondary pneumonia, etc. In yet other cases, life is
speedily brought to a close by the sudden starting into activity
of an acute purulent meningitis. There are many other conipli-
cations and accidents which may hasten the fatal termination of
chronic meningitis.
Diagnosis.
Chronic spinal meningitis is often hard to recognize, because
the symptoms remain for a long time extremely slight, and, taken ~
as a whole, present an incomplete representation of the disease,
or are obscured by complications.
INFLAMMATION OF THE SPINAL PIA MATER. 259
When the whole of the symptoms above mentioned are pres-
ent, we shall not hesitate long about the diagnosis.
The only difficulty consists in distinguishing between the
different forms of chronic myelitis, and this difficulty is the
- greater, as the two diseases are so often combined with one
another. The following guide is offered: Pain and stiffness in
the back, general pain in the extremities, extensive symptoms
referring to the roots, a slight degree of paralysis, equably dis-
tributed, and change in intensity dependent on change of position
of body, are symptoms which speak strongly in favor of menin-
gitis. The absence of increased tendinous reflex actions, of obsti-
nate contractures, of painful muscular jerkings, may be inter-
preted in the same sense. Myelitis must be thought of, when
severe paralysis and aneesthesia are present, the pains are slight,
the tendinous reflex actions are exaggerated, and considerable
contracture, etc., is present.
If there is palsy with great atrophy, without any disturbance
of sensibility or pain, our first thought must be of myelitis of
the anterior gray substance.
From tabes dorsalis, as implying the symptoms of gray de-
generation of the posterior columns, chronic spinal meningitis is
very easy to distinguish ; the points to notice are the character-
istic lancinating pains, ataxia; disturbances of muscular sensi-
bility, etc. But it should not be forgotten that both diseases are
very often combined, producing a mixed group of symptoms.
In determining the nature of the disease which causes the
spinal meningitis, we are guided by general considerations. The
diagnosis of the location in the lumbar, dorsal, or cervical region
has already been mentioned.
Prognosis.
The disease is in general a grave one; a cure is hard to ob-
tain, especially in rather old and tedious cases. But improve-
ment and cure have occurred, even in seemingly hopeless cases,
so that the prognosis is not absolutely bad, even in severe cases.
We may always remember that the chronic inflammation of
the spinal membranes need not be a continuous and limitless
260 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
process; that it is very susceptible of arrest and repair; that the
possibility of repair depends essentially upon the organization,
calcification, retraction, which may have taken place in the pro-
ducts of inflammation, but that, even after these have taken
place, others may often be expected in the course of time, which
give rise to considerable improvement of function. ;
The prognosis may be made by taking such facts into ac-
count, and with them the patient’s age, constitution, and powers
of resistance, state of nutrition, the causes, and the possibility of
removing them, the anatomical changes already developed, the
intensity of the symptoms, the results of treatment, etc. We
must, however, avoid indulging in too great hopes of curing the
disease. |
Treatment.
The causal indication is the first to be attended to. To avoid
needless repetition, we would refer to the given list of causes,
the proper remedies for which are easily inferred ; and we will
in this place only emphasize the necessity of carefully treating
the acute form. We ought always to try to cure it completely,
should observe the strictest watch during convalescence, should
not let the patient return too soon to the exertions of his calling,
should guard him from exposure to cold and other injurious
things ; by these precautions many cases of chronic spinal men-
ingitis might be prevented. |
In the treatment of the disease when developed, antiphlogo-
_ sis is to be used very sparingly. We shall seldom effect much
by bloodletting, energetic derivation to the intestine, etc., in
such a chronic disease as the present. Yet there are cases in -
which these remedies deserve a trial. In robust, well-nourished
persons, when the symptoms are rather decided, the pain of the
back severe, etc., it will be suitable to, apply every week or two
from ten to fourteen moist cups along the spine; for feeble pa-
tients the application will be restricted to dry cups once or twice
aweek. Similar principles and special indications (as habitual
constipation, hemorrhoids, etc.) will guide us in the use of pur-
gatives.
Teta wn Tt)
sina
INFLAMMATION OF THE SPINAL PIA MATER. 261
Derivation to the skin is praised by almost all writers. Noth-
ing seems more suitable for such cases than the repeated appli-
cation of large blisters to the back. Brown-Séquard advises to
do this every fortnight. The mild derivatives (sinapisms, pus-
tulating ointments, friction with oil of turpentine and croton
oil, painting with iodine, etc.) may be used in light cases and
for the sake of change. The moxa or white-hot iron (burning in
streaks along the spine) will be used only in severe and desperate
cases.
Of the drugs, the most justly celebrated is iodide of potas-
sium ; it is given for a considerable time in the usual doses. It
will be best to abstain from mercury in these chronic cases,
unless syphilis exists. Nothing remarkable is to be expected
from ergotin and belladonna. If we have cause to suspect the
existence of an abundant serous exudation, we may employ diu-
retics. | ¢
In many cases warmth seems extremely useful; warm gar-
ments, furs, and the like, warm wraps, frictions with warm oil,
etc., are praised.
Upon this fact seems to depend in part the unquestionable
advantage of baths, which have effected many notorious cures in
chronic spinal meningitis. Warm baths of all sorts, indifferent
and brine-baths, gaseous brine-baths and chalybeate-baths, etc.,
may here be used. Braun, who has examined this point with
care, states the rule for using them as follows: the baths should
in general be protracted ; the more indifferent the spring, the
longer may be the duration; the more abounding in salts and
carbonic acid, the more should the bath be shortened. The tem-
perature should at first be very carefully regulated ; if myelitic
complications exist, the higher degrees should be avoided, but in
pure meningitis they seem the best borne, which may account
for that dangerous credit which many warm springs have ac-
quired in spinal paralysis. An enlightened diagnosis should be
invoked in support of such treatment.
In very obstinate cases we may try vigorous cold-water treat-
ment, especially the wet pack, alternate cold and warm douches
on the back, moor-baths, and hot sa7td-baths.
Of the effect of the galvanic current in chronic spinal menin-
962 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
gitis, we do not yet possess full information. It is extremely
probable, a priori, that the catalytic effect of the current will be
strikingly useful in this disease. An observation by Hitzig’
seems to confirm this most clearly ; the result was obtained by
using descending stabile currents. My own experience in the
matter is also very favorable, but my observations are too few in
number to render a final decision possible. <A trial of galvanic
treatment (chiefly by stabile currents to the spine, with succes-
sive action of both poles) is certainly always indicated, and may
very well be conjoined with the use of baths.
Much can also be done to relieve symptoms. For pain, the
usual sedatives; for paralyses, anesthesia, atrophy, etc., elec-
tricity ; for weakness of the bladder, ergot, nux vomica, elec-
tricity ; for anemia and cachexia, tonics, iron, quinia, strength-
ening diet, a little wine, etc. The diet must be mostly tonic,
adapted to promote and hasten the change of tissue. The habits
are to be governed by the patient’s condition and circumstances,
and may be regulated by the general directions given at page 196
et seq.
Tn all cases, after a cure has been attained, it is absolutely
necessary to maintain a long watch over the health and habits in
all respects. For a subsequent treatment, many cases will be
benefited by electricity, cold-water cures, a mountain climate,
and the milder sea-baths.
5. Tumors of the Spinal Membranes.
Ollivier, loc. cit. 8d ed. p. 517.—Cruveilhier, Anatomie pathol. livraison. XXXIL
pl. 1. XXXV. pl. VI.—Haasse, loc. cit. 2. Aufl. p. 731.—Rosenthal, loc. cit. 2.
Aufl. p. 346.—Hammond, loc. cit. 3d edition. p. 517.—Leyden, loc. cit. I. p-
443.—Virchow, Geschwiilste. I. pp. 386, 428, 514; IL. pp. 92, 120, 345, 354,
461.— Charcot, Lecons sur les mal. du syst. nerv. II. Sér. IL. fase. Paris, 1873.
—Jaccoud, Les paraplégies et l’ataxie du mouv. Paris. 1864. p- 236.—Brown-
Séquard, Lectures on Paralysis of the Lower Extremities, etc. 1861. p. 92.
Athol Johnson, Fatty Tumour Connected with the Interior, etc. Brit. Med. Journ.
1857.— Virchow, Bésartige, zum Theil in der Form des Neuroms auftretende
Fettgeschwiilste. Virch. Arch. 1857. XI. p- 281.—Traube, Fiinf Falle von
1 Virchow’s Archiv. 1867. Bd. XL.
TUMORS OF THE SPINAL MEMBRANES. 263
Riickenmarkskrankheiten. Charité-Annalen. IX. 1861. (Gesamm. Abhandl.
Il. b. p. 994.)—Whipham, Tumour of the Spinal Dura Mater, Resembling
Psammoma, etc, Trans. Path. Soc. XXIV. 1873. p. 15.—Benj. Bell, Tumour
of the Pia Mater, etc. (fibro-nucleated growth). Edinb. Med. Journ. Oct., 1857,
p. 331.—Loewenfeld, Faserig. Sarkom an d. Wurz. der zwei ersten Sacralnerven
links. Wiener med. Presse. 1873. No. 31.—L. Benjamin, Neurom innerhalb der
Riickenmarkshiiute. Virch. Arch. 1857. XI. p. 87.— Seitz, Pseudoplasma
medull. spin. Deutsche Klinik. 1853. No. 37.—Charcot, Hémiparaplégie déter-
minée par une tumeur, etc. Arch. de Phys. 1869. II. p. 291.—Baierlacher, Zur
Symptomatologie der Geschwiilste am R,-M. Deutsche Klinik. 1860. No. 31.—
Meschede, Sarkom am R.-M. Ibid. 1873. No. 32.—7'h. Simon, Tumor im Sack
der Dura spinal., die Cauda comprim., etc. Arch. f. Psych. u. Nervenkr. V.
p. 114. 1874.—Simon, Paraplegia dolorosa. Berl. klin. Wochenschr. 1870. Nos,
35 and 36.—Duvaine, Traité des entozoaires, etc. Paris. 1860. p. 666.—Bar-
tels, Echinoc. innerhalb des Sacks der Dura spin. Deutsches Archiv. f. klin.
Med. VY. p. 108. 1869.—Béhier, Compress. de la moélle épin. par un kyste hy-
datique. Arch. gén. Mars. 1875. p. 340.— Westphal, Cysticerken des Gehirns und
R.-M. Berl. klin. Wochenschr. 1865. No. 43.
Of the new formations within the spinal canal, the most
important and frequent are those proceeding from the spinal
meninges.
They mostly originate in the dura, and develop upon its outer
or inner surface; many new formations, however, spring from
the arachnoid or pia, and remain limited to these membranes.
The latter are not always the point of origin ; neoplasms arising
from the neighboring parts often extend to the membranes, in-
volve them in a secondary way, and then produce effects like
those of primary meningeal tumors.
It results from the narrowness of the space within the canal
that the tumors usually found are of inconsiderable size, but
that they very soon begin to awaken the most active disturb-
ances through irritation and compression of important intra-
spinal tissues.
Most of the tumors reach only the length of two to four centi-
metres, rarely that of eight to ten, within the canal; their thick-
ness is from one to three centimetres. Of course, secondary
tumors, and such as send out branches through natural or arti-
ficial foramina in the spinal column, may reach a much larger
size. -
The form is usually oval, that of an olive, or something so ;
964 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the rate and direction of their growth, and hence also the general
character of the symptoms, depend chiefly upon the nature of
the tumor. It is said to have been observed that such tumors
assume a more vigorous growth during pregnancy.
In enumerating meningeal tumors, we shall for practical rea-
sons not limit ourselves to new formations in the stricter sense,
but shall add many things which have the same clinical signifi-
cance, as inflammatory new formations in the shape of tumors,
animal parasites in the canal, ete.
Pathological Anatomy.
The exact histological diagnosis of many intra-spinal tumors
is far from satisfactory. It is especially hard to make out in
older observations to which of the present categories of new
formations we ought to assign them. The observations of the
last ten years, though not very numerous, show the existence of
the following forms of tumors in the spinal meninges :
Fibroma and jfibro-sarcoma.— Usually small oval tumors,
three to five centimetres long, two to four thick, springing from
the dura or the pia, and situated now within, now without the
sac of the dura. They consist of connective tissue, with more or
less abundant cells, spindle-cells, round cells (transition to sar-
coma).
Sarcoma.—Occurring in all possible forms, as hard and soft,
fibrous, or cellular ; often with formation of cysts, cysto-sarcoma
(observations of Baierlacher, Leyden, and others). Originates
more rarely from the dura, more frequently from the soft mem-
branes; is more usually of a longish shape; not seldom lobular,
with a nodulated surface; considerable vascularity, and the usual
histological characteristics of sarcomatous new formation.’
Myzxoma has been found by Virchow, Traube, and others in
the spinal meninges. It originates almost exclusively from the
arachnoid or the pia, and is a soft, juicy, lobulated tumor of
moderate size and pale color. It may be pure; more frequently
it is a mixed product, a lipomatous or sarcomatous myxoma, ete.
| See Virchow, Geschwiilste. II.
TUMORS OF THE SPINAL MEMBRANES. 265
To the same series of new formations belongs psammoma,
found by Whipham, Cayley, Charcot, Bouchard, and others—a
sarcoma with granular concretions of lime imbedded in it. Usu-
ally a small roundish or olive-shaped, smooth or lobed tumor, in
most cases originating from the soft membranes.
Lipomata have repeatedly been found in the vertebral canal,
either caused by proliferation of the perimeningeal fatty tissue
(Athol Johnson, Obré, Virchow), when it is situated outside of
the sac of the dura, or originating from the soft membranes, and
situated within the sac of the dura.
An enchondroma as big as a hazel-nut, firmly adherent to the
dura and the connected vertebra, has once been found by Vir-
chow, and declared to be probably congenital.
Osteoma, the formation of new bone, in the form of the so-
called cartilaginous disks, is extremely common in the arachnoid,
but in this form cannot be considered a tumor, and has no clini-
cal importance. Ossification of the dura also occurs only in the
diffuse form.
Multiple fibrous melanoma has been seen in the spinal canal
by Virchow and Sander.
The name of newroma has been given to many new formations
occurring in the spinal canal, on the nerve-roots, especially on
the cauda equina (Benjamin, Virchow). These are mostly the
so-called false neuromata, and occur either singly or in numbers.’
Carcinoma proper seems very rarely to spring from the spinal
membranes ; I, at least, have had knowledge of no unquestioned
case of primary carcinoma of this region, excepting the older
and less reliable observations of ‘‘fungous’’ or ‘‘cancerous”’
growths. The tumors are almost always secondarily developed
by extension from the vertebree or other neighboring parts, or by
metastasis from other organs. Such secondary carcinomata not
seldom appear in the vertebree, in consequence of primary cancer
of the breast.
We have spoken under meningitis of the formation of miliary
tubercle in the membranes of the cord.
With these are associated the tumors which originate in
>
1 See Vol. XI. p. 599 et seq.
966 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
inflammatory, hemorrhagic, and other processes in the spinal
membranes or the neighboring parts. Such are peripachymenin-
gitic exudations, with or without caries of the vertebree, those
hard, circumscribed growths, of a purulent or. caseous nature,
of which we have before spoken, and which are so common in
Pott’s disease ; also the greenish-yellow, bacony, scrofulous exu-
dations between the dura and the vertebral column; and the
hematoma of the dura mater, originating in pachymeningitis
interna hemorrhagica,
The syphilomata which are occasionally found in the spinal
membranes are of a somewhat similar nature (Wilks, Virchow).
They have been little studied; they usually consist of gummata
of the dura or the pia. Bet
Finally, we have to speak of the parasitic new growths which
occur (though rarely) in the spinal canal. )
Cysticercus cellulose has been found once by Westphal in
the sac of the dura; there were numerous cysts in the lumbar
portion, some free in the fluid, some firmly enclosed in the meshes
of the arachnoid ; a few also in the thoracic and cervical portions.
Numerous cysts in the brain. Only one of them contained a
head. Clinical symptoms referred to the spine had been present.
Echinococcus has been found more frequently (thirteen times
in all) by Davaine, Cruveilhier, Lebert, Foerster, Rosenthal,
Bartels, etc. The development of most of the cysts took place
externally to the dura, and often led to considerable tumors out-
side of the vertebral canal. In only two cases (Esquirol and
Bartels) did they develop within the sac of the dura. They
differ in size, and present the usual characteristies of colonies of
echinococcus.
With this we close our enumeration—perhaps an n imperfect
one.
Respecting the seat of meningeal tumors, we need not add
much. They may occur at any part of the canal, may compress
the cord in front, behind, or at the side, may include various
numbers of pairs of nerve-roots, etc. Each case will differ in
these respects, but one thing is tolerably important and charac-
teristic, namely, that the disease always occupies a quite limited
and definite locality.
TUMORS OF TITE SPINAL MEMBRANES. 267
But, for the purpose of understanding the clinical symptoms
and the entire course of the disease, it is of much importance to
attend to the consecutive changes which always, though in vary-
ing degree, accompany the formation of tumors in the spinal
canal.
The nerve-roots in the region of the tumor are sometimes
found swollen, reddened, softened by inflammation, sometimes
thin, flat, grayish and translucent, atrophied and degenerated,
according to the duration and extent of the process.
The cord itself always experiences some degree of compres-
sion, which may change it to a flat, ribbon-shaped string, or, at
least, produces a local indentation, more or less deep. Simple
atrophy of the portion compressed is seldom the only change.
It is much more common to find at the compressed point marked
inflammatory symptoms (myelitis from compression), which can
be followed but a short distance upward, and often a good way
downward. The medulla is in a state of whitish or reddish soft-
ening, is full of small hemorrhages, and exhibits under the mi-
croscope many granular corpuscles amid the débris of nerve-
elements. This change continues to a variable distance down-
wards in the white substance, and more especially in the gray
also. Cruveilhier once found the whole peripheral portion of
the cord in a state of purulent degeneration.
The examination of the hardened cord in these cases regularly
shows secondary degeneration, ascending in the posterior col-
umns, and descending in the postero-lateral (see farther on, IL.,
No. 19). Simon has also found this ascending degeneration in a
tumor of the cauda equina.
In the membranes of the cord we almost invariably find signs
of chronic inflammation (thickening, opacity, pigmentation, hy-
pereemia, etc.) of various extent. In correspondence with this,
an increase of the spinal fluid (hydrorrhachis) is pretty constant.
In the peripheral nerves and muscles, degenerative atrophy
is not rare; usually in those nerve-districts whose roots are either
directly included in the new formation, or are directly connected
with degenerated portions of the gray substance.
Such further alterations as are foun® on the bodies of those
dead of meningeal tumors—bed-sores, cystitis, extreme maras-
2968 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
mus, changes of internal organs, etc.—will be described here-
after
Etiology.
The causes of meningeal tumors are usually obscure. It
seems to be established that surgical injuries are the most likely
to produce them ; cases have been observed where the first symp-
toms occurred after a fall or blow upon the back, or spine, ete.
Exposure to cold has been assigned as the cause of the dis-
ease in a number of cases, and, as it seems, with sufficient reason,
It is remarkable how often it is recorded that the first symp-
toms appeared during childbed, shortly after delivery.
Observations by Cruveilhier and Kohts render it probable that
excessive mental excitement, violent fright, may give the impulse
to the formation of meningeal tumors.
Finally, vertebral disease, the tuberculous and serofulous
diathesis, and syphilis, are among the causes of meningeal tu-
mors, as follows from the preceding enumeration of the forms.
The entrance of animal parasites is effected in the usual way by
swallowing the eggs, or the proglottides of the various species
of tape-worm.
It is seen that these scanty facts leave a large part of the eti-
ology of meningeal tumors in obscurity. |
Symptoms.
The general outline of the symptoms usually caused by me-
ningeal tumors may be drawn in a few words.
If the disease begins (as it often does) quite in a latent and
insidious way, the development of the tumor is usually first in-
dicated by the presence of pain in certain nerve-districts, which
increases in severity. Abnormal sensations in the trunk (feel-
ing of a girdle) and the extremities, paresthesia, anesthesia,
partial paralyses, are associated with the above—all at first
localized in the same nerve-districts. Painful stiffness of a
definite portion of the spine indicates more directly the seat of —
disease,
After a period of various length, often after years, paraplegia
TUMORS OF THE SPINAL MEMBRANES. 269
follows, and increases; it begins as a progressive paresis, often
unilateral, like Brown-Séquard’s palsy, but usually making
rapid progress across the body, and ending with absolute sensory
and motor paralysis. The disease rarely remains stationary at a
point of moderate severity, but usually goes on to extremes; and
after great suffering, attended by all the horrible circumstances
of the severest spinal paralysis, palsy of the bladder and rectum,
cystitis, extensive bed-sores, general marasmus, etc., the patient
is brought to a miserable end.
Although the individual features of this sketch are by no
means characteristic of meningeal tumors when taken separately,
yet, when considered as a whole, they often enable us to recog-
nize and to localize the disease with some accuracy.
Upon closer consideration we find two groups of symptoms,
distinguishable both by their succession in time and by their
pathogenetic significance. These are:
1. Symptoms of local irritation and compression of the nerve-
roots and the membranes jirst involved in the tumor.
2. Symptoms of irritation and compression of the cord itself,
and of consecutive myelitis (myelitis by compression).
Those of the first group are the earliest, and often precede the
paraplegia by months and years; their character of course dif-
fers in each case according to the location, direction of growth,
and rate of growth of the tumor; so that no exhaustive state-
ment can be made. But the numerous varieties may be inferred
from the general scheme. All these symptoms arise from irrita-
tion or compression of the nerve-roots, from consecutive irritation
of the meninges, and, to some extent no doubt, from commencing
irritation of the cord itself.
Violent pains are next observed, the lancinating, tearing,
boring character of which proves their excentric origin. They
may remain confined toa single point, or attack a single nerve-
trunk; hence, according to the seat of the disease, they either
surround the trunk like a girdle at various levels, or invade the
upper or lower extremities, of one side or both. They may ex-
tend suddenly or by degrees to neighboring nerve-districts, are
often increased by movement of the spinal column, and seem to
be made worse by sudden changes of weather (Bell). These
970 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
symptoms are so intimately associated with those of compression
of the cord by tumors, that Cruveilhier distinguished paraplegia
dolorosa, due to compression of the cord, from paraplegia non
dolorosa, caused by primary disease of the cord. |
Paresthesie also occur, corresponding to the extent of the
pains—the sensations of tingling, formication, numbness, dead-
ness, etc., either in the form of a girdle or limited to certain
regions of the extremities.
If motor roots are first exposed to the influence of the tumor,
separate muscular twitchings, spasms, may appear at the be-
ginning.
These symptoms of irritation are almost always accompanied
by distinct, sometimes very active pain in the back, localized in
the neighborhood of the tumor, and usually accompanied by a
local stiffness of the spine. Leyden points out the fact that the
movement of the spinal column is often difficult and painful in a
certain direction, because this motion one a greater pressure
upon the tumor.
In the further course of the disease symptoms of paralysis
appear sooner or later, corresponding to the locality of the dis-
ease ; circumscript anesthesia, often coinciding with the distri-
bution of nerves which are especially painful (anesthesia dolo-
rosa), local paralyses and pareses of the corresponding muscular
groups, atrophy, etc., compose an extremely complicated and
varied group of initial symptoms. |
It needs only to be indicated how various are the phenomena
of this first group in connection with different seats of disease ;
how when the cervical region is the part attacked, for example, —
one upper extremity may first be seized by pains, pareesthesia,
partial palsy and atrophy, before the symptoms of compression
of the cord appear; how, when it is the dorsal region, the dis-
ease will be introduced by intercostal neuralgias, paroxysms of
visceral pain, zoster, etc.; how, finally, when the lumbar region
is involved, all the above disorders may appear, now in the dis-
trict of the sacral, now in that of the lumbar plexus, and put on
a great diversity of form. Numerous and instructive examples
of this are upon record.
When the symptoms of the first group have existed for an
TUMORS OF THE SPINAL MEMBRANES. 271
uncertain length of time (weeks, months, often several years),
they are succeeded by symptoms of the second group, derived
from the continuous pressure upon the cord, and usually from
myelitis also (which hardly ever fails to be present); these be-
come more and more distinct, and change the scene in a very
disagreeable way.
The development may be rapid or slow; it often occurs with
almost suddenness in a few hours, and in such case is nearly
always due to secondary myelitis, as it is seldom we can suppose
so rapid an increase of the pressure of a tumor. The compres-
sion is often limited at first to one lateral half of the cord, which
may give rise to the characteristic symptoms of Brown-Séquard’s
hemiplegic lesion (paralysis of the side of compression, anes-
thesia on the opposite side ; see the section on Unilateral Lesion,
II., No. 14.) for a longer or shorter time. Or the compression
may occur on the anterior or the posterior surface of the cord,
the result of which is, that in the former case the motor phenom-
ena, in the latter the sensory, not only preponderate, but often
are exclusively present for a time.
After a variable time, the palsy invades all the paths in the
portion of the cord adjoining the tumor, and we have the symp-
toms of extreme compression of the cord. We shall describe
them fully in the section on ‘*Compression of the Cord ’’ (see
farther’on, II., No. 5), and will therefore mention here only the
most important in order to complete the description, referring
for all details to that section.
First of all there is severe paraplegia; motility and sensi-
bility more or less completely paralyzed, up to the level cor-
responding to the seat of the tumor; the limitation of these
paralytic symptoms upwards is variously strict. The bladder is
paralyzed ; at first the symptoms of retention are prominent, and
later those of incontinence, with continuous dribbling. The
sphincter ani is also paralyzed.
Violent pains in the parts below the seat of lesion usually
follow. Although the doctrines of physiology are opposed to
the supposition that such excentric pains could originate in com-
pression or irritation of the cord itself,yet many observations (as
those of Whipham, Leyden, Brown-Séquard) show that violent
272 ELRB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
pain of that kind in the legs may be caused by tumors seated in
the upper dorsal or the cervical region. It is certain that in
most cases the palsied parts are at times the seat of very severe
pains, perhaps due to secondary myelitis.
In the motor apparatus also, the symptoms of irritation do
not fail to accompany those of complete palsy ; muscular twitch-
ings, spasms, and contractions—at first temporary, then perma-
nent—occur, while the muscles, at first quite relaxed, become by
degrees tense and rigid (secondary degeneration of the lateral
columns). ‘
In many cases there isa remarkable increase of reflex actions.
Slight cutaneous irritation produces free and vigorous muscular
contractions, powerful flexion or extension, active clonic tremor,
more marked in the lower extremities, especially when the tumor
is seated at an elevated point. If, however, the gray substance
is compressed by the tumor (when located in the lumbar region),
the reflex actions are wholly wanting. The same is the case
when the gray substance is deprived of its functions by second-
ary descending myelitis. For this reason, in the later stages, we
often see the reflex activity diminish and disappear, when pre-
viously it had been exaggerated. The tendinows reflex acts also
seem considerably increased.
The nutrition of the muscles is affected in nearly the same
way ; at first it is well kept up, but afterwards severe atrophy
appears. The electrical reaction behaves in the same way ; at
first well preserved, it may afterwards sink and disappear.
Paralysis of the bladder may lead, after a while, to cystitis,
with ammoniacal decomposition of the urine and the presence
of abundant pus. The absolute immobility of the patient, who
is almost always forced to retain the dorsal decubitus, and the
frequent befouling of his person with urine and feeces, etc., give
rise to gangrenous bed-sores on the sacrum and buttocks, tro-
chanters, heels, etc., which often make unchecked progress and
produce the most shade destruction.
Chills, with very high temperature—a more or less continuthil
Jever—appear. This, and the loss of fluids caused by the suppu-
rating sores, and the loss of sleep and appetite from continual pain
and abnormal sensation, continually increase the patient’s anzemia
TUMORS OF THE SPINAL MEMBRANES, 273
and cachexia, and cause a marasmus which of itself is sufficient
to produce the fatal result. Death usually occurs in a state of
sopor, with a rising temperature, and often after a very pro-
longed agony. In other cases the patient’s sufferings are brought
to an end by bronchial catarrh or pneumonia, or an acute menin-
gitis caused by bed-sores, or other diseases.
According to the seat of the tumor, the rapidity of its growth,
the patient’s power of resistance, the sequence of these symp-
toms may be rapid or slow. If the seat is high in the cervical
region the course is usually very rapid, paralysis of the respira-
tory nerves producing early death by suffocation.
Course, Duration, Termination.—The course is usually slow
and insidious, especially at the beginning, and the first period of
the disease may last several years. With the occurrence of
paraplegia the second period commences; this often comes on
rather quickly, in a few days or one or two weeks, but may
require a much longer time. In a few cases it is effected quite
suddenly, and is then usually dependent on myelitis—as in a
case by Ollivier, in which advanced softening was found after
death.
After paraplegia has appeared the progress is usually more
rapid, but even at this point years may pass before death occurs.
This, of course, depends on the rate of growth of the tumor and
the height at which it is situated. Temporary improvement is
occasionally mentioned, and great fluctuations in the severity of
symptoms may be observed; such are usually referred, for the
most part, to the state of the compressive myelitis, but in part
also to changes in the volume of the tumor caused by variation
in the amount of blood contained, processes of softening, changes
in the direction of growth, etc.
The entire duration cannot always be easily determined,
owing to the uncertainty as to the date of commencement. Some
cases have terminated fatally in eight or ten months, while others
run on for one, three, or five years; and cases of much longer
duration—extending to fifteen years—have been observed.
The termination is almost always in death in the manner:
described. A permanently stationary condition or improvement,
or cure, israrely seen. Yet the possibility of such an event, at
VOL. XIIL.—18
274 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
least for certain forms, cannot be denied. In syphilomata and
scrofulous tumors, in inflammatory new formations, in cysticerci
(by shrinking or calcification), it may certainly be admitted, and
in the case of others may be held an open point. It will cer-
tainly be hard to prove such an event, both because the diagno-
sis during life is very obscure, and because in cases which have
recovered, it will seldom happen that the spinal canal will be
opened, post-mortem.
Diagnosis.
The diagnosis of a meningeal tumor is sometimes quite easy,
but usually very difficult, and for a long time uncertain. When
the symptoms as above given develop quickly and promptly,
and with their full characteristics, or if the disease has passed
into the second stage, there is usually no great difficulty. But
previous to this point, years of uncertainty and guess-work may
pass. And, on the other hand, in cases with slightly marked
symptoms, the disease may possess an unlucky resemblance to a
great variety of circumscript diseases of the cord, rendering a
distinction impossible.
The diagnosis chiefly depends on the demonstration of a slowly
developed compression of the cord (see farther on, II., section 5),
which has been preceded by the signs of a circumscribed ir-
ritation or compression of certain portions of the roots. It
should be particularly noticed that the symptoms point only to
a progression of the paralyzing lesion transversely to the cord,
while an extension in the longitudinal direction is not percepti-
ble, at least not upwards, while a descent of the process of mye-
litis is not rarely observed. This, however, does not make much
change in the symptoms.
When we have made out the existence of a tumor with some
degree of certainty, we may consider ourselves prepared to attack
the second and more difficult question as to the nature of this
tumor. In settling this question, we are often entirely deprived
of guiding-points—especially as the position of the cord renders a
direct examination in most cases quite impossible. In many cases
something may be found to base_a diagnosis upon, and in these,
TUMORS OF THE SPINAL MEMBRANES. 275
after a careful estimation of all circumstances, we shall be obliged
to follow general pathological principles.
We shall infer, for instance, a peripachymeningitic exudation
if Pott’s disease or a marked scrofula exists; a carcinoma, if
there is cancer of the vertebree or primary cancer of some other
part; a syphiloma, if syphilitic infection can be demonstrated ;
an echinococcus, if the parasite has been found in other organs,
or tumors containing the cysts are demonstrated near the spine ;
a neuroma, if neuromata are found in peripheral nerves, etc. In
most cases, however, we shall be forced to confine ourselves to
guesses.
It is easier, in most cases, to define the precise seat of the tumor,
or, if there are several of them, at least that of the uppermost.
This is done by following the rules we have repeatedly given, and
which will be stated more precisely below, depending on the
local distribution of the symptoms of irritation and paralysis.
We may here add a word upon the tumors of the cauda equina, which usually
proceed from the meninges, and have, in every respect, a great resemblance to those
which are situated higher and affect the cord proper. They are hard to distinguish
from the latter, but may be in many cases, perhaps, if it is borne in mind that
tumors of the cauda produce exclusively nerve-root symptoms, and that the signs of
compression of the cord, of secondary myelitis, etc., are absent. The higher the tu-
mor, the nearer it approaches the lumbar portion of the cord, the harder will it be to
draw the distinction. In respect to tumors seated lower, the following points may be
attended to: thé seat of the pains (which in such cases often attain enormous vio-
lence) is strictly localized in certain nerve-districts; all nerves leaving the spinal
canal above the tumor are free; thus, in myxo-sarcoma telangicctodes of the
cauda, I observed the pain strictly limited to the district of the sciatic, while the
crural and the.dorsal nerves were perfectly free; constant violent pain in the
sacrum. If palsy occurs, the reflex actions necessarily cease at once. Spasms are
seldom observed; more frequently contractures. Atrophy of the muscles occurs
rather frequently. The palsy and anesthesia, by their localization, often give us
the opportunity of fixing the upper limit of the lesion. Increase of the reflex acts
and marked tendinous reflexions, do not occur. Paraplegia, palsy of the bladder,
bed-sores, etc., may develop exactly as in tumors occupying a higher seat; but the
symptoms of paralysis do not seem to belong necessarily to the disease, as is shown
in my case (just mentioned), which terminated fatally before paralysis or anssthesia
occurred,
276 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
Prognosis.
It follows from what was said of the course, that the progno-
sis of meningeal tumors is very bad in almost all cases. If there
are actual neoplastic formations, the prognosis is absolutely bad.
In the most favorable case, the disease may cease for a limited
time to make progress, or death may be delayed. The more
quickly the symptoms develop, the worse for the patient; and
the worst is in carcinoma. In some other tumors, in the inflam-
matory, scrofulous, hemorrhagic, and syphilitic forms, the prog-
nosis is more favorable, and is decided upon general principles.
If paraplegia has become complete, the case is usually hopeless.
The early or late occurrence of the fatal termination then depends
on the rapidity and intensity with which cystitis and bed-sores
are developed. The prognosis of each case will depend on the
circumstances and constitution of the patient, the possibility of
sufficient attention to his wants, on the special prominence of
certain symptoms or complications, etc.
Treatment,
This presents as little encouragement as the prognosis. For
the disease properly considered (if there exists a new formation
in the strict sense) as good as nothing can be done. Some suc-
cess is to be hoped for in inflammatory, syphilitic, scrofulous
forms. We should in general attempt to fulfil the causal indica-
tion, as far as possible.
The object of removing or diminishing the size of the tumor
has been sought in a variety of ways, but mostly without success.
All sorts of local derivatives have been tried, from painting with
tincture of iodine and blistering, to the moxa and the white-hot
iron. Internally, it will be proper to try iodide of potassium and
ioduretted mineral waters, mercury, arsenic, ete. Some improve-
ment in symptoms has been observed from the use of warm
springs and brine-baths. As long as such temporary improvement
(often lasting for quite a while) can be effected, and while the
diagnosis remains uncertain, we shall always be tempted to make
new trials.
TUMORS OF THE SPINAL MEMBRANES. 277
If the diagnosis and the seat of the tumor are quite certain,
we may perhaps consider the question of trepanning the verte-
bral column ; but it is-seldom that we shall find firm ground for
undertaking such an heroic operation. And yet the success of
this attempt is by no means beyond the limits of possibility,
especially if the tumor lies ouwfside of the sac of the dura, upon
its posterior surface. If we are forced to open the dura, the dan-
ger is much increased. At all events, the prognosis of the disease
is so desperate that we ought to take the operation into consider-
ation. Echinococcus cysts, growing from the spinal canal, should
be opened and evacuated, or extirpated.
In the great majority of cases, the chief object will consist in
general attention to the patients needs, and treatment of the
symptoms. In respect to the former, we have nothing to add to
what we said in the general part of this work. Above all, we
ought to prevent cystitis and bed-sores if possible, and to keep
up the strength of the patient.
As regards symptoms, the pains should be the first and con-
stant object of treatment; they often bid defiance to all remedies,
and enormous doses of morphine are usually required to render
the patient’s life tolerable. The entire range of narcotic and
anti-neuralgic remedies must be tried. For the paralytic symp-
toms nothing can be done directly. Cystitis and bed-sores are to
be treated upon general principles.
Addendum.
Anatomical Changes in the Spinal Membranes, without Clini-
cal Significance.
Various changes in the spinal membranes are known to pathological anatomy
which seem to produce no symptoms during life; sometimes they are senile
changes, sometimes slight incidental inflammatory or degenerative disturbances,
which remain without symptoms as long as they affect the membranes alone and do
not involve the roots or the cord. These matters are about equal in importance to
pleuritic adhesions in the respiratory apparatus
The physician, however, ought to know them, in order not to interpret things
278 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
which are usually innocent as the cause of symptoms observed during life. They
are therefore briefly enumerated in this place.
1. Bony and cartilaginous disks in the arachnoid are very often found. These
are small, roundish or angular plates, flat, from six to fifteen millimetres in diame-
ter, somewhat thicker in the middle, and sharp on the edges. Their number in the
arachnoid varies; they are especially frequent in the lumbar part and on the poste-
rior surface of the cord, often composing a literal mosaic. While Ollivier! con-
sidered them as purely cartilaginous, Virchow’ has shown that they consist of
young bony tissue, and have a structure which agrees for the most part with that of
the cartilage of bone; a striped basement substance in strata, inclosing star-shaped
bodies, and passing by calcification directly into bone-tissue. Their outer surface is
smooth, their inner more rough and jagged, so that they feel like a cat’s tongue,
In most cases they give rise to no symptoms whatever. In advanced age they
are almost always present. They are often found in young persons who have ex-
hibited no spinal symptoms. They certainly point to an irritative condition of the
meninges, especially if they exist in large numbers. They are probably referable to
slight, often-repeated irritation. The connection with epilepsy, formerly imagined
to exist (Esquirol, Ollivier), is at all events very doubtful.
2. Diffuse ossification of the spinal membranes occurs now and then, but seems
destitute of clinical significance. Diffuse ossifications have been described in the
dura (Andral, Virchow), and small osteophytic elevations are also seen in the same
membrane; the deposition of brain sand [corpp. arenosa] in the exudations with
thickening of the dura (pachymeningitis arenosa*) may perhaps be included here.
3. The pigmentation of the pia may often reach so high a degree as to become
pathological. Pigmented corpuscles of connective tissue are often found in the
pia soon after puberty, especially in the cervical region. In marked cases this may
give rise to a diffuse, slightly brownish, smoky gray or blackish coloration.4 A
gradual transition from this state to actual melanoma has been observed. The
simple pigmentation is destitute of pathological importance, and has no demon-
strable connection with inflammation, or with epilepsy, as was formerly supposed.
4, Small tumors of all sorts may exist innocuously. Fibromas, cysts, melanomas,
neuromas, etc., from the size of a hemp-seed to that of a pea, have been repeatedly
observed in the cauda and the membranes without accompanying symptoms. This
is very easily understood.
5. An increased amount of spinal fluid must not be regarded as a necessary
cause of decided disturbances of function.
Such an increase is most frequent (hydrorrhachis externa ®) in the meshes of the
arachnoid in connection with atrophy of the cord. As long as this has the char-
acter of normal spinal fluid, its increase is not of any great importance. But if it
is turbid, of a reddish or whitish tinge, contains numerous cell-elements, blood-
' Loe, cit. 3. Aufl. IT. p. 466 seqq. 3 Virchow, ibidem. II. p. 117.
? Geschwiilste. II. p. 92. *Tbidem. IT. p. 120.
5 Virchow, Geschwiiste. I. p. 175.
HYPERZMIA OF THE CORD. 279
corpuscles, etc., its increase is due to an increase of irritation or to a considerable
blocking of the circulation of the spinal membranes, and then represents simply
a portion of the general morbid process. But even then there is no reason for
referring the cause of severe symptoms exclusively to the pressure of the increased
volume of spinal fluid, as was formerly often done.
II. Diseases of the Spinal Cord proper.
Introductory.—Before entering upon the special considera-
tion of these diseases, it will be suitable to give a reason for the
order and distribution of the material which we have adopted.
We cannot pretend, in the present state of our knowledge, to
make a strictly scientific division of diseases of the spinal cord.
To base such a division upon strict principles of pathological
anatomy would be completely impossible, as we are in the dark
with reference to the significance of many processes, and in many
diseases are ignorant of any anatomical basis.
A division by special localities is equally impossible, for in
many diseases we are quite ignorant of the exact locality, and in
other cases such an arrangement would involve a great deal of
repetition.
We must, therefore, resort to such methods as are convenient.
It seemed to us that for practical purposes we ought to pre-
sent as full an account as possible of the important parts of
spinal pathology, without too much detail or repetition. The
principle adopted is simple and intelligible, and sufficiently con-
sistent with the rules of logic.
In the jirst group, comprising eleven sections, we shall speak
of the processes which occupy, or may occupy, the entire trans-
verse section of the cord in a diffuse way ; processes which do
not, at any rate, either necessarily or regularly, imply a limita-
tion to certain portions of the transverse section. They may
extend longitudinally to various distances. They comprise hy-
pereemia, anzemia, and hemorrhage of the cord, acute severe trau-
matic lesions, and slow compression of the cord (Nos. 1-5).
Then follow three diseases: concussion of the cord, spinal irri-
tation and spinal nervous debility (Nos. 6-8), in which we are
980 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
aware of no anatomical changes, but are allowed to suppose at
any rate fine disturbances of nutrition, which, more or less dif-
fused in the transverse and longitudinal directions, are certainly
not attached to certain parts of the transverse section.
In Nos. 9-11 we shall present the inflammation of the cord
(acute and chronic), simple softening, and that peculiar anatomi-
cal change commonly known as sclerosis in patches—processes
which likewise do not derive their characteristic features from
their connection with any certain portion of the transverse sec-
tion.
In the second group (Nos. 12-16), we shall treat of those forms
of disease, as far as known, which are marked by their more or
less strict localization in certain portions of the transverse sec-
tion of the cord, while their extension in the longitudinal direc-
tion may greatly vary and change. To this class belong the
degenerative processes in the posterior columns, in the lateral
columns, and the lesions which are limited to one lateral half of
the cord; also the acute and chronic processes confined to the
gray anterior cornua.
Under No. 17 we shall describe acute ascending paralysis, a
form of disease still perfectly obscure, which, for the better un-
derstanding of it, we shall place after the above-named diseases.
The placing of tumors, secondary degenerations, and malfor-
mations of the cord (Nos. 18-20) at the end of this series is justi-
fied by their less frequent occurrence and importance, and the
impossibility of including them directly in either larger group.
Finally, in No. 21, we present a number of scattered facts,
which have an undoubted, though in many cases an obscure con-
nection with the pathology of the cord, and which deserve to be
collected as material for the further development of the subject.
As inducements to further investigations and researches, they
may be granted a little space.
1. Hyperemia of the Cord.
We have already spoken of this, as indistinguishable from
the same condition of the membranes, either by anatomical or
ANEMIA OF THE CORD. 281
clinical tests ; and would refer the reader to the complete account
given on page 199 et seq.
2. Anemia of the Cord.
Hasse, loc. cit. 2. Aufl. p. 652.—Hammond, loc. cit. 8d edition. p. 896.—M. Rosen-
thal, 1. c. 2. Aufl. p. 290.—Leyden, 1. c. Il. p. 27.—Jaccoud, Les paraplégies
et l’'ataxie du mouvement. Paris, 1864. p. 293 et seq.
NV. Stenon, Element. myologie specimen. Flor. 1667.—Kussmaul and Tenner, Un-
ters. iiber Ursprung und Wesen der fallsuchtartigen Zuckungen bei Verblutun-
gen, etc. Molesch. Unters. zur Naturl. III. 1857. p. 59.—Schiffer, Ueber die
Bedeutung des Stenson’schen Versuchs. Centralbl. f. d. med. Wiss. 1869.
Nos. 37 and 38.—Ad. Weil, Der Stenson’sche Versuch. Diss. Strassburg, 1873.—
Romberg, Lehrbuch der Nervenkrankh. 2. Aufl. I. 3. p. 2.—Barth, Oblitérat.
compléte de l’aorte. Arch. gén. 1835. VIII. p. 26.—G@ull, Paraplegia from
Obstruction of the Abdom. Aorta. Guy’s Hosp. Rep. 3d series. III. p. 311.
1858.—Cumings, Paraplegia from Arteritis. Dubl. Quart. Journ. May, 1856.—
Panum, Zur Lehre von der Embolie. Virch. Arch. XXV. 1862.—Brown- |
Séquard, Lectures on the Diagnosis and Treatment of the Principal Forms of
Paralysis of the Lower Extremities, London, 1861.—Sandras, Traité des mala-
dies nerveuses. Paris, 1851.—Service of Grisolle: Paraplégie apres une métror-
rhagie considérable. Gaz. des hdp. 1852. No. 108.—Moutard-Martin, Para-
plég. causées par les hémorrh. ut¢rines ou rectales. Soc. méd. des hép. 1852.
Union méd. 1852.—Abeille, Etudes sur la paraplégie indép. de la myélite.
Paris, 1854.— Van Bervliet, Obsery. de paraplég. chlorotique. Annal. de la soc.
méd. de Gand. 1861.—WMordret, Traité prat. des affect. nerveuses et chloro-
anémiques. Paris, 1861.
Definition.—By anzemia we understand a diminution in the
amount of blood contained in the cord; and this may consist of:
a. Diminution or complete suspension of the arterial supply
to the cord—ischemia ; or,
b. Deficiency of blood in the cord, owing to the diminution of
the total amount of blood, and bad crasis (oligeemia, hydreemia,
etc.), and usually named anemia without further definition.
The first form has been experimentally studied, and has been
in single cases made the object of clinical study.
The second form is still less distinct clinically, owing to the
frequent want of prominence of the spinal symptoms, and to
simultaneous disturbances, cerebral and otherwise, crigmiating in
the aneemia, and obscuring the spinal symptoms.
982 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
It is plain that there are many transitional forms between —
these two, and that a sharp distinction is not always feasible,
although we shall attempt to make it in the following presenta-
tion. Both forms lead to the same result, although in some
cases it may be developed quickly and in others slowly; the
nutrition of the substance of the cord will suffer more or less,
and this will bring about the corresponding disturbances.
Pathogenesis and Etiology.
The conditions which may produce a marked predisposition
in certain persons to anzemia of the cord are not fully studied.
Various points may, however, be mentioned which deserve
future attention. For instance, congenital narrowness of the
calibre of the circulation, shown by Virchow to be so frequent an
occurrence in chlorosis ; also congenital or acquired weakness of
the heart ; and finally, an undue excitability of the vaso-motor
nerves, So common in nervous persons, which may sometimes be
most marked in the cord. It is a fact which may be connected
with these circumstances, that the female sex seems specially
predisposed to certain forms, at least, of spinal anzemia. Dis-
eases of the vessels of the cord also, which are of quite frequent
occurrence, doubtless give rise to a certain predisposition to
anemia. I am inclined to refer to anemia of the cord those
slight attacks of feebleness of the lower extremities which are
found in old people with marked atheroma of the arteries.
The direct causes of spinal anemia are better known.
The first group embraces all those causes which produce a
contraction or closure of the afferent arteries of the cord (para-
plégies ischémiques of Jaccoud). Of these we must first name
compression, thrombosis or embolism of the abdominal aorta
above the point of departure of the lumbar arteries. It leads to
a severe ischemia of those segments of the cord which receive
branches from the corresponding lumbar and intercostal arteries.
It has very long been known that compression of the abdominal aorta is fol-
lowed very quickly by paralysis of the posterior half of the body (Stenson’s experi-
ment). The paralysis occurs a few moments after the compression begins, and was
ANAMIA OF THE CORD. 283
referred by a.s the earlier observers to a peripheral disturbance of the nutrition of
nerves and muscles. Kussmaul and Tenner have, however, shown that anemia of
the cord leads to palsy much more rapidly than anemia of the nerves and muscles.
Schiffer has tested the question again, and has decided that anemia of the cord
itself is certainly the immediate cause of the palsy, that the nerves and muscles in
this case remain excitable for a long time, and that in case of compression at a
lower point, the paralysis occurs much later. It is also true that when the com-
pression lasts a considerable time, paralysis of the cauda equina, the peripheral
nerves and muscles follows. A. Weil has contirmed Schiffer’s statements in all
essential points. Such ischzemic paraplegis have been seen to occur in the human
subject, in the rare case of thrombosis and embolism of the aorta (Barth, Gull,
Leyden, Tutscheck, and others), although it is not always possible to decide whether
their origin is spinal or peripheral.
Thrombosis and embolism of given spinal arteries can only
lead to quite circumscribed ischemia, owing to the numerous
arterial supplies which the cord possesses.
This cause has been studied experimentally by Panum, but in man has been
only accidentally observed, and its pathogenetic import is not yet sufficiently de-
fined, Leyden has found capillary embolism of the cord in ulcerous endocarditis.
It is still uncertain whether spasm of the spinal vessels can
produce anzemia of the cord; the fact is not well established,
though not quite improbable. We may assume that a direct
irritation of the vaso-motor paths concerned produces this kind
of ischemia; but the theory has been more generally accepted
that irritations of peripheral organs, due to all sorts of causes,
may produce such vascular spasm in the reflex way ; and this
may be the origin of a great many of the so-called ‘‘ reflex paral-
yses.”’
The latter view has been developed into a theory of ‘reflex paralysis” by
Brown-Séquard in particular. The peripheral irritation causes a contraction of the
spinal vessels, of various duration, which gives rise to palsy and a more or less per-
manent disturbance of nutrition in the cord, as has been observed by Kussmaul and
Tenner, and by Schiffer, to occur after simple compression of the aorta, if contin-
ued for a sufficient time.
Although it is not certain that such a permanent and severe spinal vascular
spasm occurs, as is demanded by Brown-Séquard’s theory, and although on the
other hand many “‘reflex paralyses” can be refefred to severe disturbances of nutri-
tion, yet a transitory spasm of the spinal arteries is by no means inconceivable.
984 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Vaso-motor spasms of the skin of the extremities may last for hours and daye,’ and
why not in the cord also? And if such athing occurs, severe disturbances must
occur in the fine and delicate processes of nutrition of the central apparatus.
It is self-evident that mechanical pressure upon the cord may
produce ischemia in a corresponding portion; in such cases,
however, the symptoms are referable rather to pressure upon the
nerve-elements than to compression of the blood-vessels.
The second group of direct causes embraces all such as di-
minish the total amount of blood, or cause a decided change in
its composition, with a tendency to oligocythemia, hydremia
and allied disturbances. (A portion of Jaccoud’s paraplégies
dyscrasiques. )
Upon the whole, the existence of severe spinal symptoms,
especially of paralyses, in these conditions is comparatively rare,
and the causal relation between the anzemia and the paralysis
which follows is not always perfectly clear. It seems at first
strange that the lower extremities should be almost exclusively
affected ; but a closer consideration shows, as Jaccoud has admi-
rably stated, that the fact is probably due to the greater claims
usually made upon the activity of the legs at all times, which
causes any general weakness to show first in them. It will also
remain undecided in many cases whether and to what extent the
symptoms of weakness depend on anzemia and disturbances of
nutrition in the peripheral nerves and muscles. For this reason
cases must be read with some caution. |
Several cases are described in which paraplegia followed great
loss of blood, as in parturition, metrorrhagia, bleeding from the
kidneys and intestine, epistaxis, etc. Jaccoud quotes such cases
from Grisolle, Moutard-Martin, Abeille, Landry, and others.
A similar effect is produced by great loss of blood, severe
acute diseases, inanition, etc., which injure the nutrition of the
cord by producing great anzemia. .
In chlorosis, states of weakness and palsy have been observed
and referred to anemia of the cord; such cases are rather fre-
quent, though not so in comparison with the frequency of chlo-
rosis itself. Jaccoud quotes such from Dusourd, Bervliet, Bou-
oe
' See Nothnagel, Vasomotorische Neurosen, Deutsches Arch, f. klin. Med. IL.
ANEMIA OF THE CORD. 285
chut, Mordret, Landry, and others, and includes the paraplegia
of pregnancy in the list. It appears that only quite severe cases
of chlorosis cause such paraplegia.
Pathological Anatomy.
Anemic portions of the cord look pale, bloodless, white ; no
points of blood appear on their cut surface, and no full vessels
are to be seen; the gray substance is strikingly dull in color, and
sinks a little upon the section ; the white is often found very soft
and semifluent, and pushes out above the cut surface. There
are, however, reports of cases in which the substance of the cord
was found somewhat firmer and more resistent than usual.
Perhaps these were different stages of the same change.
The membranes also appear pale, their vessels partly empty
and not easy to see.
A distinct contrast to this is afforded by those sections of the
cord in which the circulation is retained, which look of a rosy
color and are harder in consistence ; an increased injection, with
extravasations of blood, is often observed in the neighborhood of
anemic portions.
In general anzemia the cord is usually anemic also.
It is not always easy to avoid confusing these phenomena
with post-mortem appearances ; anzemia will therefore be con-
sidered to have existed during life only when all the circum-
stances which produce it in a corpse can be shown to be absent,
such as a certain position, cadaverous swelling of the medul-
lary substance, ete.
In thrombosis and embolism of the small spinal vessels it is
often possible to find the point of occlusion. Red softening
exists in the region supplied by the plugged artery, and in its
vicinity collateral fluxion. This has been found chiefly in ani-
mals. Tuckwell has found similar appearances in man. Leyden
observed microscopical embolic foci in ulcerous endocarditis.
If the ischemia is protracted, secondary changes occur—
white and yellow softening of the corresponding portion of the
cord, localized breaking-down, stasis of blood, etc. The minute
986 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
changes in nutrition which appear in a short time are not acces-
sible to a pathologico-anatomical examination.
Symptoms.
Before describing aneemia of the cord, let us consider such
facts as are derived from experimental physiology, and which,
at least in the case of the acute ischemic form, furnish us abun-
dant information.
When the aorta is compressed, motor and sensory palsy of
the legs immediately occurs, the reflex acts cease, the bladder
and rectum seem paralyzed. When the circulation is restored,
improvement in these respects is slow in proportion to the dura-
tion of the compression.
Precisely the same symptoms occur in man after embolism of
the aorta—rapid palsy of the legs, sphincters, reflex function,
etc. Gull’s case, in which he observed paralysis to occur in a
few minutes, is an especially good instance of paraplegia from
aortic obstruction. In most other cases of this class it is less
easy to affirm that the paralysis originates from spinal angemia;
it is rather probable that the disease has a peripheral origin
(see the cases of Romberg, Cumings, Leyden, Tutscheck, et al.).
If the contraction of the aorta develops by slow degrees, the
disturbances are of a gradual and less severe nature—slight feel-
ing of numbness and of a limb asleep, weakness of the lower ex-
tremities, which are easily fatigued when severe exertions are
made. ‘The symptoms of closure of the aorta become more and
more distinct—absence of pulse in the crural arteries, coldness
and cedema of the feet, enlargement of collateral arteries, ete.—
symptoms which in acute cases appear very quickly.
Here must be included a series of cases which present the symptom of inter-
mitting lameness or palsy. In these no change is observed while the patient is at
rest; but when he takes a brisker walk than usual, it is followed by distinct weak-
ness or even palsy, which disappears when he takes rest, and again returns when
he renews his muscular efforts. Such symptoms have been observed in horses, and
are accounted for by occlusion of the aorta. A similar thing has been seen in man _
(Charcot, Frerichs—intermittent palsy in one lower extremity), the cause of which
is also doubtless referable to the closure of one iliac or the aorta. But these seem
RET Ka
ANEMIA OF THE CORD. 287
to be only cases of peripheral palsy; the muscles, imperfectly supplied with fresh
blood, become incompetent to their duty where severe exertions are demanded,
while they are still able to perform a slighter task.
All that has been said applies only where the ischemia is sit-
uated in the lumbar region of the cord. We know nothing in
regard to the symptoms of ischemia of the cervical part. Clo-
sure of both vertebral arteries might be followed by ischeemia in
this case also; but the derangement of the cerebral functions
and those of the medulla oblongata would then probably be so
severe as to mask the spinal symptoms, and death would follow
speedily.
The symptoms of vaso-motor ischemia of the cord must be
the same, but they can hardly be so severe. We know nothing
with precision in regard to them, excepting those symptoms of
“reflex paralysis’? which are said by Brown-Séquard to origi-
nate in this way. It is said to be characteristic of these paraly-
ses that they originate in peripheral irritation, that variations in
the severity of such irritation are followed by corresponding
fluctuations in the symptoms of palsy, and that the latter often
disappear when the former cease. It is evident how imperfect
is this characterization.
Anemia originating in thrombosis and embolism of small
arteries probably gives rise to. merely local and subordinate
symptoms, about which nothing is known definitely. If large
spots of softening are formed, the symptoms of circumscribed
destruction of the cord follow, which will vary somewhat accord-
ing to the seat of lesion; we shall come back to these in the sec-
tion on Softening of the Cord, No. 10, farther on.
In the second group of cases of spinal anzemia the number of
symptoms of anzemia is so great, involving most of the organs of
the body, as to make it hard to sift out those proper to the affec-
tion.
The most constant seem to be those of motor weakness—
weakness and great fatigue, which forbids all severe exertions,
slight tremor when even the least muscular work is performed,
and in the higher degrees, severe paresis, and at last paralysis.
All this usually begins in the lower extremities, and extends
very gradually to the trunk and arms.
988 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
The sensibility is usually intact; but paresthesia of every
sort, pain, and hypereesthesia or slight anesthesia occur. The
reflex actions are often exaggerated ; only in the severest cases
are they depressed. The sphincters do not seem to be usually
affected, unless the severest anzemia with full paraplegia has
been developed.
At the same time, the most marked symptoms of general
anemia or developed chlorosis exist.
It is said to be a marked characteristic of this form, that the
symptoms are improved by continued lying down, which favors
the flow of blood to the cord; changes of circulation produce
the same effect upon the severity of the symptoms. It is impor-
tant to note in conclusion that a tonic treatment with iron and
stimulants quickly improves such cases.
Hammond has tried to prove that the so-called spinal irritation depends on a
local hypereemia of the posterior columns. We shall return to this point in speak-
ing of spinal irritation (see farther on, No. 7).
Course, duration, termination.—The disease may begin rap-
idly and acutely, as in embolism, severe loss of blood, ete. At
other times it is slower and more gradual, as in thrombosis, chlo-
rosis, etc.; the symptoms at first do not appear until certain
efforts are made, but become by degrees more distinct and per-
manent until the disease is fully developed. :
In its further course the patient either recovers rapidly, by
the establishment of collateral circulation or regeneration of the
lost blood, or perhaps by relaxation of a vaso-motor spasm ;
Or, after long fluctuation, a slow recovery occurs, especially
when the circulation becomes free after having been disturbed
for a sufficient time to leave considerable impairment of nutri-
ticn ;
Or, finally, return to a normal state is impossible, the cord
softens, producing all the symptoms of severe spinal paralysis,
in the midst of which death at last occurs.
Of the duration of the disease nothing need be said, as it may
vary very greatly according to the cause, the possibilities of
repair, the development of secondary changes of nutrition, ete.
= i
- ‘
Ee: ee
ANZMIA OF THE CORD. 289
Diagnosis.
We are not entitled to infer the definite existence of spinal
anzemia from the above symptoms, unless the causes are clear.
The acute ischzemic form often commences quite like a spinal
hemorrhage or an acute myelitis ; the diagnosis becomes proba-
ble only when the aorta can be proved to be closed, or a great
loss of blood has recently occurred; and it may be confirmed by
the rapid and favorable course of the disease. We have already
said that an intermittent character of the paralytic symptoms
could not probably be referred directly to anzemia of the cord.
The chronic anzemic forms (dyscrasic) resemble chronic myeli-
tis, or very slow forms of chronic meningitis, etc. If, however,
chlorosis or severe general anemia exists, we shall naturally
think first of anzemia of the cord. The fact that the horizontal
position relieves the symptoms may perhaps be made of use in
the diagnosis; but usually the decisive test will have to be fur-
nished by the result of treatment.
Vaso-motor ischemia is probably hard to distinguish. Believ-
ers in Brown-Séquard’s theory of reflex paralysis will refer to
it when peripheral irritation exists (diseases of the organs of uri-
nation or digestion, or of the uterus, etc.). The idiopathic forms
require some further study and_proof.
Prognosis.
This depends chiefly on the causes, and on the possibility of
removing them. We shall, therefore, have to decide the ques-
tion on general principles.
Of itself, spinal anemia is nothing serious. If it has not
lasted long, or has never been extreme, the prognosis is quite
good ; especially so in chlorosis.
But a severe anemia may badly impair the nutrition of the
cord, even when the disease has lasted but a short time, and may
cause injuries which require a long time for their repair. Experi-
ments have sufficiently proved this, and we ought, therefore, to
be cautious in making the prognosis of, such cases.
If it be impossible to restore the circulation, and if softening
VOL. XIII.—19
290 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
has once occurred, the prognosis is bad, provided large portions
of the cord are affected. If there is softening of small portions
of the cord, the prognosis should depend on the size and location
of such spots.
Treatment.
Here the first point is the causal indication. If we succeed
in removing the causes of spinal anzemia, the chances of restora-
tion increase considerably. The reader is, therefore, merely
reminded of the treatment of aortic thrombosis and embolism
(proper position, stimulation of the function of the heart, etc.),
of chlorosis and anzemia (tonics and iron), and of general nerv-
ousness ; of the removal of sources of peripheral irritation, ete.
These measures will generally include the chief part of the treat-
ment. |
As direct measures for the relief of anzemia of the cord, we
would recommend a suitable position, in order to favor the flow
of blood to the cord. Brown-Séquard strongly recommends the
dorsal decubitus, with raised head, arms, and legs; and this
should be maintained during the night, and several hours in
the daytime.
Drugs which increase the flow of blood to the cord, especially
strychnia, opium, and nitrite of amyl. Brown-Séquard recom-
mends strychnia above all others, and Hammond strongly sup-
ports the recommendation ; he gives it in increasing doses (0.002-
0.015, [35 to ¢ of a grain], three times a day), or, still better, in
combination with phosphorus (extract of nux vomica 0.02 [4 of a
grain], phosphide of zinc 0.006 [-1, of a grain] ).
Galoanization of the spine, with the object of dilating the
vessels of the cord and improving the spinal nutrition. Ham-
mond especially recommends the ascending stabile current.
Application of warmth to the back, by means of hot sand-
bags, or Chapman’s bags filled with hot water. For vaso-motor
ischemia, alternate cold and hot douches are recommended.
We shall also seek to fulfil the symptomatic indications ©
(relief of pain, paralysis, disturbances of circulation, etc.) by the
usual remedies and methods.
t
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7
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SPINAL APOPLEXY. 291
The diet and regimen must be governed by the existing indi-
cations and circumstances.
3. Hemorrhage in the Substance of the Spinal Cord—Hea-
matomyelia (Haematomyelitis) — Hemorrhagia Medulle
Spinalis—Spinal Apoplexy.
Compare the repeatedly quoted works of Ollivier (II. p. 167), Jaccoud ( p. 251),
Hasse (p. 667), Hammond (p. 440), M. Rosenthal (p. 292), and Leyden (IL p,
54). Also
E. Levier, Beitr. zur Pathologie der Riickenmarksapoplexie. Diss, Bern, 1864 (con-
taining all the older cases).—Hayem, Des hémorrhag. intra-rhachidiennes. Paris,
1872 (list of cases complete to that date).—Breschet, Hématomyélie. Arch. de
méd. XXV. 1831.—Grisolle, Rev. hebdom. des progr. des sci. méd. 1836. No.
3.—Monod, De quelques maladies de la moélle épin. Bull. de la Soc. anat.
1846. No. 18.—Cruveilhier, Anatom. pathol. livr. III. pl. Vi.—G@endrin, De
l’apoplexie rhachidienne. Gaz. des hdp. 1850. No. 48.—M. Trier, Hosp. Med-
delelser. Bd. IV. 1852 (quoted in Levier. Schmidt's Jahrb. Bd. 78. p. 293).
—Lebeau, Cas Whématomyélite. Arch. belg. de méd. milit. Janv. 1855.—
Barat-Dulaurier, Sur les hémorrh. de la moélle. Thése. Paris, 1859.—Duriau,
De l’apoplexie de la moélle épin. Union méd. 1859. Nos, 20-25.—Brown-
Séquard, Paralysis of the Lower Extrem. p. 86. 1861.—Colin, Hémorrh. de la
moélle. Soc. méd. des hép. 1862.—Mouton, Consid. sur ’hémorrh, rhachid.
These. Strasb. 1867.—Schuetzenberger, Apoplexie spinale. Gaz. méd. de Strasb.
1868. No. 5.—Koster, De pathogenie der apoplex. medull. spin. Nederl. Arch.
voor Geneesk. IV. p. 426. 1870.—Gorsse, De Vhémorrh, intramédull. ete,
These. Strasb. 1870.—C. O. Joerg, Fall von Spinalapoplexie. Arch. d. Heilk.
XI. p. 526. 1870.—Bourneville, Hémorrh. de la moélle 6p. Gaz. méd. de Paris.
1871. No. 40.—Liouville, Hématomyélie avec anévrysmes. Soc. de Biolog.
1872.—ZHrb, Ueber acute Spinallihmung. Arch. fiir Psychiatrie u. Nerven-
krankh. V. 1875. Beob. 5. p. 779.—H. Hichhorst, Beitr. zur Lehre von der Apo-
plexie in die Riickenmarkssubstanz. Charité-Annalen I. (1874) p. 192. Berlin,
1876.—Z. Goltdammer, Zur Lehre von der Spinalapoplexie. Virch. Arch. Bd,
66. 1876.
Definition.—The above titles include any kind of extravasa-
tion of blood in the substance of the cord proper. This is as rare
as meningeal hemorrhage, one important reason for which is cer-
tainly the low and comparatively constant pressure of the blood
in the small spinal arteries. “
The intra-medullary hemorrhages are seated almost exclu-
sively in the gray substance; their occurrence in the white sub-
992 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
stance is rare, and perhaps is never spontaneous and primary.
Their extent is usually small, but is often considerable, and may
reach to the whole length of the gray axis.
In these diffuse cases, it seems at present quite doubtful
(Charcot, Hayem, Koster) whether the affection is a primary
idiopathic hemorrhage, and not rather a hemorrhagic myeli-
tis. This is certain, at least, that a great deal has been classed
as hematomyelia which is not included under spontaneous and
primary bleeding ; such cases will have to be sifted in future. It
is, no doubt, correct that in many cases of hematomyelia there
is simply a myelitis complicated with hemorrhage (myelitis cen-
tralis hemorrhagica); but this ought by no means to be so ex-
tended as (with Hayem) to include ad/ bleeding in the substance
of the cord, and make it depend on previous myelitis. We are
decidedly of the opinion, particularly upon the ground of clini-
cal symptoms, that primary hemorrhage of the cord also occurs,
though the way for it may often be prepared by the occurrence
of slight alterations in the vessels or the cord. A case which
seems to us to be very convincing in this regard is the one lately
published by Goltdammer.
The chief symptoms, and the course of the disease, are so
alike in both forms that we may treat of them together. We
shall, however, return to the inflammatory hemorrhages of sh!
litis at a later point.
Pathogenesis and Etiology.
Our knowledge of predisposition to hemorrhage of the cord
is very scanty. The small number of cases hitherto reported
seem to show that youth and middle age are the most frequently
attacked (as the largest number occurred between the ages of ten
and forty), in opposition to cerebral apoplexy, the frequency of
which increases with advanced age.
Men are attacked much oftener than women, probably on
account of their modes of life.
It is not known how far the occurrence of the bleeding is fa- —
vored by the existence of heart disease (hypertrophy of the left
ventricle), spinal curvature, ete.
SPINAL APOPLEXY. 293
It is, however, certain that disease of the spinal vessels
(thickening, fatty deposits, increase of the nuclei in the walls,
aneurysmal dilatation—Liouville) constitutes an important pre-
disposing cause. The same is true of chronic affections of the
cord proper (chronic myelitis, progressive muscular atrophy,
tumors, etc.), which often are brought to a sudden close by
hemorrhage. The influence of these circumstances may reach so
far as to give rise to apparently spontaneous bleeding, for which
reason we shall again speak of them among the direct causes.
Among these direct causes we have to name, in the first place,
surgical injuries. Spinal apoplexy has been known to be caused
by a fall or blow upon the back, by vertebral fractures and dis-
locations, by violent shocks in riding, by a fall down-stairs, etc.,
without any direct traumatic lesion of the cord.
In the second place, all circumstances which produce a sfrong
active congestion of the cord. Such are exposure to cold, sexual
excesses and masturbation, extreme exertions of body, and the
like. Fluxions originating in the collateral way ought also to be
included, as the cases of spinal apoplexy following retention or
suppression of the menses (Levier, Schuetzenberger), or sup-
pressed. hemorrhoidal bleeding, or those which occur in the
neighborhood of inflammatory processes in the vertebra, the
dura, etc.; and with these should be included the spots of red
softening which originate in embolism of the spinal arteries.
And finally, inflammatory congestion, which so often leads to capil-
lary hemorrhage in acute central myelitis and similar conditions.
Anything which produces a disproportion between the pres-
sure within and that without the blood-vessels may give rise to
hemorrhage in the cord. When the pressure of the atmosphere
is rapidly lessened (in going out of caissons where the air is com-
pressed, used in the construction of bridges, or out of diving-
bells), symptoms have been seen which indicated spinal apo-
plexy, but this has not yet been confirmed by autopsies. A
considerable increase of the blood-pressure acts in a similar way ;
such increase occurs in the case of excessive cardiac action, or in
a more passive way it is due to impediments to the circulation in
diseases of the heart and lungs, to sudden severe bodily exertion
in lifting heavy burdens, in severe spasms, ete.
294 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Another group may be formed of those causes which lessen the
resistance of the walls of the blood-vessels, and thus give rise to
bleeding. Here should be mentioned the aneurysmal dilatations
of minute vessels, as found by Griesinger and Liouville; the
fatty degeneration, thickening, multiplication of nuclei, etce., in
the walls of the small arteries, which are often found in micro-
scopical examination of the diseased cord; perhaps also the
chronic processes of softening and inflammation in the cord, and
tumors of the cord (especially the soft myxoma and myxosarco-
ma), in the interior or vicinity of which bleeding so often occurs.
We must include here also the bleeding which in rare cases
accompanies hemorrhagic affections (scorbutus, hemorrhagic
small-pox, etc.), or acute infectious diseases (typhoid, yellow
fever, malarial diseases, etc.) )
Pathological Anatomy.
The bleeding is mostly confined—in many cases exclusively
so—to the gray substance, and in it attains very various dimen-
sions. It may involve the gray cornua or the entire transverse
section of the gray substance, and may extend to various dis-
tances longitudinally. Bleeding in the white substance is much
rarer, and is almost always combined with bleeding in the gray.
Two sorts of extravasation may be distinguished by their vis-
ible characteristics, which may coexist, but in origin and appear- —
ance are essentially different.
1. The hemorrhagic (or apoplectic) clot—We find a clot of
blood, of variable size, as big as a pea, an almond, or at most a
nut; often showing through the pia as a bluish lump, while the
pia is pressed up and often burst by the pressure, so that blood
is found in the subarachnoid space. The clot itself is composed
of blackish red blood, coagulated, and sometimes fluid in the
centre. The substance of the cord is broken down to a corre-
sponding distance, and forms a sort of ragged wall around the
clot. An envelope of white substance commonly surrounds the
clot ; it is tinged with blood (red or yellowish) to a greater or less
distance, so that the boundary between the clot and the sound
= —_
SPINAL APOPLEXY, 295
tissue is largely obliterated. The clot sends out processes to
various distances in the gray substance, and between the bundles
of white fibres. |
The clot is almost always greater lengthwise of the cord; the
globular form is usual only in very small extravasations ; con-
siderable portions of the gray columns are commonly affected, pro-
ducing what is called a tubular hemorrhage. One single clot is
what is usually found, but several, or many, sometimes occur.
The cervical and upper dorsal region is by far the most fre-
quently affected, though of course not always.
The microscope shows a great number of blood-corpuscles in
all stages of decomposition and change; pigment granules and
pigment crystals, fibrin, broken-down medullary elements, glob-
ules of myelin, and usually granular corpuscles also.
The clot undergoes a series of further changes in time; it
either thickens and slowly dries up to a crumbly, caseous lump,
the origin of which is denoted by its color and the presence of
crystals of heematoidin, or the process of softening and fluidifi-
cation occurs, so that at the last a hard capsule of connective
tissue is found filled with serous or atheromatous contents.
Smaller extravasations may doubtless be absorbed, for the most
part, and leave behind only a small cicatrix of connective tissue,
colored ochre-yellow by deposits of crystalline pigment.
Secondary disease of the cord is very often found in the
neighborhood of the clot. This most frequently consists of soft-
ening, which extends to various distances up and down, often to
nearly the whole length of the cord. Hemorrhagic softening of
the gray substance is especially frequent, by which it is changed
into a porridge-like mass, sometimes reddish black, sometimes of
a chocolate color, and sometimes of an ochre-yellow (see the
drawing in Cruveilhier) ; in these cases there probably always
exists a primary central myelitis. But simple white softening
also occurs in the neighborhood of the clot; it is to be recog-
nized by its characteristic appearance to the naked eye, and
microscopically by the numerous granular corpuscles, broken-
down nerve-fibres and ganglion-cells, the vessels in fatty degen-
eration, and the proliferation of neugoglia. In older cases we
find secondary ascending and descending degeneration of the
996 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
posterior and lateral columns, presenting the same characteristics
as in other limited disease of the cord (Goltdammer).
29. Hemorrhagic injiltration or softening ; inflammatory hem-
orrhage. This likewise occurs in the gray substance exclusively,
and is either limited to certain cornua or extends over the entire
section, but rarely spreads to the white substance. It has been
seen with an extent of a few centimetres, and again, reaching the
whole length of the cord.
The gray substance is changed to an atheromatous mass, red-
dish brown, dotted with darker, blackish red points, and small
coagula; the blood is intimately mingled with nerve-substance.
Around about the place, at various distances, the cord is tinged
unevenly of a rusty or ochre color.
The microscope shows essentially the same elements that exist
in the clot, but with a greater prevalence of granular corpuscles ;
traces of growth of connective tissue and of histological changes
in the nerve-fibres and ganglion-cells are also found.
The latter can usually be traced in the gray matter far beyond
the limits of the hemorrhagic infiltration ; they comprise soften-
ing, accumulation of granular corpuscles, thickened and swollen
axis-cylinders, like strings of beads, enormously swollen ganglion-
cells (Charcot), abundant ‘proliferation of connective tissue,
excess of blood in the smallest vessels, some of which are en-
larged into ampulle (Liouville), while in other cases their walls
are thickened and degenerated—in a word, acute central mye-
litis. .
Of the further changes occurring in such hemorrhagic infiltra-
tions nothing precise is known, for autopsies are usually made at
an early period.
Capillary hemorrhages proper—small punctated extravasations, easily recognized
—are rather common; they are not specially important, and give rise to no clinical
symptoms. They constitute, however, a frequent element in important processes,
softening, and the like. In their most developed form they are simply equivalent
to hemorrhagic infiltration. Eichhorst has lately examined under the microscope a
remarkable case of hematomyelia with widely-distributed capillary bleeding, and
has given a careful description. We are not able, however, to agree with him in
considering this case as a primary hemorrhage, as there existed paraplegia, accom-
panied by fever, gradually extending upward, and in a few days leading to death.
SPINAL APOPLEXY. 297
Changes in the spinal meninges are not specially essential
accompaniments of intra-medullary hemorrhage. There is al-
most always hyperemia, corresponding to the seat of hemor-
rhage; rarely ecchymoses.
The peripheral nerves and muscles often undergo a marked
degenerative atrophy ; this depends on the seat of lesion, and
probably on the destruction of the trophic centres of these or-
gans.
The alterations in the other organs are the same as in the
other forms of severe spinal paralysis (see the chapter on Myeli-
tis). :
Symptoms.
Although the number of observations is somewhat small,
yet it is possible to draw a tolerably fair outline of spinal apo-
plexy.
The attack degins quite suddenly in many cases, and with
fulminant symptoms ; the patient is struck with violent pains
and sudden paraplegia, and falls without loss of consciousness.
The hemorrhage often occurs in sleep, and the patient awakes
paralyzed.
But the disease does not always begin so very suddenly, be-
ing often preceded by premonitions, which either consist of the
symptoms of spinal congestion (pain in the back, excentric pain
and paresthesia in the limbs, great weariness and prostration,
hypereesthesia of the skin, etc.), lasting perhaps for days and
weeks, or the symptoms of acute central myelitis (general mal-
aise, fever, violent pains, formication, the sensation of a girdle,
of heaviness and numbness, distinct weakness in the extremities,
weakness of the bladder, etc.), and these usually last hours or
days, until the apoplectic paraplegia appears.
One specially characteristic feature of spinal apoplexy is the
way in which a complete and severe paraplegia will develop in
the course of a few minutes or an hour; this is usually intro-
duced by a violent pain, either localized or extending over the
entire spinal column, but usually disappearing after the palsy
has become complete.
998 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
Such patients are found by the physician with complete and
absolute palsy of the legs, or the palsy may extend upwards over
the trunk and even to the upper extremities ; then the respira-
tory muscles are palsied, and the patient becomes a picture of
helplessness, breathing painfully and imperfectly with the aid of
the diaphragm. The paralyzed muscles are perfectly lax, offer-
ing not the slightest resistance to passive movements,
In rare cases the paralysis is incomplete, some movements being left, or there is
paresis only. In one case a single upper extremity has been seen palsied (Bourne-
ville); hemiplegic paralysis is also rare, and always affects the upper extremity
more than the lower. All this depends on the position and extent of the hemor-
rhage.
The motor paralysis is accompanied by anesthesia more or
less complete in respect to all possible sensory impressions; this
has the same distribution as the motor paralysis. It is obvious
that this disturbance may vary in degree, and is subject to ex-
ceptions; but a certain amount of anesthesia is seldom or never
absent.
Paralysis of the bladder and rectum is equally regular ; at
first there is complete retention of the urine, requiring the em-
ployment of a catheter, and afterwards various forms of inconti-
nence ; the stools are evacuated involuntarily and unperceived.
Marked vaso-motor paralysis has been found in well-observed
cases. Levier found a rise of temperature in the paralyzed lower
half of the body (flexure of the knee), which equalled 0.2—0.5—
1.0—2.0° Centigrade as compared with the axillary measure-
ments; a symptom which, if it be of long duration, points not
merely to a simple severance of the vaso-motor paths, but also
to a destruction of the vaso-motor centres in the cord. Levier
found the cutaneous perspiration absent in the paralyzed parts.
The reflex actions vary much according to the seat of lesion ;
they are completely suspended when the gray substance is
wholly destroyed to its lowest point; if the seat of the hemor-
rhage is higher, they may also disappear at the first moment,
owing to the shock, but soon return, and may become much
exaggerated. In a few cases priapism is given as one of the
symptoms.
SPINAL APOPLEXY. 299
While the lower half of the body is thus severely affected, the
upper half may be perfectly normal and healthy, the arms may
act normally, consciousness, intelligence, the functions of the
‘cerebral nerves remain quite intact. At the most, slight febrile
symptoms appear during the first few days.
It is somewhat striking that the symptoms of irritation are
so much in the background. Pain in the back seems the most
frequent, and may be localized or extensive; the spine is little or
not at all sensitive to pressure, a high degree of such sensitive-
ness being probably limited to myelitis.
Although symptoms of motor irritation, as twitching and
partial spasms, are observed in the first moments of the hemor-
rhage, yet at a later period they become very inconsiderable, and
spasmodic symptoms are almost entirely confined to the non-
paralyzed parts, thus marking the progress of the fundamental
lesion ‘or the supervention of secondary affections. Parzsthe-
size may be wholly absent in the paralyzed parts; the patients
do not feel their limbs, or only feel them as a dead weight; in
other cases tingling or similar symptoms are felt in the paralyzed
regions.
In the succeeding days and weeks these symptoms increase
in a very troublesome way.
The first threatening symptom is usually the rapid appear-
ance and the steady progression of gangrenous bed-sores on the
sacrum, the trochanters, the heels, and other places exposed to
pressure. This untoward event may occur in a few days, often
in its most acute form.
The urinary excretion is altered, the discharge soon becomes
bloody, purulent, albuminous ; the severe palsy of the bladder
leads directly to alkalescence of the urine, cystitis, and pyelitis
with their sequele.
It follows, of course, that these severe disturbances are always
accompanied by marked fever. Chills occur, pyzemic and septi-
ceemic symptoms are developed from the bed-sores, and rapidly
consume the patient’s strength.
The paralyzed muscles become atrophic, sometimes very
rapidly ; and the atrophy is accompanied by a loss of faradic
excitability, or the appearance of the reaction of degeneration
300 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
in the muscles. A few muscles become rigid or contracted,
especially when secondary changes in the cord occur at a late
period ; spontaneous spasmodic jerkings, with exaggeration of
reflex action, usually precede the appearance of these symptoms.
But if the lesion is located high, the nutrition of the muscles and
their electrical excitability may remain nearly intact, as in the
case of Goltdammer.
The reflex actions disappear by degrees, often quite rapidly
and completely ; this is especially the case in central myelitis,
when it spreads downward.
It is usually hard to recognize the symptoms of secondary
myelitis ; violent pains, twitching movements and jerks, the
formation of contractures—all this often in parts not affected by
the palsy—such are the symptoms which belong to this affection.
It is evident that this description applies in full only to the
more severe cases, with large effusion, but must undergo various
modifications according to the seat, size, and cause of the hemor-
rhage. It seems superfluous to attempt a full presentation of
these ; the reader will be able by reflection to see for himself the
special symptoms of a small limited hemorrhage ; for instance,
that in the anterior cornua it will produce mainly symptoms
of local paralysis, in the posterior cornua perhaps very incon-
siderable symptoms, etc. It should in particular be stated that
in many such cases, with small hemorrhage, the symptoms are
so indecisive, so destitute of characteristic traits, as to furnish
no means whatever of forming a diagnosis of hemorrhage. This
is in entire accordance with what we know of spinal pathology.
Hayem gives the name of chronic spinal apoplexy to the cases in which the
hemorrhage is an accompaniment of existing chronic spinal disease. He quotes
the cases of Massot (progressive muscular atrophy), Nonat (chronic central myelitis),
Lancereaux (peri-ependymal myelitis). In all these, the symptoms of bleeding
were more or less acute in their appearance. In our opinion, a hemorrhage in the
cord cannot be chronic. Such cases are simply instances of the supervention of an
acute complication (hemorrhage) upon a chronic spinal disease; not at all of a
chronic form of spinal hemorrhage.
ete ee Ee ee ee ee ee ee
ee
~tw
ms
SPINAL APOPLEXY. 301
As to the characteristic symptoms as dependent on the
locality of the bleeding, we will content ourselves with a few
words.
If the Zumbar region is affected, the symptoms of palsy and
anesthesia are restricted to the lower extremities, bladder, and
rectum ; reflex actions are absent; rapid atrophy of the muscles
with reaction of degeneration, bed-sores at an early period, will
rarely fail to be present.
If the thoracic region, the symptoms extend higher up on the
trunk. The expiratory muscles are palsied, and those which
compress the abdomen; reflex actions may be retained for a
time; atrophy of the muscles is tardy.
If the cervical region, all four extremities are affected. A
portion of the inspiratory muscles is palsied; pupillary symp-
toms may be present; the reflex processes and nutrition depend
on the downward progress of the lesion. If the bleeding occurs
above the origin of the phrenic nerves, a rapid death by asphyxia
is inevitable. '
In a few cases (Monod, Oré, Breschet—quoted in Levier) the
hemorrhage has been found restricted to one lateral half of the
cord, with the characteristic symptoms of Brown-Séquard’s spi-
nal hemiplegia (paralysis of the side corresponding to the lesion,
anzesthesia of the other side). -
Course, duration, termination.—The course depends on the
size and location of the hemorrhage, and in part also on the
immediate cause. In severe cases, especially of diffuse central
bleeding, the fatal termination occurs very soon through paraly-
sis of respiration ; or secondary changes, acute gangrenous bed-
sores, pyzemia, and septicemia soon cause death amid fearful
suffering. Charcot believes that a true hematomyelia is always
fatal, but we cannot assent to this.
If the bleeding is small, the case may be protracted a very
long time, until at last death occurs from bed-sores, cystitis,
fever, marasmus, and other complications.
Partial recovery often occurs ; the lesion in the cord becomes
cicatrized, and is restored to as normal a condition as is possible.
Motility and sensibility return, at least in part; the bed-sores
heal, the vesical palsy disappears, and the general health is
302 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
good. But usually some muscles or groups of muscles remain
paralyzed and atrophied.
Complete cure is doubtless rare, and only possible when the
clot is very small. It is difficult to prove that it has taken place,
although reports of cases and autopsies are very decidedly in
favor of it. |
The duration must vary greatly. Rapid cases terminate in a
few minutes, hours, or days, while less severe ones require weeks,
months, or even years before death appears, or a moderate degree
of improvement is gained.
Diagnosis.
This is chiefly based on the sudden and very rapid invasion
of paraplegia without much motor irritation, upon the émmedt-
ate severity of the symptoms, and the very severe and protracted
course of the disease. The decision may be supported by the —
existence of a reasonable cause, by certain prodromic symptoms,
the absence of fever, and the elevation of temperature in the pal-
sied parts.
The diagnosis may, at any rate, be difficult in slightly marked
or complicated cases, and the disease may be confounded with
various others which resemble it.
It is hardly possible to mistake it for cerebral apoplexy. The
retention of consciousness, the absence of all symptoms of paral-
ysis of cerebral nerves, the paraplegic form assumed by the dis-
ease, the paralysis of the sphincters, etc., must guard us from
this. And even in difficult cases, such as certainly occur, we
shall not fail to make a correct diagnosis if we carefully attend
to the symptoms. |
The diagnosis from meningeal hemorrhage will usually be
easy (see above) ; in the latter there are active symptoms of irri-
tation, hyperesthesia and pain, violent spasmodic symptoms,
while paralysis is less prominent; the disturbances of sensibility
are quite slight, and the course of the attack is rapid and favor-
able. In hematomyelia the severity of the paralytic symptoms
is very striking, while the phenomena of irritation are quite in
r=
ee ed
SPINAL APOPLEXY. 303
the background; bed-sores appear quickly; the disease is severe,
often fatal, and often leaves incurable palsy behind.
The chief difficulty is that which attends the diagnosis from
acute central myelitis, especially as the hemorrhagic form of the
latter is included in spinal apoplexy. In both cases there is a
destruction of the central gray substance, and the only point of
distinction consists in the rapidity with which the symptoms
develop. The paraplegia requires hours or days for development
in simple myelitis, in hematomyelia minutes or quarters of an
hour. The same is true, of course, in hemorrhagic myelitis.
We may say that the greater the rapidity of development, the
more prominent is the element of hemorrhage. In distinguishing
central myelitis from spontaneous hematomyelia, we must at-
tend to some other points; myelitis begins with symptoms of
irritation, pain, slight spasm, the vertebra are sensitive to pres-
sure, fever may be present, and anesthesia and paresthesia, par-
tial palsy and weakness of the bladder precede the occurrence of
severe paraplegia. The ascending spread of central myelitis may
also be contrasted with the stationary nature of the symptoms in
hemorrhage. By the aid of these points we may distinguish
hematomyelia from central myelitis, and in the latter we may
separate the simple from the hemorrhagic form.
Poliomyelitis anterior acuta (or acute spinal paralysis) in
adults is often quite like hematomyelia. It may, however, be
sufficiently distinguished by the usual presence of fever at the
commencement, the entire absence of all sensory disturbances,
the absence of palsy of the bladder and of bed-sores.
The diagnosis from 7schemic paraplegia will usually be easy ;
although at the beginning it much resembles hemorrhage, yet
severe ischzemic paraplegia occurs only in cases of obstruction of
the aorta, and the latter may easily be recognized by the pathog-
nomonic symptoms of absence of the femoral pulse, and dis-
turbed circulation in the legs, etc.
The diagnosis of the level of the seat of hemorrhage is made
by attending to principles already stated.
304 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Prognosis.
Although we by no means agree with Charcot’s view of the
usually fatal character of hematomyelia, yet the prognosis is
almost always very serious. Large central hemorrhages are
always fatal. The same is true when the seat is at a very high
level.
If the first few days and weeks pass without bringing very
severe complications, the prognosis becomes gradually more
hopeful. But complete recovery is rarely to be expected.
But even when the disease appears favorable, and the symp-
toms are slow in developing, a turn for the worse is always pos-
sible. Besides the formation of bed-sores, the chief thing to fear
is the ascending spread of central myelitis.
Small circumscribed hemorrhages are certainly less dangerous
—if they can be recognized at all during life.
For the rest, a prognostication cannot be made in any case
without a careful weighing of all circumstances.
Treatment.
The prophylactic measures are inferrible from the etiology.
Such causes as can be reached will be attacked. Retained or
suppressed menses, a cessation of hemorrhoidal bleeding, heart-
disease, congestion of the cord, etc., will also receive careful
attention. It is especially needful to inquire whether the symp-
toms are related to a central myelitis, in which case all means
will be used, including large bleedings, cold applied to the back,
powerful derivation, mercury, iodide of potassium, etc.
For the hemorrhage itself, little can usually be done; by the
time the physician arrives, it will (unless very considerable) usu-
ally have ceased of itself. It will, however, be proper to take
measures for preventing a recurrence or an extension to other
parts of the cord, especially when signs of plethora, of excited
action of the heart, of severe spinal congestion are present; we
should then proceed with vigor to the employment of local and
general bloodletting, free application of cold, maintenance of a
———
WOUNDS OF THE CORD. 805
quiet position upon the side or abdomen, with the internal use
of digitalis or ergot (or still better, subcutaneous injections of
ergotin), purges, application of warmth to the extremities ; these
are the remedies here applicable, and from which the proper
selection must be made in each case.
Afterwards we have to treat the sequelee. Secondary myelitis
must be checked by the use of such means as are indicated in
the appropriate section. But the chief object will lie in the pre-
vention of severe trophic disturbances, cystitis, bed-sores, etc.,
which are the most threatening complications. Nothing but the
most careful and self-sacrificing attention can accomplish this ;
for directions see the General Division of this work (p. 192 et
seq.)
If the first weeks pass without serious results, we may at-
tempt to promote the resorption of the extravasation and the
repair of secondary myelitis by iodide of potassium. For the
same purpose we would advise the use of lukewarm baths, warm
springs, and brine baths, or a moderate cold-water cure, and
above all, the scientific application of galvanism.
The latter is also the chief remedy for the palsies, atrophies,
and anzsthesias which remain even after comparatively favor-
able cases. ;
Special indications may of course arise in each case, which
need not be enumerated here.
4. Wounds, Crushing or Tearing of the Cord (Acute Trau-
matic Lesions).
Ollivier, loc. cit. I. p. 246.—J. Hahn, Paraplégies par cause externe ou traumatique.
These. Strasb. 1866.—-Leyden, loc. cit. I. pp. 310 and 321; IL pp. 84 and
139.—M. Rosenthal, 1. c. p. 331.—H. Gurlt, Handbuch der Lehre von den
Knochenbriichen. II. 1. 1864.—Zente, Recovery from Fracture of the Spine.
Amer, Journ. Med. Sci. 1857. Oct. p. 361.—Ruehle, Greifsw. med. Beitr. 1863.
I. p. 12.— Vogt, Liihmung der vasomotorischen Unterleibsnerven nach Riicken-
marksverletzung. Wlirzb. med. Zeitschr. VII. p. 248. 1866.—Quincke, Einige
Fille excessiy hoher Todestemperatur. Berl. klin. Wochenschr. 1869. No.
29.—Fronmueller, sen., Die Riickenmarkszerreissung. Memorabil. 1870. No.
12.—M’ Donnel, Fracture of the Spine. Dublim Quart. Journ. 1871. Vol. 51.
p. 215.— W. Mueller, Beitr. zur pathol. Anat. und Physiol. des R.-M. Leipzig,
806 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
1871. Beob. 1.—Nieder, Lowered Temperature in Injury of Spinal Cord. Med.
Times. 1873. I. p. 154.—Steudener, Zur Casuistik der Herzwunden (Schuss
auch durchs R.-M.). Berl. klin. Wochenschr. 1874. No. 7.
We here include a large group of disturbances, in the full
consciousness that the bond which unites them is somewhat
loose. All, however, have one thing in common; they possess
an acute traumatic lesion of the substance of the cord, which
leads to a destruction of the organ, usually limited as to its longi-
tudinal extension, of variable extent in the transverse direction,
‘and inevitably followed by a traumatic myelitis, similarly local-
ized. This circumstance imparts to all these lesions (they in-
clude wounds by cutting, stabbing, and shooting, compression,
crushing, and tearing of the cord) a great general resemblance,
which from a practical point of view justifies their association in
one group.
Etiology.
Severe traumatic lesions of the cord are hardly possible, un-
less the bony envelope, the spinal column, is injured at the same
time.
There are but few spots (in the upper cervical and the lumbar
regions) where the instrument of offence or the foreign body can
reach the cord without injuring the spine, by passing in through
the vertebral fissures.
It may be regarded as a very rare occurrence for severe trau-
matic lesions of the cord to take place without considerable in-
jury to the bones or the soft parts.
By far the most common and important causes of these
lesions of the cord consist of fractures and luxations of the
vertebrae. All injuries which occasion these fractures or luxa-
tions may, therefore, be regarded as remote causes of lesion of
the cord.
Wherever fracture of a vertebra occurs, with displacement ot
the fragments towards the vertebral canal, wherever in luxation
the vertebree are so transposed as to narrow the vertebral canal,
there it is inevitable that severe lesions of the cord, compression
and crushing, or even local destruction and tearing apart, should
—o »
WOUNDS OF THE CORD. 307
occur. Owing to the width of the spinal canal and the loose
attachment of the cord, a considerable intrusion is necessary
before the latter is likely to be injured ; and yet the lesions we
have mentioned are among the most common sequele of frac-
- tures and dislocations of the vertebrae. Hence the great danger
connected with these surgical events.
We have no space here, nor are we called upon. to enter upon any details respect-
ing the causes and the occurrence of vertebral fractures and luxations, the displace-
ments which occur, their degree and direction, and their consequences. The reader
is referred to the proper works on surgery, especially the exhaustive treatise by
Gurlt. It is sufficiently evident that lesions of the cord may occur in cases of appa-
rently spontaneous injury to the vertebree, such as the sudden breaking down of
carious bone.
That these traumatic lesions may occupy any conceivable sit-
uation is plain; they have been observed from the atlas and axis,
the fracture and dislocation of which are usually so rapidly fatal,
down to the lumbar spine and even the sacrum, in any of which
regions the cord or the cauda equina may be more or less in-
volved.
In the second place, we would mention gunshot injuries of |
the cord, which form an important chapter in military surgery.
They are probably always complicated with gunshot fracture of
the vertebree, and the lesion of the cord is due either to the latter
or directly to the entrance of the ball into the medulla. These
cases, therefore, always involve complicated fractures of the ver-
tebree, with wounds which are often gangrenous, contain various
foreign bodies, etc.; in short, all possible unfavorable circum-
stances.
Not every shot which strikes the spine is equally dangerous
to the cord; the lesion is not rarely confined to meningeal hemor-
rhage, concussion, etc., which are infinitely less dangerous than .
actual wounds of the cord.
Stabs and cuts of the spinal cord are rarer. Blows from
knives, swords, and daggers have been repeatedly observed to
enter the cord, the point of the instrument having entered the
canal either by dividing the vertebral arches or by passing
through the intervertebral spaces. Whe injury may vary in
extent ; the point may have merely entered, or the cord may be
308 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
eut through in various ways, partially or wholly. The foreign
body (point of a sword, broken knife-blade) may then remain
sticking in the cord or vertebree. In like manner, in fractures,
pointed fragments of bone may injure the cord and maintain a
permanent irritation.
. Finally, severe concussion of the body, such as is produced
by a heavy fall on the back, rump, or feet, or by the striking of
heavy bodies upon the back, has been observed in a few cases to
be followed by considerable lesions of the cord (extravasation,
destruction, etc.) without injury of the vertebral column. Thus,
Fronmueller found a complete mashing of the dorsal medulla of
the extent of three and one-half centimetres in a person upon
whose back a heavy beam had fallen without injuring the spinal
column. These cases may also be counted in with the severest
forms of spinal concussion, and can only be distinguished from
the latter by the coarse anatomical lesion. Parrot once found
the cord of a new-born infant torn apart by excessive traction
during labor.
Pathological Anatomy.
The lesions of the spine and other neighboring parts which
cause or accompany injury to the spinal cord need not occupy
us further; we refer our readers to the text-books on surgery
and pathological anatomy.
In the cord itself we observe various phenomena :
1. Simple incised or punctured wounds. At first a wound of
various size and depth, filled and closed with curdled blood ;
the edges of the cut often projecting over the pia. A foreign
body (point of a knife or dagger, splinter of bone) is often found
. in the wound. The size of the wound differs: it involves various
portions of the transverse section of the cord, one or the other
white column, more or less of the gray substance; often one
lateral half is severed, rarely the whole (J. L. Petit, Vogt).
In a few days, and at subsequent periods, the edges of the
wound are still further protruded, are colored a brown-red, and
more or less covered with pus ; their vicinity is hypereemic, more
or less softened ; filled with little extravasations of blood; puru-
¢ fi Pt
te
eee See an DO LENS RET
WOUNDS OF THE CORD. 309
lent infiltration or actual abscess of the cord israrer. The menin-
ges, at the same time, are reddened and inflamed, covered with
fibro-purulent exudation, and abound in capillary hemorrhages ;
at a distance they are opaque, thickened, adherent; the spinal
fluid is increased, turbid, reddish.
It has often been demonstrated in animals, and is probable,
though not sufficiently proved, in the case of man, that in favor-
able instances the edges of the wound heal, and a cicatrix of
connective tissue repairs the injury. It is not yet certain how
far the nerve-elements are restored.
2. Crushing of the cord produces a softening and disintegra-
tion corresponding to the size of the crushing body, usually
associated with hemorrhage, but not always with tearing of the
meninges. The medullary substance is changed into a soft black-
red or chocolate-colored mass, sometimes rather grayish, com-
posed of blood and débris of nerve-substance, showing its color
through the pia, which is suffused with blood to a greater or
less extent. The crushed spot is usually flat, constricted, and
thin.
Great hyperemia presently appears in the parts adjoining,
with progressive inflammatory softening; the medulla swells,
the outlines seen in section become obliterated, the consistency
of the medulla diminishes; it. imbibes at first a reddish, after-
wards a yellowish tint, and is full of small extravasations. The
microscope shows in the immediate vicinity many granular-cor-
puscles, detritus of myelin, decomposed blood-corpuscles, pig-
ment, and blood-crystals; also inflammatory swelling, and after-
wards break-down of nerve-fibres, axis-cylinders, and remnants
of ganglion-cells ; in short, the ruins of the medullary substance
mingled with the products of its own acute traumatic inflam-
mation.
After a few weeks, a thin, gray-yellow, semi-fluid mass is
found at the place which was crushed, partially enclosed in a
structure of young connective tissue; the swelling of neigh-
boring parts continues, they are closely adherent to the mem-
branes, their color is grown paler, and is now a grayish yellow ;
a distinctly demonstrable simple softening is prolonged to some
distance above and below. The lower portion of the cord is
810 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
especially apt to be found softened throughout its whole extent.
Actual abscesses are seldom found. The characteristic secondary
degeneration of the posterior and lateral columns, ascending in
the former and descending in the latter, is a pretty regular oc-
currence. :
If the wounded man lives longer, the destroyed medulla is
by degrees absorbed, and in its place a sort of cicatrix is formed
of young connective tissue, abounding in fluid, which grows
harder and encloses here and there cystic spaces of various size.
A full regeneration of the nerve-substance is not known to occur
in man.
3. Complete severance of the cord is recognized by the fact
that the two ends of the cord are separated by a space which
may amount to three centimetres or more, in which case the pia
is, of course, also torn, while the dura may remain uninjured, or
nearly so.
The space is filled with a semi-fluid mass, partly composed of
blood, at first dark, afterwards rather of a chocolate or gray
color. Inflammatory softening occurs, as after crushing, and
extends more or less upward and downward. If the patient lives
long enough, the commencement of cicatrization and junction of
the ends may be observed.
4. Hemorrhagic destruction of the substance, caused by
simple concussion, is quite like a hemorrhagic softening with all
its consequences.
The secondary changes in the other organs of the body, bed-
sores, cystitis, disease of the kidneys, etc., are the same as in
other forms of severe spinal paralysis, and. will be more fully
described under myelitis.
Symptoms.
For the sake of distinctness in the presentation, we make two
groups, the one (a) containing comparatively slight injuries of
the cord, the simple incised and punctured wounds ; the other
(2) embracing all the more serious lesions, squeezing, crushing
and tearing of the cord. Tt need hardly be said that between
these two classes there exist transitions, and numerous analogies,
WOUNDS OF THE CORD. 311
both as respects the anatomical changes and the symptoms,
course, and termination of individual cases.
a. The symptoms which indicate that an injury by cutting,
or stabbing, in the neighborhood of the spine, has penetrated the
cord, will be at first those of partial or total interruption of con-
duction in the cord, which extends to the portions behind the
seat of injury, and is not merely confined to the district of the
nerve-roots which lie at the point of injury.
This interruption of conduction may vary in extent and dis-
tribution, according to the seat and extent of the injury. Almost
all the experiments in the physiology of the cord consist in the
infliction of such simple injuries by section, and all varieties of
symptoms may be imagined in connection with them.
At the moment the injury is received, there is usually a
motor paralysis of various extent in the form of paraplegia, or
spinal hemiplegia, or hemiparaplegia, or even paralysis of the
trunk, and all four extremities. With this is- usually asso-
ciated sensory paralysis, due to the injury, and correspondingly
of very various extent. It may be paraplegic, or may be lim-
ited to one side, and in the latter case is upon that opposite to
the lesion and the motor palsy ; it may be quite circumscript ; it
may affect certain qualities of sensation only, as the sense of
touch, the muscular sense, etc. Jn cases of very restricted lesion,
hyperesthesia (in the form of a girdle, or otherwise distributed)
is often found.
If the injury is of any considerable extent, paralysis of the
bladder and rectum is always present; at first with complete
retention of urine, which soon gives place to equally complete
incontinence, while the evacuation of feces takes place involun-
tarily and unperceived. Close examination usually detects also
vaso-motor palsy (elevation of the temperature of the skin, in-
creased redness) in the regions affected by the motor palsy.
The reflex actions are usually totally suspended at the first
moment under the shock of the injury, but soon return, and
may become exaggerated. This depends, of course, upon the
seat of lesion.
If we add to this the girdle-pains which are usually present,
corresponding with the seat of lesion, and due to injury of the
212 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
roots, and the symptoms which depend on injury of the bones
and soft parts, we have a pretty complete picture of the condi-
tion of the patient during the first few days after the accident.
This, however, is soon complicated by the symptoms of sec-
ondary traumatic myelitis. Usually the inflammation is trans-
verse in its distribution, covering nearly the whole breadth of the
cord, but having little extension in the longitudinal direction.
The fever usually lasts but a few days. Striking symptoms of
irritation now commonly appear ; pains encircling the trunk like
a girdle, active pains in the paralyzed parts, hyperesthesia of
various extent in the skin, also spasmodic conditions, twitching
and contractures of single muscles and groups. The palsy at the
same time increases rapidly in the transverse direction without
extending much upwards, 7. é., it seizes by degrees upon the
motor paths passing the injured spot, which were at first unaf-
fected (the sensory and vaso-motor paths, bladder, rectum, etc.),
without any considerable change in the upper limit of the lesion.
The reflex actions are decidedly increased, but may at a later
period cease entirely, when the process has extended to the bot-
tom of the cord. If foreign bodies remain in the wound, the
symptoms of irritation reach a still higher point, with very
severe pains, violent spasms and contractures. |
At a later period bed-sores, with all their consequences, ap-
pear—pyemia and septicemia, cystitis, etc.
According to the height at which the lesion is situated, othe
symptoms may arise to complicate the case; we need not men-
tion them all. The higher the injury, the more prominent are
the disturbances of respiration, and the more threatening their
import.
6. The symptoms which, accompanying severe lesions of the
spine or other places, indicate that the cord is crushed or torn,
are usually those of complete and very severe paraplegia. The
posterior portion of the body is absolutely paralyzed, with cor-
responding complete anesthesia, limited quite sharply -above;
the reflex actions are depressed or suspended, seldom increased ;
the bladder is paralyzed to a severe degree, causing retention of
urine and frequently an enormous distention of the organ; the
intestine is paralyzed, producing meteorism ; the rectum is para-
Eee ee ee ee
————
WOUNDS OF THE CORD. 3138
lyzed, with involuntary evacuations; the vaso-motor paths are
paralyzed, with elevated temperature in the posterior half of the
body, and in many cases, in men, more or less severe and persist-
ent erections of the penis; the excretion of urine is lessened or
suppressed, etc. To this add (to complete the picture) the symp-
toms due to fracture of the vertebree, or the like, as pain, immo-
bility, displacement, etc.
All these symptoms follow naturally from the lesion of the cord. The motor,
sensory, and vaso-motor palsies are direct consequences of the interruption of con-
duction in the cord. The suppression of reflex acts which is found even where
the reflex centres are not directly injured, is the result of the severe shock suffered
by the cord; after the lapse of some hours or days the reflex centres recover, the
reflex actions reappear, and may even exhibit considerable increase if circumstances
permit. The same is true of the vaso-motor centres, especially for those which
preside over the evacuation of urine, situated in the lumbar cord; the shock, com-
bined with the crushing, paralyzes these centres first, whence the complete retention
of urine in the excessively distended bladder, which exists even in cases where the
lumbar cord is not the seat of the crushing lesion. If the centres recover, occa-
sional complete evacuations of the bladder occur quite involuntarily, and usually
unperceived ; thus, Steudener found a powerful contraction of the bladder occur-
ring regularly as soon as the catheter in the urethra irritated the fossa navicularis—
a phenomenon which is in perfect accordance with physiological facts observed by
Goltz. At a later time the urine begins to drip continually.
The priapism which is so frequent an occurrence in severe fractures of the verte-
bree is far more difficult to explain. It is most common in connection with crushing
of the cervical portion, rarer with that of the dorsal region, and never occurs with
fractures from the third lumbar vertebra downwards. In many cases the erection
has been observed directly after the injury; ejaculation at the same time has oc-
curred in a few cases. The erection is either powerful, or lax and incomplete; it
is either not felt at all, or is painful; at a later period it may diminish, and may
be again produced by catheterism or other irritations.
—It is not hard to form a plausible theory of the occurrence of this phenomenon,
based on known facts; though it must be confessed that the subject is obscure in
several respects. It is best explained by the assumption of an irritation, at the
point of lesion, of those paths leading from the brain, the duty of which is to ex-
cite the centre for erections in the lumbar cord. If it be objected that the centres
in the lumbar cord are usually paralyzed at the outset, and that the complete paral-
ysis of the bladder is in contradiction with the assumption, it may be answered
that the symptom of priapism is common, in proportion to the remoteness of the
lesion from the lumbar cord, and in proportion to the probability that the latter
region retains its activity; and further, that the excitability of the centres for
erection need not be equal to that of the centres for the bladder; and that we are
314 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
ignorant of the precise condition of the latter centres and their reflex excitability,
in cases of permanent erection. If we take into view the symptom of ejaculation,
which can certainly be nothing but a symptom of irritation, the assumption of irri-
tation of the paths which give rise to erection will be found the more plausible.
We cannot see how in such cases priapism can be regarded as a phenomenon of
paralysis, unless it be of vaso-motor paralysis. At a later period—and perhaps at
the beginning in many cases—there is no doubt that reflex irritation (as that origin-
ating in a distended bladder, the introduction of a catheter, bed-sores, etc.) may
give rise to, and sustain, the erections.
If the above group of symptoms should allow the slightest
doubt of the existence of a severe lesion of the cord, if the case
should at first be taken for one of severe simple concussion, a few
days’ delay will usually bring full evidence of the real condition.
At that time fever appears; the symptoms of acute traumatic
myelitis become more and more distinct ; bed-sores appear, and in-
crease rapidly and steadily ; if the lumbar region is crushed, there
is rapid atrophy of the leg-muscles with loss of electrical reac-
tion; the urine becomes bloody, purulent, ammoniacal, ete. The
temperature, especially when the cervical region is crushed, often
rises continuously and to an excessive height (43°-44° C. [109° to
111° Fahr.], Brodie, M’Donnel, Quincke, and others)—the rise
which occurs in the neuro-paralytic agony. In other cases,
when the dorsal portion has been injured, the temperature has
been abnormally low for some days before death (Nieder). For
the interpretation of these symptoms we refer to page 128 et seq.
Thus the most severe cases are rapidly brought to an end by
complications—such as palsy of respiration, disturbances of cir-
culation, pyzemia, neuro-paralytic agony, and so forth.
The disease is by no means, however, always so severe ; there
are cases of partial crushing, where a fortunate accident has
Saved a portion of the transverse section from destruction, of
which the result is partial paralysis (Ollivier, Obs. 25 and 26).
The entire process is milder and less dangerous. This is not the
place even to touch upon all the possible cases of such partial
lesion; we need only say that the literature of the subject of
fractures of the vertebrae contains cases of all possible degrees of
Severity.
The symptoms differ, of course, in correspondence with the
level at which the lesion may be seated.
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WOUNDS OF THE CORD. 315
If the cervical portion is affected, death usually occurs at
once, if the lesion is at the height of the first or second cervical
vertebra, é. g., in luxation of the odontoid process ; and death
is almost as speedy when the lesion is above the origin of the
phrenic nerves. All four extremities are then paralyzed, while
the respiration is so difficult as only to be maintained by the
forced and anxious action of the auxiliary muscles of respira-
tion ; the speech and voice are weak, and swallowing is difficult.
If the cervical enlargement below the phrenic nerves is the seat
of lesion, the expiration is chiefly affected ; the legs are wholly
paralyzed, the arms more or less completely so; the sensibility
of the arms may be partially retained ; reflex actions are retained,
often exaggerated ; M’ Donnel even saw co-ordinated reflex actions
(the left hand, in a state of absolute palsy, made a movement to
seize the genitals during the act of catheterization) ; priapism is
very frequent ; life may be retained for a considerable time.
If the lesions are in the dorsal region, the arms are free, and
the trunk is palsied, up to an uncertain height ; the legs are more
or less paralyzed, often unilaterally, with crossed anzesthesia ;
the expiration is less impeded, the voice and speech are some-
what affected ; the reflex actions are retained and exaggerated in
the subsequent course of the disease; the bladder and rectum
are paralyzed ; priapism is somewhat rare ; bed-sores follow.
In lesion of the Zwmbar region the arms and a great part of
the trunk are free. The legs, bladder, and rectum are totally
paralyzed ; respiration is not impeded ; reflex actions of all sorts
are totally extinct; no erections ; rapid atrophy of the muscles,
and extinction of their electrical reaction. The symptoms of
lesion of the cauda equina are quite similar; but the freedom
or the implication of certain nerve-paths, especially those belong-
ing to the lumbar plexus, often enables us to refer the seat of
lesion to the cauda equina.’
a
1 Cf. Hrb, Ueber acute Spinallihmung bei Erwachsenen. Arch. f, Psych. u. Ner-
venkrankh. V. p. 785. Beob. VI.
316 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
Course, Duration, Termination.
There are hundreds of physiological observations which show
that improvement, and even cure, may occur in the first and
slighter form of lesion (simple incised wounds of the cord).
Goltz and Freusberg have kept dogs alive for many months, even
when the dorsal cord had been completely severed by a cut;
they observed, however, no occurrence of regeneration. |
An absolutely fatal termination, therefore, even in man, can
hardly be predicted ; indeed, there are numbers of cases of un-
doubted lesion of the cord, in which a comparative cure was
effected and life was retained for many years. Such are the
cases of cure of a probable punctured wound, given by Ollivier,
and of various incised wounds, by Brown-Sequard and others.
These, however, are the exceptions, which must not be looked
for unless in slight injuries. If such is to be the result, the
symptoms of myelitis do not become severe, they soon pass off,
and the outer wound closes; the symptoms of palsy are relieved
in part, and in part remain, so that a more or less complete cure
is by degrees obtained. The importance of the functional repara-
tion of the lesion, urged by Schiff (p. 64 above), can hardly be
overlooked.
Usually, however, the secondary myelitis continues to increase,
the paralysis increases, bed-sores, with their unfortunate conse-
quences, appear, and the fatal end is reached after more or less
protracted sufferings.
The second and more severe form is almost always fatal. When
the cord has been thoroughly crushed or torn in any part it is
hardly possible to conceive of regeneration; and even if life be re-
tained, in a number of cases, for weeks or months (M’ Donnel, two
months; Steudener, fifteen weeks; Page, in a case of severance of
the convict cord between the fifth and sixth vertebre, even fif-
teen months), yet the ultimate result is pretty certain, and occurs
with the usual symptoms of severe spinal palsy. It is a matter
of course that death may occur in a few hours or days after the
injury by paralysis of respiration, shock, or similar occurrences.
Is a cure ever effected ? and is it possible in any severe spinal
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WOUNDS OF THE CORD. 317
lesion? The opinions of physiologists are divided upon this point
(see above, pp. 64, 65). There are no convincing proofs in the
case of man. In the instance given by M’ Donnel, a sort of cica-
trix was found at the close of two months, but not a trace of
nerve-tissue could be found in it. Ollivier’s observation (No. 18),
and Lente’s case, are strongly in favor of the repair of lesions of
moderate severity.
Diagnosis.
It is not difficult to recognize an injury of the cord by the
preceding symptoms.
In case of simple injury to the meninges, by puncture or in-
cision, the occurrence of meningeal apoplexy might give rise to
the mistaken diagnosis of an injury of the cord. The former will
easily be recognized by the symptoms of irritation, which are
prominent at the outset—pain, spasmodic phenomena—and by
the slighter degree and the greater diffusion of the paralysis ;
and finally by its rapid and favorable course.
In severe injuries of the cord, the existence of spinal apoplexy
may be suspected ; but it is of no importance to determine it, asa
crushing of the cord is doubtless always attended by hemato-
myelia, and the symptoms and course of the two diseases are
essentially similar.
Cases of severe concussion of the cord may usually be re-
cognized by the absence of a clear demarcation of the anes-
thesia and the palsy, by the subsequent course, the absence of
bed-sores, etc. If dislocations of the vertebrze can be proved to
exist, the crushing of the cord will become more probable.
Prognosis.
This will readily be inferred from what has been said. It is
very dubious, even in the slightest cases of injury, and we should
be prepared for a fatal result through secondary myelitis ; but
there is still some hope.
In all severe cases of crushing and tearing of the cord, death
is almost absolutely certain, sooner or later. But there are excep-
318 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
tions, as has been before said, in the case of slight and very
partial lesions only.
Treatment.
The first thing to be attended to is a careful treatment of the
external injuries (wounds, fractures, and luxations of the verte-
bre), for the details of which we refer to the hand-books of sur-
gery.
The injury to the cord introduces a very important element
of danger in all these cases ; in most instances it is the cause of
death ; we ought, therefore, to make every effort to relieve it or
to promote functional recovery. In addition to the ordinary
surgical methods, we shall often have to consider the propriety
of trepanning the spinal column for the relief of compression of
the cord, the removal of fragments of bone, replacement of the
ends of the fractured bone, etc. We need not, however, discuss
the value or the feasibility of trepanning, or its indications, for
which we can refer to the work of Gurlt. And yet we believe the
operation is indicated wherever there is good reason to hope for
gaining anything in the treatment of the dislocation which caused
the lesion of the cord ; and such gain would be more probable in
fractures of the arches of the vertebra, as fragments of the bodies
can hardly be reached. We can scarcely ever expect any direct
result, as the injury to the cord is not from simple compression,
but usually from crushing or tearing. Yet the removal of dis-
placed fragments will at least increase to some extent the chances
of life. We should not, therefore, hesitate, in so almost hopeless
a case, to undertake an operation not of itself very dangerous, if
there is any possibility of relief. The physician must carefully
weigh all the chances; it is certain that in all severe cases the
operation will do little harm, and perhaps some good.
In the second place, we have to consider remedies for ¢rau-
matic myelitis, local (or if necessary general) bleeding, cold,
ergotin, and belladonna, frictions with mercurial ointment, ete.
(See the Treatment of Acute Myelitis.)
By far the hardest task will consist in the personal attentions
to the patient, those, namely, which are required for the preven-
SLOW COMPRESSION OF THE CORD. 319
tion of bed-sores and cystitis, which usually destroy life. Two
contradictory requirements are usually present: absolute quiet,
for the surgical injury, and frequent change of posture, for the
prevention of bed-sores. We must try to do what we can with
water-pillows, air-cushions, pillows pushed in alternately on op-
posite sides, cushions stuffed with chaff, great cleanliness, posi-
tion on the face, etc., as circumstances dictate.
The treatment of the vesical symptoms, the fever, marasmus,
pains, etc., depends on general principles. "We should compare
the treatment of acute myelitis.
5. Slow Compression of the Cord (Chronic Traumatic Lesion
of the Cord).
Compare the works of Ollivier (I. p. 387), Hasse (p. 735), Jaccoud (Des paraplégies,
etc.), Brown-Séquard (Paralysis of the Lower Extremities, etc. 1861), M. Rosen-
thal (p. 813), Leyden (I. pp. 213-311; Il. p. 147). Also
Charcot, De la compress. lente de la moélle ép. Legons sur la mal. du syst. nervy. II.
Sér. IL. fase. 1873.—Bouchard, Compress. lente de la moélle. Dictionn. ency-
clop. des sc. médic. II. Ser. Tom. VIII. p. 664. 1874.—C. Hawkins, Cases of
Cancerous, etc., Disease of the Spinal Column. Med. Chir. Transact. XXIV. p.
45. 1841.—Vogel und Dittmar, Deutsche Klinik. 1851. Nr. 88,—TZ?raube, 5
Fille von Riickenmarkskrankheiten. Charité-Annalen. IX. 2. p. 129. 1861.—
Ruehle, Zur Compression des R.-M. Greifsw. med. Beitr. I. p. 5. 1863.—
James Young, Case of Temporary Paralysis. Edinb. Med. Journ. May, 1856.—
Ogle, Case of Paraplegia, etc. Transact. Path. Soc. XIX. p. 16. 1868.—A.
Joffroy, Cas de fract. de la colonne vert. Arch. de Phys. I. p. 735. 1868.—
Leudet, Curabilité des accid. paralyt. conséc. au mal vert. Mém. de la Soc. de
Biol. 1862-1863.—Michaud, Sur la méning. et la myélite dans le mal vertébr.
Paris, 1871.—Charcot, Anat. pathol. et trait. de la parapl. liée au mal de Pott.
Gaz. méd. 1874. No. 49.—A. Courjon, Paraplég. dans le mal de Pott. Paris,
1875.—Z£. Rollett, Wien. med. Wochenschr. 1864. Nr. 24-26.—De Giovanni,
Storia di un caso di paraplegia, etc. Riv. clin. di Bologna, 1870. No. 12.—
Leyden, Ueber Wirbelkrebs. Charité-Annalen. XI. 3. p. 54. 1863.—M. Rosen-
thal, Wiener med. Presse. 1865. Nr. 42-45; Zeitschr. f. prakt. Heilk. 1866.
Nr. 46-51. Tripier, Du cancer de la colonne vertébr. Paris, 1866.—7h. Simon,
Paraplegia dolorosa. Berl. klin. Wochenschr. 1870. Nr. 35 und 36.
Definition.—Numerous as are the conditions which we em-
brace under this title, yet all have this in common, that a@ power
acting from without upon the cord (and the nerve-roots) com-
390 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
presses it very slowly and gradually in a limited longitudinal
extent, giving rise to a series of characteristic symptoms which
in all cases may be recognized by their essential features, and
often are the first to call our attention to the commencement of a
severe affection.
These symptoms, however, are not usually produced by the
pressure as such, or exclusively, but by the subacute or chronic
transverse myelitis which develops almost invariably at the
point of compression and by the secondary degeneration of the
cord, extending upwards and downwards.
The essential lesion is, therefore, a circumscribed transverse
myelitis, the so-called myelitis from compression ; and we
should not devote a separate section to it, were it not that it
forms a connecting link between very various morbid states origi-
nating in the spinal column and its contents, and that the symp-
toms of myelitis from pressure compose a very important feature,
common to all those forms of disease.
Etiology and Pathogenesis.
Any circumstance which very gradually narrows the spinal
canal, usually in the way of organic growth, and thereby leads
to a slowly increasing local compression of the cord, may become
a cause of myelitis by compression.
We have already mentioned an important part of these
causes, viz., meningeal tumors. To avoid repetitions, we would
refer to what has been said above (see page 262 et seq.) upon this
point. We here repeat that a gradual compression of the cord
may be occasioned not solely by the so-called neoplastic tumors
proceeding from the spinal membranes, but equally well by
meningeal tumors formed by inflammatory and hemorrhagic pro-
cesses, parasites, and the like, and by tumors which originate in
the perimeningeal tissue. All these tumors have one thing in
common, that their expansion is very soon checked by the nar-
rowness of the canal, and that they then begin to exercise an
increasing pressure upon the cord. It is self-evident that this
pressure may affect the cord in various ways and from different
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SLOW COMPRESSION OF THE CORD. 321
sides, and may thus produce a great variety of symptoms, but
the essential conditions remain the same.
It may be questioned whether the intra-medullary tumors,
those developing within the substance of the cord, ought to be
counted among the causes of compression. They do not act
from without, and therefore differ somewhat in their symptoms.
It is characteristic of them that the cord is gradually compressed
from one point of its transverse section, with myelitis as a gene-
ral accompaniment ; for which reason the characteristic initial
symptoms relating to the compressed roots are absent, and those
of compression of the cord begin at once. For all details we
refer to the section on tumors of the cord, and premise only this
remark, that all sorts of intra-medullary tumors may produce
the symptoms of myelitis by pressure—as glioma, sarcoma,
myxoma, tubercle, syphilitic gummata, cysts (hydromyelus and
syringomyelia), etc.
By far the most important cause is that furnished by diseases
of the vertebral column. The most frequent of these, and also
the most frequent cause, on the whole, of myelitis from com-
pression, is caries of the spinal column (Pott’s Disease, Spondy-
larthrocace). We need not describe this particularly, for it is
fully treated of in the text-books of surgery ; our present object
is confined to inquiry as to the manner in which it may give rise
to a slow compression of the cord.
In the first place, the wasting and sinking of the bodies of
the vertebree produce kyphosis, which may give rise to a bend-
ing and narrowing of the vertebral canal, with compression of
the cord. This is certainly very rare, and only occurs in ,exces-
sive kyphosis. Enormous angular kyphosis may occur without
any symptoms of compression of the cord; and on the other
hand, the paraplegia accompanying kyphosis often disappears
altogether without the least change occurring in the latter; and
finally, there are cases of vertebral caries without any kyphosis,
which are nevertheless accompanied by paraplegia. The kypho-
sis is not, therefore, the sole nor even the chief cause of compres-
sion of the cord.
In most cases this compression is produced by the inflamma-
tory exudation which accompanies the caries. The masses of
VOL. XIIL—21
2992 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
pus produced by caries, and in particular the fungous granula-
tions, accumulate between the dura and the bodies of the ver-
tebree and press the dura inwards ; they produce a pachymenin-
gitic growth and thickening of the dura, causing a contraction of
space in the vertebral canal (Charcot, Michaud; see also the very
artistic illustration in Ogle). The dura is thickened ; its outer
layers especially are changed to a proliferous mass of young
fibro-plastic tissue, partly undergoing caseous metamorphosis,
which either surrounds the dura at one point like a ring, or
presses it from one side against the vertebral canal to the extent
of ten, fifteen, twenty millimetres or more. The nerve-roots at
the place are more or less implicated, thickened, swollen, in-
flamed, etc. Simple caseous pus-deposits may become a cause
of pressure, or the protruding intervertebral cartilage, or sepa-
rated and displaced fragments of bone.
In the second place, carcinoma of the vertebre should be
mentioned as a frequent cause of compression, chiefly observed
in old persons. The primary as well as the secondary disease
may act in this way; the latter quite usually follows primary
cancer of the breast, but also that of any other organ. Not all
cancers of the vertebree produce spinal symptoms; that depends,
of course, upon their location, size, and the direction taken in
growing; but when cancer attacks the arches of the vertebree
and the nerve-roots which pass between them, when it has at-
tacked, softened, and thoroughly rotted the entire bodies of ver-
tebree, when it presses in to the vertebral canal, seizes on the
spinal membranes and grows directly against the cord itself, then
the characteristic spinal symptoms usually appear, and the form
of compression known as paraplegia dolorosa, with most acute
pains, is developed.
There are several diseases of the vertebree, much inferior in im-
portance to the preceding, which may occasionally lead to com-
pression of the cord. Such are exostoses of the vértebree growing
into the canal; osteoma ; syphilitic new formations of the bone;
also dry arthritis of the vertebrae, when it leads to considerable
swelling of the articular processes, osteophytic growths, deposi-
tion of bone, etc. Here must be mentioned also the thickening
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rer oa ad am
SLOW COMPRESSION OF THE CORD. _ 323
of the odontoid process of the axis, anchylosis of the vertebra,
and all similar affections. |
Finally, it remains to be said that external tumors of all
| sorts, growing towards the vertebral column, and entering the
vertebral canal by any natural or pathological opening, may
give rise to pressure of the cord. Such are echinococci, sarco-
mata, aneurisms, etc.
All these causes (with the partial exception of intra-medul-
lary tumors) have one element in common, namely, that they
push on very gradually against the cord, reaching jirst the ner ve-
roots and meninges, irritating and afterwards compressing them,
and thus giving rise to a group of most characteristic symptoms,
which belong to the first period of development.
The cord itself is then attacked ; it is exposed to a gradual
‘compression which interferes with and interrupts the conduction.
Nor is this all, for after the compression has lasted a longer or
shorter time (usually a very short time—sometimes even before
paraplegia exists—Charcot, Michaud) inflammatory changes
appear; myelitis is developed, at first confined to the seat of
compression, but usually extending over the whole transverse
section of the cord. With the compression and its concomitant
myelitis, very characteristic symptoms are associated, belonging
to a second stage of the disease. In most cases these symptoms
seem to be connected with the appearance of myelitis.
' The question whether compression may exist alone without
myelitis, and may of itself produce the paraplegic symptoms, or
whether pressure-myelitis is a necessary condition, is somewhat
a superfluous one. It is certain that compression—especially
if it be acute—is capable by itself of giving rise to the seve-
rest paraplegia, which, if the compression be speedily and suc-
cessfully removed, may disappear in a comparatively short time,
as in the oft-quoted cases of Ehrling and Brown-Séquard. It is,
however, equally certain that in the very great majority of cases
every protracted compression of the cord is very soon compli-
cated by pressure-myelitis; it does not seem probable to us that
this myelitis is the result of an ischeemia produced by compres-
sion, an ischemic softening, but we consider it as the direct
consequence of the irritation of compression acting upon the
324 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
elements of the tissue. Finally, it seems equally certain that in
many cases the mere irritation of tumors pressing against the
spinal membranes (carcinoma, etc.) is enough to produce mye-
litis without actual compression. We therefore see that the
pathogenesis of the symptoms commonly known as compression
of the cord may be of several sorts; they may arise through com-
pression alone, or through compression and the consequent mye-
litis, or finally through myelitis alone.
In conclusion, if the compression is not soon relieved, and if
myelitis is once established, secondary degeneration and sele-
rosis of the cord supervene, as in the case of every transverse
myelitis (see farther on, No. 19), invading in a strictly regular
way the various divisions of the cord above and below the point
of compression. These in their turn lead to other definite symp-
toms, which may be considered as forming a third period of the
disease.
Pathological Anatomy.
The pathologico-anatomical changes which belong to the pri-
mary lesion (vertebral disease, tumors, etc.) cannot be described
here for want of space; the reader is referred to the text-books
of pathological anatomy and surgery. We have mentioned a
few chief points under the etiology, and it remains here only to
describe what is directly concerned with the cord and its appen-
dages.
The meninges are often hy pereemic, opaque, thickened, adher-
ent to the neighboring parts; often covered with deposits of va-
rious thickness, which have much to do with the production of
compression ; often, however, they are remarkably little changed,
are smooth, and simply pushed a little from their usual position.
The nerve-roots are almost always more or less involved in
the morbid processes. They may be closely united with the
tumor or the exudation, or may appear one with it; at first they
are usually swollen, hyperemic, inflamed, their fibres are in a
state of fatty degeneration and beginning to break down, and
this may be traced into the cord (neuritis); at later periods the
LOW COMPRESSION OF THE CORD. 325
roots are atrophied, pale, gray, degenerated, and nearly reduced
to a connective tissue abounding in nuclei.
In carcinoma of the vertebree, especially, the nerves and nerve-
roots are reddened, swollen, fuller of fluid; rarely atrophied, and
still more rarely directly involved in the cancerous growth. Sim-
ple contact with the malignant tumor is sufficient to produce
severe neuritis.
The substance of the spinal cord is more or less flattened and
thinned at the point compressed, is often reduced to a slender
cylinder, hardly the size of a quill, or to a flat, ribbon-shaped
string. The compression is sometimes greater from the front,
sometimes from behind, sometimes from one side, and thus the
cord gets a distorted, irregular look. The place compressed va-
ries extremely in length; above and below it the cord is some-
times of its usual thickness, and sometimes rather thickened in a
club-shape. The consistence of the compressed spot is usually
lessened at first (inflammatory softening), but afterwards may be
increased (sclerosis). The place is anemic, pale, often presenting
no distinct change to the naked eye; usually, however, the out-
lines seen in cross-section are quite indistinguishable, the medulla
is cloudy, or, at a later stage is gray and translucent.
Microscopical examination shows—if the compression has
lasted some time—a considerable increase and thickening of in-
terstitial connective tissue at the place, and mingled with this are
many granular corpuscles, often also corpora amylacea, while the
walls of the vessels are thickened and in a condition of fatty
degeneration; the axis-cylinders are often swollen, while some
are broken down or have disappeared ; in the ganglion-cells of
the gray substance there may be observed swelling, the forma-
tion of vacuoles, pigthent-deposit, and often a breaking down and
disappearance (Michaud, Joffroy). In a word, there is chronic
transverse myelitis, chiefly interstitial, extending over the greatest
part or the whole of the transverse section.
The myelitic changes extend beyond the place crushed, and
may be observed above and below at various distances, with
diminishing intensity.
At a short distance from the spot, these changes usually appear
confined to clearly defined portions of the transverse section, and
396 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
in these may be followed up and down almost the whole length
of the cord. These are the well-known secondary degenerations
(Tuerck, see farther on, No. 19). Above the compression, the pos-
z
Fie. 5.
Compression of the
Dorsal Medulla,
Diffuse myelitis at the
point of compression
(4); the right half is
More compressed than
the left. Above, secon-
dary ascending degen-
eration in the fasciculi
graciles (1—3); below,
descending degenera-
tion of the lateral col-
umns to the sana
tance (Michaud).
terior columns are affected, higher up the fasciculi
graciles alone, and in the latter the disease often
ascends as high as the medulla oblongata. In
the lower segment the lateral columns alone are
affected, and chiefly their posterior part ; the dis-
ease descends in this to the conus terminalis.
The change may often be recognized in fresh pre-
parations with the naked eye by the translucent,
grayish, or slightly yellowish tinge of the tissue,
but more usually the altered tissue cannot be
recognized with certainty until the cord has lain
some time in chromic acid, when it acquires a
lighter color. With the microscope, interstitial
proliferation of connective tissue, and degenera-
tion of nerve-fibres are to be seen. In a few cases
the degeneration has been seen ascending in the
lateral columns also, usually but for a short dis-
Commonly the degeneration is
not uniform in the two sides. The illustration
(Fig. 5) gives a good view of the typical distribu-
tion of these alterations.
The myelitic process often extends to great
distances in the gray substance also, especially
downward, but in this situation requires close
microscopic examination to detect it; the charac-
teristic signs consist of sclerosis of connective tis-
sue, thickening of the arterial walls, atrophy and
disappearance of the nerve-elements, pigmenta-
tion, etc. This process is important in explain-
ing many later symptoms.
In severe cases all these processes make prog-
ress; there are consecutive changes in remote
parts of the body (muscular atrophy, degenera-
tion of peripheral nerves, cystitis, bed-sores, etc. ), which hasten
the fatal result.
-
SLOW COMPRESSION OF THE CORD. 327,
In more favorable cases it is possible for restoration and full
recovery to occur; this is certainly true in vertebral caries, and
would doubtless apply to other cases if the cause of compression
were removed. In such an event there must be a regeneration and
restoration of nerve-elements, at least in part, at the point of
compression. The processes, however, have not yet been fully
studied. Charcot and Michaud have examined such a case in
which recovery had occurred ; the seat of compression was very
distinct, its transverse section was much smaller than that of
other portions of the cord, and it looked gray, as if degenerated.
The microscopical examination showed the presence of much con-
nective tissue, among which there were a great many nerve-fibres,
normal in appearance, though slender ; they must certainly have
been diminished in number. In the gray substance, which was
much reduced in size, there were found some, though not very
numerous, ganglion-cells. Little is known of the more delicate
changes in these processes of restoration; it is probable that the
axis-cylinders of some nerves are not destroyed, and clothe them-
selves with a fresh medullary sheath when the pressure is re-
moved. Further examination of the subject is to be desired.
Symptoms.
It is important to remember from the outset that two chief
groups of symptoms are to be distinguished in compression of
the cord, upon which may be based a division of the disease in
two stages.
In the first group are included all the symptoms proceeding
from lesion of the parts situated externally to the cord, espe-
cially the nerve-roots, meninges, bones, etc. They may also be
designated as prodromal symptoms (symptémes extrinséques,
Charcot). This group furnishes the symptoms which are usually
decisive of the differential diagnosis of the various causes of com-
pression, while those of the second group are nearly the same in
all cases, with the exception of such variations as depend on the
level at which they occur in the cord, or the portion of the trans-
verse section which is occupied. )
This second group embraces all the symptoms which are de-
398 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
rivable from compression of the cord itself, and from the myelitis
caused by pressure (symptémes intrinséques, Charcot). They
are nearly alike under all possible causes, as above stated.
The succession and development of the symptoms of these
two groups will give the characteristic signs of the disease.
This being premised, the general symptoms are as follows.
After those of the primary disease (as Pott’s Disease, vertebral
cancer, etc.) have existed for some time, or even before they have
been observed, the first evidence that the contents of the verte-
bral canal are attacked consists in certain symptoms of irritation
of all the organs contained in the canal, the periosteum, menin-
ges, and especially the roots of the spinal nerves. Pain of vari-
ous sorts and degrees of violence, pains in the form of a girdle,
excentric neuralgias in almost any spot (but holding constantly
to that spot), open the scene; a great hyperesthesia of those
portions of skin which correspond to the distribution of the pain
may be added, but often disappears to make room for a corre-
sponding anesthesia, often limited to a few islands of skin—or
both conditions may subsist together. Severe pain in the back,
local stiffness of the spine, great sensitiveness of the spinous
processes, are seldom absent. The neuralgic pains are often
accompanied by herpetic or bullous eruptions of the skin. To
these are afterwards added (especially when the lesion occupies
the cervical or lumbar enlargement) states of motor irritation in
the districts of the nerves whose roots are first implicated, as
twitching, spasm, tonic spasm, and contracture; weakness and
paralysis is soon added, confined to certain muscles or groups
of muscles, to one extremity or the other, and often accompanied
by great atrophy and loss of electrical excitability. It must be
observed that these sensory and motor symptoms are located in
the same, or adjacent nerve-districts, and therefore may be re-
ferred to a single source of disease.
If the original causal lesion then declares itself by such signs
as progressive kyphosis, congestive abscesses, pain strictly local-
ized in the spine, external swellings of various sorts, etc., the
diagnosis of the disease may be considered as already made
out.
This prodromal period may differ very greatly in duration ; it
SLOW COMPRESSION OF THE CORD. 329
may last months or years; its symptoms always precede for
some time those of compression of the cord; they are absent
only in case intra-medullary symptoms are prominent, when the
symptoms of pressure may be the very first to be noticed.
The latter, belonging to the second stage of the disease, con-
sist at first of a paralysis, of more or less rapid development,
usually in the form of paraplegia, more rarely in that of hemi-
plegia, and in the latter case usually developing into paraplegia.
The first symptoms of paralysis are often preceded for a time by
paresthesia in the lower half of the body; tingling, furriness,
sensations of burning or cold, girdle-sensations, etc., are described
by the patient. The order in which the sensory and the motor
symptoms appear depends on the direction from which pressure
is first felt ; those which first appear may exist some time before
the other set follows. Those of the motor class, however, very
soon become more marked than the other set; the preponderance
of motor paralysis is quite a characteristic trait in the picture of
myelitis from pressure. The paralyzed muscles are first com-
pletely relaxed and softened, the joints are relaxed, and obey
every passive movement without resistance. At the same time
there is considerable increase of the reflex actions, both cuta-
neous and tendinous, in the paralyzed lower extremities, except
when the lumbar swelling is the seat of pressure; the slightest
irritation gives rise to the fullest reflex movements, convulsive
twitching, and the like, in grotesque contrast with the absolute
motor paralysis.
The paralysis of the bladder and rectum is often delayed, but
if there is any considerable compression, it is sure to occur; the
symptoms are the well-known ones of involuntary discharge.
As the disease progresses, the muscles, at first quite lax, be-
come by degrees tense and rigid, and are attacked by twitchings,
or transient tonic spasms; contractures appear, at first tempo-
rary, afterwards permanent; the lower extremities continue in
a permanent position of extension, which afterwards gives place
to flexion. At the same time there is an additional increase of
reflex action ; the tendinous reflexions especially gain in inten-
sity, every slight dorsal flexion of the foot produces the most
active clonic movement of both lower extremities, often a con-
380 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
vulsive tremor, etc. The nutrition of the muscles may remain
intact for a time, or they may emaciate.
At this point the cases divide ; those of a ih severe sort
remain for a long time of about the same severity ; slight im-
provement gradually appears; the anesthesia is the first to
diminish ; the functions of the bladder are better regulated ; the
power over a few movements returns, increases by degrees; in
short, the improvement may go on step by step to full recovery.
In severe cases, however, the symptoms become worse; the
paraplegia remains complete; bed-sores appear on various
places, cystitis, fever, general marasmus follow, and amid inde-
scribable sufferings the patient sinks into his grave.
Let us now analyze the symptoms, and attempt to refer them
to the existent anatomical desions.
The most constant and most important of the prodadaal
symptoms is without doubt that of pain. It has a great deal
that is characteristic ; it is confined to very distinctly marked
nerve-root districts, being in the beginning often localized in a
line or a point ; it is neuralgiform, lancinating, and often (in con-
nection with marked neuritis) rather of a burning character. It
is very distinct in carcinoma of the vertebrae, where it occurs in
severe paroxysms, especially by night, is soon beyond the con-
trol of narcotics, and gives the patient fearful torments. A vari-
ety of eruptions of the skin often appear in the district of the
cutaneous pain.
Without doubt these pains should be referred to the movin
ical irritation, and most especially to the consequent neuritis of
the sensory roots; this irritation is brought about by the in-
crease of the compression, the sinking together of the ik i
and the narrowing of the intervertebral foramina.
As all these matters may differ in each case, it is readily seen
that the degree and extent, intensity, character, and commence-
ment of the pain may differ greatly in individual cases. We
refrain from entering further into the details.
It is without doubt to the same cause—mechanical and inflam-
matory irritation of the sensory roots—that the hy pereesthesia is
due which we observe in many cases, found usually in the parts
where the pain is distributed, and varying greatly in character.
SLOW. COMPRESSION OF THE CORD. 331
A further lesion of the roots is indicated by the anesthesia
occurring in their district of distribution, which may assume the
form of a zone, or be restricted to certain cutaneous nerves, or to
quite isolated spots of skin, according to the number of fibres
compressed.
The symptoms of motor irritation and paralysis in the initial
stage are referable to quite analogous states of the anterior roots.
Tremor, spasms, cramps, permanent uniform painless contrac-
tures occur here, and alternate with paresis or paralysis of cer-
tain muscles and groups of muscles, or coexist with them. The
location of these disturbances varies according to the seat of
lesion ; they will be noticed at an early period if the compression
acts upon the roots passing off from the cervical or lumbar swell-
ing, because in that case considerable disturbances at once ap-
pear in the extremities.
The fact that the motor and the sensory disturbances are
referable to nerve-roots occupying nearly the same level in the
cord is one which has been observed in many spinal diseases, but
is especially distinct in this.
If the compression and neuritis of the anterior roots becomes
severe, the now complete paralysis of the corresponding muscles
is followed by progressive atrophy, and with the atrophy there
is very closely associated a corresponding diminution and loss
of faradic excitability, which, as will be seen upon closer exami-
nation, is only a portion of the reaction of degeneration.
It hardly need be said that in these paralyses from pressure
on the roots the reflex actions are always extinguished, and that
this circumstance is not without value in the diagnosis. |
In the second stage the symptoms of motor paralysis are the
first and the most prominent. In fact, paraplegia is often
enough the first symptom that indicates the severity of the dis-
ease. It may develop with more or less rapidity ; a few hours
or days are often sufficient, but usually weeks are required ; the
patient feels his legs growing heavier, he drags them in walking ;
the toes catch at the least obstacle ; his knees double under him,
and so walking and standing become impossible ; at last there is
a complete loss of all movement, even in the lying posture. The
muscles remain perfectly lax, soft, and non-resistant under pas-
832 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
sive movement. Their electrical reaction is unchanged; their
nutrition is at first quite unimpaired.
All this is perfectly intelligible when referred to the gradually
increasing compression of the cord, with its accompanying mye-
litis; the slight initial symptoms of weakness may without hesi-
tation be referred to compression, while a more rapid increase of
paresis, a relatively rapid development of paralysis, is undoubt-
edly due to myelitis. At a later date, of course, the proportion
of the influence of the two elements upon the origin of the com-
plete paralysis cannot easily be estimated. As the disease is
always circumscript at the beginning, the nutrition and electric —
reaction of those muscles whose nerves originate in the inferior
(intact) portion of the cord will remain perfect until a descending
affection of the gray substance threatens their functions.
As in most cases the compression takes place from the front
of the cord (Pott’s disease), it is readily seen that the motor dis- _
turbances will be the first to appear, and will for a long time
outweigh the sensory. |
In a minority of the cases, the compression is limited to one-
half of the cord, leaving the other more or less intact. The
paralysis then takes the form of spinal hemiplegia or hemipara-
plegia ; if the compression of the affected half is pretty complete,
it may be associated with a crossed anesthesia, and give rise to
the characteristic unilateral lesion (see below, No. 14). Usually,
however, after a longer or shorter time, the myelitis will extend
over the entire transverse section, and complete the paraplegia.
The paralysis not infrequently begins in the form of a cervical
paraplegia, z. e., the upper extremities are first and completely
palsied, while the lower are nearly or wholly free at first. This
condition may be due to the fact that the lesion occupies the
level of the cervical enlargement, and in this place first attacks
the anterior roots for the upper extremities; in this form of
palsy, muscular atrophy and absence of reflex actions form a
characteristic feature. Or, if the lesion is situated in the upper
part of the cervical cord, it may happen that the motor paths in
the antero-lateral columns which belong to the upper extremity
are at first exclusively attacked by the compression, and those
for the lower extremities at a later period. This might perhaps
SLOW COMPRESSION OF THE CORD. 333
be explained by supposing the former to lie nearer the surface of
the cord than the latter, and thus to be sooner affected by pres-
sure and myelitis. In this case the reflex actions are retained in
the upper extremities also.
Finally, in a few rare cases, a so-called recurrent paralysis
has been observed, that is, an upward extension of the paral-
ysis above the point of compression; eé. g., in compression of
the dorsal region, extension to the upper extremities. This is
explained by the ascending myelitis, which often occurs, and in
some cases by the very rare occurrence of ascending degeneration
of the lateral columns, which may extend to the cervical enlarge-
ment (Michaud).
The sensory disturbances are not usually so marked as the
motor, at least in the beginning. The development of paraplegic
symptoms is often preceded for a varying period by paresthesia
(tingling, formication, burning, etc.), which may cover the whole
body, and often continue without a break, or recur during the
later course of the disease. They are sometimes due to compres-
sion of the posterior columns, and sometimes are signs of com-
mencing myelitis in the posterior columns and the gray substance.
The same cause may be assigned for the pains, which often
appear during the later course of the disease ; these have not the
lancinating, neuralgiform character, but are rather an intense, dif-
fuse sense of pain, burning, boring, pressure, etc., extending over
the whole of the lower extremities. I have repeatedly observed
them in the paraplegia of vertebral caries, and Michaud ascribes
them to the myelitic irritation of the gray substance.
Charcot describes also an abnormal irradiation of pain and
pareesthesia, a peculiar dysesthesia, which is produced by vari-
ous sensory irritations; it is a singular painful vibrating feeling
in the lower half of the body, the same for all sensory impres-
sions; this sensation must also be referred to the disease of the
gray substance. |
Symptoms of anesthesia are most constant, though they may
vary greatly in amount; the anesthesia is usually incomplete,
and not rarely presents a certain contrast to the severity of the
motor paralysis; Courjon states that the sensibility is never
quite destroyed in vertebral caries, though this certainly occurs
834 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
‘in other forms of paralysis from compression. <A retardation of
sensory conduction is also often observed. All these symptoms
are very simply explained by the different degrees of compres-
sion and of myelitis, by the eresier or less implication of the
gray substance, etc. |
There is very little said of vaso-motor paralysis in the omnia
reports of cases; only Hawkins states that he has observed a
constant elevation of the temperature of the paralyzed half of the
body in a case of compression of the dorsal medulla. It is con-
ceivable that the slow progress of the interruption of conduction
in the cord may give the vaso-motor centres, situated in the lum- -
bar region, time to develop sufficient activity to avoid serious
-vaso-motor disturbances.
Paralysis of the bladder is usually a subordinate feature of
compression-myelitis, especially when seated above the lumbar
enlargement; it then seldom appears early or in a severe form.
‘This depends on the seat and severity of the lesion, the integrity
of the centres in the cord, etc. ; all shades of severity may be
observed. The severest cases are those which accompany a pres-
sure-myelitis of the lumbar medulla. The same is true of paral-
ysis of the rectum.
The condition of the reflex functions is especially ‘atresia "7
an exaggeration of their activity is one of the most constant
symptoms of pressure-myelitis, provided that the portions of
gray substance which preside over the reflex actions are not dis-
eased.
The first thing which attracts notice is the increase in the
cutaneous reflex actions, the lightest touch upon the skin pro-
vokes a vigorous reflex jerk; if the skin is pressed or pinched
more strongly, active and powerful movements of the entire
extremity are made, which often extend to the other inferior
extremity, or, in their severest form, terminate in a convulsive
twitching and shaking of the limbs, which may continue some
time. | |
The reflex actions originating in other parts are also: in-
creased ; every evacuation of the bladder or the rectum, the
introduction of a catheter, etc., is accompanied by active, often
painful, jerkings of the limbs. Irritation of the skin of the inner
SLOW COMPRESSION OF THE CORD. 300
surface of the thigh, or of the urethra, has been seen to produce
reflex erection of the penis.
The tendinous reflexions, however, are most markedly devel-
oped in such cases, and it is in myelitis from pressure that they
‘are to be best studied. The lightest tapping of the patellar ten-
‘don or the tendo Achillis, the tibialis posticus, the tendons of
the flexors of the knee, gives rise to reflex actions; the same is
often accomplished from the periosteum of the bones and from
various fasciz ; powerful pressure of the patella downwards pro-
duces reflex clonus in the quadriceps ; the slightest dorsal flexion
of the foot produces that clonic tremor of the lower leg, which in
its highest degree extends to the whole leg, and then to the
other leg, and terminates with an intense tremor of both legs,
lasting some time.
Nothnagel has recently stated that all these reflex actions
may, in favorable cases, be inhibited and arrested by a powerful
pressure upon one of the great nerve-trunks of the lower extrem-
ities.
It can hardly be doubted that this increase of reflex activity
must be referred to two circumstances: first, interruption of the
conduction to the brain, which interferes with the function of the
fibres for inhibition of reflex action; and secondly, hyperemia
and inflammatory stimulation of the gray substance. It is not
at present possible to determine the part taken by each of these
circumstances in increasing the reflex action.
It is interesting that a reflex action originating in a tendon,
the centre for which is situated in the compressed region, may
become extinct, and may afterwards reappear when the motility
has returned and the pressure-myelitis is cured.
I have observed this in a case of kyphosis of the lumbar region, in which the
upper part of the lumbar enlargement was evidently compressed. As long as the
paraplegia continued, the tendinous reflexions from the ligamentum patelle and
the adductor tendons were completely extinct, while in the whole sciatic region
they were considerably increased. After four months the paralysis disappeared,
when the reflex actions from the ligamentum patelle and the adductor tendons re-
appeared.
‘Another step in the disease of the cord is indicated by rigid-
ity of the muscles. .We have seen that at first they are com-
336 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
pletely relaxed. In a few days, however, or more usually in a
few weeks, or still later, the muscles begin to be attacked by
twitchings and slight spasms; they assume a condition of ten-
sion, oppose to passive movement a gradually increasing oppo-
sition, and at last contractures appear, at first transient, then
permanent, which affect the disease in a characteristic way.
Usually these are at first contractions in extension ; the legs lie:
stretched stiff and straight side by side, the feet in the position
of varo-equinus, the knees stiff and pressed together. Ata later
period, especially in vertebral caries, contractures in flexion al-
ways occur; the hip and knee-joints are strongly bent, the knees
drawn up, the heels to the buttocks, the legs often crossed and
locked. At first the contractures are comparatively easy to
reduce, but return whenever the traction is taken away ; after-
wards they resist all external force.
It appears quite certain that these motor symptoms are refer-
able to disease of the lateral columns, that they belong to the
descending degeneration and sclerosis of the postero-lateral col-
umns. They seem to be more marked in myelitis from pressure
than in most other forms of the disease.
Trophic disturbances are not very prominent in myelitis from
pressure, as long as certain sections of gray substance (in the
cervical and lumbar medulla) are not directly affected. The
nutrition of the muscles then remains intact a long time, and so
does their electrical reaction ; at the most we observe emaciation,
caused by want of activity and by the general depression of the
nutritive processes.
The case is otherwise when the lumbar or cervical enlargement
is affected, or when the secondary myelitis of the gray substance
extends upwards or downwards to those parts ; the consequences,
then, are rapid and great emaciation of the muscles, loss of
faradic excitability, and the appearance of the reaction of de-
generation.
In a few cases, affections of the joints and skin have been
caused by pressure-myelitis.
Bed-sores are usually confined to the severer cases. The same
is true of cystitis and other consequences of retention of urine.
After this review of the chief symptoms, we have to say a few
SLOW COMPRESSION OF THE CORD. 337
words of the variation in symptoms which is due to the differ-
ent seat of the compressive lesion.
The case is most complicated when the lesion occupies the
cervical part of the cord. And here, again, we can form two
subdivisions, according as the cervical enlargement, or the part
of the cord above it, is the seat of compression.
In the latter case (compression of the upper part of the cervi-
cal cord), the disease not rarely begins with pain in the occiput,
stiffness of the whole neck, obliquity of the head, inability to
nod and turn the head, and so forth. The paralysis often begins
and continues in the upper extremities (paraplegia cervicalis),
while the lower are wholly or comparatively free. At a later
time there is palsy of all four extremities. The reflex actions are
retained in the upper extremities. Other symptoms, however,
now appear, which are quite characteristic of this seat of lesion,
and are due to implication of the nerve-paths there situated.
Such are: oculo-pupillary symptoms, either paralytic myosis
(from paralysis of the corresponding paths in the cervical me-
dulla), or spastic mydriasis (from irritation of the corresponding
paths), either unilateral or bilateral; respiratory disturbance,
from implication of the respiratory paths ; gastric disturbances,
repeated vomiting, difficulty of swallowing, continued hiccup,
to be explained by implication of the vagus, spinal-accessory,
and phrenic. In many cases a striking and permanent retarda-
tion of the pulse has also been observed, down to 48-20 beats in
the minute, accompanied by fainting-fits with complete cessation
of pulse; these symptoms have been referred to irritation of the
vagus (Charcot, M. Rosenthal); and finally, epileptic attacks
have often been seen when the compression was situated at this
point.
If the cervical enlargement is compressed, the initial symp-
toms of pain, anesthesia, spasm, palsy, atrophy, are localized
in the upper extremities ; these are also the first to be affected,
and the lower extremities follow later. The absence of reflex
phenomena, and the atrophy which soon invades the upper ex-
tremities (see above, description of Pachymeningitis Cervicalis
Hypertrophica, p. 221 et seq.), constityte decisive proof that this
is the seat of disease. In this form, also, one or several of the
VOL. XIII.—22
338 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
above-named symptoms may appear (changes in the pupils, dis-
turbances of respiration, retarded pulse, etc.), and complete the
picture of the disorder.
The portion most frequently the seat of compression is the
dorsal region. The symptoms are very characteristic: girdle-
pains, intercostal neuralgia at various levels of the trunk, para-—
plegia up to the corresponding level, reflex actions in the lower
extremities retained and increased, nutrition of the muscles and
their electrical excitability intact, etc.
If the Zwmbar region is affected, the paralysis is confined to
the lower extremities, the bladder, and rectum ; the initial symp-
toms are localized in the lower extremities; reflex actions are
absent, the muscles are permanently relaxed, are mostly atro-
phic, exhibit the reaction of degeneration, etc. The paralysis
of the bladder and rectum is complete, and severe at an early
period.
It scarcely need be mentioned, that the diagnosis of the loca-
tion may be sustained and confirmed by various symptoms con-
nected with the vertebree—kyphosis, swelling, painfulness, etc.
If only one lateral half of the cord is compressed, the charac-
teristic symptoms of Brown-Séquard’s unilateral lesion appear:
motor paralysis and hypereesthesia, and increased temperature
on the side of the lesion, bounded above by a zone of anesthesia,
while on the opposite side of the body there is (crossed) anzes-
thesia. (See below, No. 14.)
Course, Duration, Termination.—All depends on the nature
of the primal lesion. In meningeal and intra-medullary tumors
(see the section on these) the disease almost always goes on with-
out stopping to its termination ; death comes sooner or later,
after months or years, and always amid the painful accompani-
ments of severe spinal paralysis—bed-sores, cystitis, fever, ma-
rasmus, etc.
The same is true in cases where vertebral carcinoma or other
malignant tumors are the cause of compression, except tliat in
these the fatal result is usually much more speedy.
But it is otherwise in vertebral caries, which is by far the
most common cause of spinal compression. In most of these,
the course is comparatively favorable. A good many perish by
= ,' % a An, 7). a
wre *
Ee
SLOW COMPRESSION OF THE CORD. 339
the ordinary process of severe paraplegia, bed-sores, pyzemic
fever, etc.; but the disease usually runs on more slowly to its
end, with remissions and exacerbations, often after an apparent
cure, if the vertebral disease is lit up afresh by an accident, a
surgical injury, a severe cold, etc.
In more favorable cases, the paraplegia remains unchanged
and uniform for a considerable time (two, five, to ten months,
one to three years) ; bed-sores do not appear, or, if they do, are
healed. Finally, a slow improvement begins; a few movements
can at times (for example, when in the bath) be executed by the
paralyzed parts; then they are resumed permanently, grow
stronger, the contractures disappear, sensibility improves, the
function of the bladder is again controlled by the will, the excess.
of reflex action diminishes. The patient then succeeds in stand-
ing, and by degrees learns to walk, at first with crutches, then
with a stick, and then without help. Thus he may be completely
restored ; but a number of months is always required for the pur-
pose. Such kyphosis as is present may remain without any
change ; evidently nothing has occurred but a diminution of the
exudation in the spinal canal, by which a resumption of use, and
repair of structure, has been rendered possible.
The result is not always so completely favorable. Restora-
tion may remain imperfect ; partial paralyses and contractures,
local atrophy and anzesthesia, weakness and clumsiness in the
use of the limbs, remain. Such persons are always in danger of
a relapse, and any external injury may arouse the sleeping dis-
ease.
Diagnosis.
The entire group of symptoms, their beginning and succession,
usually enable us to decide with ease that a slow compression of
the cord exists. Of characteristic importance are the initial root-
symptoms, which give warnings for a long time previous; and
afterwards, the more or less rapid occurrence of paraplegia with
increased reflex action, with muscles at first entirely lax, after-
wards more rigid, etc.
The only point which usually pieacnts difficulties is that of
840 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the cause of the compression. In many cases it will be quite im-
possible to ascertain the cause, as in small exostoses of the ver-
tebree, in meningeal tumors, etc.
In the ordinary cases, the points of diagnosis will be furnished
by the external circumstances, those belonging to the primary
disease as such, although these will not always insure a correct
decision. We will give some instances.
Pott’ s disease usually presents the symptoms in their typical
form, and the actual cause of them cannot be ascertained unless
other symptoms, especially characteristic of spondylitis, are
present—the gradual formation of kyphosis, especially if angu-
lar ; painfulness of movements of spine; great tenderness of spi-
nous processes when touched ; severe pain when the electrodes of
a galvanic current are placed close to the diseased vertebra (M.
Rosenthal) ; abscesses of congestion; youth on the part of the
patient, especially if he be scrofulous; in older persons, a pre-
vious traumatic lesion, etc.
In vertebral carcinoma, the violence of the initial pains is
usually regarded as characteristic, but there are so many excep-
tions to the rule that this circumstance ought to be allowed, at
most, only to establish a suspicion. The girdle-pains and other
pains of excentric origin are often of fearful violence, and occur
in paroxysms, especially by night. Great hyperesthesia usually
exists in the painful region, together with all other possible root-
symptoms. The localization of the pain in the back close to the
vertebral column is said to be characteristic (Gull). If, in addi-
tion, there exist a local pain in the vertebree, progressive, round
curvature of the column, symptoms of compression of the cord,
an external prominence and general cachexia, the diagnosis be-
comes plainer, and the more so if a primary cancer can be shown
anywhere else (as, for instance, in the breast)—the search for
which should be a first duty. Yet it is possible to confound this
affection, in its first stages, with almost any other one which com-
presses the roots. |
In respect to meningeal tumors we have mentioned the most
important points above (p. 262 et seq.); they are usually charac-
terized by slow development, and also, to some extent, by the
absence of every symptom of vertebral disease.
ee ad —
——— ae. se
a ee er eee
SLOW COMPRESSION OF THE CORD. 341
In regard to the intra-medullary tumors we shall speak more
in detail farther on (see No. 18). It is doubtless extremely hard, in
most cases, to distinguish them from cases of circumscript trans-
verse myelitis of spontaneous origin. We merely remark here
that the initial symptoms of irritation of the roots are usually
absent, and that they open with symptoms of pea moeeran and
myelitis caused by pressure.
The diagnosis of the rarer causes of compression of the cord—
gout of the vertebrae, exostoses, syphilitic new formations, aneu-
risms, etc.—is made from the signs which are applicable to these
diseases, though their uncertainty is well known.
Prognosis.
This follows easily from what we have stated, and depends in
the first instance upon the fundamental disease. Carcinoma of
the vertebree, tumors of the meninges, exostoses, etc., are never
recovered from. If they lead to compression of the cord, the
prognosis is very bad, or absolutely fatal, and the most that can
be hoped for is some modification of the duration of the disease,
depending on the original cause and the greater or less rapidity
of its progress. j
Cases due to compression by syphilitic formations, perimenin-
geal exudations, and vertebral caries, are curable. The question
whether restitution and repair of myelitis from compression is
possible must be answered decidedly in the affirmative. Wher-
ever the cause of compression is capable of removal, the cure of
the paraplegia may be expected.
This seems to be far from. uncommon in Pott’s disease.
Among six cases of paraplegia from vertebral disease which have
come under my observation in the past year, five, including two
adults, have been cured or decidedly improved, and only one has
terminated fatally. A similar result is reported by a great
many (Leudet, Charcot, Courjon, and others). Accordingly,
the prognosis of such paraplegias is to be stated as compara-
tively favorable, with a certain reservation. A good recovery
may be especially looked for in ygung, pretty well-nourished
persons, in whom the disease of the bone has not assumed con-
842 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
siderable dimensions, or led to large abscesses of congestion, and
who also are not very scrofulous. Complete recovery, with the
exception of the permanent deformity of the spinal column,
seems to be a possible thing. In many cases, however, we must
be content with an imperfect recovery.
Treatment.
Little can be said of this. In cases of severe lesion (carci-
noma, exostosis, meningeal tumor, etc.) there is simply nothing
to do, and we must be content with a symptomatic treatment for
the relief of pain and other discomforts, and for prolonging the
patient’s life as much as possible.
The only object which repays treatment is formed by the
cases of spondylarthrocace ; a steady persistence in the use of
rational means will often lead the disease to a more favorable
course and gradual recovery. It is not our object here to enter
into details regarding the treatment of vertebral caries, but only
to cast a passing glance upon it.
First of all, the spine should be kept in repose as nearly as
possible, for which purpose rest in bed for months on the face or
back is necessary. Apparatus for support or protection of the
spine may be very useful in cases where movement is unavoida-
ble, or is required for other reasons, or, finally, when the im-
provement has made a certain degree of progress, and the spine
requires still further care. The physician must be earnestly
warned of the danger of those mechanical manipulations which
are so often employed by ignorant orthopedists and bandagers
for straightening the spine and relieving the curvature. It is
quite certain that kyphosis is not usually the cause of para-
plegia.
In general, a tonic treatment is to be reeoommended—good,
abundant diet, such as is specially suited to scrofulous patients,
fresh air, iron, quinia, cod-liver oil. Jor the disease of the bone
itself, preparations of iodine are much in favor ; iodide of potas-
sium, or still better, iodide of iron, and externally, painting with
tincture of iodine, or friction with strong iodine ointment. In
a yy —— TT ’ «
SLOW COMPRESSION OF THE CORD. 343
proper cases, leeches or cups may be applied to the spine.
Derivatives, vesicants, moxze are great favorites. The white-hot
iron has lately been repeatedly advised as peculiarly efficacious
in Pott’s disease (by Charcot, and others). Every two weeks, on
each side of the curvature, from two to four eschars are to be
made of the size of a half-mark piece (sixpence sterling), and
passing through the entire skin. Strikingly good results have
been observed from this treatment even in late stages of the dis-
ease. Brine-baths or warm sea-baths may support this treatment
in many cases.
For the myelitis from pressure little can be done until the
cause of compression is removed. In the cases, which have been
before described, where the cause is not removable, we had
better not undertake any treatment for the relief of myelitis.
In vertebral caries, also, we should do best to put off this
branch of the treatment until the compression begins to dimin-
ish; but inasmuch as this point cannot be defined, and as the
hope of doing good is likely to influence us at an early date, we
shall usually find ourselves justified in employing the customary
remedies for the relief of chronic and subacute myelitis (cf. be-
low, Treatment of Myelitis). These include local bloodletting,
derivatives, frictions with mercurial ointment, the exhibition of
iodide of potassium, pencilling with iodine, etc.
When the process of regeneration has begun, there are various
remedies which may possibly hasten it, as the continued use of
nitrate of silver, iodide of potassium, iodide of iron, quinia, |
strychnia (used with the utmost caution), moderate hydropathic
measures, and most especially the galvanic current. Ollivier (p.
481) gives a case, in which galvano-puncture was apparently fol-
lowed by good results. I have acquired the impression from
my own experience that a moderately strong galvanic current,
applied in the stabile way to the point of lesion, decidedly favors
the restoration of the spinal functions. I place the poles upon
the spine, one above, the other below the seat of disease, and
pass a weak current, at first in one direction and then in the
other, for two or three minutes in all, once a day. I have never
seen this do harm. Patience and perseverance are of course
required for this.
344 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The symptomatic treatment of the chief special symptoms
(pain, spasm, atrophy, bed-sore, cachexy, cystitis, etc.) is gov-
erned by general rules.
When a cure is effected, the patient should be strictly warned
against fresh injuries, which might bring on a relapse of his com-
plaint.
6. Concussion of the Spinal Cord—Commotio Medulle Spi-
nalis.
Abercrombie, Diseases of the Brain and Spinal Cord. German tr. by G. v. d.
Busch. 1829. p. 520.— Ollivier, L. c. I. p. 488.—Leyden, L. c. II. p. 92.—Holmes,
System of Surgery. Vol. II. p. 238.—Clemens, Die Erschiitterung des R.-M. und
deren Behandlung durch Elektricitiét. Deutsche Klinik. 1863-65.—Lidell, On
Injuries of the Spine, including Concussion of Spinal Cord. American Journ.
of Med. Sci. Oct. 1864.—Hrichsen, On Railway and other Injuries of the Ner-
vous System. Germantr. by Kelp. Oldenburg, 1868.— Webber, Recovery after
Four Years’ Paralysis, following Railway Injury. Boston Med. and Surg. Journ.
July 18, 1872.—Morgan, Injuries of the Spine, Result of Railway Concussion.
Med. Press and Circular. Jan. 1873.—Scholz, Ueber Riickenmarkslihmung und
deren Behandlung durch Cudowa. 1872. p. 76.—Hrichsen, On Concussion of
the Spine, Nervous Shock, and other Obscure Injuries of the Nervous System.
London, 1875.
Introduction and Definition.—Under the term, ‘‘ Concussion
of the Spine,’’ we include those cases in which energetic trau-
matic influences (falls, blows, collision, etc.) have given rise to
severe disturbances of the function of the cord, without any
' considerable visible anatomical changes in the latter. Slight
changes, small capillary extravasations, etc., probably exist in
such cases, but they do not seem to constitute the proper es-
sence of the disease; for the most part, the anatomical change
is quite negative, and we do not yet know what changes, if any,
constitute the basis of the concussion proper.
In the preceding chapters we have considered cases in which
Severe traumatic injuries have given rise to coarse anatomical
lesions—hemorrhages, crushing, hemorrhagic softening of the
cord, etc. We have now to deal with cases in which this does
not occur, and yet there are severe spinal symptoms. Whether
these two classes of cases are different only in degree, and may
eS —— -
=
CONCUSSION OF THE CORD. 345
gradually run into one another, we will not try to decide ; but it
does not seem very probable to us. Werather incline to the
view that the concussion of the cord is a very peculiar kind of
disturbance, and that more or less of it is usually present in
those severer lesions, but concealed to some extent by the symp-
toms. We may here assume a similar relation to that which
exists between concussion and contusion of the brain ; the for-
mer being a condition unaccompanied by any certain and con-
stant anatomical changes, and the latter involving crushing and
destruction of brain-tissue. 7
We may here include with safety the conditions which have
been named shock of the spinal cord.
The diagnosis is in many cases so uncertain, and the want of
satisfactory evidence from autopsies so great, that the history of
the disease is still surrounded by darkness. We shall, there-
fore, be as brief as possible, consistently with the great practical
importance of the subject.
Etiology and Pathogenesis,
The most usual cause consists of a fall of moderate height
upon the feet, buttocks, back, and less frequently on both arms
outstretched and stiff. I have observed the symptoms in two
ladies, produced by a fall on the ice and on a polished floor; a
fall on the buttocks caused by slipping down stairs is often men-
tioned as a cause.
A blow from a heavy body in motion, striking the spine or
trunk, acts in quite the same way.
A sudden shock to the whole body produced by the sudden
cessation of a rapid motion—as occurs in a collision between
vehicles—is a common cause of concussion ; of late years railway
accidents have played a very prominent part in such injuries,
the rapidity of their movement essentially increasing the force of
the shock. They sometimes seem to produce quite special forms
of concussion, and have been carefully studied, especially in
England, where the suits for damages against the railway cor-
porations have given them a very great practical importance.
The action of any of these mechanical causes may be limited
3846 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
more or less to a portion of the cord, when the spinal column
has been directly struck; but it may extend to a great part
or the whole of the cord, if the shock has been indirect, or has
affected the entire system at once. Severe symptoms do not
always follow directly upon the accident ; they are often delayed
for weeks or months, and may not appear until some other in-
jury has been received. We must then assume that the shock
has only produced a certain tendency to disease of the cord.
All these mechanical causes may produce a more or less con-
siderable lesion of the soft parts or the spinal column; which is
quite a matter of accident.
Besides the mechanical causes, there are others capable of
producing symptoms very like those of concussion of the cord,
which we will not omit.
Clemens speaks of excessive coitus, conjoined with unusual
excitement, or suddenly interrupted, or practised in the upright
posture, as a not infrequent cause of a certain sort of concussion
of the cord, said to be indicated by sudden weakness, collapse
of muscular force, and subsequent severe spinal symptoms.
Violent mental excitement, especially fear or anger, is con-
sidered to play a similar part, and the paretic symptoms which
often follow such excitement are referred to the cord; but the
nature of the connection is quite obscure, and seems to us to be
effected rather by congestion or myelitis, than by a change re-
sembling concussion.
Finally, there is no doubt that a stroke of lightning often
causes a general shock, in which the spinal cord participates,
and which causes speady death. The person struck often re-
covers, but with paralysis, paraplegia, etc., for various periods
of time, for which no anatomical basis has been found. A sort
of concussion is, therefore, supposed to be experienced in such
cases by the central nervous system, and in a few cases by the
cord especially. We cannot form an exact idea of it at present.
The pathological anatomy of concussion of the cord is ex-
tremely imperfect. |
In many cases which are examined at an early period, nothing
at all is found in the cord, or at most one or two small unimport-
ant extravasations of blood. Leyden reports a case which ended
gee ep SP er or es
CONCUSSION OF THE CORD. 347
fatally in five days, in which the most careful examination dis-
closed no alteration of the cord.
In other cases anatomical changes are found, which are not
severe enough to be considered causes of death; large and small
clots, crushings, softenings of the cord in various places, etc.
In cases which terminate in death after a long time, chronic
inflammatory changes may be found ; it is supposed nowadays
that chronic meningitis and myelitis, and various forms of gray
degeneration and sclerosis, may gradually develop out of con-
cussion ; but this is not determined with sufficient precision.
It is, therefore, rather rash to entertain a decided opinion re-
garding the proper nature of concussion of the cord. It seems
to be certain that the anatomical report is a negative one. The
most common view, therefore, is that which supposes only molec-
ular changes in the finer nerve-elements to have occurred, giving
rise either to an immediate and complete functional paralysis of
the latter, or forming the commencement of further disturbances
of nutrition, which at a later time may result in degenerative
inflammation. H. Fischer’ has recently attempted to develop, in
a complete form, another view of the cause of shock and concus-
sion. He considers that which is known to surgeons as shock to
be nothing more than a traumatic reflex paralysis of the vascular
nerves ; the concussion of the brain simply a shock localized in
the brain, a traumatic reflex paralysis of the cerebral vessels.
Scholz has applied this view directly to concussion of the spine.
We cannot see that Fischer’s argument is convincing ; it is
hard to understand why, in so severe a shock, the vascular nerves
alone should be paralyzed, to the exclusion of the other nervous
elements; we rather believe that the latter are affected to at
least as great a degree. This of course shakes the foundation of
Scholz’s application of Fischer’s hypothesis to the cord.
For the present our opinion is that the molecular disturbance
is the chief element in concussion. Such anatomical changes as
may be present in individual cases are accidental and not essen-
tial adjuncts. It is perfectly evident that concussion of the cord
must very often be complicated with contusion, hemorrhage
within its substance, ete. a
1 Volkmann’s Samml, klin. Vortr. ‘Nos. 10 and 27.
348 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
A very interesting statement has been made by Erichsen '—although it is not at
present quite easy to interpret—to the effect that persons who are sleeping at the
moment of a railway accident do not, as a rule, receive a concussion of the nervous
system. ‘Those sitting with their backs to the direction from which the shock
comes, are the most severely injured. The same author draws an excellent com-
parison between the effect of a violent mechanical impression upon the cord, and
the loss of magnetism in an iron bar which is struck with a hammer.
Symptoms.
The phenomena of concussion of the cord may vary very
much ; there are many circumstances which influence it, such as
the nature and the severity of the traumatic lesion, the degree of
individual resistance, perhaps also neuropathic influences, the
external circumstances as regards the care received, and the rest
taken, with a variety of other matters.
In fully developed cases the essential point lies in the pres-
ence of a sudden, more or less complete loss of the spinal func-
tion ; if the concussion is local, this may be confined to the parts
below the point of shock ; if diffuse, it may extend to the greater
part of the body. We observe accordingly a more or less exten-
sive paralysis and anesthesia, coldness, cyanosis, weakness of the
pulse, disturbance of respiration, retention of urine, etc. In some
cases there is a gradual and imperceptible shading from slight
weakness and relaxation to the severest palsy.
After some minutes, hours, days, or even weeks, movement
and sensation return slowly ; often there is no other phenomenon
developed until recovery is complete; more often, however, a ~
sort of stage of irritation follows, to which chronic inflammatory
Spinal disease may be added; the latter may under some cir-
cumstances last a long time aia result badly.
Not every case, however, begins with severe symptoms ; there
exists a class of cases which ought, without doubt, to be included
here, which, commencing with the most trifling symptoms, after-
wards develop into a serious chronic spinal disorder.
The result is the production of a great diversity among the
individual cases of concussion of the cord. For convenience we
present here the following principal groups in outline :
1 On Concussion, etc. p. 120.
"9 ™
“on
t*
CONCUSSION OF THE CORD. 849
a. General and very severe symptoms at the instant of in-
jury. Death in a short time. Severe form of shock.
The patient, after receiving some severe injury or other, is
found completely paralyzed in all his extremities, with distinct
- anesthesia, great prostration, often, though not always, with dis-
turbance of consciousness, with involuntary evacuations. The
pulse is very small, weak and slow, the skin cool and pale, or
slightly cyanotic, the respiration disturbed, dyspnoic, etc.
In a few hours or days death occurs amid general prostra-
tion, increasing collapse, and paralysis of the respiration and
circulation. |
In this class must be included the cases of severe injury to
the cord which end fatally in a day or two without any visible
lesion (as crushing) which should necessarily involve death.
These disturbances are plainly due to a severe molecular con-
cussion of the substance of the cord, whereby its internal nutri-
tion is impaired and arrested.
b. Severe symptoms at the moment of receiving the injury.
Cure in a short time. Slight shock.
Immediately after the accident the patient is found, usually
in full possession of consciousness, complaining of severe and
general pains in his body or in the lower half of it. The lower
extremities, less commonly- the upper also, are more or less
severely paralyzed ; usually there is anesthesia also, but the
latter is not always present, and often is but slight. The blad-
der is not always paralyzed. There are no symptoms of spasm.
If such a case is seen within a moderate time after the accident,
the reflex function, especially that connected with the tendons,
may be found exaggerated, and the electrical reaction in the
paretic parts may be increased or depressed.
In a few days improvement appears ; the patient regains the
power to stand and walk, but slowly, hesitatingly, feebly, and
with tremor. The pains disappear; improvement makes rapid
progress, and in a few weeks the recovery is complete. As an
example of this form I repeat the following case in brief.
Johann Schaefer, set. 55, day-laborer, four weeks ago fell a distance of twenty
feet from a tree, landing on his feet and buttocks. He was not unconscious, but
was paralyzed immediately, and had to be carried home. The following symptoms
350 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
were there observed: violent general pains in the loins and legs. Legs quite para-
lyzed and immovable for about a week, when improvement gradually commenced,
so that the patient can now walk a couple of steps. The sensation of the legs was
always good ; no anesthesia was observed. Evacuation of the bladder always nor-
mal. Stool retained the first day, afterwards regular. The pains have disappeared
by degrees, but the legs still tremble and are stiff.
Present condition.—The patient can scarcely walk two steps, and does it slowly,
hesitatingly, dragging his feet, but without ataxia. Standing on the toes or on one
foot is very difficult. Both legs tremble when he stands. Sensibility of the lower
extremities quite normal. Cutaneous reflex functions retained. Tendinous reflex
function strikingly active. No distinct atrophy of the legs. The electrical excita-
bility of the nerves and muscles of the lower extremities is remarkably depressed,
without qualitative change. Sphincters and upper extremities quite normal. No
change in the back and vertebral column. Region of sacrum somewhat sensitive to
pressure.
The galvanic treatment (to the spinal column and legs) was wonderfully success-
ful; after a few sessions the patient was able to walk quite well, and was discharged
cured after twenty-two (daily) sessions. The electrical reaction was again almost
normal.
c. Severe synuptoms at the first ; followed by a protracted ill-
ness of some years’ duration ; recovery in most cases.
Shortly after the accident, the patient displays great weak-
ness, which rapidly increases to a paralysis of various extent,
often embracing all the extremities. With this are associated
acute pains, more or less diffuse, often chiefly located along the .
Spine, in the back of the neck, and loins. Pareesthesia occurs;
cutaneous anesthesia is not usually very marked. Retention of
urine and retardation of pulse occur. In many cases an impli-
cation of the brain is indicated by unconsciousness and vomiting
at the first ; or by an increased irritability of mind afterwards.
Slow and gradual improvement occurs; great weakness of
the extremities, slight atrophy of the muscles, acute pains and
great sensitiveness remain. The extremities are cool and livid, |
the vertebral column is painful to pressure, and often excessively
sensitive. The patient is obliged to learn to walk by slow de-
grees. After a long time—often years—a. condition which ap-
proaches recovery is attained ; but the patient always remains
irritable and sensitive, and has to guard against injury. The
following may serve as an illustration :
CONCUSSION OF THE CORD. 351
Miss X., aged twenty, in April, 1872, slipped and fell on a polished floor, com-
ing down on her seat. She immediately felt a severe pain in the back of the neck
and loins, with great weakness, but was able to go into another room. In a quarter
of an hour she vomited, the pains increased, there was severe paresis of the entire
body, so that she could not even raise her head. All efforts to move were extremely
painful, and she was excessively sensitive to light. Vertebre very sensitive to pres-
sure; numbness of hands and feet, oppression of the chest, weak and slow pulse;
such were the leading symptoms at first. Urine retained only during the first day.
In the third month she begins to be able to lift her head a short time; the feelings
of precordial distress disappear; afterwards the movements of hands and feet are
recovered. At the beginning of September the patient can walk a few steps, if
supported. Improvement very slowly progressing.
At the beginning of June, 1873, I found the patient a fresh, healthy girl in
appearance, but with very excitable nerves. In walking—for which a slight support
is required—a marked slowness and difficulty in performing the motions strikes the
observer. Her back seems weak, and vacillates in various directions. In a few
minutes she sinks upon her knees, and is forced to sit down. Standing is accom-
plished tolerably well for a considerable time. Sitting without a support for the
back is possible only for aishort time. No ataxia. Given movements are easily
executed with the legs, but without force. Arms and head quite free from symp-
toms. No difficulty with the bladder, no sense of constriction, no palpitation of
the heart. Sensibility normal everywhere; slight numbness is said to be felt occa-
sionally in the soles. Spinal column straight, easily moved. The spinous pro-
cesses of the cervical and upper dorsal vertebree, and those of the lumbar vertebre,
are very sensitive to pressure.
Galvanic treatment is carefully commenced, and is followed by a rapid and
progressive improvement. By the middle of August the patient can walk quite
securely without a stick. She then makes use of the cold-water treatment in
Switzerland, from which she returns with fresh improvement. Another five weeks’
course of galvanic treatment is also attended by good results. The patient was
fully cured in the course of the year 1874, and in 1875 was married.
ad. Very slight symptoms at the beginning ; a severe progres-
sive spinal disease develops after a longer or shorter time. Re-
sult doubtful.
At the first moment—e. g., if a railway collision—the symp-
toms are very insignificant. The patient has a sensation of hay-
ing been severely shaken, a momentary weakness, perhaps some
confusion of mind, but soon recovers, picks himself up and walks
about, dismisses apprehension from his mind, and goes on his
journey. |
On the next day, or several days later, or even after weeks
352 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
and months, more threatening symptoms set in, perhaps pre-
ceded for a considerable time by very slight and unnoticed
premonitions. A general depression of strength, sleeplessness,
slight mental indisposition, tendency to shed tears, etc., may be
noticed ; the patient cannot attend to his usual business; pains
uppear in the back and limbs, and gradually increase.
Out of these symptoms a group gradually develops, which is
very far from being identical in given cases, but which in general
presents the following as its chief features: increasing weakness
of the legs, which may reach different degrees of severity ; the
gait is uncertain, straddling, stiff, and dragging ; uncertainty in
standing, indications of disturbed co-ordination are often present.
Stiffness of the back and the general attitude. Back painful,
especially when moved ; some of the spinous processes extremely
sensitive. Girdle-sensation, paresthesia of all sorts, anzesthesia
of various degree and location, and often hypereesthesia. Weak-
ness of the bladder, diminution and loss of sexual power. Im-
paired general nutrition, pale sallow complexion, changed ex-
pression of countenance. Marked atrophy in certain muscles
and groups of muscles, often quite extensive. Disturbances of
circulation, bluish complexion, cold extremities, etc.
With these are usually conjoined symptoms which point to a
disturbance of the cerebral functions ; broken, poor sleep, timid-
ity and irritability, weakness of intelligence, impairment of
memory and of power to work, change of character, constriction
of the head, increased irritability of the senses, ete.
These are essentially the marks of a very slow meningo-my-
elitis, associated with more or less considerable disturbances of
the cerebral functions. |
The subsequent course of the disease usually fluctuates a
good deal. Periods of apparent improvement and comparative
health alternate with those of downward progress. On the
whole, a gradual loss usually occurs; a favorable result is sel-
dom seen; but cases occur in which, after a very long time, the
_ disease has considerably improved, or at least has ceased to make
progress. :
This category is largely composed of the cases which Erichsen —
has so admirably described; they-have been observed more fre-
CONCUSSION OF THE CORD. 353
quently of late, especially as a consequence of railway accidents,
and have acquired a great practical importance in connection
with the latter (railway-spine of the English), They may, how-
ever, equally well follow other severe concussions of the body,
and especially of the back. Clemens describes a similar case, in
which, after a fall from a scaffolding, atrophy and paralysis
began to appear three-quarters of a year after the accident. The
two last observations by Scholz are excellent instances of this
form of concussion. ‘There are various cases of progressive mus-
cular atrophy originating in surgical injury which might be in-
cluded here.
Diagnosis.
It isa matter of no small difficulty to establish a concussion
of the cord with certainty, since the symptoms, especially at the
beginning, possess a very close resemblance to those of slight
hemorrhages or contusions of the cord.
The entire group of concussions of the spinal cord is still ©
somewhat doubtful and undefined, and by many is only retained
in order to serve as a receptacle for certain cases which cannot
otherwise be easily interpreted. We shall make an attempt at a
stricter definition.
The distinguishing character of concussion is the fact that, in
consequence of some one of the above-mentioned causes (espe-
cially a traumatic lesion), severe disturbances of the functions
of the cord occur, while at the same time. the entire course of
events shows the absence of any severe anatomical lesion, such
as often actually follow such accidents.
The case may then take one of two forms: either (1) severe
disturbance quickly appears, most severe immediately after the
injury, and is followed in a comparatively short time by improve-
ment, disappearance of the grave symptoms, until recovery is
complete; or (2) no symptoms appear at first, or at most only
trifling ones, the functions of the cord are comparatively free,
the idea of a severe anatomical lesion of the cord seems inadmis-
sible, and yet after a longer or shorter time severe and increasing
disturbances do follow, which indicate a profound affection of
VOL. XIII.—23
854 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the cord. In both cases we shall be compelled to assume the
existence of molecular changes due to the traumatic lesion.
Either class, however, may give rise to mistakes.
Cases of the first class may be mistaken for crushing and
contusion of the cord, with hematomyelia and hzematorrhachis.
The symptoms of all these may be very much alike at the begin-
ning ; but it is not impracticable to draw the diagnosis. Concus-
sion agrees with crushing and tearing and with hematomyelia,
in the severity of its initial symptoms, its paralysis, etc. ; but its
course is much more rapid and favorable. This point is entirely |
decisive. When, therefore, an apparently severe paraplegia
comes to a favorable ending in a few days or weeks, without
bed-sores, etc., we should assume the existence of concussion.
The rapidity of recovery and the favorable termination belong to
hematorrhachis and to concussion; but the initial symptoms
are different, being usually more severe in concussion. In he-
matorrhachis the preponderant symptoms are those of pain and
spasm ; the paralysis is slighter; in concussion the opposite is
usually the case.
The hypothesis of a concussion may be favored by the follow-
ing circumstances: distribution of the paralysis over the entire
spinal region without the corresponding disturbance of respira-
tion and the rapidly fatal result which are the regular conse-
quences of crushing of the cervical region ; paleness and coolness
of the skin, small, retarded pulse, absence of dislocation or
fracture of the vertebrae, absence of pain and stiffness of the
back at the commencement, etc.
Cases of the second class are not essentially distinct from
those of myelitis or myelo-meningitis with a slow beginning,
and are to be known only by the cause—the immediate and un-
questionable connection of the symptoms with some traumatic
or similar cause. The concussion should then be regarded only
as the cause and starting-point of an organic disease.
We believe that the points of view we have taken will enable
the reader to form at least a more correct judgment and a clearer
definition in many cases of concussion of the cord. Much re-
mains to be done in this respect ; the first thing consists in col-
lecting accurate reports of cases, avoiding, more carefully than
CONCUSSION OF THE CORD. 355
has hitherto been done, the intermixture of other sorts of
lesions.
The diagnosis will have to remain very obscure in many cases ;
it will of course be the most difficult, where with the concussion
there exists at the same time some severe lesion, as crushing or
bleeding of the cord. In such cases it will often be impossible
to make an accurate diagnosis; but in many a careful sifting of
evidence will perhaps succeed in distinguishing the two classes
of injury. The diagnostic evidence will here consist in the dis-
appearance of the symptoms of concussion from a part of the
body—a reduction, as it were, of the functional disturbance to
that point where it is properly commensurate with the anatomi-
cal lesion.
Prognosis.
In the severest forms of concussion of the cord, Known as
shock, the prognosis is always very grave. The lighter cases of
this sort mostly recover; if improvement rapidly occurs, and
good care is taken of the patient, the prognosis will be quite
favorable. It is, on the whole, not very bad, when compared
with the severity of the brief initial symptoms.
At all events, cases with severe initial symptoms seem to be
the very ones which warrant a favorable prognosis as compared
with those whose development is slow (Erichsen).
But even in protracted and sluggish cases, the prognosis is not
absolutely unfavorable. If distinct myelitic or meningitic symp-
toms appear, the prognosis must be made as for these diseases ;
but even in the latter case, an attack which originates from con-
cussion in a comparatively well person admits of a more favor-
able prediction than one of spontaneous origin. But when the
improvement ceases, when after one or two years of rational treat-
ment it makes no further progress, recovery is hardly to be ex-
pected.
If there is a severe anatomical lesion along with the concus-
sion, such a lesion determines the prognosis when the danger of
shock is over. .
356 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Treatment.
According to the form assumed, the treatment must vary.
In many cases the most urgent indications are those for ¢reat-
ment of shock. We must first make a most careful examination,
must observe the pulse, the respiration, etc. A quiet and easy
place to lie, warmth to the body, covering with warm clothes,
rubbing the skin, are the first things to attend to. Then, in most
cases, stimulants must be given in full doses; we should select,
according to circumstances, wine, coffee, tea, hot spirit and water,
cognac, and the like; or such drugs as aromatic spirit of ammo-
nia, ether, musk, camphor, etc. In severe and threatening cases,
strong cutaneous irritation is indicated, large sinapisms and vesi-
cants, the faradic brush, ete. It must be decided by further ex-
periments whether the subcutaneous injections of strychnia em-
ployed by Leyden will be serviceable.
Bloodletting, formerly very popular, must always be used
with care in such cases; we may employ it in certain cases of
robust persons, of full habit of body, if their pulse is strong, the
temperature normal or increased, the spinal column decidedly
painful at one point, or if we suspect some anatomical lesion, etc.
We shall rarely have reason to use general bloodletting; the
local will usually suffice. :
In the second place, we shall have to treat symptoms of reac-
tion. Here, too, absolute rest in a suitable position is required ;
if the patient does not bear lying on the side or face, he may lie
on his back upon a couch tilted down at its foot (Erichsen).
According to the violence of the symptoms, we shall then have to
use the ordinary remedies for hypereemia of the cord, for slight
meningitis and myelitis—cold, moist or dry cups, derivation to
the skin and intestine, ergot, iodide of potassium, etc. __
A careful watching of the period of convalescence is necessary
after these symptoms have passed away. The patient must care-
fully avoid all injurious things; especially, he must strictly
abstain from bodily and mental excess of work, sexual excesses
or excitement, colds, unusual jarring of the body (as by long
drives, driving in bad roads, etc.) ; and he must be careful to get
enough sleep. Recovery can often be favored by careful friction
SPINAL IRRITATION. 357
with cold water, by moderate use of the galvanic current (ascend-
ing and stabile through the spinal column), or peripheral fara-
dization ; by the careful use of chalybeate spring-baths abound-
ing in carbonic acid (Cudowa, Schwalbach, etc.); also, by the
internal use of tonics, iron, quinia, cod-liver oil, etc. Strychnia
should not be resorted to until all the symptoms of irritation are
past. Patience is necessary, as many of these cases last a des-
perate while.
It remains to speak of the treatment of the seguela@, tedious
and often severe, which follow so many cases of concussion of
the cord. In most of these cases the treatment of chronic myelo-
meningitis will be appropriate. Quiet, and a well-ordered life,
are of the first importance, and after this we may attend to the
administration of special remedies, according to the usual princi-
ples—of which the chief will be the galvanic current, derivations
to the skin, and iodide of potassium. Erichsen praises the effi-
cacy of a combination of corrosive sublimate and quinia. The
preparations of strychnia and iron will not be called for until a
later period, when things have taken a favorable turn. The
mineral springs are of especial importance in these cases ; a pro-
per selection is difficult to make, in the present state of our
knowledge. Therme, especially the hotter ones, seem decidedly
injurious, while moderate and careful cold-water cures seem dis-
tinctly useful. Scholz praises the Cudowa springs as the chief
resource in most cases of concussion of the cord; he states the
indications somewhat thus: Cudowa is indicated in all pure, un-
complicated cases of concussion; in the later periods it is espe-
cially indicated when there are few inflammatory symptoms, even
in marked paralysis and anesthesia. Cudowa is nearly useless
for distinct meningitis.
In all circumstances, the treatment of these severe and pro-
longed cases requires great care and skill.
7. Functional Irritation of the Spinal Cord—Spinal Irrita-
tation.
Stiebel, Rust’s Magazin. XVI. p. 550. 1823.—C. Brown, On Irritation of the Spinal
Nerves. Glasg. Med. Journ. No. 2. May, 1828.—T7: Pridgin Teale, A Treatise
358 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
of Neuralgic Diseases dependent upon Irritation of the Spinal Marrow, ete. 1829,
—Hinterberger, Abhandlung iiber die Entziindung des R.-M. u.s. w. Linz,
1831.— W. and D. Griffin, Observations on Functional Affections of the Spinal
Cord, etc. London, 1834.— Ollivier, 1. c. II. p. 209. —Stilling, Physiologische und
pathol. etc., Untersuch. iiber die Spinalirritation, Leipzig, 1840.—Tuerck, Ab-
handlung iiber Spinalirritation. Wien, 1843.—G. Hirsch, Beitr. zur Erkenntniss
und Heilung der Spinalneurosen. K6nigsberg, 1843.—Hisenmann, Zur Spinal-
irritation. Neue med.-chir. Zeitung. 1844. No. 1.—A. Mayer, Ueber die Un-
zulissigkeit der Spinalirritation als besondere Krankheit. Mainz, 1849.—Die
Lehre von der sog. Spinalirritation in den letzten 10 Jahren. Archiv der Heilk.
I. 1860.—Romberg, Nervenkrankheiten. 3. Auflage Bd. I. p. 184. 1853.—
Wunderlich, Handb, der Pathologie und Therapie. 2. Aufl. III. p. 28. 1854.—
Azenfeld, Des névroses. Paris, 1863. p. 284.—Radcliffe, Reynolds’ System of
Medicine. II. p. 640. 1868.—Beard and Rockwell, A Practical Treatise on the
Uses of Electricity. p. 350. 1871.—Hammond, |. c. p.397. 1873.—Leyden, 1. c.
Il. p. 3. 1875.
Introduction and Definition.—A good deal of change has
taken place in the views entertained respecting the existence, the
pathological position and significance of the group of symptoms
which has been so well known by the term ‘‘spinal irritation”
since the time of Brown (in 1828). Sometimes greatly overrated,
its importance and frequency exaggerated beyond limit, and
used as a common term for many most heterogeneous forms of
disease in which pain of the back and sensitiveness of the verte-
bre happened to be present, spinal irritation has been considered.
one of the commonest of diseases ; while again, at the time when
pathological anatomy was made the sole judge of everything, it
was entirely denied recognition, or regarded as at most a frequent
and’ rather meaningless symptom, so that it has almost passed
from the memory of the present living generation of physicians.
No one, however, who has had much practical experience and
who understands how to observe, can have failed to see that
there is a considerable number of cases which by no means
deserve to be confounded with hysteria, as has commonly been
done ; and which, on the other hand, do not agree with the other
forms known to us, especially the ordinary spinal complaints,
while they exhibit a sufficient mutual resemblance and agree-
ment.
Such cases occur chiefly in the female sex. They are charac-
i i i ete a ee ee
SPINAL IRRITATION. 8359
terized by a great irritability of the sensory functions, with motor
weakness and debility, in which one of the most constant symp-
toms is pain in the back and great sensitiveness of many spinous
processes to pressure. In these cases the group of symptoms, as
a whole, and the general course, unite to exclude with certainty
any coarse anatomical lesion of the nervous system.
These diseases, which are distinguished by the great incon-
stancy of the symptoms, and a great variety in the localization
and the apparent nature of the case, but which possess certain
essential features in common, we will name ‘‘spinal irritation,”’
and we justify the use of the term by claiming that the disease it
represents is sufficiently characteristic in form. It must be ad-
mitted that the term is only a symptomatic one, as long as the
pathological anatomy is so completely in the dark.
We would state plainly, that the idea of spinal irritation
involves its own complete series or group of symptoms ; and that
all other known forms of disease, especially all organic diseases
' and tangible anatomical lesions, must be excluded. Thus we
throw out all those cases which have so much confused our ideas
of spinal irritation, in which the simple presence of spinal pain
and tenderness have been supposed to prove the existence of
spinal irritation. Spinal pain occurs in numberless diseases—
hysteria, intermittent fever,.many affections of the thoracic and
abdominal organs (compare Tuerck’s instructive presentation) ;
but this does not imply that spinal irritation is present in these
diseases. In hysteria, the entire series of symptoms often occurs,
and so do, not infrequently, all other possible neuroses (intercos-
tal neuralgia, migraine, spasm of the diaphragm, etc.). Never-
theless, spinal irritation does occur in an isolated form, and
deserves separate consideration. It is the duty of diagnosis to
establish in each case the independence or the secondary nature
of the disease.
We have no more right to refuse to spinal irritation the claim
to a separate existence, simply on the ground of the want of a
known basis of anatomical lesion in the cord, than we have to do
the same in acute ascending paralysis, in tetany, and many
other diseases which betray an equally imperfect knowledge of
pathological anatomy. 5
360 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
At all events, we believe that in the statement we are going
to make, we shall present forms of disease with which practition-
ers are well acquainted, and for which neither the diagnosis of
‘‘hysteria,” nor general ‘‘ nervousness,” nor any known ana-
tomical form of disease, sufficiently accounts.
Etiology.
The female sex is very much predisposed to the disease. The
number of women suffering from spinal irritation is far greater
than that of men; yet the disease occurs in men also. Youth is
also decidedly liable; very much the greater number of cases
occur between the fifteenth and the thirtieth year. Finally,
hereditary neuropathic tendency plays a very considerable part.
Among the direct causes it is usual to enumerate everything
which excites and weakens the nervous system, and depresses
its power of action. This includes strong psychical impressions,
great excitement of the feelings, fright, grief, care, unfortunate
love, violent passions, etc.; also excessive bodily exertions, severe
marches, watching by night, work by night, etc. ; in like manner,
great sexual excitement and excesses, onanism in excess, con-
tinued and frequent sexual excitement without gratification ; and
finally, bad food, imperfect formation of blood, exhausting dis-
eases, losses of blood and fluids. All these things may pro-
duce spinal irritation.
Intoxication with alcohol or opium, traumatic agencies, cold,
etc., are also named as occasional causes.
At the time when every patient with pain and tandiernel of
the spine was considered to have spinal irritation, numberless
diseases of the peripheral organs, and especially those of the
intestine and uterus, were considered as giving rise to a symp-
tomatic form of spinal irritation, as it was called. Such a thing
is now no longer spoken of. |
As we do not yet know what takes place in the cord in cases
of spinal irritation, and as the pathological anatomy of the dis-
ease does not at present exist, it is hard to form a reasonable
idea of the nature of the action of all these causes. We gladly
omit all statements regarding the pathogenesis of the disease.
SPINAL IRRITATION, 361
Symptoms.
The development is usually gradual. Slight pain and dis-
comfort in the back appear, especially between the shoulder-
blades—at first only upon unusual occasions, during excitement
or fatigue; by degrees they become more permanent and require
less and less to produce them. ‘To these are added all kinds of
excentric pains, increased nervous irritability, loss of general
power, etc., and all this increases until the disease is fully dev-
eloped.
Often, however, the development occurs quickly—in a few
days, especially when very powerful influences have some upon
predisposed persons. ,
The disease then presents the following general aspect :
The patient is oppressed by a more or less troublesome sense
of illness ; a general malaise, increased psychical irritability, has
seized upon her. In most cases she complains especially of pain
in the back, situated in various spots, but most frequently be-
tween the shoulder-blades, next in the back of the neck, less fre-
quently in the loins. It grows more severe when any movement
or exertion is made, and in the exacerbations of the disease.
An examination usually discovers at the spot mentioned a
great sensitiveness to pressure, tapping, the passage of a hot
sponge, electricity, and other irritations. This sensitiveness may
be so great that the lightest touch calls forth loud expressions of
pain, the weight of the clothes becomes intolerable, and leaning
the back against anything impossible. The skin of the affected
portions of the back is usually very hyperesthetic, but the spi-
nous processes themselves are usually very sensitive to pressure.
The degree and character of the pain differ greatly in individual
cases ; the pain is commonly described as a more or less severe
sense of aching, which often lasts a considerable time beyond the
effect of the irritation. Hammond describes, in addition, a deep-
seated pain of the back, which, he says, is produced by pressure
on vertebree which are not sensitive, by movements of the spinal
column, by standing, etc.
To this are added a crowd of other symptoms ;. but what most
troubles the patient is the pain felt in various parts of the body :
362 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
neuralgiform pains, now in the upper extremities, or the occi-
put, or face; now in the trunk or viscera, assuming the form of
various visceral neuralgiz ; again in the lower extremities, pelvic
region, bladder, or genitals; pain often of great violence and
severity, sometimes fleeting, sometimes more permanent, and
often brought back by slight causes. ,
With these pains paresthesie are often connected; tingling,
formication, a sense of burning and heat, often of cold also; but
these are less prominent. The same is true in a still greater
degree of actual anesthesia; it seems to be very seldom ob-
served.
Marked disturbances of motility are regularly observed—
above ‘all, great weariness and exhaustion upon slight efforts ;
the patient has lost all endurance in walking, can walk but a lit-
tle way, and presently not at all, on account of the intolerable
pain the act occasions. Most patients therefore find it agreeable
to lie on the back, and usually continue thus. Manual occupa-
tions, such as knitting, sewing, piano-playing, writing, etc., are
more and more restricted, and at last are quite suspended, chiefly
owing to the pain produced in the back or limbs. No real paral-
ysis usually exists ; all movements are possible, but provoke vio-
lent pains; and there is no power of endurance. The nearest
approach to palsy consists in a moderate general paresis, occur-
ring in but few cases; proper paralysis is not one of the symp-
toms of spinal irritation.
On the other hand, much is said of spasmodic symptoms;
fibrillary twitchings, spasms of some muscles, choreoid move-
ments, singultus, etc., are often observed. Even permanent con-
tractures, epileptic attacks, etc., are said (probably without
truth) to have been observed as consequences of spinal irritation.
Vaso-motor disturbances are also very frequent; most pa-
tients exhibit an abnormal irritability of the vessels, and easily
turn red or pale; most of them suffer from marked coldness of
the hands and feet, which are often of a bluish, cyanotic color.
Functional disturbances of the vegetative organs, of a great
variety of forms, are also very common; eructations, nausea,
even vomiting occur; palpitations of the heart are very frequent;
disturbances of breathing, spasmodic cough, etc., are less com-
SPINAL IRRITATION. 363
mon; while vesical spasm, increased desire to urinate, abundant
discharge of pale, clear urine, are more frequent, but actual
palsy of the bladder and rectum does not seem to occur.
Finally, a symptom, which seems quite a regular one, is that
of increased psychical irritability and depression, with more or
less sleeplessness ; there is often some dizziness, noise in the
ears, inability to read continuously, owing to the appearance of
muscz and disturbances of vision, etc. |
The physiognomy of the disease is thus seen to be very com-
plex. In fact, individual cases also differ greatly. We may try
to divide them into three classes, according as the symptoms
point to the upper, the middle, or the lower parts of the cord
as the chief seat of suffering.
If the upper portions are principally affected, the pain of the
back and spinal tenderness are chiefly localized in the cervical
vertebree. The prominent symptoms are those referred to the
head, giddiness, sleeplessness, disturbances of the senses, pains
in the occiput, and pains in the district of the brachial plexus ;
nausea, vomiting, palpitations, hiccup, etc., are not rare; motil-
ity in the upper extremities is usually impaired.
If the dorsal portion is affected, the chief symptoms in addi-
tion to those in the spine are intercostal neuralgia, gastralgia,
nausea, dyspepsia, etc.; the lower extremities usually take a
large part in the disturbances of motility and sensibility.
If the lumbar portion is chiefly affected, the leading symp-
toms are neuralgia in the lower extremities and the pelvic organs,
spasm and weakness of the bladder, cold feet, weakness of the
legs, etc. 3
A certain generalization of the disease is not uncommon,
when the spine is painful in several places, often quite gene-
rally, and the disease is complicated by all kinds of peripheral
symptoms. :
Course, duration, termination.—We have already described
the way in which the disease begins. Its cowrse is usually very
fluctuating. Improvement and relapses alternate in the most
irregular way ; the chief symptoms and the spinal tenderness are
sometimes felt in one place, sometimes in another; a relapse
often occurs without any visible ause, and so does improve-
364 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
ment; it is here that we must be most on our guard against illu-
sive successes.
Many cases run a comparatively acute course, grow rapidly
worse, and as rapidly improve and recover.
In most cases, however, the disease is extremely slow and
chronic, and its duration is stated in months and years; there
are some patients who suffer more or less from occasional attacks
all their life, and who are exposed to a relapse on the slightest
occasion.
Nevertheless, a cwre may be regarded as the rule; if proper
measures are taken and the causes avoided, this may be ex-
pected in the majority of cases. Much patience will doubtless
be required, and the many relapses may often greatly prolong
recovery.
Whether spinal irritation may in bad cases result in the de-
velopment of severe spinal diseases, does not seem to us suffi-
ciently ascertained. The observations are almost all of an elder
date, and give no sufficient guaranty against the confusion of
the first stages of severe spinal lesion with functional irritation
of the cord. This question, therefore, can only be decided by
further careful observations. The entire doctrine of spinal irrita-
tion requires a renewed revision by means of careful and criti-
cally sifted clinical observations.
Until this is done, we shall not be in a position to entertain a
better founded opinion upon the nature of spinal irritation
than we now possess. We can scarcely doubt, it is true, that
the structures within the spinal canal are the proper seat of the
disease, and the entire list of symptoms makes it most probable
that the cord itself is in a condition in which it performs its
functions badly. The assumption that the meninges are the first
to be affected, and the nerve-roots and the cord suffer second-
arily, has little support.
But we possess no direct: observations to show what sort of
changes occur in the cord. The pathological anatomy of spinal
irritation does not exist ; the few autopsies which we possess are
not always uniform, and some of them certainly do not relate to
cases of this disease. We are therefore thrown back upon
guesses and hypotheses regarding the real nature of the change
SPINAL IRRITATION. 365
in the cord in spinal irritation. Such hypotheses are numerous,
but we have not the time to spare for them. The contradictory
views that are entertained by authors are well illustrated by the
fact that Ollivier and (in part) Stilling also refer spinal irritation
to hyperemia of the cord, while Hammond affirms with the full-
est conviction that it is due to anzemia of the cord, and especially
anemia of the posterior columns, and that the ultimate cause
for it may possibly exist in the sympathetic (vaso-motor) sys-
tem; Beard and Rockwell assume at one time anemia, at an-
other hyperemia as a cause, while Hirsch and many other wri-
ters see in spinal irritation nothing but a so-called dynamic
disease, a functional disorder of the cord, without organic change
in it—an irritation which may be due to very various causes.
All these opinions may be defended and attacked with power-
ful reasons, but we need not try to sit in judgment on them, as
‘the conclusion could only be that we know nothing definitely at
present.. The most probable seems to us to be a purely func-
tional disturbance of certain nervous elements of the cord, in
company with which hyperzemia and anemia of the cord may
probably appear when the vaso-motor. paths are reached by the
disturbance; but this whole question, it seems to us, awaits a
solution.
. Diagnosis.
It will not be very hard to recognize spinal irritation when
the entire group of symptoms as above given is present; when
the pain in the back and the sensitiveness of the spine are
accompanied by many changeable excentric symptoms, motor
weakness, great psychical irritability, or marked paralysis or
anesthesia; when no organic changes exist, and a remarkable
disproportion between the intensity of the subjective symptoms
and the objective can be demonstrated ; and where, finally, great
fluctuations in the course of the disease are observed.
We ought not to try to settle the diagnosis too soon, nor
Should we acquiesce in it until, after careful examination and
estimation of all circumstances, the other possibilities have been
excluded. In doing this we shoul@ bear in mind the following:
366 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
The diagnosis from hyperemia of the cord is so difficult, that
cases were formerly often mistaken one for the other. The long
duration of the disease will furnish the most important argu-
ment in favor of spinal irritation ; in severe hypereemia, paralysis
is rarely absent. Hammond recommends as a test remedy a sub-
cutaneous injection of strychnia, which is believed to do good in
spinal irritation, and harm in hypereemia.
The distinction from meningitis spinalis will also often be
difficult. But in the latter the stiffness and painful tension of
the muscles of the back, the pain in the spine, which especially
occurs during movement, the fever, late paralyses, etc., may fur-
nish very useful diagnostic points,
_ Meningeal tumors in their first stage, among the primary
symptoms of which are found pain in the back and excentric
neuralgia, will best be known by the stability of the symptoms,
by their permanent localization in well-marked nerve-paths, and,
at a later stage, by the paralytic symptoms.
The diagnosis from myelitis will usually be made soon. In
this disease only deep pressure on the spinous processes is pain-
ful; there is no circumscribed cutaneous hyperesthesia in the
vertebral region, but there is the girdlé sensation, very early and
marked anzesthesia and palsy, vesical paralysis, often. painful
contractures and spasms, which are absent in spinal irritation.
The unfavorable termination of the disease, the absence of the
general nervous condition so common in spinal irritation, are
likewise in favor of myelitis.
The distinction from hysteria will be impossible in many cases,
as both diseases possess many similar features, and spinal irrita-
tion not rarely occurs in connection with hysteria. The specific
hysterical symptoms of globus, general spasms, definite forms of
paralysis, etc., do not belong to spinal irritation; and the pecu-
liar mental traits so characteristic of hysteria—whimsical obsti-
nacy, irritability, etc.—are also absent. A full consideration of
the circumstances in each case will often furnish some decisive
diagnostic points, while in other instances we shall have to admit
the existence of both diseases together.
From newrasthenia spinalis, which is described in the follow-
ing section, and which has an undeniable general resemblance to
SPINAL IRRITATION. 367
spinal irritation, the present disease differs by the fact that symp-
toms of sensory irritation preponderate, that extreme sensibility
of the vertebree is present, and that the disease occurs chiefly in
the female sex. (See the diagnosis of spinal nervous weakness. )
The marks which distinguish spinal irritation from vertebral
caries and other coarse lesions of the spine need not be stated
here.
Prognosis.
This is generally held to be favorable, although such is not
always the case. In all circumstances we should remember that
the disease is usually chronic, may last many months and years,
and relapses are very frequent.
Life is in no danger; but most of the patients are doomed to
a long and tedious illness, they are cut short in all their enjoy-
ments, are plagued with tormenting pains, and so forth—circum-
stances which certainly deserve mention in making a prognosis.
Treatment.
This is a difficult subject. The disturbance of nutrition in the
cord is not so easily to be removed ; and the patient is usually
irritable, changeable, weak of purpose, so that it is often very
hard to secure the necessary persistence and energy in treatment.
First of all, we must try to remove the causes. By reference
to the list already given, it will appear what is implied by this.
In the direct treatment, the chief object doubtless consists in
improvement of the nutrition and tone of. the nervous system,
especially the spinal cord. The first thing to prescribe is, there-
fore, in most cases, a general tonic regimen: good food in
abundance, a not too sparing use of spirituous drinks (the Eng-
lish recommend them in large doses, and Hammond orders stimu-
lants such as brandy and rum). As tonics, guinia and iron,
preparations of zinc, and cod-liver oil may be used. A great deal
of fresh air is indispensable to all the patients; active and pas-
sive exercise in the open air is therefore always indicated, but
this should not be overdone, as fréyquent. repose in the horizontal
868 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
posture is often necessary. When it can be had, the air of
mountains and forests is to be sought; a moderate cold-water
treatment supports these tonic measures, and will be especially
valuable when applied in a high mountain climate.
Strychnia (with other preparations of nux vomica) enjoys a
special reputation with many physicians for the cure of this
affection. It is given alone, orin suitable combination with other
medicines. Thus, Hammond advises a combination of extract of
nux vomica, half a grain (0.03), with phosphide of zinc, one- —
twelfth of a grain (0.005), given several times a day. A mixture
of iron, quinia, and nux vomica in various forms seems often
useful. |
Another important remedy is the galvanic current. Ham-
‘mond ascribes great successes to it, and I have also observed some
good results. The best plan seems to consist in passing an as-
cending stabile current through the vertebral column, including
the painful portions between the two poles. The current ought
not to be very strong, and the duration of the applications must
be short. The negative pole, acting directly on the painful ver-
tebre, has often been found to be of value. Many patients of
this class will be benefited by the methods of general faradization
and central galvanization. (See above, p. 181 et seq.)
Finally, derivatives have long enjoyed a general reputation,
The best place for application seems to be directly upon the
affected spots, the most painful parts of the spine. Many
wonderful reports are made of the successful application of blis-
ters, tartar-emetic ointment, oil of turpentine, veratrin ointment,
etc. A repeated and continued use of these remedies is, how-
ever, often necessary. In less severe cases, dry cups suffice, and
moxee or the hot iron will be resorted to very rarely.
We should be careful about drawing blood from the spine,
which was formerly so much in vogue. With most patients this
does not agree; though in some cases, when the person is very
robust and of full habit, or when there are signs of congestion, it
may be very suitable.
A symptomatic treatment is required for the pains in the
back and other neuralgiform symptoms. Hammond recom-
mends opiates especially ; the application of hot water or sand
SPINAL NERVOUS WEAKNESS. 369
along the spine may also be tried ; also bromide of potassium,
blisters, and other derivatives, faradization, galvanization etc.
For weakness, electricity is of special value.
8. Functional Weakness of the Spinal Cord.—Spinal Nervous
Weakness.—Neurasthenia Spinalis.
Beard and Rockwell, Practical Treatise on the Uses of Electricity, etc. 1871.
p. 294.—Russel, Cases of Paraplegia induced by Exhaustion of the Spinal Cord.
Medical Times. Oct. 31, 1863; May 25, 1867.—A. Bourbon, De V’influence du
coit et de l’onanisme dans la station sur la production de paraplégies. Paris,
1859.—Leyden, 1. c. IL. p. 22.—Hrb, Bericht tiber die Versammlung mittel-
rhein. Aerzte am 18, Mai, 1875, in Heidelberg. Betz’ Memorabil. 1875. 5.
Heft.
Introduction and Definition.—Every physician encounters
cases in the course of his daily practice, chiefly if not wholly
originating in the higher walks of life, which may affect either
one of the various departments of the nervous system. As a
rule, there is no anatomical basis for them; and certainly, any
severe anatomical changes seem to be excluded by the entire
nature and course of the symptoms observed. Such are the cases
which have been classed together under the name of ‘‘ nervous-
ness,’ **nervosismus,’’ ‘‘ nervous weakness,’’ etc., and are com-
monly regarded with some mistrust by physicians. Beard and
Rockwell have given a very good description of them, and have
proposed the name newrasthenia (weakness of the nerves).
It is desirable to examine these cases more closely, and form
them into classes. Careful observation quickly shows that this
nervous weakness is capable of assuming various forms, and
affecting different parts of the nervous system. In some cases
the entire nervous system is more or less affected ; in others the
brain is chiefly affected, and in others still, the functions of the
cord. It is this latter, the spinal form of neurasthenia, that we
wish to speak of.
Abundant experience has shown me that these cases are not
Tare, and are of great practical consequence. For they cause
much anxiety, not only to the patient, but also to the physician,
owing to the striking resemblance*they possess to the first stage
VOL. XIII.—24
8370 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
of severe disease of the cord. It is of course important to decide
this question as early as possible, as the prognosis of the two dis-
eases must be very unlike.
We therefore understand by spinal nervows weakness those
diseased conditions in which marked and unquestionable dis-
turbances of the functions of the cord exist, for which no consid-
erable anatomical basis can be found or assumed ; a disease,
therefore, which must at present be classed among the functional
disorders.
Whether, and how often, this condition may lead to actual
organic disease of the cord, cannot be known at present ; from my
experience I infer it to be rarely the case. The symptoms, how-
ever, are not infrequently present during the early period of ana-
tomical lesions of the cord, though probably always associated
with other disturbances, which enable us to recognize the com-
mencement of the real disease.
It cannot be denied that this complaint has a close resem-
blance in many respects to spinal irritation, the subject of the
previous section ; and the opinion might perhaps be defended,
that this disease is essentially, for the male sex, that which corre-
sponds with spinal irritation in females. Nevertheless, charac-
teristic differences will be seen as the description is given; I
believe that the two diseases, though related, cannot be regarded
as identical. It would be very desirable to lay out a better divi-
sion and classification of these spinal ‘‘neuroses’’ by means of
accurate clinical and symptomatic study, in order to promote
the pathology of such an obscure subject.
What follows professes only to be a first step in this direc-
tion. Few accounts of the disease are recorded in print; I find
an exquisite case briefly described in O. Berger;* Scholz* de-
scribes one under another name; that which Leyden describes as
** spinal irritation from loss of semen” belongs for the most part
to this class; so does much of what has been described as the
results of spermatorrhcea, etc., in regard to which see Cursch-
mann’s excellent account in Vol. VIII. of this Cyclopedia.
’ Zur Pathogenese der Hemikranie. Virch. Arch. Bd. 59. p. 385. 1874.
* Ueber Riickenmarkslihmungen und deren Behandlung in Cudowa. p. 21.
SPINAL NERVOUS WEAKNESS. 371
Etiology.
A predisposition to this affection is most common in the male
sex ; and males are attacked in much larger numbers. Youth
and middle age are also most exposed to the disease.
The chief contingent to this army of sufferers comes from
neuropathic families, in which psychoses, hysteria, and other
neuroses are well-known guests. The upper classes are also
more affected than the lower, though the latter are by no means
spared.
Finally, all the direct causes of the disease (to be named
presently) may increase the predisposition, or perhaps cause it.
Among these direct causes, I am able from experience to
name three as particularly active.
Excessive mental efforts may often produce the spinal form
of neurasthenia—such as are made in the pursuit of a profession,
or in severe mental toil, especially by night; a similar effect is
produced by grief and excitement, violent excitement of the affec-
tions and passions, gaming, etc., in predisposed persons.
A much more frequent and important cause is found in sexual
excesses ; onanism begun very young and long continued; ex-
cessive coitus. I have often seen the entire series of symptoms
develop in otherwise healthy men after very great sexual ex-
cesses, and again disappear in a few weeks under suitable ob-
servances. ‘The standard of sexual ‘‘excess”’ is of course very
varying; but, for the individuals in question, excess usually
begins with comparatively moderate performances, Excesses of
a less degree, but protracted, are often also at fault, and the
affection not rarely appears after the honeymoon. In predis-
posed individuals, frequently repeated sexual excitement without
gratification acts similarly ; and the practice of having connection
in the standing posture, mentioned by French authors, seems
not less injurious.
Excessive bodily effort seems to be a less potent cause; yet
long forced marches, mountain climbing, etc., are often men-
tioned as causes.
The injury is most distinct when several of the above causes
coexist—e. g., great mental and bodily overwork, with disturb-
872 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
ance of the nightly rest (hence, the disease is not infrequent
among physicians); or when, amid great mental exertions,
sexual excesses are indulged in, etc.
It is not yet certain whether there are other causes; but it is
probable that severe exhausting diseases, bad food, and other
circumstances which depress the powers of the nervous system,
may be active in this direction.
Symptoms.
The description of these is based almost exclusively upon the
patients’ subjective complaints. The persons affected are usually
young or middle-aged men; they complain chiefly of a set of
motor disturbances, principally consisting of a striking weak-
ness and rapid fatigue of the lower extremities. They have
constantly the sensation of great exhaustion of the legs, such as
well persons only feel after making considerable exertions of
body ; this is perceived even in bed in the morning. They are
incapable of walking or standing for a long time; a continuance
in the standing posture is especially apt to make them tired.
After more severe exertions, the great fatigue is accompanied by
occasional tremor of the legs, and such a remarkable stiffness of
the members as a well man would only feel after a very severe
march. Unaccustomed efforts, even of a very moderate degree,
are remarkably apt to produce that peculiar muscular pain, the
origin of which is so obscure.
I refer to that well-known pain in the muscles which frequently occurs in
well men after very active and unaccustomed muscular efforts, as when one rides, |
practises gymnastics, takes mountain walks, etc., after a long period of intermis-
sion. It usually appears about twenty-four hours after the exertion, is associated
with slight swelling of the muscle and sensitiveness to pressure, and is produced by
every contraction of the muscle affected. The essential nature of the pain is not
yet known. Such a pain occurs in patients of the present class, after comparatively
very slight exertions.
Similar symptoms of quick exhaustion and want of endur-
ance are observed in the arms, but much less in degree than in
the legs.
With this is associated a variety of disturbances of the sen-
SPINAL NERVOUS WEAKNESS. 373
sory organs. One of the most common is a peculiar pain in the
back, seemingly localized in the muscles of that part, and appear-
ing whenever certain movements are made, as of bending the
spinal column forward or backward, or certain movements of
the shoulder ; and often in breathing or swallowing. The pain
is not very intense, and varies greatly in its occurrence and posi-
tion, rarely remaining for any length of time in one place. It is
increased or brought on by slight exposure to cold, a draft of
air, and probably also by excesses in Baccho aut Venere.
A diffused sensation of burning in the skin of the back is
often observed, especially between the shoulder-blades ; this is
usually accompanied by sensitiveness of some of the spinous
processes, just as in spinal irritation. In other cases, pain in the
loins is observed.
In the extremities, especially the lower, this excessive feeling
of fatigue often increases to that of slight shooting and tearing
pain in the districts of certain nerves. These pains are usually
not very severe, and pass away rapidly ; they chiefly occur dur-
ing movement and after unusual exertion. Some of the muscles,
also, are not infrequently stiff and painful. In such cases there
are seldom or never any defined and violent pains of the well-
known lancinating sort (see above, p. 75-6).
Marked paresthesia is also very rarely spoken of; many
complain of a slight numbness or formication, especially in con-
nection with great cold of the feet. A medical man, or one who
knows and dreads the symptoms, is apt to speak of this.
Cold hands and feet are very commonly complained of; they
are probably due, for the most part, to vaso-motor disturbances.
The feet, in particular, are often icy cold, and can hardly be
warmed, even in bed. The feeling of burning in the feet is rare, °
and if it occurs, is associated with an actual rise of local tem-
perature.
The disturbances of the sexual functions are usually very
striking; they commonly take the form of irritable weakness ;
the power of erection and of performing the act are lessened ; the
ejaculation takes place too quickly, and a repetition is impossi-
ble. The act is usually followed by remarkable prostration,
restlessness of the limbs, and the like; or the man falls into a
—
374 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
half-slumber and a profuse perspiration, etc. All the symptoms
usually increase after the passion has been gratified, unless the
greatest moderation has been used, or even after repeated sexual
excitement. Pollutions or spermatorrhcea do not constitute a
regular feature of the disease, unless they previously existed,
and are to be considered as causes of the disease. Their oceur-
rence, however, often aggravates the trouble, and they are much
dreaded by the patient.
~The functions of the bladder are usually quite normal; in
some cases 2 little dribbling is spoken of. The sphincter ani acts
properly. Trophic disturbances of the lower extremities, and
bed-sores and the like, never occur.
With these regular and common symptoms we often find a
number of others which indicate a wide extension of the nervous
weakness. Among these we should mention sleeplessness, not
usually very troublesome, but often peculiar inform. The patient
wakes, after a few hours’ sleep, with a sense of great uneasiness
in his limbs, and cannot fall asleep for some hours after; in the
morning he feels unusually prostrated. In some cases there is a
certain sense of constriction of the head, timidity, often a re-
markably womanish disposition, a tendency to weep, etc. I have
seldom heard complaints of vertigo. The higher functions of
the brain, memory, intelligence, etc., and the organs of special
sense, remain perfectly normal. The power of mental work may
be unimpaired, but is usually weakened by the patient’s hypo- |
chondriacal depression.
The vegetative functions are unimpaired, on the whole; the
disturbances most frequently observed are those of the digestive
apparatus—dyspepsia, tendency to constipation, flatulence, etc.
There is frequent complaint of palpitations, and a sense of con-
striction.
The general sense of iliness is very great. Most patients
are hypochondriacal in their feelings, are in dread of tabes,
etc.; if a physician is the sufferer, he is apt to let his mind
dwell on this anticipation, and to be made wretched by the
thought. |
The general nutrition is usually somewhat impaired ; the pa-
tient loses some flesh, gets .a sallow look, and becomes a littlo
SPINAL NERVOUS WEAKNESS. 375
anemic. There is always great sensitiveness to cold and severe
changes of weather.
As compared with all these complaints, the objective symp-
toms—and this is a decisive point—are excessively slight, in fact,
almost wholly negative. The closest examination shows no trace
of disturbance of motility; all movements are performed easily
and securely; the finest and most complicated actions can be
executed ; the patient stands on one foot, or with closed eyes,
quite perfectly ; only the power of endurance in muscular action
is weakened,
In like manner there exists not the least disturbance of sensi-
bility. There is usually no sensitiveness of the spinous processes.
The reflex functions of the skin and tendons are usually normal.
There is no atrophy, no change of electrical reaction. The only
distinct symptom that can be found is, in many cases, a moder-
ate degree of anzemia, a changed, suffering expression. ‘
The closest objective study, therefore, discovers no change \
whatever that can stand in any relation to the patient’s subjec-/
tive complaints.
Of course, not all cases are alike, for many variations in the
character of the disease occur; various symptoms may be absent,
or may be more distinct in one case than in another; but the lead-
ing features of the disease will probably be traced in most cases.
I select from my list of recorded cases (of which I possess more than two dozen)
the following one as an example: The patient, a wholesale merchant, aged thirty-
five, belongs to a neuropathic family; two sisters were in the insane asylum; a
brother has a tendency to melancholy and nervous complaints; he himself has
been a long time “nervous.” Married at twenty-three; he has three children; he
says that he indulged a good deal in the sexual act, perhaps too much, but never
observed any ill results from it. He has often been to bathe in the ocean, with
temporary benefit. He has a great deal of work; at least eight hours a day in his
office, occasionally going into a close, damp warehouse. All the nervous symptoms
have slowly increased ; they have been about as follows for four weeks past:
Great general sense of fatigue—this is very marked in the morning in bed; ina-
bility to walk for a long time, or, if he does it, it is followed by great fatigue and
active tremor of the legs. When moderate exertion of an unwonted sort is made,
there are severe muscular pains on the following day (as lately, after skating for fif-
teen minutes). No tottering or uncertainty of gait; no vertigo. Some sense of
fatigue in the arms, uncertainty in writing.
>
376 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
No pains, no numbness or formication in legs or arms. No headache; only a
frequent sense of pressure on the vertex. Intelligence and memory good ; depressed,
hypochondriacal state of feeling. Occasional disagreeable feeling in the back, but no
real pain. Suffers much from cold feet, which formerly was never the case. Great
sensitiveness to cold; after exposure he feels slight shooting pains in the limbs.
Sleeps badly ; usually wakes about three o’clock and remains awake for two or
three hours, with great prostration and restlessness of limbs.
Vesical functions quite normal. Sexual functions distinctly altered in the last few
weeks ; sexual excitability increased, ejaculation too early, erection insufficient ;
after coitus a sense of exhaustion, with excitement and restless half-sleep.
Tendency to shed tears ; unusual timidity and want of self-possession ; noticeable
confusion when he is conscious of being observed. Frequent palpitation, and some
shortness of breath when he ascends stairs. Appetite and stools good.
Objective symptoms.—An apparently strong and well-nourished man; internal
organs all sound. Motility quite normal by objective tests. Stands with closed
eyes very well. No disturbance of sensibility. Cerebral nerves all normal. Slight
anzmia.
He was ordered quinine and iron; cold friction in the morning ; movement in
the open air; strong diet; moderation in business and sexual act; afterwards a
period of residence in a high mountain region.
Half a year later the patient returned from Switzerland and called upon me;
he was considerably improved. The strength and endurance of the legs are decid-
edly greater, and his temper is much more cheerful. He walks his four or five
hours every day and seldom suffers from tremor, still less from pain of the muscles.
He has no cold feet, and his sensitiveness to cold is less. He sleeps much better,
though not perfectly well. Sexual functions the least improved of all. Head never
troubles him. ‘Temper much improved ; he has no disposition to weep.
After another half-year the greater part of the morbid symptoms had dis-
appeared.
Course, duration, termination.—The disease usually begins in
a very gradual and insidious way, yet sometimes it happens
that it develops quite rapidly; some injury, a severe exertion,
an excess, may bring the disease to an outbreak, when in the
course of a few days or weeks it may reach a certain severity.
In such acute cases there is during the first few days a marked
and general sense of being ill, prostration, loss of appetite, ete.
The symptoms usually increase gradually for weeks and
months, and then remain more or less stationary. Great fluc-
tuations, considerable transitory improvements, are rare; but
slight fluctuations in the intensity of the symptoms are common.
If a proper treatment and regimen are then adopted, gradual
SPINAL NERVOUS WEAKNESS. 377
improvement occurs; but months and years may pass before the
last traces are removed. Intercurrent febrile affections often
seem to have a favorable influence upon the disease and to hasten
recovery. Traces of the disease may last many years. Relapses
are not uncommon, and are often occasioned by fresh injurious
exposures of a trifling nature.
Iam unable to state whether there are incurable cases, and
whether the disease may last a great many years. At all events,
cases occur of sufficient severity to compel the patient to give up
business and avoid society, and to make his existence wretched.
I am also in doubt whether the disease can pass into any
tangible chronic form of spinal disease (myelitis, sclerosis, gray
degeneration). I have not observed such an event, and have
never had to modify my diagnosis in the direction indicated.
But only continued experience can decide.
Of the essential nature of the disease, I think we are not yet
prepared to express an opinion. We are far too little acquainted
with the pathology of many morbid processes of the cord, to
allow ourselves to express a distinct opinion regarding the foun-
dation of the disease here described.
A few remarks may, however, be allowed.
A spinal difficulty may naturally and reasonably be thought
of, in connection with the symptoms described ; the simultaneous
occurrence of sensory and motor difficulties in both legs, the
vaso-motor disturbances, the pains in the back, and especially
the disturbances of the sexual function, which are most easily
explained by increased excitability and weakness of the centres
in the lumbar cord, are so strongly in favor of the spinal location
of the disease, that other possibilities (as, for example, that of an
affection of the cauda equina) sink into the shade by its side.
The hypothesis of a spinal affection certainly seems to us the
most acceptable.
Furthermore, the disease can only be a functional disorder
in the ordinary sense of the term. In favor of this we have the
absence of all objective disturbances, the absence of all paralytic
symptoms, and the usually favorable course. In such circum-
stances it is hardly possible to suppose a considerable anatomi-
cal change in the nervous or interstitial structure of the cord ;
378 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the most would be, perhaps, a disturbance of circulation, hyper-
zemia, or anzemia of the cord. The regularly accepted descrip-
tion of these forms, however, does not agree with that of neu-
rasthenia spinalis. I must admit that the hypothesis of anzemia
of the cord is very plausible. But it is impossible at present to
confirm this hypothesis in any way, and it must remain an open
question.
It seems most natural to recur to fine disturbances of nutri-
tion in the cord, such as we are still obliged to assume in so
many diseases of the nervous system. 3
The term ‘‘irritable weakness”’ (reizbare Schwache) agrees
best with this notion, and in our description the weakness is
quite prominent. We do not know at all what may be the
nature of the processes of nutrition which cause the symptoms.
We, however, believe that we are certainly entitled to locate
them in the cord, especially the lower portion, the lumbar region.
The most obvious view is that which supposes that the physio-
logical fatigue of the nervous elements, which always occurs
after severe and protracted irritation, becomes exaggerated and
assumes a fixed form. In such a case we may suppose that the
fatigue of the nervous elements does not become repaired in the
prompt manner which is usual under physiological conditions.
Diagnosis.
The decision will be based chiefly on the great disproportion
between the acute subjective complaints of the patient and the
almost negative result of objective examination. The absence of
each and every disturbance of motility and sensibility, of all
symptoms which indicate an anatomical lesion of the cord, must
give probability to the supposition of a purely functional dis-_
turbance. If in addition there exist general nervous weakness,
sleeplessness, psychical irritability, a neuropathic constitution,
and other etiological elements. (especially that of undue sexual
stimulation), the supposition then becomes much more probable.
A good deal of practical experience and accuracy in examination
is always necessary, and a long period of observation will often
be necessary before we are clear in our minds.
SPINAL NERVOUS WEAKNESS. 379
A few remarks upon the points of diagnosis in reference to
the better-known diseases of the cord will be useful here.
From a commencing tabes, which is the disease most usually
suspected, spinal neurasthenia can be distinguished with tolera-
ble ease.
The absence of lancinating pains, of pareesthesiz and disturb-
ances of sensibility, of the girdle-sensation, of tottering when the
eyes are shut or in the dark, of motor uncertainty, of ataxia,
will suffice. The study of the tendinous reflex action will per-
haps furnish an important point, if it should appear that this
reaction is absent in the early stages of tabes.
From active hyperemia of the cord we may distinguish spi-
nal neurasthenia by the absence of pain, of cutaneous hyper-
eesthesia, of symptoms of motor irritation, and probably also by
the long duration of the disease. From passive hyperemia, by
the absence of paretic symptoms, of the feeling of heaviness in
the legs, and probably also by the causes of the disease.
From incipient myelitis the diagnosis will be rendered possi-
ble by the absence of parzesthesiz and anesthesia, of paresis and
paralysis, of weakness of the bladder, ete.
The distinction from spinal irritation will often be less easy
to make. If we consider that the latter is more characterized by
symptomis of sensory irritation, that in it the dorsal pains, neu-
ralgias, sensitiveness of the_vertebre, etc., are in the foreground,
while in spinal weakness the motor disability, the sexual weak-
ness compose the chief subjects of complaint, we shall usually be
in the right way. It must be admitted that there are cases of
ambiguous signification which stand, as it were, half-way between
the two forms of disease, and possess somewhat of each.
In no case can we state the diagnosis with certainty until after
a most careful objective examination and a weighing of all cir-
cumstances, and, if possible, an opportunity for watching the
case some time.
The prognosis is very essentially influenced by these circum-
stances. It is favorable, as compared with that of organic dis-
eases of the cord, which somewhat resemble it in symptoms.
In most cases the patient recovers when the causes are re-
moved and a suitable regimen of life is observed. Much time is
380 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
required for this, and the patient must submit for months, or
even years, to many a deprivation of ordinary enjoyments. If he ~
will do this, his powers, and especially those of the mind, may
remain considerable, provided that great regularity of life is ob-
served, and all excesses are avoided.
In almost all cases, however, patients will have to suffer some
loss of the former enjoyments of health ; they remain a long time
—perhaps always—in the category of ‘‘nervous’’ persons, and
must look forward to a relapse of their disease with every fresh
exposure to injurious influences.
If the hereditary tendency is very great, if there are unfavora-
ble external conditions, permanent causes, the prognosis will of
course be much less bright. The disease then continues, but
without, as it seems, involving immediate danger to life. As re-
gards the possibility of the development of anatomical lesions,
we cannot at present render an opinion.
Treatment,
The causal indication must be satisfied, first and foremost.
The excessive claims upon the nervous system must be decidedly
forbidden, and in most cases it is really necessary to interpose a
period of absolute rest from harmful occupations. The arrange-
ments for this will differ in each case, according to the existing
cause.
Especial attention is required by the regimen and diet of the
patient. He must live a regular and healthy life in every respect,
and must continue this plan with the greatest perseverance. He
must work little, and only at fixed hours, with frequent interrup-
tions ; must go to bed early and sleep as much as he can; must
have an abundance of strong, easily digestible food, at not too
great intervals ; spirituous drinks are allowable in moderation ;
much moving about in the open air (but never to the point of ex-
haustion, and with proper alternations ; walks, mountain climb-
ing, skating, gymnastics, etc.) is absolutely necessary ; patients
who are very easily exhausted must sit a great deal out of doors
in a good air; the sexual act must be restricted as much as possi-
ble, but need not be absolutely forbidden in most cases, or but
Paice,
SPINAL NERVOUS WEAKNESS. 381
for a time; sexual excitement without gratification must be
avoided as much as possible.
Of the plans of treatment for the direct relief of the disease,
the use of a moderate cold-water cure, well graduated to the
patient’s strength and sensitiveness, deserves especial mention.
Rubbing down with partly warmed water, gradually made colder,
washing of the back, of the feet, and sitz-baths are the most
suitable, and usually soon impart an increase of vigor and power.
Douches and very cold applications should be avoided.
I have found the mowntain air no less efficacious in many
cases ; a considerable time passed among high mountains, gradu-
ally going to higher stations, does such patients a great deal of
good, and quickly improves the power of their lower extremities.
It is well to combine this air-cure with a moderate water-cure,
when possible. In selecting a place, its altitude, the quality of
the service, and the convenience of the walks must be regarded ;
there is no lack of very suitable places in Switzerland and Tyrol.
The galvanic current has also an important place among the
remedies for spinal nervous weakness ; it is applied to the back
in the usual way (best in the ascending direction, stabile, with
change of the position of the electrodes—current not too strong),
and may also be applied directly to the legs, and perhaps to the
genitals also. Most patients bear it well, and are improved by it.
Of drugs, almost the only ones in use to be recommended are
the preparations of ivon and guinia; their forms and combina-
tions may be very various. It is often useful to combine them, in
the way recommended by. Hammond (see the previous section),».)
with small doses of nux vomica or strychnia; but it is well
to be cautious. According to circumstances, other tonics may be
used.
We shall often have to decide upon the choice and applica-
bility of daths. For anemic and debilitated persons, the chaly-
beate baths will be indicated; patients who require much protec-
tion, who are very sensitive to cold, should at first be sent to the
thermal brine baths (Rehme, Nauheim, etc.), rather than to a
cold-water cure. Sea-baths are a most excellent after-treatment
for patients who are used to the water and have a good digestion.
Under all circumstances, these cures must be followed out
ae
a)
889 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
steadily and repeatedly for a long time, for the complaint is
very slow and does not yield to the first attack.
Symptomatic indications, such as arise from the presence of
sleeplessness, pain, spermatorrhcea or pollutions, impotence, di-
gestive disorders, etc., should be treated with the customary
remedies.
9. Inflammation of the Spinal Cord—Myelitis.
Harless, Diss. inaug. de myelitide. Erlangen, 1814.—KJohss, De myelitide. Halae,
1820.—Funk, Die Riickenmarksentziindung. Bamberg, 1825.—A/bers, Beob.
auf d. Gebiete d. Pathol. L 8. 73. 1836.—Ollivier, 1. c. IL. 8S. 302. 3. Aufl. —
Abercrombie, Krkh. d. Gehirns u. R.-M. Deutsch von G. y. d. Busch. 1829. 9.
474.—Cruveilhier, Anatom, patholog. 18385. 42. Livr. 32 u. 38.—Marcel, Diag-
nost. et nature du ramolliss. blanc d. 1. moelle épin. Gaz. méd. d. Paris. 1854.
No. 52.—Hvan Reeves, Acute Myelitis. Edinb. Med. Jour. I. 1855, 1856. p. 305
and 416.— Oppolzer, Acut. Entziind. mit part. Erweichung d. R.-M. Spitalszeit.
1860. No. 1-3.—Brown. Séquard, Lect. on Diagn. and Treat. of the Prin. Forms
of Paral. of the Lower Extrem. London, 1861.—Koehler, Monographie d.
Meningit. Spinal. 1861. Beob. 17 u. 18.—Mannkopf, Fall von acut. Myelit
Berl. klin. Woch. 1864. No.1; u. Tagebl. d. 40. Vers. Deutsch. Aerzte u.
Naturf. etc. 1865.—Juccoud, Des paraplégies et de l’ataxie du mouv. Paris,
1864.—Armin. Levy, De myelit. spinali acuta, Diss. Berolin, 1863.—77ommann,
Untersuch. iiber die normale u. patholog. Anatom. d. R.-M. I. 1864. IL 1867.
—Engelken, Beitr. zur Pathol. d. acuten Myelitis. Diss. Ziirich, 1867.— P. A.
H. Sachse, Ueber Myelit. etc. Diss. Berlin, 1867.— Voisin, Meningo -myélite
aigué. occas. p. 1. froid. Gaz. d. hép. 1865. Nos. 25-30.—Harley and Lockhart
Clarke, Fatal Case of Acute Progress. Paral. from Softening etc. Lancet. 1868.
Oct. 3.—Keen, Softening of the Spinal Cord, etc. Amer. Jour. of Med. Sci.
July, 1869. p. 128.—Hasse, Krkht. des Nervensyst. 2. Aufl. S. 696.—Ham-
mond, Diseases of the Nervous Syst. 3d edit. p. 456.—M. Rosenthal, Klinik
d. Nervenkrkht. 2. Aufl. S. 296.—Zeyden, Klinik d. Rtickenmarkskrkht. IL. 8.
115.—Dujardin-Beaumetz, De la myélite aigué. Paris, 1872.—G. Hayem, Des
hémorrhag. intrarhachid. Paris, 1872.—Hayem, Deux cas de myél. aigué cen-
trale et diffuse. Arch. de Physiol. VI. p. 603. 1874.—(. Westphal, Ueber fleck-
weise oder diseminirte Myelitis, Arch. f. Psych. u. Nerv. IV. S. 338. 1874.—
Bernheim, Artikel: Myélite im Dict. Encyclop. des Sci. médic. IL. sér. T. VIII.
p. 674. 1874.—Duchenne (de Boulogne), Electris. localisée. 3e édit. 1872. p.
459.—Hallopeau, Etudes sur les myélites chron, diffuses. Arch. génér. d. méd,
6. sér. T. XVIII. u. XTX. 1871, 1872.—C. Lange, Fall von Myel. interstit. chron.
Hosp. Tid. 14. Aarg. 8. 85. Virchow-Hirsch, Jahresb. pro 1871. II. 8. 77.—
Frommann, Fall von Wirbelcaries u. Degenerat. des R.-M. Virchow’s Arch.
MYELITIS, 383
Bd. 54, 1872.—Rob. W. Tibbits, Case of Myelitis. Med. Times, 1871. May 13.
—Hallopeau, Etude d. 1. sclér. diff. periependymaire. Gaz. m¢d, 1870. Nos.
80-35.— Vulpian, Cas d. méning. spin. et d. sclérose corticale annulaire, etc,
Arch. d. Physiol. II. p. 279. 1869.—Martineau, Inflammat. aigué général,
de 1, substance grise d. 1. moelle. Union méd. 1874. Nr. 30.—Feinberg,
Ueber reflect. Gefiissnervenlihmung u. Rtickenmarksaffection nach Ueber-
firnissen der Thiere. Virchow’s Arch. Bd. 59. 8. 270. 1874.—Schueppel, Fall
von allg. Aniisth. Arch. d. Heilk. XV. S. 44. 1874.—Tvroisier, Deux cas de
lésions sclér, de la moélle ép. Arch, d. Physiol. V. p. 709. 1873.—Joffroy,
Faits experim. pour servir a l'histoire de ]a myélite. Gaz. méd. de Paris, 1873,
Nr. 36.—Charcot, Sur la tuméfact. des cellules nerv. motrices et des cylindres
axiles, etc. Arch, d. Physiol. IV. p. 93. 1872.—C. Lange, Bidrag til etc. Hosp.
Tid. 16. Aarg., Schmidt’s Jahrbb. Bd. 168. 8, 238.—Raymond, Myél. de la
région dorsale. Gaz. méd. 1874. No. 9.—/". Raymond, Myélite de la rég. cer-
vicale. Progrés méd. 1875. No. 17.—Gérin-Rose, Myél. aigué généralisée.
Union méd. 1875. No. 90.—LZanghans, Myelitis d. grauen Commiss. etc. bei
Lepra anesth. Virch. Arch. Bd. 64. 1875.—Hamilton, On Myelitis, etc. Quart,
Journ. of Microsc. Sci. Oct. 1875. p. 334.—Pierret, Note sur un cas de myél.
a rechutes. Arch. d. Physiol. VIII. p. 45. 1876.—JZaveran, Obs. d. myél. centr.
subaigué. Ibid. VII. p. 866. 1875.—P. Baumgarten, Eigenth. Fall von Paralys.
ascend. acut. mit Pilzbildung im Blut, Arch. d. Heilk. XVII. S. 245. 1876.—
Lewin, Paraplegie in Folge von acut. Myelitis u. cl. Behandlung derselben.
Deutsche Klinik. 1875. Nr. 11.—See also the literature of multiple sclerosis,
sclerosis of the posterior columns, Jateral sclerosis, poliomyelitis anter. acuta et
chronica, etc., in the succeeding chapters of this work.
Introduction,
Myelitis constitutes unquestionably the most extens.ve and
important chapter in the pathology of the medulla spinalis.
Any one who possesses eyen a superficial knowledge of the sub-
ject, will be able to appreciate the difficulties which confront us
in the attempt to furnish a comprehensive and classical account
of it.
The material at hand bearing on inflammation of the spinal
cord and affections that are classed with it, is immense and in
the critical sifting and arrangement of this material we meet
with difficulties that cannot be overcome. These are encountered
chiefly in the domain of pathological anatomy, many and per-
haps most of the questions which come within the limits of this
department being still in process of development. It is as yet
884 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
impossible to define accurately the boundaries of inflammation
of the spinal cord in both its acute and chronic forms, and to
decide exactly what does and what does not fall within them.
Some authors do not hesitate to class almost all the forms of
acute as well as chronic disease of the cord, which will be de-
scribed in the following chapters, under the head of Inflamma-
tion. They regard tabes dorsalis, the so-called lateral sclerosis,
multiple sclerosis, progressive muscular atrophy, spinal paraly-
sis of children, myelitis centralis, chronic atrophy of the cord,
and secondary degeneration of it, as mere subvarieties or different
localizations of one and the same inflammatory process. Others,
on the contrary, hold that a number of these processes, such as ~
simple and degenerative atrophy, softening, sclerosis, gray de-
generation, and the like, are entirely distinct from and independ-
ent of inflammation.
Hence, the additions made by one party to the great mass of
material bearing on the disease, are detached and diverted in
different directions by others. It is as yet impossible to foretell
when the elucidation of the facts and opinions will take place.
Of late, however, all the anatomical and clinical investigations
have aimed at this goal, and they have already thrown much
light on some of the doubtful points.
We need, above all things, searching histological studies of
the diseased spinal cord, to enable us to comprehend the gene-
sis and the histological development of the different processes.
There is, moreover, great need of further elucidation and a more
exact definition of the general pathological conception of inflam-
mation, in order to show what should be comprised under the
head of inflammation of such an organ as the spinal cord. It is
especially necessary that we should learn how chronic inflamma-
tion of the cord is to be defined, and how it is to be distinguished
from, or in what genetic connection it stands to, the other forms
of chronic disease, viz., atrophy, degeneration, softening, sclero-
sis, etc. Not till these steps have been gained, will it be possible
to determine positively what forms of disease are to be classed
under the head of myelitis, and to describe accurately the clini-
cal histories of the different forms.
The necessities of practice, however, demand a dogmatic pres-
MYELITIS. 385
entation of the subject, and the practical physician has a right
to insist, that it should be in accord with the present state of our
knowledge, however incomplete that may be, all disputed ques-
tions being avoided as far as possible. This idea has guided and
influenced us in the preparation of the following account of the
disease. It is both short and incomplete, but in extenuation of
the latter we must plead the difficulty of the subject, and of the
former the shortness of the space allotted us.
History,
An accurate history of the growth of medical knowledge on
the subject of myelitis would be almost the same thing as a his-
tory of the pathology of the spinal cord in general. That does
- not enter into our present task. Nor is it at all necessary for us
to investigate the question whether the ancients—Hippocrates,
Aretzeus, Galen, and others—had or had not any definite con-
ception of myelitis, There can be no doubt that they repeat-
edly met with the disease, but they did not differentiate it
sharply from other affections. We find in their works more or
less recognizable descriptions of both the acute and the chronic
forms of myelitis.
Our more accurate bitibriteigle of the inflammations of the spi-
nal cord dates only from the end of the last and the beginning of
the present century. Here, too, it was P. Frank (1792) who gave
the impetus to more accurate investigations. Spinitis, rachi-
algitis, and the like, were the terms then applied to the more
acute forms of the disease. At a later period, the term ‘‘ myeli-
tis,’? which is now universally employed to designate inflamma-
tion of the spinal cord, was introduced, mainly through the
works of Harless (1814) and Klohss (1820).
In the third decennium of this century, the epoch-making
works of Ollivier (1st Edit., 1821) and of Abercrombie (1828)
appeared and placed the subject of myelitis on a firmer founda-
tion. These authors were the first to point out the intimate con-
nection of softening with the acute form of the disease. After
this the subject remained in statu quo for along time. During
the fifth and sixth decennia the attention of physicians was grad-
VOL. XIII —25
286 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
ually directed more to the chronic forms of the disease. Among
the valuable contributions of this period, we must mention
Tuerck’s discoveries concerning the secondary degenerations, and
Romberg’s account of tabes dorsalis, but, above all, the admira-
ble observations and investigations of Duchenne (of Boulogne).
This last-named author described in a classical manner the clini-
cal histories of chronic spinal paralyses, locomotor ataxia, pro-
gressive muscular atrophy, etc.
The development of the pathology of the spinal cord did not,
however, receive any great impetus until the beginning of the
seventh decennary, when it began to make rapid progress under
the influence of improved methods of physiological and_histo-
logical investigation. In this accelerated development the sub-
ject of myelitis played a prominent part. We must here extol
especially the works of Brown-Séquard. The publications of
Oppolzer, Levy, Mannkopf, and others, on acute myelitis, are
also deserving of special mention, while the pathological ana-
tomy of the subacute and chronic forms of myelitis was cleared
up very greatly by the valuable contributions of Frommann (1864
and 1867). From this time forward we have to chronicle a rapid
advance in the knowledge of the acute and chronic forms of
inflammation of the spinal cord, which became the object of zeal-
ous study in France and England, as well as in Germany. Broad
foundations, on which to build up the edifice of acute myelitis,
were laid by the works of Engelken, Charcot, Dujardin-Beau-
metz, Hayem, Westphal, J. v. Heine, and others, but it was
nevertheless the chronic forms of the disease which attracted the
most earnest attention of scientific men. Our knowledge of these
has been greatly advanced by the admirable works of Friedreich,
Westphal, Leyden, Frommann, Th. Simon, and others, in Ger-
many ; of Lockhart Clarke, Gull, and others, in England; and
of Duchenne, Topinard, Jaccoud, Charcot, Vulpian, Hallopean,
Joffroy, Michaud, Pierret, and others, in France.
The school of the Salpétriére, under the direction of Charcot
and Vulpian, has unquestionably played the most prominent
part in the furtherance of this development. We have to thank
it for numerous admirable works, full of new discoveries and
fruitful thoughts. Germany, too, has furnished during recent
MYELITIS. 387
years a number of excellent works. (Compare the histories of
tabes dorsalis, multiple sclerosis, and spinal paralysis of children.)
Finally, we must also mention the claims of the electro-therapeu-
tists, especially those of Germany, whom we must thank for
many valuable advances, not only in the treatment, but also in
the pathology of myelitis.
In describing myelitis, it seems to us for many reasons expe-
dient to distinguish two principal forms of the disease, viz., the
acute and the chronic. These two forms run into one another in
many points, but as a general thing they present noticeable dif-
ferences, chiefly in regard to their course, but also in regard to
their pathological anatomy and their clinical manifestations.
The different forms and subvarieties of the disease, of which
there are not a few, will be only briefly alluded to here, as we
shall return more fully to them at a later period.
A. Acute Inflammation of the Spinal Cord—Myelitis Acuta.
Definition.—We understand by acute myelitis all the varie-
ties of acute inflammation of the substance of the spinal cord,
which rapidly lead to serious disturbances, and are usually, if
not always, attended by fever.
We have to deal here with rapidly developing inflammatory
changes, which affect the connective substance as well as the ner-
vous elements of the cord, but of which all the histological steps
are not yet thoroughly understood. The usual result is a rapid
destruction of the histological constitution of the cord, which
almost always takes the form of softening, and is of course
accompanied by abolition of the function of the affected part.
In the present state of our knowledge, it is scarcely possible
to make an accurate subdivision of the disease into parenchyma-
tous and interstitial acute myelitis.
Acute myelitis may present itself in different forms, according
to its exact seat. It may also follow very different courses. It
is true that the development of the disease and of the disturb-
3888 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
ances of function caused by it, is in almost all cases very rapid,
but of the cases which prove fatal, it is only in a small number
that the subsequent course of the disease is as rapid as its com-
mencement. On the other hand, a speedy recovery is very rare ;
usually the disease runs a more or less protracted course, and
either terminates in death or sinks into a chronic affection.
Etiology and Pathogenesis.
The comparative rarity of acute myelitis accounts in a mea-
sure for our lack of knowledge concerning its causes. It is
only ina small number of the cases that we can succeed in dis-
covering a tangible cause, and even in them its mode of action
usually remains enveloped in mystery. Many cases apparently
originate spontaneously, without any exciting cause at all. In
such cases the cord has been subjected to the action of irritants
which are entirely unknown to us.
Very little is known concerning the conditions which produce
an increased predisposition to acute myelitis. The male sex
seems to be more subject to the disease than the female. It is
said that the greatest number of cases occur during youth and
middle age, between the ages of ten and thirty years, but still
there is a particular form of acute myelitis, the so-called spinal
paralysis of children, which is essentially and almost exclusively
a disease of childhood. Many authors hold that this form of the
affection is connected with dentition, but the correctness of the
opinion is questionable. |
It seems to us that it would be more correct to class sexual
excesses, the practice of coitus in the erect position, severe
bodily exertion and the like, with the predisposing than with
the exciting causes of acute myelitis.
Of the latter the simplest and the easiest to study are inju-
ries, to which the spinal cord is so frequently exposed, and
which may result from the most various external agencies. All
sorts of injuries of the cord, such as those produced by punctur-
ing and cutting instruments, by fractures and luxations of the
vertebra, contusions, etc., form the regular starting-point for the
acute traumatic myelitis which we have already described in
=
=! '
c ss
a ae
MYELITIS. 389
No. 4, Part 1, p. 305. This traumatic myelitis has also repeat-
edly been the subject of experimental investigations.
Next in order come the cases, in which a slow compression of
the spinal cord is the starting-point of a myelitis. This com-
pression may be due to lesions of the most various sorts. (Comp.
above, No. 5, Part 1, p. 319.) It is true that some of the com-
pressing agents which come in question here, are more liable to
excite the subacute and chronic forms of myelitis. When, how-
ever, the agent which produces compression of the cord, is at the
same time of an irritating nature, e. g., carcinoma, the inflamma-
tory exudation in caries of the vertebra, etc., changes are not
infrequently produced, which unquestionably belong to acute
myelitis. This brings us to those forms of acute myelitis which
are due to the transmission of inflammatory processes from
neighboring organs and tissues, without the intervention of com-
pression of the cord. The principal, and practically the only
important, disease belonging in this category is acute meningitis
spinalis, which is almost invariably attended by more or less
extensive implication of the cord itself. We have already spoken
of this peculiarity in the chapter on Leptomeningitis Acuta, Part
1, p. 233.
Catching cold is unquestionably one of the most important
and most frequent causes of acute myelitis. The cases in which
exposure to some one of the more severe causes of colds, such as
sudden cooling of the overheated body, a fall into water, sleep-
ing on the damp earth or in snow, etc., has been followed imme-
diately by the symptoms of acute myelitis, are too numerous to
leave any doubt of the potentiality of this cause. (See the obser-
vations of Ollivier, Oppolzer, Voisin, and others.) Dujardin-
Beaumetz believes that the frequency of the disease among bakers
can be ascribed to the fact, that their work exposes them in an
unusual degree to colds.
The question whether excessive bodily exertion must also be
classed among the exciting causes, cannot as yet be decided.
Perhaps it acts only as a predisposing cause. At all events, it
seems to have a certain etiological significance, when combined
with exposure to the causes of colds; every war, and especially
every winter campaign, furnishes examples which illustrate this.
390 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
The same may also be said of the different varieties of sexwal
CXCESS.
Acute myelitis is not unfrequently developed as a complica-
tion or sequel of acute diseases. It has been observed in con-
nection with typhus, the acute exanthemata, acute rheumatism,
severe puerperal diseases, etc.; most frequently, however, in con-
nection with variola (Westphal). In this last case the myelitis has
set in at a variable period after the outbreak of the primary dis-
ease, in a few rare cases not until several weeks afterwards.
Baumgarten recently reported a remarkable case, in which infec-
tion with bacteria (from malignant pustule) was in all probability
the cause of an exceedingly acute myelitis.
Among the chronic infectious diseases, syphilis can unques-
tionably cause acute myelitis. A question may be raised as to
whether we have to deal in this case with a specific luetic process,
or with an ordinary non-specific myelitis of which the syphilis
has been only a predisposing and distant cause. It is at all
events certain, that myelitis running a rapid course, is observed
with unusual frequency among syphilitic patients. Our own
observations lead us to agree with Hayem, who claims that
syphilis is an etiological agent of decided importance.
Continued suppression of the menses, sweating of the feet,
and hemorrhoidal bleeding play a more or less doubtful réle in
the etiology of acute myelitis. | |
Violent emotions seem in many cases to have been really the
starting-point of myelitis. At least some isolated cases have
been reported (by Leyden, among others), in which the first
symptoms of myelitis showed themselves immediately after some
intense psychical movement, such as fear, anxiety, or anger.
Finally, irritations and diseases of peripheral organs must
also be mentioned among the causes of acute myelitis, although
the cases in which they are really the agens morbi are compara-
tively rare. For instance, a certain proportion of the so-called
reflex paraplegias, which are developed in connection with dis-
eases of the urinary and digestive apparatuses and of the uterus,
or with irritations and inflammations of the peripheral nerves,
the joints, etc., should really be classed as acute myelitis. This
fact and the pathogenesis of reflex paralyses have already been
MYELITIS. 391
discussed In more than one chapter of this work, and we may
refer the inquirer to them for further information.’ Here, we will
only mention the fact that Feinberg’ has recently succeeded, by
varnishing the skin of rabbits, in exciting an acute affection of
the spinal cord, which at all events closely resembles inflamma-
tion. He regards it as reflex in nature and secondary to the
severe irritation of peripheral sensitive nerves, and ascribes it to
paralysis of the vaso-motor centres. After all has been said,
however, we must admit that we have very little positive knowl-
edge concerning the pathogenesis of reflex paraplegias, and
unfortunately our knowledge of the pathogenesis of myelitis
due to other causes is equally deficient. The traumatic cases
and those secondary forms due to extension of inflammation
from neighboring tissues, are the easiest to comprehend. When,
however, we seek to explain the manner in which catching cold
or emotional disturbance produces myelitis, or the mode in
which it is developed in connection with acute diseases, or with
syphilis, etc., we can only bring forward more or less gratuitous
theories, which it would be useless to discuss here.
Pathological Anatomy.
Frequently a spinal cord which is the seat of acute inflam-
mation, presents very little or even absolutely no macroscopic
change.* There is not the slightest reason to doubt, that the
disease has on innumerable occasions been overlooked at the
autopsy. In fact, we can scarcely ever be absolutely certain
that an acute myelitis exists, until a microscopic examination
has been made.
In the macroscopic examination the most striking peculiarity
is the diminution in the consistence, the softening, of the cord
(myelomalacie). This change is so constant, that softening has
been generally, but very incorrectly, identified with acute in-
flammation. That the two processes are not identical, is evident
—
1 See Vol. XI. and Vol. XII.
2 Virchow’s Archiv. Vol. 59. p. 270.
392 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
on the one hand from the fact, that every softened cord is not
inflamed, and on the other from the fact that inflammation of the
cord does not always terminate in softening. It would be better
consequently to discard entirely the use of the term ‘‘softening,”’
to designate inflammatory processes. I must at all events pro-
test most earnestly against: the promiscuous employment of the
name myelomalacia as a synonym for myelitis. That term
should be reserved for processes of softening pure and simple.
The inflammatory changes, which we will consider first, vary
greatly as regards their localization in the spinal cord. Acute
myelitis has its seat and starting-point most frequently in the
gray substance, a fact which depends probably on the vascular
richness of this portion of the cord. It may extend to a greater
or less distance in a vertical direction, and may penetrate more
or less deeply into the white columns. This is the form which,
since the time of Albers, has been usually designated as myelitis
centralis.
It may spread very rapidly through the gray substance, and in a short time
involve the greater part, or even the whole of the gray axis—diffuse central myelitis
(Hayem). When the white columns are also involved to a marked extent, so that
the entire cord is more or less implicated in the inflammatory process, the affection
may be called myelitis diffusa. Strictly speaking, however, this is a rare oc-
currence.
Not unfrequently the entire thickness of the cord is affected
for a longer or shorter distance. The diseased part may in such
cases be several inches in length, but the inflammatory process is
usually not equally intense throughout its whole extent. This is
the form which is now ordinarily described as myelitis trans-
VET Sa.
When the centre of inflammation is less extensive, so that it
involves only a small portion of the cord both vertically and
transversely, it is termed myelitis circumscripta. Here we have
to deal with a small spot of inflammation buried somewhere in
the substance of the cord. Not unfrequently, however, we meet
with several of these small spots in the same cord. Cases have
been observed (Westphal), in which the myelitis presented itself
in the form of numerous foci scattered throughout the entire cord
ie pt ,
ar rie i) at
MYELITIS. 393
and separated from one another by healthy tissue—cases in which
the disease was widespread, but attacked only circumscribed
and scattered spots. This is called myelitis disseminata.
Finally, that form of the disease which is secondary to menin-
gitis, affects principally the peripheral layers of the cord, pene-
trating more or less deeply and extending vertically to a variable
distance—myelitis peripherica.
The appearances presented by the affected spots vary greatly
according to the stage of the myelitis, and in part also accord-
ing to the special peculiarities of the process in the individual
cases—always provided there are macroscopically demonstrable
lesions. We must here distinguish different stages.
1. The stage of hyperemia and commencing exudation (red
softening). We do not often meet with this stage of the disease
at the post-mortem table. The opportunities to study it are fur-
nished most frequently by those cases in which the inflammation
is secondary to severe traumatic lesions, or by cases of myelitis
centralis, which run a rapidly fatal course.
At the affected spot a slight, and in rare cases a marked, swell-
ing can be recognized. On section, the transverse markings are
found to be blurred and indistinct, and the cut surface not unfre-
quently presents a variegated, marbled appearance. The red
color of the tissue, which is due to the hyperemia, is usually very
marked ; it may vary from a slight rosy injection to a deep red,
reddish brown or chocolate color, when more or less numerous
capillary hemorrhages are added to the often very intense hyper-
zemia. The inflamed spots are almost always unusually moist
and soft ; they swell up above the level of the cut surface. The
softening may be so great that the tissue is reduced to the con-
sistency of pap. In very rare cases we observe a slight increase
in consistency at this stage, probably on account of infiltration
of the interstitial tissue with a firmer exudation. Hayem has
reported an instance of this. In some few cases we can see with
the naked eye, or with the help of a lens, a distinct deposit of
294 ERB.—DISEASES OF THE SPINAL CORD AND ITs ENVELOPES.
exudation in the affected spot; it takes the form of whitish or
yellowish, clouded or glassy, colloid streaks or rings, which are
imbedded in the septula or poured out around the vessels. The
meninges in the neighborhood of the affected spot also frequently
present the signs of hyperemia and inflammation.
In preparations hardened in chromic acid, the myelitic spots can usually be much
more readily distinguished from the healthy tissue by their different (brighter yel-
low) color, than in the fresh cord. The inflamed parts, moreover, harden slowly
and badly, and on section they appear friable, crumbly and not coherent, and do
not present sharply defined markings. The smaller spots of myelitis in particular, as
well as the secondary degenerations, are very sharply and distinctly mapped out by
this discoloration.
2. The stage of fatty degeneration and of resorption (yellow
and white softening). As the disease progresses, the affected
spot becomes constantly paler and more and more softened. Its
color changes gradually from red to yellow; this change is due
partly to the diffusion and alteration of the coloring matter of
the blood, partly to the fatty degeneration of the medullary
sheaths and the formation of masses of fat-granules, and partly
to the cessation of the hyperemia. Through the influence of
these three agencies, but particularly in consequence of the ac-
cumulation of fatty detritus, the color becomes progressively
whiter, and the entire substance assumes a creamy or milky ap- ©
pearance. The softening has meanwhile made rapid progress, the
medulla swells up very much above the cut surface, acquires a
pappy or even a more fluid consistency, and often flows out of
the sac of the pia entirely. This softening is caused principally
by the fluid exudation from the vessels, acting in concert with
the destruction of the nerve-fibres. This exudation may possibly
present certain differences in different cases, which would account
for the varying degree of the softening, or even for its entire ab-
sence. Of this, however, we have no positive knowledge.
At last nothing remains of the diseased spot but the vascular
network and a portion of the hypertrophied septa, between which
is a softened mass that can readily be pressed out, or which per-
haps flows out without the help of pressure. In consequence of
the progressive resorption of the nerve-substance and the fat-
ee ae
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4 ' * 4“ i
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MYELITIS. | 395
granules, the spot gradually assumes a more grayish color, and
finally becomes smaller and depressed.
Actual suppuration occurs very rarely in acute myelitis. "When abscess of the
cord does form, it is generally secondary to a severe traumatic lesion or to suppu-
rative meningitis. In spontaneous myelitis, on the other hand, suppuration is ex-
ceedingly rare, and has only been observed in a very few cases.
3. The terminal stage (formation of cicatrices or cysts, in-
duration, sclerosis, etc.).
The resorption of the softened masses continues until finally
all the fluid portions have completely disappeared. Nothing
remains but the vascular and connective tissue networks, which
are in part thickened and hypertrophied; they form a more or
less dense, shrivelled, grayish, semi-transparent cicatrix, which
is often flecked with pigment. This cicatrix unites the portions
of the cord that have remained healthy. In some rare cases a
restoration of the nerve-tissue takes place ; after a certain length
of time small, dark-bordered, regenerated nerve-fibres can be de-
monstrated in the cicatrix. In this way also a restoration of
function can be brought about, as happened in one of Charcot’s
cases. This fortunate result seems, however, to occur more read-
ily in the subacute and chronic forms.
Not unfrequently more or less extensive collections of fluid
are left behind in the framework of the cicatrix, and lead to the
formation of single or multiple, large or small cysts, They usu-
ally contain a muddy fluid resembling milk, or more frequently,
serum. |
In many cases, on the contrary, the interstitial, supporting
framework becomes in course of time greatly hypertrophied and
consolidated. It increases in thickness and density, the vessels
become larger and their walls thicker; the previously softened
spot becomes firmer and denser, gray and semi-transparent, and
presents a marked contrast in color and consistency to the sur-
rounding parts. Here we have the commencement of harden-
ing, or sclerosis. When the interstitial growth of connective
tissue persists, and extends in a slow but progressive manner to
the neighboring parts of the coxd, which were previously either
healthy or very slightly changed, and when it propagates itself
896 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
there, leading to a gradual destruction of the nervous elements,
we have before us the transition into chronic myelitis. This is
a frequent occurrence. In almost all cases of myelitis which do
not prove rapidly fatal, this transition takes place at some late
period of the disease.
The macroscopic examination, as a rule, reveals also an ém-
plication of the meninges in the inflammatory process. The
signs of it are cloudiness of the membranes, infiltration with
serum, cellular elements or pus (often only discovered at the
microscopical examination), thickening, adhesions, capillary ex-
travasations in addition to extreme hyperemia, etc. The spinal
fluid is usually increased, somewhat cloudy and reddish, but it
is sometimes entirely unchanged. The condition of the roots of
the nerves is regulated by that of the pia; they are sometimes
softened, loosened and swollen, sometimes atrophic, gray, trans-
lucent and indurated. |
In the later stages, in addition to the actual centre of inflam-
mation, we often meet with the so-called secondary degenera-
tions, of which we have already repeatedly spoken: ascending
degeneration in the funiculi graciles, and descending in the pos-
terior lateral columns, etc. In many cases of acute myelitis the
disease does not last long enough for their development, but they
are rarely wanting in the cases that become chronic. The transi-
tion from myelitis to secondary degenerations can often be traced
very accurately in successive transverse sections.
. The microscopical examination is, however, of supreme im-
portance for the understanding of the pathological processes
which take place here. The cord should be examined microscop-
ically, both in the fresh state and after it has been hardened by
the usual methods. The changes are seen to affect the nerve-
fibres and the ganglion-cells, as well as the connective tissue
framework and its vessels.
In the first stage we find marked dilatation of the capil-
laries and small arteries, and more especially of the small veins ;
they are distended with blood, and not unfrequently enveloped’
in layers of white and red blood corpuscles arranged in the form
ofasheath. Here and there larger collections of red corpuscles
are found (capillary extravasations), The walls of the vessels
—
MYELITIS. 397
are thickened and studded with fat-granules and granule-cells,
presenting exudative and plastic infiltration. Hayem describes
particularly a glassy, colloid exudation, which surrounds the
vessels like a sheath in a layer of varying thickness, and which
is also found disseminated elsewhere in the tissue.
Baumgarten seems to have seen something very similar—a hyaline, firm, glassy
exudation in the tissue of the gray substance, about the vessels and in the anterior
longitudinal furrow—in his interesting case of acute central myelitis, which was
probably due to infection with the poison of anthrax.
Marked changes are always found in the newroglia. The
fibres of the reticulum are thickened and swollen, the network
is much denser and more distinct, and it is in part filled with
nuclei and cells. The glia cells themselves are swollen and in-
creased in number; they often contain several nuclei, and are
sometimes, like the thickened connective tissue septa, infiltrated
with colloid masses. Even in this stage we generally find
granule-cells in greater or less numbers, partly in the immediate
neighborhood of the vessels, partly scattered irregularly in the
interstitial tissue and its meshes.
The changes in the nerve-fibres are also very striking and im-
portant. The fibres, in general, present irregular contractions
and enlargements; the medullary sheath has in places broken
down into globules or larger irregular fragments, and has become
granular; in many fibres it has entirely disappeared, or has
united with the axis-cylinder to form a single, homogeneous
mass. The azis-cylinders themselves, as is evident from the
observations of Frommann, Charcot, Hayem, Joffroy and others,
are frequently swollen, and often attain enormous dimensions.
They present large, spindle-shaped swellings and bulging, club-
shaped fragments ; they are streaky, clouded, studded with gran-
ules, brittle, and apparently in a state of granular degenera-
tion. The thickening of the axis-cylinder can be very readily
seen in transverse sections, in which they are often found lying
together in groups. Isolated swollen axis-cylinders are also
found lying in the midst of unchanged nerve-fibres.
The ganglion-cells are also involved in the inflammatory
changes. They are swollen, often to a very considerable size,
; ee
“#
298 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
looking then as if they were puffed up. Their substance is
clouded ; in the beginning the nucleus and nucleolus are usually
intact, but in a few instances they are in process of division.
Sometimes we observe glassy swelling of the cells, and a develop-
ment of vacuoli in them. Their processes are also swollen,
clouded, irregular in shape, and in part destroyed. At a later
period the cells disappear before the advancing processes of de-
struction.
In the second stage we find the nervous elements fully in-
volved in the process of destruction: the nerve-fibres are broken —
down into fragments ; the medullary sheath is in a state of fatty
degeneration, and the axis-cylinder altered or destroyed. The
ganglion-cells are partly melted down and destroyed, partly
atrophied and reduced to small glistening scales, without demon-
strable structure. The connective tissue framework is loosened
and softened by the fluid exudation, the development of cells
and fatty degeneration. The walls of the vessels are thickened,
very rich in nuclei, filled with fat-granules and frequently sur-
rounded by thick layers of granular cells. The semi-fluid pulpy
mass formed by the inflamed and softened cord, contains also
numerous lumps and drops of myelin, the remains of blood-cor-
puscles, colorless cells, pigment-granules, fine granular detritus,
and, above all, numerous fat-granule-cells. These fat-granule-
cells form usually the most striking constituent of the softened
myelitic mass, and attract the attention of the observer at
once; they are especially distinct when the cord is examined —
in the fresh state. They are found deposited about the ves-
sels, and in the spaces left empty by the destruction of the
nerve-fibres and axis cylinders, and also in the septa of the neu-
roglia. This extensive distribution of these cells indicates of
itself that they are produced in different ways; it is, in fact,
probable that some of them are formed from young cellular ele-
ments which have taken up fat, while others can be ascribed to
fatty degeneration of the glia cells, and still others to fatty de-
struction of the nerve-fibres and the spindle-shaped swellings of
the axis-cylinders (Hayem, Th. Simon).
In the third stage we find in the affected spot, which is now
engaged in an effort at cicatrization, a sclerotic connective tissue
‘'
MYELITIS. 399
with numerous nuclei and neuroglia cells. At this period Deiter’s
cells often become very distinct and prominent; they are often
large and possess numerous processes. The vessels are dilated,
and their walls thickened. The ganglion-cells are mostly atro-
phied. Sometimes numerous small, delicate nerve-fibres, with
thin medullary sheaths, can be seen.
Occasionally cysts are found, surrounded by a more or less
dense layer of connective tissue, and usually also traversed by a
large-meshed, connective tissue network. ‘Their contents are
partly muddy, partly serous; microscopically, nothing can as a
rule be discovered in the fluid, except detritus.
In the stage of transition to sclerosis and chronic myelitis,
the increase of the interstitial tissue becomes particularly dis-
tinct. The threads of the reticulum become wider and thicker,
the spider-cells are enlarged and increased in number, the
vessels are thickened, the nerve-fibres and ganglion-cells are
involved in degenerative atrophy. The tissue contains relatively
few fat-granule-cells, but, on the other hand, it contains large
quantities of corpora amylacea.
When secondary degeneration exists, it presents the usual
well-known histological characters, which will be described in
detail in a subsequent chapter (No. 19).
A priori, the usefulness of experimental investigations of these conditions would
seem self-evident. Unfortunately, however, the attempts to clear up the subject in
this way have been but few in number, and have furnished no important, or at all
events no conclusive results.
Strange to say, the numberless experimental sections of the spinal cord per-
formed by physiologists, although undoubtedly on every occasion followed by
traumatic myelitis, have not hitherto been utilized to any extent worth mentioning,
for the study of this affection.
Dujardin-Beaumetz describes some experiments performed by Hayem and Liou-
ville, who sought to excite myelitis by applying iodine or glycerine to the outside
of the cord, or by injecting them into its substance; also some experiments under-
taken by himself in connection with Grancher, in which mechanical injuries were
employed to excite the inflammation. The results of these experiments are, how-
ever, very unsatisfactory. Joffroy made some similar experiments on dogs, and
obtained the same histological changes as those which have been here described as
belonging to the acute myelitis of men.
The investigations of Feinberg and Tso those of Klemm, who endeavored to
produce myelitis in a reflex manner or by means of a neuritis migrans, have not
400 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
made any important addition to our knowledge of the histological genesis of the
myelitic changes.
A sumewhat more comprehensive series of experiments was set on foot by Ley-
den, but his account of the results obtained, which was published in his ‘ Klinik
der Riickenmarkskrankheiten,” is only fragmentary. He experimented on cats and
dogs, and employed exclusively injections of Fowler’s solution into the cord, the
result being almost always a suppurative myelitis. As, however, this variety of the
disease is exceedingly rare in man, the experiments are not of much yalue for the
elucidation of the subject of acute myelitis in the buman subject. Moreover, the
reports that have thus far been published by Leyden, contain no conclusive in-
formation concerning the manner in which the process is developed, the relation
of the minute histological changes to each other in point of time, and the part
taken by the different tissue-elements in the process. Still, we have learned many
things from these experiments. They have proved, for instance, that an injury of
the sort here mentioned can produce an intense myelitis, which may extend beyond
the point of irritation; that the process presents varying degrees of intensity in
one and the same experiment; that the affection diminishes in intensity as it re-
cedes from the point of irritation; that this diminution in intensity is indicated
on the one hand, by a tendency to localization in scattered, circumscribed spots,
and on the other, by a preponderance of the connective-tissue growth over the
softening, liquefaction and suppuration; that multiplication and swelling of the
nuclei of the neuroglia, swelling of the nerve-fibres and axis-cylinders, disappear-
ance of the medullary sheath and development of granule-cells, must be regarded
as the first signs of a commencing acute myelitis, etc.
In the latest experiments of Hamilton on cats, only the first days of acute trau-
matic myelitis are taken into consideration. He found among other things, that
rounded bodies separate from the swollen axis-cylinders and either degenerate into
colloid bodies, or give rise to an endogenous brood of young round cells (pus-
cells), He also observed swelling and cloudiness of the ganglion-cells, multiplica-
tion of the nuclei of the neuroglia, collections of cells in the walls of the ves-
sels, etc.
It is certainly desirable and even necessary that these experiments should be
repeated with modifications, that myelitis should be produced in other ways,-so as
to bring the results more in accord with the lesions in man, and to furnish a
more complete periscope of the process in its different modifications and its various
degrees of intensity.
We must here mention briefly some special forms of acute
myelitis. First of all, we will speak of myelitis centralis acuta.
In this form the softening and liquefaction affects pre-eminently
the gray substance, which flows out when the cord is divided,
leaving a cavity behind. The spinal cord is somewhat swollen
throughout its entire extent, and on section the transverse mark-
MYELITIS. | 401°
ings are seen to be greatly blurred. Hayem describes this form
in the following words: diffuse inflammation of the gray sub-
stance, more or less diffuse hyperemia of the white substance ;
small, band-shaped foci of inflammation in the latter; more or
less intense, meningitic changes.
When this form possesses a hemorrhagic character, we have
the myelitis centralis heamorrhagica, which Hayem designates
by the term hematomyelitis. It is characterized by a more or
less abundant extravasation of blood, which appears either in
the form of a marked hemorrhagic softening, affecting chiefly or
exclusively the gray substance, or in the form of hemorrhagic
foci of varying sizes, which may extend into the white substance.
The tissue in the neighborhood of these foci, both above and
‘below, is in a state of myelitic softening, that may extend
throughout almost the entire length of the medulla.
The acute myelitis without softening, which Dujardin-Beau-
metz terms myelitis hyperplastica, also deserves special mention.
Its essential characteristic is an increase of the interstitial tissue,
which becomes unusually dense and very rich in nuclei. The
septa are wider than usual, and the vessels are thickened ; there
are a few granular cells. The consistence of the cord is normal
or somewhat increased. This form seems to occur principally in
small spots (Westphal’s myelitis disseminata), and to indicate in
general a slighter degree of intensity in the inflammatory pro-
cess. It is sometimes observed also in the neighborhood of spots
of acute softening. It should probably be classed rather with
the subacute forms, which constitute an intermediate step be-
tween acute and chronic myelitis.
The changes in the other organs of the body, in acute myelitis,
require only a brief enumeration. In the peripheral nerves we
find in many cases—especially in central myelitis—degenerative
atrophy in its different stages of development. In the muscles
supplied by these nerves, we find also the characteristic signs of
the first stages of the same process (proliferation of the nuclei,
slight atrophy of the fibres, etc.).
The mucous membrane of the urinary bladder is in many
cases swollen, flecked with hemofrhages and in a state of catarrh ;
in the severest cases it is infiltrated with diphtheritic exudation.
VOL. XIII.—26
402 ERB.—DISEASES OF THE SPINAL CORD AND ITs ENVELOPES,
and presents foul, sloughy ulcers. Sometimes similar changes
are observed in the ureter extending into the pelvis of the kid-
ney, and in not a few cases the kidneys have been found filled
with metastatic abscesses. According to Hayem, a part of these
originate from collections of vibriones. it ae
The changes characteristic of decubitus acutus in its different
stages of development, are usually observed on the skin covering
the sacrum and the nates, the trochanters, and other spots ex-
posed to mechanical pressure. (Compare Part I., p. 121.)
Other pathologico-anatomical changes, which are more or less.
accidental, do not require special consideration here.
Pathology of Acute Myelitis.
Symptoms.
The general clinical history of acute myelitis is so manifold
and changeable, and so different perhaps in each individual case,
that we can only attempt to give here its most common features.
Later on these will be filled out in many particulars while con-
sidering the symptoms in detail.
Even in its mode of commencement the disease is very variable.
Sometimes it is preceded by general malaise and slight febrile
movement, while in a few cases it commences with a chill, which
is followed by the usual febrile symptoms: headache, general
depression, dragging pains in the limbs, loss of appetite, ete.
Frequently the scene is opened at once by spinal symptoms.
In these cases the symptoms which first attract the attention of
the patient are usually disturbances of sensation: pareesthesie,
formication, etc., in the extremities, a girdle-sensation or perhaps
a girdle-pain at the level of the seat of disease, pain in the back
and tenderness over certain spinous processes, sometimes pain-.
ful, dragging sensations in the bladder and rectum, gastralgiec
pains and the like. These are sometimes, but not always, accom-
panied by motor symptoms of irritation: twitchings of certain
muscles or groups of muscles, violent tremor, partial clonic
spasms and in some special cases even general convulsions.
ia i
:?
ry
4
5
MYELITIS., 403
Sometimes an isolated paralysis of the bladder is the first
symptom.
Very soon, however—sometimes after a few hours, or on the
next day—the characteristic paralytic symptoms make their
appearance. Of these, the motor paralysis is the first to appear ;
it is more or less complete and involves a variable number of
muscles, usually taking the form of paraplegia, but not unfre-
quently assuming other forms.
Paralysis of the sphincters usually sets in soon after this.
It often appears very early, simultaneously with the motor para-
lysis, but in some cases it does not occur until long afterwards.
It may, however, be entirely wanting.
The same may be said of the paralysis of sensation. In all
Severe cases it sets in very early and is complete; there is then
usually complete anesthesia of the lower half of the body up to
a certain height, which is sometimes marked by a pretty sharply
defined line. In milder cases the anesthesia may be less com-
plete and less extensive, and finally in certain forms of the dis-
ease (poliomyelitis anterior), it is entirely wanting.
The reflex excitability varies according to the seat of the
disease. It may be rapidly and completely destroyed in the
paralyzed part, or it may gradually diminish as the disease
progresses, or it may remain normal, or finally it may be very
considerably increased, occasionally attaining an astonishing de-
gree of intensity.
For most cases of acute myelitis the rapid extension of the
paralysis through the cord in a horizontal direction, the com-
plete paraplegia, is to some extent characteristic; not less
so in many cases, is its rapid extension in a vertical direction,
the rapid ascent of the paralysis towards the head, the acute
ascending paralysis. These peculiarities depend on the variety
and localization of the disease in the individual cases. In
sharp contrast to them, there are others in which the paralysis
attains its acme in the very commencement, never extending
subsequently.
In almost all.the severe cases, vaso-motor paralyses, cystitis
and pyelonephritis, and extensive bed-sores which are often acute,
set inearly. All these complications may, however, be absent.
404 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The same is true of the atrophy of the paralyzed muscles, and»
of the loss or modification of their electrical excitability.
The subsequent cowrse of the disease varies greatly in the dif-
ferent cases and forms:
1. It may be rapidly progressive and Jatal. In this case,
after a few days of continuous fever with the symptoms of an
ascending paralysis, death takes place from a rapidly develop-
ing asphyxia.
2. Or the disease may run a slower and less violent course ;
the fever remains moderate or disappears entirely, but cystitis
and bed-sores are developed, bringing in their train fever, emaci-
ation and exhaustion, and the patients succumb after weeks or
months of suffering.
8. Or the acute affection may be transformed into chronic
myelitis ; the paralytic symptoms persist with slight variations
in intensity, until at some later period a slow exacerbation sets
in, and the affection then runs the usual course of a chronic
myelitis. |
4. Or an improvement sets in, which, however, always fre-
mains incomplete. The myelitic process ceases, but not until it
has irreparably destroyed a certain number of the nervous ele-
ments of the cord, as a result of which a more or less extensive
defect, such as paralysis, atrophy, contracture, anchylosis, or the
like, is left behind. The general health, however, becomes and
remains good, and the disease which he has passed through
exerts no further influence on the length of the patient’s life.
5. Or finally—and this is perhaps the rarest termination of all
—complete recovery takes place. Several reported cases demon-
strate that this favorable termination is at all events possible.
A rapid improvement sets in, and, after the expiration of a
longer or shorter period, all the bodily functions are completely
restored. Convalescence is usually somewhat protracted.
As has been stated, this clinical picture, which contains only
the most general features of the disease, can be modified in many
ways, the necessary result of which has been the differentiation
of various forms of acute myelitis, to which we will return later.
Before doing so, however, we must describe somewhat more
closely the individual symptoms.
a ae ae a a ’
MYELITIS. | 405
Among the disturbances of sensation the symptoms of irri-
tation, in consequence of the complaints of the patients, usually
assume the greatest prominence. -In a few rare cases they are |
entirely wanting, or are so slight that the patients do not speak
of them, unless closely questioned about them. Violent shoot-
ing pains are not commonly present in acute myelitis, a point of
importance in the differential diagnosis from meningitis. They
do occur, it is true, especially in the initial stage, but usually
disappear soon, seldom persisting for any length of time. They
appear sometimes in the form of neuralgic pains surrounding the
trunk like a girdle at a variable height, sometimes as a circular,
hoop-like, burning sensation in the skin, or they may consist of
dragging, tearing, boring or burning sensations in the limbs.
Pressure and movement do not usually aggravate these pains in
the extremities. They are very commonly accompanied by pain
in the back, extending over a more or less extensive area, and
also by tenderness over several of the spinous processes. This
can sometimes be recognized by passing hot and cold sponges
over the spine of the back. On the other hand, various parees-
thesis belong to the more constant symptoms of the disease.
One of them is the well-known unpleasant sensation of con-
striction as by a girdle, which is experienced not only on the
trunk, but also in the extremities and joints. Feelings of ten-
sion or swelling, and of cold or heat, pricking and sticking sen-
sations, formication, etc., are experienced over more or less ex-
tensive cutaneous areas, particularly in the lower extremities.
Gradually the feeling of numbness and furriness and the loss
of sensation become more and more prominent as the anzesthe-
sia becomes more distinct. True hyperesthesia is rarely pres-
ent in acute myelitis, and when it is, is probably due usually
to a complication with meningitis. It does, however, occur also
in unilateral circumscribed myelitis, on the same side as the
motor paralysis. Charcot describes, under the name of dyses-
thesia, a peculiar, diffuse, painful, vibrating sensation, which
is produced by touching any circumscribed spot on the skin,
and may extend to the entire extremity and even to both lower
>
extremities.
The symptoms of sensory paralysis are not usually slow in
406 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
making their appearance, though they too may be permanently
absent. The anesthesia may be more or less extensive and com-
plete; the paralysis of sensation is sometimes only partial, or
there may be merely a slowness in the conduction of sensations.
Severe pains are not unfrequently complained of in parts that
are entirely deprived of sensation—anesthesia dolorosa. Iso-
lated, jerking, shooting pains, accompanied by spasmodic twitch-
ings of the muscles, are very common in the paralyzed parts.
The explanation of all these symptoms is undoubtedly to be
sought in the development and progress of the inflammatory
changes in the spinal cord. The initial symptoms of irritation
are to be ascribed to the inflammatory and hypereemic irritation
of the nerve-elements in the gray and white substances, the later
symptoms of paralysis to the destruction of these elements and
their compression by the inflammatory exudation. The girdle-
sensations depend probably on the involvement of the posterior
nerve-roots in the inflamed spot; the parzesthesiz and anesthe-
size of the posterior half of the body, on the involvement of the .
sensitive tracks situated in the gray substance and in the poste-
rior white columns. Since these sensitive tracks lie for the most
part within the gray substance, or at all events must pass through
it for a certain distance, it is easy to account for the usually in- —
tense and complete anesthesia in acute central myelitis. Fur-—
ther, the well-grounded assumption, that the sensitive tracks run
principally or exclusively in the posterior half of the gray sub-
stance and the posterior and lateral white columns, explains
sufficiently the fact, that in myelitis involving only the anterior
portion of the gray substance (e. g., in the spinal paralysis of
children), disturbances of sensation are entirely wanting. In the
circumscribed, disseminated, and peripheral forms of -myelitis,
the degree of the disturbance of sensation will depend solely
on the extent to which the sensitive tracks are involved in the
pathological changes in the cord.
The motor disturbances also present irritative and paralytic
stages. To the former belong, in the first place, the twitchings
of individual muscles or of entire extremities, which often occur
in the initial period, and the spasmodic contractions of the: mus-
cles, which sometimes increase to a condition of tetanic rigidity ;
MYELITIS. 407
also the convulsive movements of the extremities, and finally
the initial general convulsions, which occur almost solely in chil-
dren. Much more constant and more important, however, are
the symptoms of motor paralysis, the development of which
stamps the clinical picture of acute myelitis with such a charac-
teristic impress. The paralysis may be developed with such
enormous rapidity, that we speak of an apoplectiform myelitis.
Cases have been observed, in which complete paraplegia was
developed during one night, within a few hours, and even in less
than an hour. It is, however, only in the hemorrhagic form of
myelitis that the paralysis can develop fully within the space of
a few minutes, just as it does in apoplexy of the cord. This
rapid development is the rule particularly in central myelitis ;
in the other forms of the disease, a longer period may be neces-
sary for the production of the paralysis. In such cases the mus-
cles are always perfectly flaccid ; the limbs hang or lie as if they
were dead, and when raised fall like the limbs of a corpse.
Later in the disease, if the patient survive, the symptoms of
irritation may again make their appearance in the affected limbs.
Isolated spontaneous twitchings of the muscles are observed,
which are often accompanied or excited by severe shooting pains.
A state of muscular tension, or spasmodic tonic contractions of
the muscles set in, which are excited particularly by attempts at
voluntary movement or by irritation of the sensitive nerves.
Finally, severe contractures are produced, which fix the legs in
an extended or flexed position, and are frequently rendered more
intense by attempts at active or passive movements. These
symptoms, however, belong more to the later periods of the dis-
ease, and hence are more constant in the subacute and chronic
forms.
The most common form of the paralysis is paraplegia; still
hemiparaplegia, paraplegia cervicalis and isolated paralyses of
particular limbs, as well as complete paralysis of all four extremi-
ties along with the trunk, also occur. This depends, of course,
entirely upon the seat and extent of the disease.
The pathogenesis of all these motor disturbances is not by
any means perfectly clear as-yet. There can be no doubt, it is
true, that they must be due to changes in the motor nerve-tracks
408 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
in the spinal cord, but we are unable to decide positively in
every case, whether they are due to lesions of the anterior roots,
or of the nerve-tracks in the gray substance or in the lateral
columns, or to simple reflex processes. The arguments that are
advanced in support of each of these suppositions have already
been detailed while speaking of the general disturbances of mo-
tility (see Part I., pp. 79 and 97), and to avoid repetition we may
refer the reader to that chapter. It is consequently in regard to
the localization of the morbid process, that the explanation
meets with the greatest difficulties, for it is a self-evident fact
that the inflammatory changes in the cord must be capable of
producing irritative as well as paralytic phenomena in the motor
paths.
The disturbances of reflex action are especially valuable for
the interpretation and localization of the lesion in many cases
of acute myelitis. The state of the reflex activity, both of the
skin and the muscles, may vary greatly ; it may be diminished
and even destroyed, or it may be considerably increased. In —
a portion of the cases it is abolished very soon, immediately
after the development of the paralysis, and reflex actions can
no longer be excited even by severe irritants; sometimes it is
not entirely abolished, but a longer time is required for the
production of the movements; in other cases it undergoes a
very considerable increase, so that even very slight irritations
call forth the most active, reflex muscular twitchings, which
may increase to a persistent, convulsive jerking of the para-
lyzed part; or, in still other cases, it remains unaltered or is
slightly increased for a time, and then begins to diminish and
gradually becomes weaker, finally disappearing entirely. What-
ever the condition may be, it furnishes a valuable indication
of the state of the gray substance, for it is this portion of the
cord which determines principally the state of the reflex activity.
The more intact the gray substance remains, the more confi-
dently can we look for a continuance of the reflex actions.
When a portion of the gray substance, itself intact, is sepa-
rated from its connection with the brain by a more centrally
situated myelitis (e. g., the gray substance in the lumbar portion
of the cord by a myelitis located in the dorsal region), the re-
MYELITIS. | 409
flexes are increased ; hence the exaltation of the reflex excita-
bility so commonly observed in myelitis transversa dorsalis.
When the gray substance is destroyed by the disease the re-
flexes are abolished ; hence their disappearance in myelitis of
the lumbar enlargement, and more especially in diffuse central :
myelitis, in which all reflex action is usually abolished from the
very commencement. When:this destruction of the gray sub-
stance is secondary and effected at a later period of the disease
by the extension of the inflammation downwards, the reflex
activity may be at first normal or even increased, but will sub-
sequently become weaker and gradually disappear.
Hence, we shall be able in many cases to draw from the con-
dition of the reflex excitability important and relatively sure
conclusions, with regard to the localization of the myelitis in the
gray substance. We must bear in mind, however, that the reflex
actions can also be modified by changes in the anterior roots, and
that, moreover, the lateral columns probably exert an important
influence on them—facts which warn us not to make these con-
clusions too positive.
The sphincters are very frequently involved. Vesical paral-
ysis is not unfrequently one of the earliest, and sometimes even
one of the prodromal symptoms of acute myelitis. In severe
cases there is usually complete retention of the urine, which
must be evacuated by the catheter during the entire course of
the disease. In other cases there is merely incontinence of urine,
or this is the most constant symptom on the part of the bladder.
In a word, any of those disturbances which we have described
and attempted to explain in Part I., p. 182, may be observed.
Sometimes the symptoms in the beginning of the disease are
more those of irritation, spasmodic closure of the sphincter with
increased desire to make water.
The sphincter ani behaves in a similar manner; here, too, the
most constant symptoms are those of paralysis. The explana-
tion of all these symptoms on the part of the sphincters is to be
found in the localization of the myelitis ; for further particulars
we may refer to what has been said on this subject in the gen-
eral part. .
Priapism is not an uncommon symptom in acute myelitis.
410 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
Generally the erection of the penis is incomplete, but it often
persists for days, with slight variations in degree. It must be
regarded as essentially a sign of irritation, produced either by
irritation of the nerve-tracks passing from the brain to the lum-
par portion of the cord (Comp. p. 318), or by reflex excitations
proceeding from the bladder, skin, etc.
The vaso-motor disturbances in acute myelitis have not yet
been sufficiently studied. Engelken found in one case a rise in
the temperature of the paralyzed part, but most authors speak
of the extremities as being cold. Diffuse cedema of the paraple-
gic lower limbs has sometimes been observed. The perspiration
is sometimes increased, sometimes diminished in quantity. As
recent physiological investigations have demonstrated that the
vaso-motor innervation is of a complicated nature, we must wait
for more exact observations before an explanation of these dis- —
turbances can be attempted. | 4
This applies with even more force to the trophic disturbances,
which follow in the train of acute myelitis.. They are most dis-
tinct in the skin, the most striking of them being the decubitus
acutus,’ which is developed regularly and early in the severer
forms of myelitis, and occasions great danger to life. It appears
in the well-known form of gangrenous inflammation of the skin
over the sacrum, trochanters, etc., usually progresses rapidly,
and proves fatal by septic fever. When the lesion in the cord
is unilateral, the decubitus is situated on the opposite side of
the body. It may make its appearance as early as from the sec-
ond to the fifth day of the disease. For its pathogenesis we may
refer to the remarks made in Part I., p. 123.
There is not always time for the development of. trophic
disturbances in the nerves and muscles; still, even in rapidly
fatal cases of central myelitis, the first traces of the degenera-
tive atrophy have been discovered in the muscles and nerves.
When the disease has been of somewhat longer duration, the
atrophy of the muscles is not unfrequently very marked. There
' TRANSLATOR’S NoTE.—The Germans use the term decubitus to designate bed-
sores, and for the sake of convenience it has been deemed advisable to retain it in the
translation.
: (des Lyle a7
’
_
cee
MYELITIS. 411
seems to be no question that these disturbances in the nutrition
of the muscles are directly dependent on the condition of the
gray substance. Every marked disturbance of nutrition in the
gray substance leads to rapid atrophy of the muscles, and the
study of particular forms of acute myelitis (spinal paralysis of
children) has demonstrated very positively that this influence
on the nutrition of the muscles is exerted especially by disease
of the anterior horns. Hence, wherever a considerable and rap-
idly developed atrophy of the muscles exists, we must assume
an inflammation of the gray matter.
The state of the electric excitability is of great value for the
recognition of this degenerative atrophy. Whenever rapid mus-
cular atrophy sets in, or in other words in severe affections of
the gray substance, a loss of the faradic irritability of the nerves
and muscles is also observed; and, unless greatly deceived, we
may look for the development of the reaction of degeneration
(Entartungsreaction) in all such cases. Death, it is true, often
occurs so rapidly, as to leave no time for its complete develop-
ment. In the more subacute cases, however, we shall frequently
be able to demonstrate this reaction of degeneration, and in the
forms of acute myelitis in which the changes are confined to the
anterior horns of the gray matter, it is one of the most constant
phenomena. On the other hand, there are cases of acute mye-
litis in which there is absolutely no change in the electric irri-
tability, and others in which only slight quantitative changes
in the same, slight increase or diminution, can be demonstrated.
The conclusion, that in such cases the corresponding portions of
the gray substance have remained intact, cannot be questioned.
Marked alterations in the urinary excretion occur with strik-
ing rapidity in severe cases of acute myelitis. After a very few
days (two to eight), the urine is alkaline and not unfrequently
bloody ; a muco-purulent deposit, numerous triple-phosphate
crystals, etc., form very rapidly. It is not improbable, though
by no means proven, that these alterations are directly dependent
on the acute spinal affection, andenot merely the result of the
retention of urine caused by the paralysis of the bladder.
: Cerebral phenomena are not regularly or even frequently
iN present in acute myelitis. Still they are not exactly rare in the
| ‘
412 ERB.—DISEASES OF THE SPINAL CORD AND ITs ENVELOPES.
commencement of some particular forms (poliomyelitis anterior),
though they usually last only a short time. In children espe-
cially, we observe in such cases headache, delirium, and general
convulsions. It is scarcely possible to determine, however, what
part in the production of the last-named symptom is played by
the great irritability of the central nervous system of the child,
and what part by the disease of the spinal cord. |
The headache, delirium, etc., in acute myelitis may also occa-
sionally be due to the fever, or to a complicating septicemia or
uremia.
Graver cerebral symptoms make their appearance, when a
process analogous to that in the cord is established in the brain,
where it produces its characteristic local manifestations.
Oculo-pupillar symptoms are sometimes developed in cervical
myelitis. Speaking and swallowing may also be interfered with,
when the disease involves the medulla oblongata.
The disorders of the optic nerve, of the nerves supplying the
muscles of the eye and of other cerebral nerves, which play a
very prominent réle in the clinical histories of many cases of
chronic myelitis, are unknown in acute myelitis.
On the part of the digestive organs, the most constant symp-
tom is great obstipation, for the relief of which the most energe-
tic remedies are often required. It is probably due to paralysis’
of the muscular coat of the intestines. Later on this may lead
to great meteorismus, which may become so excessive as to be
dangerous tolife. In the commencement of the disease violent
paroxysms of cardialgic pain are sometimes observed; their
pathogenesis is undoubtedly the same as that of the girdle-
pains.
Little is known concerning the behavior of the circulatory
organs. ‘The pulse is usually increased in frequency. When
the myelitis extends to the cervical portion of the cord, the in-
crease in the frequency of the pulse may be very great, and
finally a state of pronounced cardiac weakness is produced.
Many patients suffer much from palpitation or irregularity in the
action of the heart, which is accompanied by unpleasant, twitch-
ing sensations in the cardiac region.
The disturbances of the respiration are better understood and
MYELITIS. 413
more important. When the myelitis is primarily located in, or
has extended to, the cervical region of the cord, they occupy the
foreground in the clinical picture, and occasion immediate danger
to life. In cases of ascending central myelitis, the gradual en-
croachment on the respiratory movements, terminating finally in
complete paralysis, can be followed with great facility. First of
all, the abdominal muscles are paralyzed, and expiration and
expectoration are impeded. Next in order, the .intercostales
and the muscles of the trunk are affected ; as a result inspira-
tion is interfered with, and the patients breathe only with the
diaphragm. When this last-named muscle is also involved in
the paralysis, the dyspnoea becomes very intense, inspiration
being carried on only by means of increased activity of the cer-
vical muscles, and death by asphyxia very soon occurs in con-
sequence of paralysis of the respiratory centres. In this way the
fatal termination can be brought about with very great rapidity
in severe cases, death often occurring in an acute attack of dys-
pnoea. Other cases, however, are more protracted, and the pa-
ralysis is then usually complicated by pulmonary hypostasis.
The pathogenesis of the respiratory disturbances requires no
special elucidation.
The general health is greatly impaired in almost all cases.
In exceptional instances the appetite is not affected and the pa-
tients sleep well, and the nutrition of the body consequently re-
mains tolerably good. Usually, however, the fever, the psychi-
cal depression, the commencing cystitis and the decubitus occa-
sion sleeplessness and loss of appetite which are soon followed
by marked disturbance of nutrition, great emaciation and finally
exhaustion.
In the commencement of acute myelitis, fever is present only
in a small number of cases. In these cases, however, it may at
once become very high, and it may remain persistently high
throughout the entire course of the disease. Sometimes it occurs
in isolated, sharp attacks, and an excessive rise of temperature —
is not infrequently observed immediately before death. In other
cases the fever is slight, never attaing a high grade, and may even
disappear entirely during the subsequent course of the disease.
To sum up, the fever in acute myelitis is in no respect charac-
414 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
teristic. As might be expected, the cystitis, pyelonephritis, de-
cubitus and septic infection very frequently give rise in the later
stages of the disease to a symptomatic fever, which exhausts the
strength of the patients.
Course, Duration, Terminations.
With regard to the course of the disease but little can be said
that will be generally applicable, on account of the great diver-
gences presented by the individual cases. This fact is suffi-
ciently evident from what has already been said, and it will be
rendered still more apparent, when we come to speak of the dif-
ferent forms of the disease.
The abrupt commencement of the disease in almost all of the
cases, and the speedy development of the symptoms up to a cer-
tain point, are to some extent characteristic of acute myelitis. It
is the rapid development of the paralytic phenomena, rather than
the presence and the degree of the fever, which usually leads us
to characterize a myelitis as ‘‘acute.’’ Itis not exactly neces-
sary for the paralysis to be developed within a few hours, in
order to justify the employment of the term ‘‘ acute,” but it
must at all events make its appearance within a few days (about
one to ten). Cases which run a slower course may be classed as
subacute, but no sharp line of demarcation can be drawn between
the two forms.
In not a few cases the commencement of the disease is exceed-
ingly abrupt. The paralysis may develop in an apoplectiform
manner, almost without premonitory symptoms, and it may
attain considerable intensity in an hour or even less. Often, pa-
tients awake in the morning with complete paraplegia, who had
retired to bed on the preceding evening feeling scarcely at all
unwell (myelitis apoplectica). Usually, however, there is a pro-
dromal stage of variable length, and after the paralysis has com-
menced, hours or days elapse before it develops into pronounced
paraplegia. In some cases, which must also be classed as acute
myelitis, a number of days elapse before this point is reached.
Sometimes the development of the disease, instead of being con-
tinuous, is interrupted by successive pauses.
bd
MYELITIS. 415
Once begun, the subsequent course of the disease is also vari-
able. In the most violent and rapid cases (myelitis centralis,
hematomyelitis, etc.) the paralysis rapidly ascends, symptoms
of asphyxia appear, and death takes place in a few days ; or the
fatal termination is brought about by the violent fever and septi-
cemia caused by the acute cystitis and decubitus, and occurs
after a somewhat longer period, at most after a few weeks.
In the less severe cases, particularly when the entire lumbar -
enlargement with or without the dorsal portion of the cord, is
affected, the course is somewhat slower. There is complete para-
plegia with paralysis of the bladder; cystitis is gradually devel-
oped, followed by decubitus, fever, cachexia and exhaustion, and
the patient succumbs after several weeks or months.
In still other cases the transition to chronic myelitis is effec-
tuated. There is then usually complete paralysis of motion, with
incomplete paralysis of sensation and paralysis of the bladder.
The symptoms remain stationary for months and years, or pre-
sent slight oscillations, being at one time better and at another
worse. Cystitis and decubitus may develop after the disease has
persisted for a variable time, but they never become very severe,
and are susceptible of being at least partly cured. Death finally
results from exhaustion or from some intercurrent disease.
In other cases, again, the disease ceases, leaving only a few
unimportant and harmless traces of its passage. The disorders
of sensation and of the bladder, and the trophic disorders of the
skin are usually entirely wanting in these cases. The general
health is soon completely restored. The only traces left by the
disease are paralysis and atrophy of one or more muscular
groups with their consequences, the patients feeling in all other
respects perfectly well. The duration of life is not affected in
any way by the myelitis. This is the termination in imperfect
TECOVETY.
Finally, complete recovery takes place in some very rare cases.
In consequence of the lack of autopsies, however, it will always
be possible for sceptics to question the correctness of the diagno-
sis in these cases. This complete recovery probably takes place
only in the milder forms of myelitis, though these are not unfre-
quently quite diffuse. This termination usually sets in early.
416 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
After the symptoms of paralysis, the fever, etc., have persisted
for one or two weeks, they undergo a slow and gradual retro-
gression, and after the expiration of a few weeks all the func-
tions of the body are completely restored. Convalescence is,
however, almost always very protracted. Medical literature con-
tains a number of reported cases which demonstrate pretty posi-
tively the possibility of this termination.
It still remains for us to point out briefly the characteristics
of the different forms of acute myelitis, as they most frequently
come under observation.
The traumatic myelitis, which develops after severe injuries of
the cord, can be regarded as the type of acute myelitis trans-
versa. It is most frequently located in the dorsal region of the
cord. Its principal symptoms are: girdle-sensation and girdle-
pain, complete paraplegia, aneesthesia, paralysis of the bladder,
preservation and increase of the reflex excitability, absence of
muscular atrophy, retention of electric irritability; in the later
stages, symptoms of motor irritation, contractures, etc.; also cys-
titis and decubitus. The persistence of the reflex excitability is
particularly important.
Acute myelitis centralis, as described especially by Dujardin-
Beaumetz and Hayem, includes the cases which run the most
rapid course. The commencement is usually abrupt and at-
tended by disturbances of sensation; complete anesthesia and
paralysis of the lower half of the body with entire relaxation
of the joints, are developed very rapidly, often in the course of a
few hours or during a night; paralysis of the bladder and rec-
tum. The extinction of all reflex excitability and the early com-
mencement of progressive muscular atrophy, with loss of faradic
irritability, are specially important. Later on, decubitus acutus,
alterations in the urine, often cedema of the paraplegic limbs
and neuropathic articular affections, more or less intense fever,
progressive advance of the paralysis upwards, early death by as-
phyxia.
The hemorrhagic form of myelitis centralis, or hematomyelitis
(Hayem), does not differ essentially from the simple form in the
commencement. It runs the same rapid course, but the very ab-
rupt appearance of the paralysis, which becomes complete in the
MYELITIS. 417
course of a few minutes, or at most of an hour or a little more,
marks the occurrence of hemorrhages. The more rapid the de-
velopment of the paralysis, the more predominant is the hemor-
rhagic element in the process. In other respects the course is
the same as in the simple form.
Hemorrhagic myelitis can only be distinguished from simple,
idiopathic hemorrhage into the substance of the cord, in those
cases in which the hemorrhage is preceded by pronounced symp-
toms of an acute myelitis; pains, pareesthesiz, girdle-sensation,
vesical weakness, muscular twitchings, commencing paresis, fever,
etc. (Compare p. 291.)
The so-called poliomyelitis anterior acuta (Kussmaul), the
spinal paralysis of children, which occurs in isolated, circum-
scribed spots in the anterior horns of the gray matter, is clini-
cally a sharply characterized form of acute myelitis. Acute
febrile commencement, often with headache, delirium and con-
vulsions ; rapid development—in a few hours or days—of motor
paralysis, which varies in area in different cases, but attains its
maximum of extension in the very beginning ; no disturbances of
sensation, no paralysis of the sphincters, no decubitus; on the
other hand, rapidly progressive muscular atrophy, with the re-
action of degeneration ; eventually, atrophy and impairment of
the growth of the bones, deformities of the joints, etc. Com-
plete restoration of the general health, early improvement of the
paralysis up to a certain point, a number of the muscles, how-
ever, almost always remaining atrophied and paralyzed, causing
permanent deformities. (Compare Section No. 15.)
In myelitis disseminata, as described by Westphal, the clini-
cal picture is naturally not so characteristic. It ordinarily causes
paraplegia, sometimes with spastic symptoms, usually with
paralysis of the bladder. The state of the sensibility is variable;
it is sometimes more, sometimes less impaired. The same state-
ment holds true of the reflex and also of the electric excitability.
Sometimes the existence of several centres of disease can be recog-
nized from the grouping of the symptoms, the exacerbations, etc.
The development of the symptoms after acute diseases, especially
variola, or in phthisical patients, etc., might direct suspicion to
this form of the affection.
VOL. XIIL—27
418 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Acute myelitis is very frequently complicated with meningitis,
myclomeningitis acuta. The addition of meningitic changes to
the myelitic affection, although unquestionably very common, is
not specially important, since the severity and dangerousness of
the disease is not essentially modified thereby. The develop-
ment of myelitis as a complication of acute meningitis is a more
serious affair. We have already, in another place (p. 226),
spoken of this condition of affairs, and endeavored to form an
estimate of its influence on the symptomatology of acute spinal
meningitis; this influence is, at all events, greater than has
been hitherto supposed. Finally, the two inflammatory pro-
cesses can set in simultaneously, so that neither one of them is
dependent on or secondary to the other. Under all these condi-
tions, the meningitic symptoms usually assume the most promi-
nent rdle in the subjective complaints of the patients, while the
myelitic symptoms are the most striking in the objective exami-
nation. In such cases the phenomena which speak for menin-
gitis are chiefly the pain and stiffness in the back, the cervical
rigidity, the pronounced hypereesthesia, the diffused pains, etce.,
while the contractures, the severe paralytic symptoms, the paraly-
sis of the sphincters, the augmented reflex activity, etc., must be
placed more to the account of the myelitis. More exact obser-
vations and investigations are, however, necessary for the clearer
differentiation of the two processes.
Diagnosis.
In the matter of diagnosis, acute myelitis resembles many
other affections of the spinal cord; the typical cases are easily
recognized, while on the other hand, the less pronounced, the
complicated and the uncommon cases are difficult to unravel.
It is easy to gather from the preceding description, what the
characteristic symptoms are, from which an acute myelitis can be
easily diagnosticated ; acute commencement with more or less
marked signs of sensitive and motor irritation, very rapid develop-
ment of complete paralysis, vesical paralysis, bed-sores, ete.
When fever is also present, and the etiological conditions are
known, the diagnosis is easy.
MYELITIS. 419
There are several other diseases with which it may possibly
be confounded. First of all we must mention paralysis ascen-
dens acuta (see farther on, No. 17), which resembles diffuse
central myelitis in particular so closely, that it is often scarcely
possible to determine to which of the two diseases the case in
question belongs. The results of recent investigations (West-
phal) have gradually forced us to the conclusion, that paralysis
ascendens acuta is a special form of disease, entirely distinct
from myelitis. The diagnostic points, which speak rather for
acute ascending paralysis, are the following: absence of con-
vulsive movements at the outset of the affection, absence of tro-
phic disturbances, a slight degree of encroachment on sensation
and preservation of electric irritability. In many cases, how-
ever, the positive diagnosis can only be made with the help of
the autopsy.
The difficulty of distinguishing acute myelitis from menin-
gitis acuta is often very great, in consequence of the frequent
combination of the two diseases. The following symptoms speak
for meningitis: high fever, severe pain, dorsal and cervical rigid-
ity, contractures, slight symptoms of paralysis, especially on
the part of the sphincters, absence of severe trophic disturb-
ances, pronounced hypereesthesia, etc. (Compare also p. 245.)
The differentiation of hematomyelia, or simple hemorrhage
into the spinal cord, from central myelitis, and particularly from
the hemorrhagic form of that affection, is often uncommonly dif-
ficult. The diagnostic points are: the very abrupt development
of the paralysis without fever or prodroma, the stationary char-
acter of the paralysis, etc. This question has already been fully
discussed in another place (p. 303).
The differentiation of myelitis from hematorrhachis, or hem-
orrhage into the meninges of the cord, is, as a rule, easier. The
very abrupt development of the affection without premonitory
symptoms or fever, the symptoms of severe meningeal irritation,
the violent pains, the dorsal rigidity, the relatively moderate
grade of the paralytic phenomena, and particularly the slight
intensity of the aneesthesia, usually characterize heematorrhachis
sufficiently. (See p. 214.)
It is scarcely possible to confound acute myelitis with hyper-
420 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
emia of the cord. The absence of fever, the slight intensity of
the sensory and motor disturbances, the frequent and rapid
variations in the symptoms, and the absence of vesical weakness
and of bed-sores, are so characteristic of the latter affection as to
almost prevent the possibility of a mistake.
The diagnosis from hysteria can scarcely present any diffi-
culties; at all events any doubt which may arise, will be cleared
up by a few days’ delay. It is unnecessary to recapitulate here
the points of the differential diagnosis. On the other hand,
many poisons produce symptoms, which may resemble the clin-
ical picture of ascending central myelitis so closely, that the
differentiation is very difficult.
The seat of the disease in the cord and its extension in the
transverse and vertical directions, can readily be determined
from the area of the paralytic phenomena, the state of the reflex
irritability, the trophic disorders, etc. As these points have
already been repeatedly discussed, we may dispense with fur-
ther consideration of them here.
Prognosis.
The prognosis varies vary greatly. In general it is unfavor-
able, because the disease is almost always severe. There are,
however, numerous exceptions to this rule.
A perfect recovery is rare. In many cases a chronic state of
disease persists, while in others the morbid process ceases, but
leaves a legacy of incurable, although relatively harmless defects.
The prognosis, at least as far as life is concerned, is often abso-
lutely favorable (poliomyelitis anterior acuta).
This much being premised, we may state that the prognosis
depends chiefly on the location and extent of the inflammatory
process. It is not correct to say, that it always becomes worse
the higher the location of the disease in the cord. Strictly
speaking, that assertion holds true only when the disease is
located in the dorsal and cervical regions; in such cases the
higher up it is located, the greater is the liability of the respi-
ratory tracts becoming affected, hence the increasing danger to
life. On the contrary, a myelitis in the dorsal region is, ceteris
MYELITIS. ; 421
paribus, more favorable than one in the lumbar region, on ac-
count of the important centres located in the latter.
It is much more correct to say, that the prognosis depends on
the extent of the cross section of the cord involved in the process ;
the more considerable this is, the more unfavorable is the prog-
nosis. It becomes worse in proportion especially to the extent
of the gray substance involved. The central and posterior por-
tions of the gray substance seem to be particularly dangerous
in this connection, for experience teaches that acute myelitis of
the anterior horns alone is not attended by any danger to life,
although it certainly annihilates the function and the nutrition
of the muscles. In myelitis of the central gray substance, on
the other hand, the prognosis is much more unfavorable, on ac-
count of the usually unavoidable development of cystitis, decu-
bitus, ete. Weare as yet unable to say how much the more or
less extensive implication of the white columns influences the
prognosis.
The extent of the longitudinal section of the cord involved in
the processes influences the prognosis in a similar manner; it
becomes worse in a direct ratio to the longitudinal extent, or, in
other words, to the length of the diseased spot. Hence a very
circumscribed, transverse myelitis is not so dangerous as the
same affection, when it extends over a greater length of the
cord. Hence, also, the unfavorable prognosis in the progres-
sive, ascending forms of the disease, and particularly in cen-
tral ascending myelitis. A longitudinal extension of the disease
in the white columns is, however, not by any means so porten-
tous.
There are various other facts which can also be made use of
for the prognosis. A very rapid development and great intensity
of the paralysis, complete paralysis of the sphincters, early and
especially acute decubitus, progressive advance of the disease
upwards, high fever, great impairment of the general health,
disorders of respiration, dyspnea, cyanosis, etc., influence the
prognosis unfavorably. On the other hand, a moderate degree
of paralysis, absence of trophic and sensory disturbances, impli-
cation of the bladder to only a”slight extent, absence of fever
and of marked impairment of the general health, commencing
492 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
improvement of some of the symptoms, etc., are signs of favor-
able portent.
The nature of the etiological influences and the possibility of
removing them, the possible occurrence of exacerbations and
relapses, the general condition of the patients, the effects pro-
duced by certain therapeutic measures, etc., must also be taken
into account in determining the prognosis.
By close attention to all of these points, we shall in many of
the cases succeed in forming a tolerably correct judgment of the
course and termination of the disease.
Treatment.
Of a prophylactic treatment of acute myelitis, there can
hardly be any question. If there be any it consists simply in
the observation of those general rules, which are in any case
necessary for the preservation of health.
On the other hand, a causal treatment is possible in many
cases. Injuries of the spinal column must be treated surgically,
and simple concussions must also receive proper attention.
Tumors of the spinal column should be removed if possible; in
these cases the acute meningitis also requires treatment. When
the premonitory signs of myelitis make their appearance after
exposure to cold, etc., the morbid process can be perhaps arrested
or mitigated by an energetic diaphoretic treatment (diaphoresis,
hot drinks, the warm bath, the pack, derivation to the back, etc.).
Where there has been excessive bodily exertion, the same end
may perhaps be attained by absolute rest in the proper position,
a warm bath, etc. Suppressed secretions, profluvia and hemor-
rhages should be excited afresh, if there be any reason to suspect
that the suppression has had any influence in causing myelitis.
The treatment of syphilis is of special importance, when an acute
myelitis is developed in its course; in such cases an energetic
mercurial treatment must be immediately commenced and be
supplemented by large doses of iodide of potassium, ‘‘ Roob Laf-
fecteur,’ etc., when the stage of the disease indicates them.
Asa rule, however, the patients do not come under observa-
tion until the disease is developed. The measures to be adopted
ee
MYELITIS. 423
then will of course vary both in nature and in activity, according
to the form and the severity of the disease. The general features
of these measures of treatment are all that we can attempt to
describe here.
In all cases that are at all severe and threatening, an energetic
antiphlogistic treatment is indicated. This is not the place to
discuss the justifiableness of the usual antiphlogistic measures.
We are, moreover, still very much in want.of actual observations
on which to base a reliable opinion as to their efficiency in acute
myelitis. Nothwithstanding this, however, in the face of so
dangerous a disease, the energetic employment of all antiphlo-
gistic measures is decidedly indicated. Active local bloodletting
from the spine may be practised by means of leeches or wet cups,
applied several times in succession; Chapman’s ice-bag, from
which Tibbits saw very good results, may be employed; the
trunk may be enveloped in, or the back covered with, cloths
wrung out in water, which should in turn be covered with
caoutchouc-paper and flannel, and should be renewed every
few hours; to these may be added the inunction of mercurial
ointment into the back and other parts of the body—a measure
of doubtful utility, but still one which is permissible in view of
its efficiency in inflammatory affections of the eye, even when
not of a specific nature. For the same reason, small doses of
calomel, frequently repeated, may be tried, and eventually also
iodide of potassium, in sufficient doses. Brown-Séquard recom-
mends, on the ground of physiological experiment, the employ-
ment of ergot and belladonna (to combat the concomitant hy per-
zemia) ; these remedies deserve a trial.
In the majority of the cases, however, a moderate derivation
to the intestines (castor oil, ‘‘aqua laxativa,’’ mineral waters con-
taining sulphate of magnesia, senna, rhubarb, colocynth, etc.),
and also to the kidneys (by the ingestion of large quantities of
water, the use of Ems or Vichy water, of acetate of potash, etc.)
is more important and more useful. Attention must be paid to
this.
One difficult question which presents itself in the treatment
of acute myelitis is, whether or not the employment of energetic
derivatives to the skin over the spinal column, is permissible and
424 ERB.—DISEASES OF TITE SPINAL CORD AND ITS ENVELOPES.
serviceable. The results obtained by their employment in other
affections, as well as in a few cases of myelitis, have been very
encouraging, but at the same time the danger of producing ulcers,
and of favoring the formation of bed-sores, and the great annoy-
ance they cause the patients, are apt to deter physicians from
using them. I believe that, when properly used, they can do no
harm and often do good. Those which act rapidly and ener-
getically should be chosen—the hot iron, or, in less serious cases,
the blister. These counter-irritants should never be applied to
places where the skin is already very anesthetic ; all parts that
are exposed to continuous pressure should also be avoided. In
severe and threatening cases (particularly in cases of ascending
central myelitis) we need not hesitate to give them a very thor-
ough trial, since the great danger in which the patients are placed
justifies the use of severe and even dangerous remedies. Here
the greatest advantage will be derived from two bold streaks
drawn with ferrum candens, or from punctiform cauterizations
on both sides of the spine, repeated every day or two. The fa-
vorable termination of Levy’s case, in which the diagnosis of
acute myelitis was in all probability correct, speaks highly in
favor of this method.
The antiphlogistic treatment must, of course, be modified ac-
cording to the age, constitution and general condition of the
patients. The more robust the individual, the more energetic
should be the antiphlogosis; in plethoric patients a moderate
venesection may even be advisable.
The galvanic current should never be employed in the acute
forms and the acute stage of myelitis. It is only in the treat-
ment of the more chronic forms, and of the residua and sequel
of the affection, that is permissible and proves valuable.
The cases reported by Lewin! and Hitzig® might possibly be adduced in oppo-
sition to this statement. In Lewin’s case, however, the diagnosis was not quite cer-
tain. Under the galvanic treatment, which was begun on the twentieth day, the
patient did remarkably well. In Hitzig’s case, the chief affection was a subacute
meningitis.
? Deutsche Klinik. 1875. No. 11.
* Virch. Arch. Band XL. p. 445. 1867.
MYELITIS. | 425
In addition to these therapeutic measures the most careful
attention must also be paid, in the first stages, to the feeding
and the nursing of the patient; his strength must be kept up,
and all the evil consequences of the disease guarded against and
combated. In this connection the following points must be at-
tended to: absolute rest as far as possible, and of course in bed;
the patient should lie often on his side or abdomen, and not ex-
clusively on his back. It would hardly be possible to enforce
the exclusively abdominal position, reommended by Brown-
Séquard. Easily digested but nourishing food; no spirits, no
tea or coffee; absolute mental quiet; avoidance of all violent
movements of the body, especially of those caused by driving ;
careful attention to the skin, which must be washed regularly.
In the milder cases a lukewarm bath may be administered. Above
all things, every precaution must be taken to prevent the devel-
opment of cystitis and decubitus ; the directions for this will be
found in the general part (Part I., p. 193).
If we succeed in tiding the patient over the first few weeks,
or the acute stage of the disease, the case may be safely left for
a time to nature, on which our chief reliance must be placed
under all circumstances. Of course, the directions given for the
diet and nursing must still be strictly followed out. We can, to
a certain extent, count on the development of a reparative action
in the organism, which will lead to at least a partial adjustment
of the derangements. In all such cases we have to deal with sub-
acute and chronic forms of myelitis, and the treatment of these
forms, which is given at length in the succeeding chapter, then
comes into play.
The time has now come for a more supporting and stimula-
ting treatment (quinine, iron, good food, wine, cod-liver oil, fresh
air, etc.), which will further the restoration and regeneration of
the tissue ; also for the employment of baths (thermal and brine
baths), or of a mild cowrse of hydropathy ; particularly, how-
ever, for the employment of the galvanic current. For detailed
information concerning the indications for these measures and
the methods of employing them, the reader is referred to the
section on the treatment of chronic Inyelitis.
Finally, specific internal remedies, such as nitrate of silver,
426 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
chloride of gold and sodium, iodide of potassium, etc., are also
indicated now. Strychnine may also be cautiously tried.
If the case be progressively improving, the patient may grad-
ually be allowed to move about cautiously. He should be put
through a course of chamber gymnastics, etc., before he is al-
lowed to go about freely.
Finally, convalescence in the cases which run a favorable
course, may be hastened by residence in a mountainous region,
or by cold-water treatment, or by sea-baths. The patients, how-
ever, must always observe great caution for a long time, and
avoid every excess, every occasion of over-exertion and any ex-
posure to cold.
The indicatio symptomatica may be furnished by the most
different symptoms. The most important, as a rule, is the care-
ful treatment of the cystitis and decubitus, the rules for which
have been given in the general part (Part I., p. 193). The relief
of the pains and of the muscular twitchings and contractures
that follow in their train, is also often very desirable. (Morphine,
bromide of potassium, chloral, etc.) Sleeplessness may also
require treatment. Against the asphyctic condition which sets
in sub finem, and the impending cardiac paralysis, the usual
irritant remedies are almost powerless. The anzsthesias, para-
lyses, atrophies, etc., which persist after the cessation of the dis-
ease, are most:satisfactorily treated by electricity.
B. Chronic Inflammation of the Spinal Cord.—Myelitis Chronica.—Sclerosis,
Gray Degeneration.
Definition.—We enter here on a domain, the limits of which
it is exceedingly difficult to mark off. For the present we must
include under the head of chronic myelitis, many affections that
will doubtless be sifted out and more sharply defined in the
course of time.
We understand by chronic myelitis JZ those slowly develop-
ing processes in the spinal cord which run a tedious, lingering
course without fever, and which in the present state of our
knowledge are ascribed to chronic inflammation. It comprises
a A
MYELITIS. 427
consequently the processes which are designated as chronic in-
flammation in its narrowest sanse, as induration, as sclerosis and
as gray degeneration; also a portion of the slowly developing
processes of softening, and perhaps some of the cases in which
cavities form in the cord.
We include here consequently forms of disease which vary
very greatly in location and extent. In this chapter, however,
we will consider only those forms which do not possess an exact
localization, but are characterized rather by irregularity in seat
and extent. The remaining forms, especially the funicular scle-
roses, etc., will be made the subjects of special chapters.
Etiology and Pathogenesis.
The question whether an increased predisposition to myelitis
exists in certain persons, has not yet been sufficiently investigated,
but it is at any rate exceedingly probable that it does. Here too,
the hereditary neuropathic constitution presumably plays a very
prominent role; numerous facts in the etiology of tabes, multiple
sclerosis, etc., indicate this. Mental and corporeal over-exertion,
dissipation, sexual excesses, syphilis, emotional excitement, care,
grief, etc., can probably also act as predisposing causes. The
disease is most common during youth and middle age, and in the
male sex.
Chronic myelitis can, as we have already seen, proceed from
the acute form. This is not an uncommon occurrence. Hence,
all the causes of the acute must also be regarded as more remote
causes of the chronic affection. The latter, however, can also be
primarily produced by these same causes. The differences in the
degree of the external injurious influences, or of the predisposi-
tion to the disease, which determine the occurrence of an acute
affection in one case, and of a chronic affection in another, are
still unknown. Of the exciting causes the following may be
briefly mentioned : catching cold, which is one of the most im-
portant, and certainly one of the most frequent causes; often-
repeated exposure, long sojourn in damp, cold localities, sleeping
on damp earth, etc., are especially dangerous. Bodily over-
498 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
exertion, especially when combined with exposure to cold; hence
the great frequency of chronic myelitis after military campaigns.
Simple concussion of the cord without direct injury has already
been mentioned (p. 846) as a possible cause of chronic myelitis ;
also gradual compression of the cord.
Whether alterations in the circulation within the cord, such
as possibly follow suppression of habitual hemorrhages (the
menses, bleeding piles, etc.), can be the starting-point of chronic
myelitis, is still doubtful. The question whether the myelitis,
which develops in persons suffering from hemorrhoids, has a
causal connection with the latter and the disorders excited by
them, or whether we have to deal here with a purely accidental
coincidence, which, in view of the commonness of piles, would
not be at all astonishing, must still be left open.
Sexual excesses are undoubtedly rather a predisposing than an
exciting cause of chronic myelitis. Still, there are several cases
on record, in which no other cause could be discovered to account
for the disease. The same remark applies to continued, depress-
ing mental emotions.
Syphilis is unquestionably a very fruitful source of chronic
myelitis. Putting out of question the syphilitic affections of
the vertebral column and the spinal membranes, and the specific
neoplasms in the cord itself, which excite myelitis only indi-.
rectly by means of the compression they exert, the occurrence
of subacute and chronic myelitis in syphilitic individuals or
in persons who had previously suffered from the disease, is so
exceedingly frequent, that the possibility of an etiological con-
nection between Iues and chronic myelitis cannot be denied.
During the last few years I have myself met with at least a
dozen such cases, some of which I dissected. It is true, that
it is still impossible to decide, whether in these cases we have
to deal with really specific myelitis, or with simple myelitis in
persons predisposed by the syphilis to chronic inflammations.
Judging, however, from the cases in which I had opportunities
to hold autopsies, an account of which will be given elsewhere
by Dr. F. Schultze, I must for the present regard the latter as
the more probable. More attention should in future be paid to
this question, which is therapeutically exceedingly important.
MYELITIS. 429
Chronic myelitis is occasionally developed as a sequel of
various acute and chronic diseases. Langhans found chronic
myelitis with softening and the formation of cavities, in con-
nection with lepra. Chronic alcoholism, chronic lead-poisoning,
and perhaps also chronic poisoning with other metals, can like-
wise lead to chronic myelitis.
Finally, its development from irritation and diseases of peri-
pheral organs must be mentioned. Most of the cases of so-called
reflex paraplegia belong in the domain of subacute and chronic
myelitis. It is unnecessary to add anything here, to what has
been already said in different parts of this work concerning the
pathogenesis of this form of disease. We will only allude toa
case recently published by Laveran, which illustrates well the
difficulty of explaining the etiological connection between the
affection of the bladder and the disease of the cord.
Pathological Anatomy.
In many cases of chronic myelitis, the macroscopic examina-
tion reveals no noticeable anomalies. The investigations of re-
cent years have left no room to doubt, that very marked and
widespread structural changes may exist in cases where the
most careful macroscopic examination discloses absolutely no
alterations either in the color or the markings, or even in the
consistency of the cord. The changes are revealed, however,
when hardened preparations of the cord are subjected to a mi-
croscopical examination. It is unnecessary to dilate on the sus-
picion, which this discovery throws on the statements of many
excellent observers, who were content to declare a cord to be
‘‘normal’’ after a mere macroscopic or, at most, a hasty micro-
scopic examination. There can be no reason to question the
truth of the statement, that it is ¢mpossible to decide positively
from macroscopic observation alone, or from a superficial micro-
scopic examination of fresh specimens, that the cord is normal in
structure.
Not unfrequently, however, chronic myelitis causes very con-
siderable macroscopic changes. These affect, on the one hand,
the consistency and, on the other hand, the color of the cord, or
430 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
of circumscribed portions of it. There is almost always an in-
crease in the consistency—a hardening or sclerosis of the cord ;
its substance is denser and firmer, and resembles coagulated albu-
men, or it may be still denser and difficult to cut, presenting a
smooth section. This hardening is usually accompanied by a
more or less pronounced gray, or yellowish gray discoloration of
the tissue—hence the much-used name, gray degeneration.
In a minority of the cases only, do we meet with more or less
extensive softening. This is observed rather in the subacute
cases, or in the earlier stages of a chronic myelitis, which has de-
veloped from the acute form. It is sometimes met with, however,
even in primarily chronic cases, é¢. g., in the one reported by
Keen. Sometimes we meet with more or less extensive and
numerous cavities, which, in a number of the cases at least, are
by several authors correctly ascribed to chronic myelitis. ’
The spinal cord in these cases rarely presents any considerable —
change in volume. An increase in volume, or swelling of the
whole or of circumscribed parts of the cord, is least frequent ;
on the other hand, a slight diminution in volume, or atrophy,
is very common. What was formerly called consumption of the
cord, atrophy of the cord, and tabes dorsalis, in the anatomical
sense of the term, are really nothing more than different forms of
chronic myelitis. In such cases the cord is atrophic and thinner’
than usual; sometimes it is greatly shrunken. This change may
be general and equable, so that the cord still presents the appear-
ance of a cylindrical structure, but it is usually limited to its
lower half; or the shrinkage may be in the antero-posterior
direction, so that the organ has a more flattened, band-like
appearance; or, finally, the surface is somewhat depressed only
in isolated, circumscribed spots, or perhaps along the entire
length of certain columns. Everywhere the gray, degenerated
tissue shimmers through the pia.
The localization and the area of the chronic inflammation
in the spinal cord may vary greatly. There may be merely
isolated foci of disease, varying in number and size, and im-
bedded in healthy tissue. They are dense, reddish-gray or gray,
often possess a gelatinous translucency, and are either sharply
defined, or gradually shade off into the healthy tissue. When
MYELITIS. 431
there is only one focus, which does not take in an entire.
cross-section of the cord, we speak of a myelitis cirewmscripta.
When, as not unfrequently happens, there are several of these
foci scattered irregularly through the cord, we have the myelitis
chronica disseminata, or sclerosis multiplex seu disseminata,
which is usually combined with an analogous, disseminated scle-
rosis in the brain.
When the entire thickness of the cord is involved, the disease,
however, being more or less limited in a vertical direction, we
have before us the very common form to which the name mye-
litis transversa has been applied. <A portion of the cord of
variable length, but usually not more than a few inches in
span, appears grayish, translucent, shrunken and atrophied;
the line of demarcation from the surrounding tissue is not
very sharply defined, especially when, as is usually the case,
secondary degeneration has set in. On section, the tissue ap-
pears more or less firm, dense and dry, or occasionally more suc-
culent and soft.
In other cases the lesion involves only small and as a rule
distinctly circumscribed portions of the cross-section of the cord,
but extends farther in a vertical direction, sometimes stretching
throughout almost the entire-length of the organ. In this last
case we have to deal with the so-called band-shaped sclerosis,
or funicular degeneration. In this form of chronic myelitis,
different parts of the cross-section may be involved. The affec-
tion may be limited to the gray substance, and may surround
the central canal in the form of a cylinder of varying thick-
ness; in this situation it not unfrequently leads to the forma-
tion of cavities—this is the so-called periependymal sclerosis,
which Hallopeau has described minutely. Or it may be con-
fined to the anterior horns of the gray matter, one or both of
which may be affected to a varying extent longitudinally: this
is the poliomyelitis anterior chronica (Kussmaul). Or it may
be located exclusively in the white columns, usually involv-
ing a large portion of their longitudinal section, and almost
always affecting both sides symmetrically. In this category
belongs the much spoken of gray degeneration of the posterior
columns ; the degeneration may involve the entire thickness of
432 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
these columns, or it may be limited to the funiculi graciles. The
sclerosis of the lateral columns, especially of their posterior
portions, and the sclerosis of the inner portion of the anterior
columns, also belong here. We will speak more fully of these
forms in another place. Finally, the chronic myelitis may also be
confined to the periphery of the cord, forming a ring-shaped zone
lying immediately beneath the pia, and corresponding to the
normal cortical layer. This form is usually combined with
meningitis. It constitutes the ring-shaped, peripheral sclerosis,
or the sclerose corticale annulaire of Vulpian.
When the chronic myelitis extends over the greater part of
the cord, it is termed myelitis chronica diffusa. This extension,
however, is usually not uniform, some portions being much
more intensely affected than others. In many cases the myelitis
is at first circumscribed, but becomes more or less diffused in
course of time.
A close examination reveals in very many cases the presence
of the secondary degenerations, which have been often alluded
to already, and which will be more fully described in another
chapter. In an upward direction, it is chiefly the ascending
degeneration of the posterior columns, reaching to the medulla
oblongata, which attracts the attention of the observer—in a
downward direction, the descending degeneration of the poste-
rior portions of the lateral columns, reaching to the end of the
lumbar medulla. The transition from these degenerated parts to
the actual myelitic centres, is usually a very gradual one.
The meninges, as a rule, take part in the chronic myelitic
process. They also present the signs of chronic inflammation—
cloudiness, thickening, adhesions, calcifications, ete. It is un-
necessary to describe these changes here.
The nerve-roots are in many cases gray, translucent, exceed-
ingly atrophic, and converted into a wavy connective tissue, rich
in fat, but containing few or no nerve-fibres. |
The peripheral nerves also are not unfrequently found ina
state of degenerative atrophy. The muscles are then in the same
condition; they appear very atrophic, pale, rich in connective
tissue, and occasionally very abundantly supplied with adipose
tissue. These points will be considered more in detail, when we
MYELITIS. ; 433
come to speak of the forms of chronic myelitis, that are most
liable to be followed by these degenerative processes.
Furthermore, at the autopsy we often find changes in the
joints (erosion, deformity or destruction of the cartilages, thick-
ening of the capsule, serous accumulations, etc.) ; more or less
extensive and often gangrenous ded-sores on different parts of
the body; marked vesical changes (hypertrophy and ulcera-
tion or diphtheritis of the mucous membrane, hypertrophy of the
muscular coat, etc.) with consecutive pyelitis and nephritis, etc.
We find also many other changes which are partly consecutive
to the severe, chronic spinal paralysis, partly symptomatic of
accidental, intercurrent diseases, but which it is unnecessary to
describe here.
We possess a great abundance of isolated observations bear-
ing on the microscopical lesions of chronic myelitis. In general,
however, there is still but little unanimity on the subject, least
of all concerning the interpretation to be placed on what has
been discovered. We cannot, of course, enter here into all the
details, since many of the points in dispute are as yet undevel-
oped, and for the practising physician of but little importance.
Neither have we to speak of the methods of investigation, as that
is a subject which belongs in the domain of pathological anat-
omy; essentially, all the discoveries have been made by the
study of hardened preparations, colored and rendered trans-’
parent by various methods.
It is probable that many different processes are still classed
together under the head of chronic myelitis. The changes enu-
merated in the following paragraphs are, however, common to
all these forms, and constitute in all probability the essence of
the process.
Changes in the connective tissue or the neuroglia: increase
in the thickness and width of the individual fibres and septa of
the reticulum ; gradual transformation of the tissue into a deli-
cately fibrous, fibrillated connective tissue. Aceording to From-
mann the fibrillee are developed within the old, enlarged neuroglia
fibres and cells. They form finally a dense tissue, composed of
delicate, fibrillated fibres, usually arranged in long wavy bun-
dles. The neuroglia-cells enlarge, and their nuclei undergo
VOL, XIII. —28
434 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
proliferation; they become more numerous and more distinct.
Nowhere can Deiter’s cells be found more perfect and more
developed than in chronic myelitis; truly gigantic specimens
with numerous processes are often found. The change consists
consequently in a gradual conversion of the normal neuroglia
tissue into a fibrillated, delicately fibrous connective tissue, ac-
companied by proliferation of the cells and their nuclei.
Changes in the nervous elements : sometimes the nervejibres
are swollen, the medullary sheath being irregularly thickened,
crumbly and in a state of commencing degeneration ; in this case
numerous swollen azis-cylinders, which present spindle-shaped
enlargements and are fused with the medullary sheaths, are also
found. More frequently, however, we find pronounced atrophy
or a starved condition of the fibres, with destruction of the
medullary sheath, sometimes by fatty degeneration, sometimes
without apparent change of this sort. The naked axis-cylinders
then often remain in statu quo for a considerable time; but
finally, they too undergo atrophy and become shrunken and de-
stroyed. Sometimes they are found stiff, brittle, very brilliant,
and indurated.
The ganglion-cells are sometimes clouded and swollen, and
contain vacuoles. More frequently, however, they are dimin-
ished in size, strongly pigmented, shrunken, atrophied and in-
‘durated, and are finally converted into small, unrecognizable,
angular structures, in which neither nucleus nor nucleolus can
any longer be discovered, and which have lost their processes.
Changes in the vessels. —The walls of the small arteries and
veins, and of the capillaries as well, are considerably thickened,
and their calibre is lessened. This of course varies very greatly
in degree in different cases. The walls, especially the adventitia,
are converted into a thick, homogeneous, often indurated mass,
presenting proliferation of nuclei, collections of fat- and pigment-
granules, and not unfrequently also granule-cells. The peri-
vascular space is filled with cells and exudation ; fusion of the
wall of the vessel with the surrounding, indurated connective
tissue ; sometimes aneurysmal dilatations of the vessels.
Appearance of heterogeneous elements : of these the fat-gran-
ule-cells (Fettkérnchenzellen) are the most frequently met with ;
MYELITIS. 435
they are sometimes numerous, sometimes scanty, at one time de-
posited around and in the walls of the vessels, at another scat-
tered through the connective-tissue septa, and again arranged in
rows, apparently in the spaces that, under normal circumstances,
contain the nerve-fibres. This very difference in distribution
indicates different modes of production.
Corpora amylacea are also usually found; they are some-
times present in immense numbers, scattered throughout the
entire tissue, but at other times only a few can be discovered.
All these things will be found in the different stages of chronic
myelitis. Not unfrequently they will all be found at the same
time in the same cord, provided different parts of it be the seat
of different stages of the process.
It is evident, that the different age of the process must
occasion characteristic differences in the histological picture.
All the details of these differences have not yet been thoroughly
settled, but still the various stages of the disease can be charac-
terized histologically about as follows:
1. The earliest stage.—Thickening and swelling of the inter-
stitial tissue; greater succulence of the tissue; proliferation of the
nuclei, slight swelling of Deiter’s cells ; commencing thickening
and alteration of the walls of the vessels; nerve-fibres rather
swollen, medullary sheath in a state of incipient degeneration ;
axis-cylinders often no longer distinct; ganglion-cells clouded,
irregularly swollen, with fewer processes, etc.; more or less
abundant fat-granule cells, and a few corpora amylacea.
2. Later stage.—More warked increase of the interstitial
tissue, close network of thick neuroglia-fibres, proliferation of
the nuclei, increase of the neuroglia-cells, great thickening of the
walls of the vessels; distinct atrophy of the nerve-fibres, a num-
ber of which have disappeared. On the other hand, the axis-
cylinders sometimes survive for a very long time (particularly
in the so-called multiple sclerosis, for which it seems to be to
some extent characteristic—Charcot, Leyden). Ganglion-cells
atrophic, sclerosed and in part destroyed; fewer fat-granule
cells, more corpora amylacea. The fissue in general, of greater
density. )
3. Last stage.—Almost exclusively connective tissue ; a dense
436 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
tissue, composed of delicate fibrillated fibres in a state of inex-
tricable entanglement, with tolerably numerous nuclei and cells ;
the latter often strikingly developed and distinct. Walls of the
vessels greatly thickened, vascular lumen narrowed or in rare
instances enlarged. Only a few, isolated nerve-fibres are still
recognizable ; the greater part of the fibres have disappeared,
and most of those which remain are atrophic; many naked
axis-cylinders. Ganglion-cells shrunken to unrecognizable ele-
ments, or entirely destroyed. Very few fat-granule cells, but
corpora amylacea, on the other hand, usually very numerous.
The entire tissue very dense, firm, dry and shrunken. These
are the appearances presented in the oldest cases, which have
lasted several or many years.
In many cases extensive cavities are found in the cord—this
is probably the terminal stage of a very chronic myelitis charac-
terized by softening. We shall return to these cavities in another
chapter.
These are the chief lesions found in chronic myelitis. When we attempt to
interpret them, various questions force themselves on our notice, the solution of
which still presents considerable difficulties. We cannot, however, well avoid de-
voting a brief space to a consideration of them.
In the first place, the question arises, whether in all these processes, we have really
to deal with a chronic inflammation? We cannot spare time for a close examination
of this general pathological question. According to the principles that are still
generally accepted, the term chronic inflammation (cirrhosis, etc.) is in accord with
the anatomical lesions, which are analogous to those found in other organs when
the seat of chronic inflammation. The matter, however, is still very open to dis-
cussion, especially the question whether the process in many cases may not be one
of simple or of degenerative atrophy. This interpretation may apply to the so-
called ‘‘secondary degenerations,” which some authors are disposed to class among
the chronic inflammatory processes (Charcot, Hallopeau). The anatomical picture
of secondary degeneration can certainly resemble very closely that of chronic
inflammation. Joffroy asserts that in experimental myelitis, he found swelling and
hypertrophy of the axis-cylinders in the actual focus of inflammation, but not in
the parts which had undergone secondary degeneration ; this would indicate a
difference in the two processes. This observation, however, requires confirmation,
especially as it contradicts the statements of other observers. In secondary degen-
eration we have to deal essentially with that form of degenerative atrophy which
occurs in the nerve-trunks, when they are cut off from their nutritive centres.
(Compare our description and explanation of this in Vol. XI., p. 412.) It is true
MYELITIS. | 437
that this atrophy also is not unfrequently spoken of as an actual inflammation ; it
must then be regarded, however, as a specifically neurotic inflammation. Very
plausible also is the theory, that in such cases there is a primary degeneration of
the nerve-fibres, the products of which exert an irritant action on the interstitial
tissue, and excite in it a slow, chronic inflammation (sclerosis). A process of this
sort might well occur primarily in many forms of the band-shaped affection, and
it would furnish a simple explanation for the fact, that interstitial, chronic inflam-
matory changes exist also in the gray degeneration. or degenerative atrophy of the
spinal cord.
This brings us to a second very important question, namely, whether the chronic
inflammatory process always has the same point of departure, be this from the con-
nective tissue or from the nervous elements? Whether, in other words, we must
assume an interstitial or a parenchymatous inflammation, or perhaps both together ?
To this question also we are as yet unable to give a decided answer. It seems both
possible and probable, however, that both forms of inflammation may occur; au-
thorities whose opinions carry weight, maintain this and claim that they possess
observations which prove it. In general, however, we have to deal here with as-
sumption against assumption. Charcot and his disciples do not hesitate to distin-
guish the interstitial myelitis or sclerosis from the parenchymatous form. In the
former it is claimed that the process begins in the connective tissue, the nerve-fibres
not being involved until the affection has reached its later stages; hence the fibres
and axis-cylinders remain unaltered for a long time (disseminated sclerosis). In the
latter, on the contrary, the process begins with irritation and degenerative atrophy
of the nerve-fibres and ganglion-cells, and involves secondarily the interstitial tis-
sue (band-shaped sclerosis of the posterior columns, progressive muscular atrophy,
probably also secondary degenerations), It is, in the present state of our knowl-
edge, difficult to demonstrate the correctness of this view. An unprejudiced exami-
nation of preparations from both forms of the disease shows that there are no
essential differences in the histological appearances, that the same alterations may
occur in both forms, and that all theories concerning the mode of their production
are more or less gratuitous.
Theoretically the thing is certainly possible and even probable, but it can by no
means be admitted as proven. It is, in fact, very difficult to decide the question
from a purely anatomical standpoint. At all events, it does not seem to us justifi-
able to confine the term chronic myelitis solely to the so-called interstitial sclerosis,
and to deny the character of an inflammatory process to the so-called parenchyma-
tous sclerosis. To us, at least, it seems better and simpler to designate for the pres-
ent all these forms together as scleroses, and to differentiate them chiefly according
to their localizations.
Another and a better differentiation will only be possible when a third ques-
tion is decided, namely, whether the pathological process in all these forms of dis-
ease, which histologically present essentially thg same picture, is actually the same ?
Whether, consequently, the different conditions described as induration, gray degen-
eration, multiple sclerosis, secondary degeneration, etc., are to be ascribed to one
488 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
and the same distinct disease, namely, chronic myelitis, of which they constitute only
different forms, or whether they represent essentially different diseases? In our
opinion it is still impossible to decide this question with positive certainty. The
French school in particular classes the secondary degenerations with myelitis and
the band-shaped scleroses. With all reverence for the value of the evidence fur-
nished by the histological appearances, we cannot repress a modest doubt of the
correctness of this view, a doubt which is based chiefly on physiological and clini-
cal considerations. There is another point on which, as it seems to me, most ob-
servers agree, and that is that the processes in tabes and multiple sclerosis are not
entirely identical, but present certain differences which cannot as yet be defined
with satisfactory precision.
There undoubtedly remains much to be done in this department, but judging
from the great strides that have of late been made in the development of the path-
ological histology of the spinal cord, we may confidently expect that the concep-|
tion of chronic myelitis will be cleared from its obscurities in a not very distant -
future.
Pathology of Chronic Myelitis.
Symptoms.
In consequence of the great diversity of the processes and
forms of disease, that are included under the term chronic myeli-
tis, it is difficult, if not impossible, to draw in connected strokes
a general clinical picture of the affection.
The following description consequently applies more to the
general type of chronic myelitis, and particularly to the so un-
commonly frequent myelitis transversa, where one large focus of
disease exists at any height in the cord, or where there are sev-
eral foci, one of which, however, determines chiefly the clinical
picture. 5
In the majority of the cases belonging in this class, there is a
slow, creeping, almost unnoticed development of spinal symp-
toms, which vary in nature and location. Sensory disturbances
are usually the first to attract the attention of the patient, but
they ordinarily discommode him but little. They consist of ab-
normal sensations in the lower, more rarely in the upper extrem-
ities, parcesthesiee, anzesthesie, and the like, which, however, are
subject to frequent fluctuations, and may even at times entirely
disappear. They are frequently accompanied by a girdle-sensa-
~~ “4
ne
MYELITIS. 439
tion in the trunk at a varying height, or perhaps also in the
extremities. Severe painful sensations are rare, as are also
hypereesthesize of any degree of severity. All these symptoms
are exceedingly variable and inconstant, and only very gradually
attain any great degree of intensity and stability.
Slight motor disturbances next present themselves and de-
velop in a very analogous manner. ‘They may, however, open
the scene. A feeling of weakness and of slight fatigue, and a
certain heaviness and uncertainty of gait, are the first symptoms
to attract notice. The patients are incapable of making any
great exertion, and very quickly become fatigued. These symp-
toms also may fluctuate considerably in intensity; they are often
neglected for a long time and ascribed to all possible causes but
the right one, until finally, in common with the sensory disturb-
ances, they assume graver significance.
Sometimes the disease commences with vesical weakness, with
slight incontinence or retention, more rarely with pronounced
paralysis of the bladder. These symptoms may exist for weeks
or months, before the other signs of the disease make their ap-
pearance. Constipation is almost always present, even in the
earliest stages of the disease.
After a time, as the disease progresses, all the above-men-
tioned symptoms are found in combination ; a slow, progressive,
or sometimes an intermittent aggravation of the symptoms is
noticed. Not unfrequently we observe a more rapid advance
of the disease, a suddeu, marked aggravation of the symptoms,
under the influence of some injurious agency, such as over-exer-
tion, exposure to cold, sexual excesses, the improper use of
baths, and the like. Finally, after the disease has lasted a vari-
able time—several months or even years—the clinical picture is
thoroughly developed, usually taking the form of typical spinal
paraplegia with all its consequences. There is distinct paral-
ysis, varying in degree from paresis to complete paralysis; it
generally takes the form of paraplegia, but may assume any other
possible form. Anesthesia of greater or less intensity is rarely
wanting. It varies in point of extension, but usually involves
the lower extremities and the trunk up to a variable height.
Partial paralysis of sensation and retardation of the sensory con-
440 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
duction occur. Paresthesie and dyseesthesie in the paralyzed
parts are not rare. Usually, however, the motor is more intense
than the sensory paralysis. The sphincters are almost always
involved ; the different varieties and degrees of vesical paralysis
are met with, and similarly there may be mere weakness of the
sphincter ani, or involuntary and unconscious passages from the
bowels. A marked increase of the reflex activity usually occurs ;
a spontaneous twitching of the muscles, which is often accom-
panied by severe pains, and muscular contractions and contrac-
tures, etc., are also met with. The sexual power is wont to ex-
pire early.
In the form of chronic myelitis, to which the above deserip-
tion chiefly applies, the reflex excitability may be lost after a
time. Progressive atrophy of the muscles, changes in the skin,
nails and joints, and chronic decubitus, with all its consequences,
may also occur. When vesical derangements exist, cystitis
rarely remains long absent. All these symptoms, however, are,
as a rule, developed very slowly, and only very kis attain
dangerous intensity and extent.
The disease may terminate in different ways. A more or less
complete recovery may very slowly take place, or the affection
may become stationary and remain so for many years, or a fatal
termination may be gradually brought about in various ways.
The clinical history is essentially the same as that of the anal-
ogous form of acute myelitis, the only differences being the very
slow and gradual development of the disease, the entire absence
of fever, and the usually excellent state of the general health of
the patient. The duration of the disease is always very pro-
tracted ; it must be reckoned by years.
The preceding clinical picture applies, as has been already
stated, only to one of the many forms of chronic myelitis. It
would require too much space, to describe in a similar manner
- the other forms, in which the seat of the disease is different, and
we must content ourselves for the present with the brief charac-
terization of them which is given below. For further particulars
concerning them, we must refer to the appropriate chapters.
MYELITIS. 441
When we analyze the individual symptoms of chronic myeli-
tis, we meet with the same pathogenetic conditions as in the acute
disease. A detailed description and minute investigation of them
would consequently only lead to needless repetitions. Still, there
are many points, which it is necessary for us to examine more
closely before proceeding further.
Among the sensory disturbances the s ymptoms of irritation
play a comparatively unimportant réle. There are cases in which
pain is entirely absent throughout the entire course of the dis-
ease. In other cases, however, very violent pains are expe-
rienced, particularly during the stage of development, or very
Severe paroxysms of pain occur at intervals during the entire
course of the disease. The spasmodic muscular contractions of
the later stages are usually accompanied by very intense pains,
and I have seen cases in which peripheral sensory irritations,
such as the dressing of a bed-sore, passing the catheter, etc., ex-
cited violent radiating pains in the back or the extremities. The
peculiar, vibrating, painful sensation produced by touching the
skin, to which Charcot has applied the term dysesthesia, is also
met with. |
The so-called paresthesie are more frequently observed :
the girdle-sensation, formication, numbness, cutaneous burning,
furry feeling, etc., are very common. Finally, anesthesia is
almost regularly developed in the later stages of the disease ;
there are cases, however, in which it is entirely or almost en-
tirely absent. The anesthesia may vary greatly in degree. All
possible forms of sensory paralysis, from mere slowness of con-
duction to the most complete anesthesia, may occur. It is not
necessary to describe these things in detail; for an explanation
of them we may refer to the general part (p. 66 et seq.).
Among the motor disturbances also, the symptoms of irrita-
tion are of subordinate importance, particularly in the first
stages. Usually there is only an occasional, slight, muscular
twitch, or a sudden twitching movement of the legs, or the like ;
there may also be slight muscular contractions and trembling of
the legs after fatiguing exertion, or when the weight is laid on
the toes.
The signs of paralysis, however, are usually much more im-
442 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
portant and more prominent. Ordinarily, the first symptoms are
marked weakness, loss of tone, and a sense of fatigue. In the
early part of the disease these symptoms are not unfrequently
relieved by moderate movement, such as walking; the patients
feel stiffer and more fatigued at starting out than after they have
walked for a time. As the disease progresses the stiffness and
helplessness become more marked and are objectively evident.
The movements are slow and stiff ; the fingers and toes, for in-
stance, can no longer be moved about quickly, or this is only
possible with the help of many associated movements. The
legs feel heavy, ‘‘as if they were filled with lead,’ and the feet
are dragged along the ground, the toes readily catching in
every slight inequality. The walk has a pronounced paralytic
character.
Gradually both walking and standing become impossible.
When the patients attempt to stand they collapse; their legs:
can no longer sustain them. Even while lying down the move-
ments become progressively weaker and less frequent, until
finally, the case terminates in complete paralysis. This may
vary greatly inform. In the great majority of the cases it takes
the form of paraplegia, but it may occasionally appear as hemi-
paraplegia or spinal hemiplegia, or even cervical paraplegia, ete.
The spastic symptoms may return again in a later stage.
First of all, a gradually increasing contraction of the muscles
sets in; this is manifest at first only during passive motion, but
it soon becomes evident also during the voluntary movements,
which are impeded and retarded by it. The characteristic ‘‘ spas-
tic’’ walk, which we have described elsewhere (Part I., p. 97), is
now developed. The muscles become more and more tense and
rigid, until finally a state of permanent and more or less marked
contracture is produced. This may affect either the extensors or
the flexors, the latter being, as a rule, attacked only in the later
stages of the disease. The adductors are likewise almost always
involved. The stiff and paralyzed limbs are not unfrequently
shaken by twitches and spasmodic movements, which either
arise spontaneously or are excited by sensory irritations. These
twitches and movements are often exceedingly active and may
resemble voluntary movements; they are often accompanied by
PO) i ee 0
ee
MYELITIS. 443
severe pains. They are most readily excited by sensory irrita-
tions: cutaneous irritation, catheterization, micturition or defe-
cation, traction on the tendons, etc. They may develop into long-
continued, convulsive tremor of the lower extremities. Sometimes
all voluntary movements are accompanied and followed by this
spasmodic muscular action.
The various, special disturbances of motion, such as the ataxia, the tremor
accompanying yoluntary movements, etc., which occur in other distinctly localized
forms of chronic myelitis, will be described more minutely in the appropriate
chapters.
All the motor disturbances are very readily explained by the
chronic inflammatory processes going on in the motor conduct-
ing tracks and central apparatus, although it is not always pos-
sible to determine the exact point in the central nervous system,
at which these processes are located. Of late it has become cus-
tomary to ascribe the spastic symptoms, which develop during
the later stages of the affection, to secondary degeneration of
the lateral columns. It cannot be denied, that there are good
grounds for this assumption.
The vaso-motor disturbances in chronic myelitis are, as a rule,
not of a very striking nature, The coldness of the feet, which is
very frequently complained of and proves very annoying to the
patients, probably belongs here, as does also the often observed,
cyanotic, bluish-red color of the lower limbs. In consequence
probably of the very slow development of the obstruction to con-
duction, the vascular innervation is able to adapt itself to the loss
of a part of its spinal centres, so that the resulting derangements
are not very marked.
The state of the reflex irritability varies. In the majority of
the cases it is increased and is very active. Very curious things
are often observed in this connection; reflex movements of the
strangest kinds are produced by irritation of all imaginable sensi-
tive regions. Tickling the soles of the feet causes active jerking
and kicking movements in the paralyzed legs; colic pains, the
introduction of a catheter, the act, of dressing a bed-sore, etc.,
may excite movements in the legs. I have seen evacuation of the
urine produced by irritating the skin of the feet, or by introduc-
| 444 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
ing the finger into the rectum; erections produced by rubbing
gray ointment into the thighs ; a discharge of faeces occur during
the dressing of a bed-sore, etc. The tendon-reflexes are also, as
a rule, abnormally active, often excessively so. The slightest irri-
tation of the tendon of the quadriceps extensor femoris causes a
reflex movement, which can readily be made to develop into
clonic spasm. The most marked clonic spasm of the muscles of
the calf can be excited by passive flexion of the foot; reflex
movements can also be produced by irritation of the tendons of
the adductors and of numerous other muscles.
- Both of the conditions which are known to lead to increase
of the reflex activity—destruction of the connection between the
reflex apparatus and the brain, and abnormal irritability of the
gray substance—may be present in chronic transverse myelitis,
It is probable that in most of the cases the increase is due to a
combination of these two conditions.
On the other hand, there are cases in which the reflex irrita-
bility is diminished, or even entirely abolished. In such cases
we must, in accordance with the views at present held, assume
either that the gray substance is very extensively involved, or
that the conducting power of the nerve-roots which come into
play, is destroyed by the myelitis.
There is an unmistakable parallelism between the state of
the reflex excitability and the state of the electric irritability of
the nerves and muscles. When the reflexes persist, the electric
excitability is also, as a rule, preserved. In the majority of the
cases, I have found the latter to be both qualitatively and quan-
titatively normal. In a few isolated cases there was a distinct
increase in the faradic and galvanic excitability (without quali-
tative anomalies) of the nerves of the paralyzed limbs; in other
cases there was an unimportant quantitative diminution of this
excitability. I am as yet, however, unable to say, whether or not.
this pathological state will afford us any assistance in determin-
ing the seat, stage, or course of the disease.
In those cases, however, in which the reflexes are abolished
in consequence of extensive implication of the gray substance,
atrophy of the muscles usually sets in, accompanied by loss of
their faradic excitability (probably with the reaction of degener-
MYELITIS. 445
ation in the majority of the cases). In certain forms of chronic
myelitis, which we can with great probability locate in the an-
terior horns of the gray matter, this state of affairs constitutes
the rule, the loss of electric irritability occurring remarkably
early and rapidly.
Further and more accurate investigations of these phenomena
in chronic myelitis are greatly to be desired.
There is a very close connection between the electric irrita-
bility and the state of the nutrition of the muscles. Usually the
latter is intact and good, and it can remain so during the entire
course of the disease. In other cases a slow, progressive atro-
phy of the muscles sets in in the later stages—a sign that the
gray substance has become more extensively involved. In still
other cases a rapidly progressive atrophy of the muscles is ob-
served, which sets in early, and is accompanied by the reaction
of degeneration. The territorial extent of the atrophy varies
greatly ; it depends on the extent of the central disease. Some-
times the upper extremities are chiefly or alone affected by the
atrophy, the lower limbs presenting simple paralysis without
atrophy. This is easily accounted for by differences in the
condition of the gray substance of the cervical and the lumbar
enlargements.
In regard also to other trophic derangements, the individual
cases vary greatly. They are entirely wanting in some forms
of chronic myelitis, of which we will presently give brief de-
scriptions; as a rule, disorders of sensation and of the bladder
are also wanting in such cases. Frequently, however, and more
especially in cases of myelitis transversa, decubitus is devel-
oped sooner or later, generally in the chronic form already de-
scribed (Part I., p. 122); sloughs form in the usual places of’
predilection, their formation being not unfrequently hastened by
more or less accidental agencies (sitting or lying in the same
position for a long time, unusually severe pressure or other me-
chanical injury, a long railroad journey, febrile diseases, etc.).
Sometimes, when the patient has not been nursed with proper
care, the attendants will be astonished by the unexpected dis-
covery of a bed-sore, which has already attained large dimen-
sions, on the nates or over the sacrum. The sore may develop
446 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
and spread with more or less rapidity, but it usually runs a
chronic course. When great attention is paid to cleanliness,
etc., the parts first affected may, after separation of the sloughs,
heal up in the course of a few weeks or months ; fresh bed-sores,
however, constantly form in other situations, often in considera-
ble numbers, or the already cicatrized spots break out afresh on
the slightest provocation. The patients, even when they are
covered with large ulcers, may, if carefully nursed, drag out a
miserable existence for a long time, until finally death ensues
from exhaustion. Under all circumstances the formation of ex-
tensive sloughs is an unfavorable sign; it marks the beginning
of the end. In some rare cases large decubitus ulcers may be-
come permanently cicatrized, even though there be no noticeable
improvement in the primary disease. I have at present one such
case under observation. With respect to the pathogenesis of the
bed-sores in chronic myelitis, we have nothing to add to the re-
marks made in the place mentioned above.
In the forms of chronic myelitis which more especially engage
our attention here, the sphincters are almost always involved in
the paralysis to a greater or less extent. The vesical functions
in particular are almost regularly impaired at an early period;
there are some exceptional cases, however, in which the bladder
remains unaffected throughout the entire course of the disease.
In many cases the vesical paralysis is the first symptom, and pre-
cedes the other manifestations of the disease often by a consider-
able period (Laveran’s case). It may present any of the different
forms and degrees which have been enumerated elsewhere (Part
I., p. 182); it may vary from slight retention of urine to complete
incontinence, or constant dribbling of urine. The variations in
the localization and extent of the myelitis explain sufficiently
these differences in the vesical symptoms. Naturally, cystitis
with all its evil consequences, which render the nursing and treat-
ment of the patient so much more difficult, does not remain long
absent under such circumstances. Pyelitis and nephritis may
set in later, and hasten the fatal termination. The functions of
the rectum usually suffer in an analogous manner to those of the
bladder.
Sexual power is usually impaired early. As a rule, it dimin-
MYELITIS. 447
ishes with more or less rapidity, and finally disappears entirely.
Notable exceptions to this rule are met with, however, particu-
larly in cases of incomplete paraplegia, and in those forms of
chronic myelitis which affect chiefly or exclusively the voluntary
motor apparatus.
The general nutrition often remains perfect for a very long
time. It is not at all rare to meet with patients, whose blooming
and well-nourished appearance presents a most striking contrast
to the state of perfect helplessness, to which they are reduced by
a complete paraplegia or some other form of paralysis. This is
to some extent characteristic of certain special forms of chronic
myelitis, which will presently be described. In all the more
severe and progressive cases, however, a constantly increasing
disturbance of the general nutrition is observed, though usually
not until after the development of cystitis and bed-sores. Loss
of appetite, fever, repeated chills, digestive derangements, pro-
gressive emaciation and finally complete exhaustion generally
constitute the final symptoms in such cases, provided some inter-
current disease does not terminate life sooner.
With regard to the disorders of the cerebral nerves and of the
brain itself, we have but little tosay. There are cases of chronic
myelitis, e. g., of tabes and multiple sclerosis, in the clinical
picture of which disorders of certain cerebral nerves, such as the
optici, the nerves of the muscles of the eye, the faciales and the
hypoglossi, occupy an important position; there are other cases,
in which psychical disturbances and disorders of speech and of
the voice are equally prominent. We will return to these symp-
toms in the appropriate chapters.. In the cases of myelitis trans-
versa, however, which interest us more especially at present,
cerebral symptoms and disorders of the cerebral nerves are usu-
ally entirely wanting throughout the whole course of the disease,
or, at most, they occur during the agony. Finally, there are
cases in which the process slowly ascends until it at last reaches
the medulla oblongata ; disorders of deglutition, speech, respira-
tion, circulation, etc., are then produced, and bring about the
fatal termination. The sequence and grouping of these symp-
toms follow naturally from the functions of the cervical marrow
and the oblongata, and it is unnecessary to describe them in
448 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
detail, especially as they present very great differences in the
individual cases.
Course—Duration— Terminations
When the chronic form of myelitis is developed from the
acute form, it is preceded by the symptoms of the latter; some
of these symptoms undergo a gradual retrogression and the gen-
eral health improves, but the paralyses, pains, contractures, etc.,
persist and subsequently become slowly and gradually more
developed.
In the other cases, we observe the slow, lingering development,
which has been briefly described above. Of course the individ-
ual cases do not resemble each other exactly in every particular,
but the fundamental characteristic of the disease always remains
the same; it is the successive, gradual appearance of the various
spinal symptoms, their development from insignificant begin-
nings which often attract little or no attention. Sometimes the
‘development of the affection, instead of being continuous, is in-
terrupted by intervals of more or less marked improvement;
these alternate with exacerbations and slight relapses, each of
which leaves its mark in an increase of the disturbances.
When the disease has attained a certain height it may remain
stationary for many months or even years, or it may slowly pro-
gress and terminate in different ways. The great multiplicity
of the morbid conditions included under the term chronic mye-
litis, makes it impossible to give even an approximate estimate
of the duration of the disease. All we can say is that it is an
affection whose duration can only be measured by years. In not
a few cases, many years elapse before the final termination is
reached, while in others the disease may persist during the life-
time of the patients, without directly threatening existence.
It very rarely terminates in recovery, and when it does the cure
is usually exceedingly incomplete. Moreover, relapses are very
liable to occur, and they furnish good reason to doubt the reality
of the cure. Various residua, such as paralyses, atrophies, par-
tial anezesthesias, deformities, vesical disorders, etc., often remain
behind permanently, even when the actual morbid process has
ae
MYELITIS. 449
undoubtedly ceased ; hence the recovery must be regarded as in-
complete.
In one relatively mild case that came under my own observa-
tion, an intercurrent ileo-typhus exerted a very favorable influ-
ence on the course of the disease. In another case, an inter-
current scarlatina seemed to exert a similarly favorable influence.
A slow progressive course, leading gradually and in different
ways to a fatal termination, is, however, so much more common
as to be almost therule. The process may slowly creep upwards,
until, at last, disturbances of deglutition and respiration set in,
and death is caused by asphyxia. Or the secondary affections
caused by the myelitis, the decubitus, cystitis, pyzemic and septi-
ceemic infection, etc., destroy the vital powers of the patient and
lead to death by exhaustion. In such cases we sometimes ob-
serve a peculiar final stage, or stage of agony, in which death is
preceded for days by high fever, chills, somnolence, delirium,
signs of collapse, etc., for which the autopsy reveals no cause.
Finally, death may be due to the development in the medulla
oblongata or in the brain of a process analogous to the myelitis,
or if may be caused by accidental, intercurrent diseases (pneu-
monia, typhus, choleraic diarrhoea, etc.).
Different Forms of Chronic Myelitis.
In what precedes we have sought to delineate the clinical his-
tory of myelitis transversa ; if we exclude from consideration
those well-marked forms, which are sharply localized in particular
parts of the cord, and to which special chapters will be devoted,
it is the most common and typical form of the affection known as
chronic myelitis in its narrower sense. To briefly recapitulate,
the typical picture of myelitis transversa is about as follows :
Slow development and persistence of spinal symptoms, which
vary according to the height at which the disease in the cord is
located; symptoms of irritation not very prominent; girdle-
pains, pains in the back and paresthesiz, indicating the seat of
the disease ; signs of sensory and motor paralyses occurring to-
gether or in succession; early development of a more or less
complete paraplegia, the upper limit of which can usually be
VOL. XIII.—29
450 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
readily determined by the disturbances of sensation and motion ;
weakness of the bladder and rectum; reflex irritability usually
increased ; general health good until the later stages, when it is
impaired te the cystitis and bed-sores.
The symptoms vary somewhat, according to the location of
the morbid process in the cord. When the lwmbar enlargement
is affected, we find complete paraplegia extending up ‘to the
hypogastric region, anzesthesia of equal extent, paralysis of the
bladder and rectum, loss of reflex excitability, and usually mus-
cular atrophy. Bed-sores develop early. :
When the process is located in the dorsal region of the cord,
paraplegia also exists, but the sensory and motor paralysis ex-
tends higher up—to the level of the nipples or even further ; the
muscles of the abdomen and back are involved. Expiration is
impeded. Paralysis of the sphincters, bed-sores, etc., as in the |
preceding form; characteristic of the dorsal affection, however,
are the often very marked increase of the reflex actions, the ab-
sence of muscular atrophy, and the appearance in the later
stages of signs of irritation, contractures etc., in the muscles.
When the cervical enlargement is the seat of the disease, the
usual initial symptoms are observed, but they affect principally
the upper extremities, and the paralysis which follows frequently
takes the form of paraplegia brachialis—the hands and arms are
affected first and chiefly, the paralysis of the legs not appearing
until later. When the affection is at its height, all the four ex-
tremities are more or less completely paralyzed. Paralysis of the
sphincters, decubitus, and increase of the reflexes in the lower
extremities, are present here as well as in myelitis of the dorsal
region; the impeded inspiration, the oculo-pupillar symptoms,
and the atrophy of the upper extremities with extinction of their
reflex activity, are, however, characteristic of the cervical affec-
tion. In consequence of the loss of their reflex activity, the
upper presenta striking contrast to the lower limbs. The electric
irritability is diminished or destroyed in the atrophied muscles. —
When only the upper part of the cervical marrow is attacked,
the clinical picture varies somewhat from the above. There is.
paralysis of all four extremities, it is true, but the nutrition of
the upper limbs remains intact, and their reflex activity is rather
Pe —~ ————s- *
MYELITIS. 451
increased than diminished. Moreover, severe disturbances of
respiration (paralysis of the diaphragm), difficulty of swallowing,
impairments of speech, vomiting, singultus, etc., occur which im-
part an exceedingly threatening character to the clinical picture.
A particularly common form of chronic myelitis is the so-called
compression-myelitis, which occurs in connection with any dis-
ease, that occasions a slow compression of the cord. We have
given a detailed account of this form of the affection in another
place (p. 320), to which the inquirer is referred. We shall con-
tent ourselves here with the statements, that the clinical pic-
ture corresponds perfectly with that of spontaneous transverse
myelitis, and that the only thing, which is at all distinctive and
characteristic of a compression-myelitis, is the existence for a
variable period preceding its development, of initial symptoms
referable to some particular portion of the cord (severe pains
and cramps, local paralysis, atrophy, or anesthesia, dorsal pain
and stiffness, local hy pereesthesia, etc.).
The form of chronic myelitis which is confined to the anterior
horns of the gray matter, poliomyelitis anterior chronica (see
Section No. 16) is, as a rule, readily recognized. It is character-
ized by a slowly increasing weakness and paralysis of the limbs,
which advances progressively from below upwards; by distinct
and sometimes rapid atrophy of the muscles, with loss of the:
faradic irritability (and probably with development of the reac-
tion of degeneration) ; by the absence, or the very slight develop-
ment of the sensory disturbances, which frequently exist only
in the initial stage, in the form of dragging and tearing pains;
also by the extinction of the reflexes, and the complete absence
of decubitus and of vesical weakness. This is the affection which
Duchenne has described under the name ‘‘ Paralysie générale
Spinale antérieure subaigué,’”’ the localization of which in the
anterior gray substance is at all events exceedingly probable.
It is as yet impossible to give an accurate clinical description
of that form of chronic myelitis, which is limited to the central
gray substance, and to which the name myelitis centralis has
been given. This form is the myélite periépendymaire of the
French, and it probably includes also a portion of the cases of
hydromyélie and syringomyélie. Many cases present absolutely
452 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
no symptoms, while others, as it appears, present the clinical pic-
ture of progressive muscular atrophy, but with more prominent
paralytic symptoms. Hallopeau ascribes to this form of the dis-
ease, circumscribed paralyses of different parts with atrophy and
loss of electric irritability, vague pains, very little or absolutely
no anesthesia, sometimes tremor, and the like. The clinical pic-
ture is consequently so exceedingly vague and uncertain, that a
positive diagnosis cannot be made from it.
In some cases the chronic myelitis gradually extends until it
involves the entire cord; it may then be termed myelitis univer-
salis progressiva. This form is characterized by progressive
weakness and paralysis of the muscles, extending slowly from
below upward, rarely in the reversed direction, while the museu-
lar contractions and contractures, and also the atrophy of the
muscles, are less pronounced ; the electric irritability disappears
slowly. The reflexes are usually diminished. There are more
or less violent pains in the back, trunk and extremities, dys-
zesthesize and pareesthesiz and later on marked anesthesia,
paralysis of the sphincters, and bed-sores. The clinical picture
is consequently essentially that of Duchenne’s ‘‘ paralysie géné-
rale spinale diffuse subaigué,’’ the individual cases, of course,
presenting countless modifications, according to the stage and
the extent of the process.
The clinical history of myelitis chronica disseminata, or
multiple sclerosis, which will be described in detail in another
place (No. 11), is in some cases very characteristic, and in others
just the contrary. The reason of this is that the grouping and
character of the symptoms depend entirely on the accidental
locations of the different centres of disease. The numerous,
concomitant cerebral symptoms, the psychical disturbances, the
peculiar impairments of speech, and the affections of different
cerebral nerves, are particularly important ; so are also the very
irregular distribution of the paralyses, the peculiar and varying
range of the anesthesia, the trembling of the limbs during volun-
tary movement, ete.
That form of chronic myelitis wich is confined to the poste-
rior white columns, and is usually designated as tabes dorsalis
(gray degeneration or sclerosis of the posterior columns), will
a eS ee ae -_
ae eee
MYELITIS. 453
be described in detail in a subsequent chapter (No. 12). It is
characterized, in the early stages, by severe lancinating pains,
slight disturbances of sensation, a girdle-sensation, and not un-
frequently by implication of the optici and the nerves supplying
the ocular muscles; in the later stages, by impairment of co-or-
dination (ataxia), weakness of the bladder and of the sexual
functions, loss of the tendon-reflexes, ete.
An essentially different clinical history is, on the other hand,
presented by that form of chronic myelitis called lateral sclero-
sis, in which the morbid process can with great probability be
located in the lateral columns. Here we have a motor weakness,
which gradually increases in intensity and range, and is accom-
panied by striking muscular contractions and contractures, and
by great increase of the tendon-reflexes. There is no ataxia, but
instead of it a markedly spastic gait; no disorder of sensation,
no atrophy of the muscles, no diminution of their electric irrita-
bility, no paralysis of the bladder, no decubitus. This form, too,
must be made the subject of special consideration (see No. 13).
Finally, it is very difficult to recognize during life that form
of myelitis which is localized in the peripheral layers of the
white substance, and which is perhaps most correctly designated
as myeclomeningitis chronica (the sclérose corticale of the French).
It may be recognized in a few cases by the fact that the symp-
toms of chronic meningitis (see p. 255) are accompanied by some-
what more pronounced manifestations of both sensory and mo-
tor paralysis. It is said that muscular atrophy, as a rule, does
not occur. These points are not very safe or reliable from a
diagnostic point of view.
Diagnosis.
The diagnosis of the different forms of chronic myelitis is
to a great extent evident from the preceding descriptions, and for
further details we may refer to the special chapters which follow.
We must make place here, however, for a few words concerning
the simple, chronic myelitis transyersa. It is characterized by
slow development of paraplegia with relatively slight irritative
symptoms, but with more or less marked disturbances of sensa-
454 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
tion and of the bladder; usually also with muscular contrac-
tions, increased reflexes, and decubitus. Hence, all, or at least
most of the paths in the cross-section of the cord are included in
the lesion, though with varying degrees of intensity. The pro-
cess, however, is limited to a relatively small area in a vertical
direction, a fact which can be most readily recognized from the
state of the reflex irritability. The affection is but slightly pro-
gressive in character, and runs a tedious course. The diagnosis
of transverse myelitis can readily be made from these points, all
the more certainly if the existence of such etiological influences
as slow compression, syphilis, and the like, can be demonstrated.
The height at which the lesion is located in the cord can usually
be easily determined from the range of the paralysis, the state
of the reflex and electric irritability and of the nutrition, etc.
The differentiation of transverse myelitis from the other forms.
of the affection, from the later stages of tabes, from lateral scle-
rosis, from multiple sclerosis, and also from progressive muscular
atrophy and from paralyses of the cauda equina, is in most
cases easy. Still there are many cases of peripheral paralysis
due to affections of the plexus or of the cauda equina, to com-
pression of a number of the nerve-roots, etc., in which the differ-
entiation from chronic myelitis is very difficult. In the diagnosis
of such cases, the co-equal extension of the motor and sensory
disturbances, the absence of all reflexes, the loss of electric irri-
tability, the limitation of the disturbances to certain isolated
nerve-territories, etc., may be turned to good account.
There still remain, however, numerous complicated and per-
haps irregular cases, in which an exact diagnosis of the special
form of the disease is downright impossible. This leads us to say a
few words concerning a point to which, despite its great impor-
tance, too little attention has been paid in practice, and to the
disregard of which a great part of the obscurity and confusion
in the accepted clinical conceptions of the disease is due. It is
the simple fact, that the myelitic processes, described in the
preceding pages as strictly localized in particular parts of the
cross-section of the cord, do not by any means always remain
limited to these particular parts, but often extend beyond them
and involve neighboring parts; that, in other words, in addi-
MYELITIS. 455
tion to the special forms of chronic myelitis, transition-forms
exist and combinations occur which are of course characterized
by combinations of the clinical histories. While, in the very
great majority of the cases, sclerosis of the posterior columns
gives rise to the typical clinical picture of tabes, while the regu-
lar form of sclerosis of the lateral columns, as a rule, remains
limited to the lateral columns and produces its own special
symptoms, while poliomyelitis anterior chronica has its own dis-
tinct clinical history, we meet in practice with not a few cases in
which the typical symptoms of tabes are combined with those of
sclerosis of the lateral columns, as well as cases in which the symp-
toms of.a, poliomyelitis anterior are added to those of a lateral
sclerosis or of a tabes. Pathological anatomy has already fur-
nished a sufficient explanation of this fact. A number of reliable
observations have been recorded, in which the anatomical exami-
nation demonstrated the co-existence of gray degeneration of the
posterior and of the lateral columns, or the combination of an
extensive lesion of the anterior gray substance with sclerosis of
the posterior or lateral columns. Careless investigations and an
insufficient acquaintance with these facts have naturally led to
the incorrect conclusion, that lesions of special parts of the cross-
section of the cord do not give rise to special groups of symp-
toms, but that on the contrary these lesions can cause sometimes
one and sometimes another set of symptoms. The knowledge
which is now possessed of the pathology of the cord, teaches us,
however, that each typical clinical picture must correspond to
some distinct anatomical lesion, and that where we meet with a
combination of different clinical pictures, we must also assume
a combination of different anatomical lesions. Valuable confirma-
tion of this statement is furnished by the striking conformity of
the typical cases of each particular form of the disease. These
combined forms are not at all rare, although they certainly con-
stitute but a small minority in comparison with the pure, typical
cases of each form. It is true, that we cannot hope to be able
to recognize these typical clinical pictures whenever met with,
even when more or less confused by combination with one an-
other, without a careful observation and study of an abundant
material. Without this preparation, the differential diagnosis of
456 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
such cases will prove very troublesome, and we shall have reason
to complain of the obscurity and ambiguity of the clinical his-
tories, while with it we shall be able to take a more decided stand,
and to resolve the combination pictures more readily into their
various component parts. That every case of this sort requires a
special diagnosis, and that countless modifications are possible,
are self-evident facts. We will return to these points again when
speaking of the individual forms of the disease.
Prognosis.
The prognosis varies very greatly in the different forms of
chronic myelitis; for details, we may refer to the appropriate
chapters. In simple chronic myelitis transversa the prognosis is
in general unfavorable. The affection is always a severe and a
dangerous one, and the best that can be hoped for is recovery
with a heritage of considerable residua. A real and complete
recovery can only be looked for in exceptional cases, where the
disease is very mild and has developed in otherwise healthy per-
sons, and where, moreover, treatment has been begun in the earli-
est stages.
Only rarely, also, will it be possible to predict a partial recov-_
ery, followed by a persistence of the status quo for many years or
until the natural end of life. In such cases a complete recovery
of power over the limbs can never be expected. In the majority
of the cases a slow, progressive course must be looked for, and
usually only a few years of life can be promised to the patients.
The prognosis will be partly determined or influenced by the
more or less progressive and ascending character of the disease,
by the tendency to aggravations and relapses which sometimes
exists, by the effect produced by certain therapeutic measures,
and finally, by the more secondary symptoms, particularly the
cystitis and decubitus which most frequently place life in dan-
ger. None of these points require a more extended considera-
tion.
MYELITIS, 457
Treatment.
Is there any prophylaxis for chronic myelitis? Unquestion-
ably, though only to a certain, very limited degree. The pre-
cautionary measures, which in general prove useful in preventing
the development of diseases of the cord, are serviceable here also.
Their employment is advisable particularly in the case of the
numerous individuals, who belong to neuropathic families, and
more especially when affections of the spinal cord have occurred
in the generations immediately preceding. In such individuals,
more even than in others, the most beneficial effects will be de-
rived from a rational hardening of the body (by means of cold
sponging, baths, gymnastics, exercise in the open air, pedestrian
excursions, nourishing diet, proper but not too warm clothing,
etc.),and from appropriate hygiene of the nervous system (proper
alternation of rest and work, avoidance of mental overexertion
and of violent emotional excitement, sufficient sleep, etc.). The
avoidance of sexual excesses, of spirituous drinks and other
irritating articles, of bodily overexertion, of the causes of catch-
ing cold, etc., will also assist to a certain extent in keeping the
spinal cord in a state of health. Unquestionably, much would
be gained in many of these cases, if the physician could induce
the individuals in question to follow out strictly the above pre-
cautionary measures. Unfortunately, however, we can rarely
succeed in this.
In respect to the cawsal indication in chronic myelitis, it is
only in isolated cases that anything can be done. In this con-
nection, the importance of a careful treatment of acute myelitis,
continued until recovery is complete, must be alluded to. In other
cases there may be some compressing agent (caries of the verte-
bree, new growths, etc.), which we must endeavor to remove; or
a syphilis, which forms the basis of the spinal affection, must be
energetically attacked ; or diseases of peripheral organs, of the
intestines, or of the urinary or sexual organs, must be subjected
to proper treatment. When, in addiéion to hemorrhoids, a ten-
dency to constipation, dyspepsia, etc., exist, the appropriate
treatment for them should be employed ; the favorable results
458 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
obtained in many cases of chronic myelitis (so-called hemor-
rhoidal tabes), by a course of treatment at saline springs, may
perhaps be accounted for by its influence on these derangements.
Usually, however, in consequence of the slow and lingering man-
ner in which the disease is developed, it is impossible to discover
any causal indication, or, if discovered, to carry it out.
For the treatment of the disease when it has developed to a
certain degree, we possess, it is true, numerous remedies, but we
must not deceive ourselves with regard to their efficiency.
Chronic myelitis, in all its different forms, is a disease from
which recovery is rare, and in the best cases slow. ‘The earlier
the treatment is begun, the better are the prospects of a favora-
ble termination. Hence, it is particularly important, that notice
should be taken of the earliest and even the most trifling of the
initial symptoms, and an energetic and appropriate treatment at
once commenced. It is better to be too careful and anxious, and
to ascribe excessive importance to trifling and perhaps harmless
symptoms, than to suffer the patient and ourselves to be de-
ceived concerning the gravity of the initial symptoms, and thus
give the creeping evil time to develop into a dangerous and un-
conquerable foe.
We shall rarely have an opportunity to employ antiphlogistic
measures. The development of the disease is much too linger:
ing to permit their employment; the symptoms of hyperemia
and irritation remain more in the background. Hence, blood-
letting, ice, confinement to bed, drastic cathartics, depressing
diet, and the like, should be avoided. These measures will only
be indicated, when subacute or acute exacerbations occur. Under
such circumstances, the treatment laid down for acute myelitis
should be employed. hi ie
The much used and often misused derivative measures will
naturally be the next to be thought of. Unfortunately, ex-
perience teaches that they prove, as a rule, of very little use. In
former times they were invariably employed, and in a very
energetic manner ; the red-hot iron was an especial favorite, and
all sufferers from spinal disease bore the marks of it in numerous
cicatrices on the back. The results produced by these measures ©
were entirely disproportionate to the frequency and energy with
MYELITIS. 459
which they were employed. The persistent employment of
milder derivatives (repeated flying or suppurating blisters, pus-
tulating salves, painting with iodine, etc.) has also proved, as a
tule, of little use. Personally I do not remember to have ever
obtained any distinct advantage from the employment of these
remedies, though, it is true, my experience with them has not
been particularly extensive. Our attention is, however, directed
to them over and over again by the favorable results they pro-
duce in other diseases, and perhaps fresh trials of them are now
more admissible, in view of the facts that we can diagnose the
different forms of the disease more positively, and can also pick
out more readily the cases which present any chance of success.
Such trials, however, should be carried out in a systematic
manner, and with exclusion of other remedies.
We recommend as a relatively harmless, and still in many
cases decidedly efficient derivative measure, the application of
dry cups along the spine, repeated every few days. Brown-
Séquard praises highly the daily employment of a hot (87-40°
C., 98.5°-104° F.) douche to the back, for two or three minutes
at a time; the stream should be nearly an inch in diameter.
In the treatment of chronic myelitis at the present day (we
are speaking now of all the forms together, referring to the
special accounts of the different forms for further details), the
chief reliance is placed on three curative agencies. These are
baths (particularly the therme, hot and cold brine baths, and to
a less degree steel-baths), hydropathy, and galvanism. We have
already (in the General Part, p. 164 et seq.) spoken at length of
these things, and endeavored to determine with some degree of
accuracy the general indications for their employment, and we
have only to add here a few points bearing directly on their
use in chronic myelitis.
In order to attain an approximately correct idea of the action
of these agents, I have made out a table from the cases of
chronic myelitis (in all its forms, inclusive of multiple sclerosis,
lateral sclerosis and sclerosis of the posterior columns), that
have come under my own observatjon, of which I have notes of
the treatment and its effects. This table includes 175 different
observations that were made on 107 different cases. It is true
460 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
that this material is not homogeneous. It contains a large
number of hospital cases, and many old and severe cases that
defied all treatment ; most of them were treated solely by elec-
tricity ; many of them have undergone several courses of treat-
ment, and have thus afforded opportunity for repeated observa-
tion. With all this, however, some important points, which I
would gladly see made the subject of further investigations, can
be gathered from this table.
In the first place, the result of my collation of facts is decid-
edly unfavorable for the indifferent therme (Wildbad, Teplitz,
etc.). Out of twenty-two cases in which these thermze were em-
ployed, there were no less than twelve which were decidedly in-
jured by them ; in these cases an aggravation of the disease set
in during or immediately after the course of treatment by baths.
Of the remaining ten cases, seven experienced no change at all,
and only in three was there any improvement; one of these was
cured. In two of the three cases which were improved, the baths
were, however, cooler, of shorter duration, and less numerous.
These observations coincide with the experience of most spe-
cialists. The results are at all events not encouraging; they
take away all desire to send such patients to the thermal springs,
which was formerly the universal custom, and is even yet fre-
quently done. If the physicians located at watering-places could —
_ be induced to publish unprejudiced and careful observations,
based on correct diagnoses, a great desideratum would be ful-
filled. At all events, I no longer risk a trial of the therme in
these cases, except when I have guarantees for the most cautious
employment of a modified course of baths. The temperature of
the bath should never be above 33°-34° C. (912-934° F.), and
prolonged immersion should be avoided. If I were to attempt to
pick out the actual cases for which the therme are suitable, I
should find myself in a difficult position. It is usually stated
that the cases with prominent irritative symptoms, with hyper-
cesthesia, with meningitic symptoms, etc., are especially benefited
by them. I must confess, however, that without further critical
observations, I cannot regard these indications as reliable. At
present I would only recommend a trial of hot baths after other
remedies have failed, and even then only with every precaution.
MYELITIS. 461
My experience has been much more favorable with the thermal
brine baths (Rehme, Nauheim). I possess notes of twenty-one
cases ; of these twelve were improved by the course of treatment,
nine received no benefit from it, but none were rendered worse.
Here, too, I am convinced that much depends on the manner
in which the treatment is carried out, on the temperature and
duration of the baths. It is advisable that they should be of
a moderate temperature (80-26° C.—86-784° F.) and not too
prolonged, and that the water should not contain an excessive
quantity of carbonic acid. Any increase in the activity of the
treatment must be made with great caution. These baths are
suitable for most of the cases. At the most, I would hesitate to
recommend them for cases attended by great irritability, violent
pains and other symptoms of irritation. '
I have had no experience at all with the ordinary drine-baths,
and very little with chalybeate and turf baths. The latter proved
useful in two cases, and detrimental in one. They are highly
extolled by many authors. In Franzensbad particularly, various
good results have been obtained by their use. This, too, is a
subject worthy of further investigation.
Concerning animal-baths, hot-sand baths, pine-needle baths, steam-baths, hot-air
baths, etc., I know very little from personal experience. In most of the cases they
are superfluous, and, when used at very high temperatures, they are actually injuri-
ous and dangerous.
On the other hand, the results of a rationally conducted cold-
water cure are exceedingly favorable. Out of twenty-nine cases of
which I have notes, the results of the treatment were favorable in
twenty-one, negative in five, and unfavorable in three. Here
too, of course, everything depends on the manner in which the
cold water is used. I cannot insist too much on the danger of
forced cures, of all severe and strongly exciting procedures, such
as the employment of water at very low temperatures, douches,
sharp slappings, etc. These measures are, as a rule, absolutely
injurious in cases of myelitis; even wet packs of the entire body
have, to my surprise, generally proved injurious. Simple rub-
bing with wet cloths, foot-baths and sponging the back, hip-
baths, half-baths with affusions to the back, local compresses to
462. ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the back left on till they become warm, etc., seem to be the
measures which are chiefly applicable. The treatment should
always be begun with moderate temperatures (20-25° C.—68-77°
F.), and we should never go below 16-12° C. (604-533° F.),
believe also that excessive prolongation of the treatment is inju-
rious. Many over-zealous hydropathists are only too often led,
by their great confidence in the water-cure, to prolong the treat-
ment to an extent that proves detrimental to the patients.
The water-cure is, all things considered, one of the most
important and most promising means of treating chronic myeli-
tis. The mistrust with which it is regarded by some authors is,
as far as my own experience goes, entirely unjustifiable. It is
suitable for almost all cases, though of course the method of
application must vary according to the peculiarities of the indi-
vidual cases. Some patients, however, cannot bear the treatment
at all; it is followed by insufficient reaction, causes chilliness,
discomfort, etc. In such cases the treatment should not be per-
sisted in. The choice of the establishment is of course a matter
of great importance. I prefer one situated in a healthy moun-
tainous locality and in a wooded region. The chief requisite,
however, is always the presence of an intelligent and competent
physician.
In recent times the galvanic current has acquired a promi-
nent position in the therapy of chronic myelitis. Out of one
hundred cases treated by it, I obtained a more or less favorable
result in fifty-two. Complete recovery ensued, it is true, only in
a few of these cases, but a very considerable and striking im-
provement was observed in quite a number of them; in most of
them, however, the improvement was only moderate. In forty-
seven of the cases the results were negative, although in some of
them the treatment was persisted in for a very long time. In
only one case was the effect of galvanization decidedly bad.
The chief part of this treatment is, of course, the direct gal-
vanization of the cord, which must be conducted precisely ac-
cording to the principles which have been exhaustively consid-
ered in another chapter (see page 178). The electrodes must
be applied differently, in accordance with the differences in
the position and extent of the focus of disease. It is best to let
MYELITIS. 463
both poles act successively, either with a stabile or with a slowly
labile current. When we have to deal with band-shaped sclerosis,
it is advisable to include the cervical sympathetic also within the
sphere of the electricity. The current used should not be very
strong, and the séances should be short. I cannot insist suffi-
ciently on the point, that the treatment, to be successful, must
be conducted with great care and skill. Great patience on both
sides is, as arule, necessary. The treatment must be continued
for months, being occasionally interrupted only to be recom-
menced after a brief pause. It is expedient to alternate or com-
bine galvanization with other methods of treatment.
It is as yet impossible to indicate the cases for which the
galvanic treatment is especially suitable. It may, indeed, be
tried in most or all cases, as we know of no positive counter-
indication. Every now and then, however, we shall meet with
patients who cannot bear, or who think they cannot bear, even
the most cautious application of the galvanic current. In such
cases the treatment must be at once discontinued.
, Little can be expected from internal medicines in the treat-
ment of chronic myelitis. WVitrate of silver, which was first
recommended by Wunderlich, is the most reliable of all of them.
In a few cases it has undeniably proved beneficial. It is impos-
sible to give the exact indications for its employment, but, as
it is in general a harmless medicine, it may be tried in most of
the cases. Brown-Séquard very urgently recommends ergot
and belladonna, both of which are said to lessen the congestion
of the spinal cord and to diminish its reflex irritability. He
gives the ergot in doses of 0.30-0.50 (gr. v.—viiss.) twice a day,
and in connection with it applies a large belladonna plaster to
the back, or gives extract of belladonna internally in doses of
0.015 to 0.02 (gr. 4-4) twice a day. The effect is said to be very
decided in many paraplegias. Jodide of potassium has rather
unexpectedly proved almost invariably useless. I at least, often
as I have prescribed it, have never seen any decided improve-
ment follow its use. Even in the paraplegias of syphilitic
patients, its curative action is often very limited. Arsenic,
too, has in my experience, as a rule, proved useless. P/hos-
phorus I have seldom prescribed ; its curative action seems to
464 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
me dubious, and its administration not entirely without danger.
Strychnine is in my opinion almost always decidedly objection-
able in chronic myelitis. In the earlier stages it is more liable to
do harm than good, and for the later stages, when the residua of
the myelitis (paralyses, etc.) are to be treated, we possess in
electricity a much more reliable as well as safer remedy.
In consequence of the long duration of the disease, the phy-
sician will often find himself tempted to employ in a tentative
manner, not only the above, but also numerous other remedies.
It will be fortunate both for physician and patient, when the
right remedy is discovered at once.
The general management, the diet and the mode of life of the
patients are in our opinion of very essential importance. These
points are still very often sinned against, partly through igno-
rance, partly through carelessness. Above all, rest and a regular
mode of life are essential; overexertion of every kind, mental
as well as bodily, must be avoided; sexual intercourse should be
confined within the strictest possible limits or completely stopped ;
all excitement, violent emotions, etc., must be prevented as much
as possible. The diet must be simple and easy of digestion, but at
the same time nutritious. Many patients are, however, benefited
by a very abundant supply of nourishment, and by cod-liver oil.
Spirituous drinks should only be allowed in small quantities.
Strong coffee and tea and strong cigars must be avoided. It is
very important that the bowels should be kept regular ; for this
purpose we must usually employ both aperients and clysters.
The patients should be strongly urged to keep as much as possible
in the open air. When practicable, a prolonged sojourn in a
mountainous region at a moderate elevation, or at the sea-side,
will be useful; it is also advisable that the winters should be
passed in the South, in the Riviera, the southern Alpine valleys,
etc. The regulation of the bodily exercise is usually a very
important question. Much harm can easily be done by ex-
ceeding the permitted amount of exercise. I have repeatedly
known patients, who had begun to improve, to be thrown back
for a long time by an unduly prolonged walk. The idea which
is entertained by many patients, that a commencing muscular
weakness and stiffness can be removed by forced exertion of the
Sar
MYELITIS. 465
muscles, must be energetically combated. I believe that patients
who are still capable of moving about, should be allowed to take
only so much exercise as they can indulge in without fatigue ;
as soon as they begin to grow tired, they must rest for a time,
and may then resume the walk or other movement.
In many cases, it is true, exercise is out of the question—the
patients are bed-ridden, paralyzed. Such patients must make it
a point not to lie always and exclusively on the back. Brown-
Séquard wants to discard the dorsal position entirely, and to
replace it by the lateral or abdominal position, but it is more
than doubtful whether it will be possible to do so. For these
paraplegic patients a wheel-chair may be used, though it is but
an unsatisfactory substitute for walking exercise. It will at least
enable them to enjoy the fresh air regularly and freely.
In most of the cases of chronic myelitis, there are also a
number of symptomatic indications that require attention.
The most important of these is unquestionably the prevention
of cystitis and decubitus; the closest attention must be paid
to this point under all circumstances. We have already dis-
cussed it at length on page 193 et seq., to which the reader is
referred.
Another frequent and important indication is the relief of the
pains—of the lancinating pains of tabes, the spontaneous and
radiating pains of myelitis transversalis, etc. These will very
frequently resist all imaginable remedies, and prove a source of
great annoyance to the physician, as well as of torment to the
patient. The most rapid relief will always be obtained from
hypodermic injections of morphine, but the dangerous conse-
quences of the constant use of this drug must deter us from too
frequent employment of the injections. After morphine the
most serviceable drugs are bromide of potassium, quinine, bro-
mide of quinine, zinc, and valerian. Cutaneous irritation, elec-
tricity (the faradic brush or galvanic current), Preissnitz’s com-
presses, applications of chloroform, and frictions with veratrine,
oil of hyoscyamus, and the like, often do good service. Similar
remedies are employed with more or less success to relieve the
manifestations of motor irritation, the painful spasms, reflex
twitching, etc. For the paralyses, atrophies, anesthesia, etc.,
VOL. XIIL—30
‘
466 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
which persist after the disease has run its course, electricity is
the sovereign remedy.
The general plan of treatment must of course, apart from the
stage of the disease, be regulated chiefly according to the indivi-
duality of the case, or the internal and external conditions of the
patient. Any causative influences that may be discovered must
be first of all removed, and the surroundings of the patient and
his mode of life regulated. In the relatively recent cases, which
are still in the early stages, the following course of treatment
may be recommended after the above points have been attended
to: mild, but nevertheless efficient hydropathic treatment, in
conjunction with the employment of the galvanic current; in
appropriate cases these may be combined with mild derivatives
(blisters, dry cups, Preissnitz’s compresses, etc.), change of air,
and a sojourn in the mountains or at the sea-side. As the dis-
ease progresses a course of treatment at the hot brine-springs, or
in a hydropathic establishment may be tried, alternating with
the treatment by galvanism; internally the persistent use of
nitrate of silver. .
In the older cases, where the prospects of recovery are much
less, a cautious alternation of the different methods of treatment
is requisite. During the winter such patients should be treated
by galvanism, and should also be made to employ cautiously
cold applications combined with frictions. In the summer the
thermal brines, cold-water treatment in the mountains, and per-
haps also the therme, may be tried. In addition to these meas-
ures, various internal remedies may be tried, the symptomatic
indications must be carefully fulfilled, and decubitus and cystitis.
must be guarded against.
Under all circumstances, the employment of psychical influ-
ences constitutes an important part of the treatment of chronic;
myelitis. The courage of the patient must be maintained, his:
confidence in the various methods of treatment strengthened,
and his hopes constantly aroused and reawakened. Unfortu-:
nately the physician must in only too many cases rest contented.
when he can succeed in this task, which is itself by no means a
Jjight one, and brighten the miserable existence of the patients:
by an occasional glimmer of fresh hope.
_MYELOMALACIA, —§, |. 467
10. Simple Softening of the Spinal Cord.—Myelomalacia.
Brown-Séquard, Lectures, etc., on Paralysis of the Lower Extremities. p- 34. 1861.
—Hennig, Fall von Erweichung des Riickenmarks. Arch. d. Heilk. L §. 188,
1860.—Leyden, L. c. Il. 8. 38, 51 ff.—Panum, Experim. Beitr. z. Lehre von d.
Embolie. Virch. Arch. Bd. 25. 8. 308. 1862.—Hasse, L. c. 2 Aufl. S. 706.—
Hammond, L. c. 3. edit. 1873. p. 463.— Willigk, Ueber d. Verhalten d. Nerven-
zellen bei embol. Processen im R.-M. Prager Vierteljahrschr. 1875. ITI. 8. 41.
—D. J. Hamilton, On Reflex Paralysis and Urinary Paraplegia. Brit. and For.
Medico-chir. Rev. Tome I. VII. p. 440. 1876.—Hm. Bertin, Ramolliss. d. 1.
moélle. Dict. Encyclop. des. Sc. méd. II. Sér. T. VILL. p. 751. 1854,
It may perhaps seem venturesome in the present state of our
Race ledge, to devote a special chapter to simple,;.non-inflam-
matory softening of the spinal cord. We are still deplorably
ignorant with regard to this affection, and hence the chapter
will necessarily be a short one. That there really is, however,
a non-inflammatory as well as an inflammatory softening of the
spinal cord, must unquestionably be admitted; it is demon-
strated both by convincing analogies with similar processes in
the brain, and by a certain number of anatomical and clinical
facts. It is in order now to describe as accurately as possible,
the anatomical changes and clinical history of this simple soften-
ing, in order to differentiate it more positively from the inflam-
matory affection.
It seems to us particularly destrabhs to protest against the
misuse of the word ‘‘softening,’’ which is at present very com-
monly applied to simple and even to acute inflammation. The
terms softening and inflammation are by no means synonymous;
not every softening is the result of inflammation, and not every
inflammation leads to softening. The latter certainly occurs as a
concomitant and a consecutive lesion in many forms of spinal
inflammation, but it is by no means an essential part of them.
We might, with just as much and perhaps even more reason,
employ the term ‘‘hyperemia,”’ or ‘‘exudation,’’ or ‘‘ fatty de-
generation,” to designate inflammation.
It is unquestionably better to discard entirely the use of the
term ‘‘softening’’? for inflammatory conditions; this would be
the best way to avoid misunderstandings. If used: at all, it
468 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
should be reserved for the simple, non-inflammatory processes
of softening, which are undoubtedly met with in the cord ; for
these, it seems to us perfectly appropriate.
It is true that the existence of these non-inflammatory changes
has not yet been demonstrated with that degree of positiveness,
which is desirable, and that we do not, as in the case of the
brain, possess experimental proofs or clinical observations equiva-
lent to them (cerebral emboli) for the most important forms of
the softening. With respect, moreover, to the histological pro-
cesses, and more particularly the points which distinguish the
simple from inflammatory softening, we are as yet to a great ex-
tent in outer darkness. Still, it seems to us that there has been
too great a tendency in recent times to class under myelitis all
lesions of the spinal cord characterized by softening, even though
the characteristic histological evidences of inflammation be by
no means always present.
A few brief remarks concerning simple softening may be made
now, principally with a view to incite others to further studies
and investigations. |
The pathogenesis of the affection is enveloped in numerous
obscurities. The softening which is due to ¢hrombosis and em-
bolism is probably the easiest to explain, in consequence of its
analogy with the corresponding cerebral process. ‘The effects of
embolism of the abdominal aorta, from which we might expect
the most valuable information in this connection, have not yet
been sufficiently studied. It has been stated, that white softening
of the cord has been found as one of these effects.
Embolism of the small arteries of the cord is very rare, and
would at all events produce only very circumscribed centres of
softening. Panum, Vulpian and others have studied it experi-
mentally, and have demonstrated the development of small cen-
tres of red softening as the result of such emboli. Leyden found
small, inflammatory foci produced by emboli, which were derived
from ulcerative endocarditis. Willigk, in his recent investiga-
tions, discovered no centres of true softening in the neighborhood
of the obstructed vessels, but found instead of softening, in some
cases a hyperplasia of the connective tissue with atrophy and
destruction of the ganglion-cells, and in others a peculiar ‘‘ col-
MYELOMALAOTA, 469
loid’’ degeneration of the ganglion-cells without increase of the
connective tissue. All this requires further study and investiga-
tion. The case of multiple thrombosis of the small vessels of the
cord, reported by Hamilton, is a remarkable one.
There is little reason to doubt that a severe affection of the
walls of the vessels, such as atheroma, calcification, or sclerosis,
diminution of the vascular lumen, etc., can also cause similar
retrogressive metamorphoses in the tissue of the cord, which
finally terminate in softening.
Second in order of importance comes the softening produced
by slow compression of the cord. We have already (p. 323)
stated, that a true myelitis (compression-myelitis, inflammatory
softening) of the affected portion of the cord is almost without
exception excited by such compression. Nevertheless, excep-
tions do apparently occur. The fact that in not a few cases of
compression of the cord, the microscope reveals in the softened
mass no granule-cells, no hyperplasia of the connective tissue,
no proliferation of the nuclei, but only swollen and disinte-
grated nerve-elements, speaks unmistakably in favor of the view
that the process is sometimes, at least for a time, one of simple
softening. There is nothing forced in the theory, that the is-
chemia of the cord caused by the compression results in simple
softening, and that this condition may persist as long as the
compressing mass does not develop strongly irritating qualities,
and implicates the cord only very gradually and slowly. This,
too, requires verification.
It is still very doubtful whether a spontaneous simple soften-
ing ever occurs. At all events, the older observations which are
adduced in favor of it, are by no means conclusive, since they
lack the microscopical examination which alone can determirie
positively the absence of inflammatory changes.
A senile softening of the cord is spoken of, but we must con-
fess that the supposed examples of it contained in medical liter-
ature do not by any means convince us of its actual existence.
Still, it is certainly possible that the vascular affections, which
are so common in old age, may o@casionally give rise to small
spots of softening in the spinal cord. At all events, however, the
fact requires more accurate authentication.
470 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
We may mention, finally, that Hammond assumes sewwal ex-
cesses to be the cause of simple softening in a few cases.
Under these circumstances there is but little that can be said
concerning the special pathological anatomy of myelomalacia ;
there is always danger of confounding the inflammatory with
the non-inflammatory foci of softening. In fact, macroscopically
they resemble each other very closely. The spinal cord is soft
and pulpy, and swells up above the level of the cut; in pure
cases it is white, and in the later stages becomes creamy, milky,
and fluid. Pronounced red softening can, however, also occur
in consequence of the blood being dammed back in the ischeemic¢
vascular territories. When the fatty degeneration assumes spe-
cial prominence, the softened spot may acquire a more yellowish
color, and present the appearances of yellow softening. At its
boundaries, the softened spot usually merges imperceptibly into
the normal tissue. |
It is difficult to decide whether the case of Hennig should really be classed as
simple softening; if it must be, it would present a sort of gelatinous or colloid
degeneration, with fatty degeneration of the vessels. .
The microscopical examination can alone furnish conclusive
evidence of the inflammatory or non-inflammatory nature of the
softened spot. Unfortunately, however, we do not as yet possess
a sufficient number of accurate reports bearing on this point.
Wherever we find a large number of cells containing fat granules,
tensely distended blood-vessels, numerous young cells, increase of
the interstitial tissue, swollen axis-cylinders, etc., we are justified
in assuming positively the inflammatory character of the process.
On the other hand, when these characteristics are wanting, and
we only find simply swollen and disintegrated nerve-fibres, gan-
glion-cells in a state of glassy swelling, a few cellular elements
and fat-granule-cells, and a small quantity of fatty detritus, we
must diagnose a simple softening. Further and searching in-
vestigations of this point are, however, very much to be desired.
The symptomatology of simple softening is also exceedingly
obscure. In the clinical histories we meet with the picture of a
more or less acute or subacute myelitis unattended by fever, and
presenting only a few non-essential modifications, that are of
MYELOMALAOCTA, 471
little help in the diagnosis. According to Hammond, tne absence
of motor symptoms of irritation is particularly distinctive of
simple softening. That this, however, does not hold true of all
cases without exception, is demonstrated by the histories of
many cases of acute myelitis.
In the commencement of the disease a sensation of numbness
and a feeling of weakness are experienced, which gradually be-
come more intense, but are not accompanied by pains, muscular
twitchings, etc. Progressive weakness of the bladder is added
to the paralysis; the anal sphincter is also affected, and the
reflex excitability seems diminished.
In the later stages of the affection we have the completes: pic-
ture, modified only in accordance with the localization of the
softened spot, of a severe sensory and motor paraplegia, with
paralysis of the sphincters, bed-sores, and the well-known termi-
nation.
According to Brown-Séquard and Hammond, the absence of
motor and sensory signs of irritation is conclusive for the diag-
nosis from inflammatory softening. According to them, there
are no pains, no spasms, no hypereesthesia, and no increase of
the reflex activity. Personally, however, we cannot suppress a
slight doubt as to the pathognomonic importance of the absence
of these symptoms, and feel ourselves forced to look to the future
for the possibility of a more exact diagnosis of simple myelo-
malacia.
The prognosis of the affection must be debldeaty unfavorable,
when the centres of softening are at all extensive. The very
small foci, which give rise only to a very limited array of symp-
toms, or perhaps to none at all, do not, as a rule, call for a prog-
nosis. |
The treatment of simple softening can also be disposed of in a
few words. It must be carried on essentially according to the
rules laid down for the non-febrile forms of myelitis without
prominent inflammatory symptoms.
Brown-Séquard recommends, besides iron and quinine, chiefly
iodide of potassium, which is best administered in a bitter decoc-
tion (cinchona, colombo, rhubarb); strychnine only withthe
greatest caution; noergot! nobelladonna! He believes, further,
472 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
that the cold douche or shower-bath to the back is indicated, as
is also confinement to the dorsal position.
In general, abundant and nourishing food, when possible
moderate exercise, and the employment of the galvanic current,
will be found advantageous.
11. Multiple Sclerosis of the Spinal Cord (and Brain).—Mul-
tiple, nodular Sclerosis; disseminated, multilocular, insu-
lated Sclerosis of the Central Nervous System.—Sclérose en
plaques disseminées.—Insular Sclerosis.
Cruveilhier, Anat. pathol. Livr. 32, 38. 1835-42.— Charcot, Klin. Vortr. tiber die
Krankh. des Nervensyst. Deutsch von Fetzer. 1874.—Hasse,l.c. 2. Aufl. 8.
708.—Rosenthal, l.c. 2. Aufl. 8. 147.—Hammond, 1. c. 3. Edit. p. 637.—Ley-
den, 1. c. IL. 8. 375.—Bernheim, Dict. encyclop. des Sc. méd. IL. Sér. T. VIL
p. 707. |
Frerichs, Ueber Hirnsklerose. Haeser’s Arch. X. 8. 334. 1849.— Valentiner, Ueber
Sklerose des Gehirns u. R.-M. Deutsche Klin. 1856. No. 14 bis 16.—Leyden,
Ueber graue Degen, des R,-M. ibid. 1863. No. 13.— Rindfleisch, Histol.
Detail zur grauen Degen. Virch. Arch. Bd. 26. 8.474. 1863.— W. Zenker,
Sklerose des Gehirns u. R.-M. Zeitschr. f. ration. Medic. 3. Reihe 24. Band.
1865. — Vulpian, Notes sur la sclérose en plaques, etc. L’Union méd.
1866. Nr. 67-72.—Charcot, Gaz. des hdp. 1868. Nr. 102, 103.—Ordenstein,
Sur la paralys. agit. et la sclér. en plaques généralisée. Thése. Paris, 1867.—
Bourneville, Mouvem. méd. 1868. Nr. 13-25, u. 1869, Nr. 27 bis 38.—Bourne-
ville et Guérard, De la sclérose en plaques dissém. Paris, 1869.—G@uérard,
Essai sur la scl. en plaques. These. Paris, 1869.— Liouville, Gaz. méd. 1870.
Nr. 19 u. 20.—Joffroy, ibid. Nr. 23, 24.—Magnan, ibid. Nr. 14. p. 183.—Leo,
Beitr. zur Erk. der Sklerose des Gehirns u. R.-M. Deutsch. Arch. fiir klin.
Medic. IV. 1868.—H. Schuele, ibid. VII. 8. 159. 1870, u. VIII. S. 223. 1871.
W. Leube, ibid. VIII. S. 1. 1870.—u. Klin. Ber. aus dem Krankenhaus zu
Jena. 1875. 8. 111.—Zenker, Deutsch. Arch. f. klin. Medic. VIII. 8. 126. 1870.
—Ebstein, Spinale Form der multipl. Sklerose. ibid. TX. 8. 528, u. X. 595.
1872.—Kelp, Ueber Hirnsklerose. ibid. X. 8S. 224, 1872.—Buchwald, ibid. X.
8. 478. 1872.— Otto, ibid. X. S, 531. 1872.—Berlin, ibid. XIV. 8S. 108. 1874.
—Engesser, ibid. XVII. 8. 556. 1876.—Baerwinkel, Arch. d. Heilk. X. 8. 590,
1869.—C. Hirsch, Deutsch. Klin. 1870. Nr. 33-38.—Radlick, Fall von Sclérose
en plaques. Diss. Berlin, 1874.—Pohl, Sklerose des Gehirns u. R.-M. Diss.
Berlin, 1874.— Westphal, Ueber eine Affection des Nervensyst. nach Pocken
u. Typhus, Arch. f. Psych. u. Nerv. III. 8. 376. 1872.— The same, Neue Charité-
Annalen. I. Jahrg. 1874. 8. 427.— Otto, Casuist. Beitr. zu den nerviés. Nach-
MULTIPLE SCLEROSIS. 473
krankh. der Pocken. Virchow-Hirsch, Jahresbericht pro 1872, II. 8. 23.—
Jolly, Ueber multiple Hirnsklerose. Arch. f. Psych. u. Nery. II. §. 711. 1872.
—OChvostek, Wien. med. Pr. 1873 u. 1874.—Allgem. Wien. med. Zeit. 1875.
Nr. 11-20.— W. Moxon, Eight Cases of Insular Sclerosis, Guy’s Hosp. Rep. XX.
p. 437. 1875.—Molliére, Sur quelques points du diagnost. d. 1. sclér. des centr.
nervy. Lyon méd. 1875. Nr. 28.—F. Schultze, Ueber das Verhiiltniss d. Paralys.
agit. zur multiplen Sklerose des R.-M. Virch. Arch, Bd. 68. 1876.—Christidis,
Ueber multiple Sklerose, etc. Diss. Wiirzburg, 1875.—Z. Killian, Ueber einen
Fall von diffuser Myelitis chronica. Arch. f. Psych. u. Nervenkrankh. VII. S8.
28. 1876.—Putzar, Fall von multipl. Sklerose des Gehirns u. R.-M. Deutsch.
Arch. fiir klin. Med. XIX. S. 217. 1877.
History.
The disease now generally known under this name has only
figured in the annals of science for a few decades, and only be-
came thoroughly understood during the last decennium. The
first minute account of the affection appeared, accompanied by
excellent illustrations, in the large atlas of Cruveilhier (1835 to
1842). A similar case, observed by Tuerck in the year 1855, was
entirely lost in a clinical point of view.
The clinical history of circumscribed sclerosis begins with the
work of Frerichs (1849), which was very greatly enlarged and
perfected by Valentiner (1856). A few years later, the pathologi-
cal anatomy of the disease was greatly cleared up by the labors
of Rindfleisch (1863), Leyden (1863), and Zenker (1865). The
French works, which followed those of the above-named investi-
gators, have, however, undoubtedly contributed most to our
knowledge of the disease. They defined more sharply the morbid
picture presented by the affection, gave due prominence to its
essential points, and secured for it a place in pathology as a
legitimate and recognizable disease. After the appearance of the
first works of Vulpian and Charcot (1866-1868), the latter in par-
ticular contributed very greatly to the enlargement of our knowl-
edge of multiple sclerosis; with the help of his pupils (Orden-
stein, 1867, Bourneville and Guérard, 1869) he has studied it in
an exhaustive manner, from almost every point of view.
About the same time there appeaged in Germany an excellent
account of a case observed by Leo, which was the first of a long
474 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
list of careful and full reports (by Schuele, Leube, Ebstein, Kelp,
Buchwald, Otto, Berlin, Engesser, Baerwinkel, Hirsch, West-
phal, Jolly, Chvostek, and others). These reports have contrib-
uted not a little to the enlargement of our knowledge and to the
elucidation of different important questions. In France, also,
numerous isolated observations have been recorded since the
above date (by Liouville, Joffroy, Magnan, and others). In Eng-
land, however, until the appearance of the recent work of Mox-
on (1875), the disease was overlooked and almost entirely
unknown.
Through the labors of the above-named writers, we have ac-
quired a pretty accurate knowledge. of the affection, especially in
its practical relations, although numerous questions of detail,
some of them not unimportant, are still in an unsettled state,
while in the domain of therapeutics in particular almost every-
thing still remains to be done. pias
Definition.—Multiple sclerosis is a form of chronic myelitis
and encephalitis.
It is characterized, anatomically, by the development of numer-
ous, insulated sclerotic nodules, varying in size, and of a chronic
inflammatory nature, which are scattered irregularly throughout
the entire cord, and usually also throughout the entire brain, but
which seem to possess, nevertheless, certain spots of predilection.
Sometimes a less intense, but more diffuse sclerosis unites the
different nodules with one another. |
Clinically the manifestations of the disease are very variable
and manifold, assuming almost protean shapes. This is the nat-
ural result of the development of the nodules in so many differ-
ent localities, which are seemingly determined by accident.
Motor pareses and paralyses are never wanting, while disturb-
ances of sensibility belong to the less constant symptoms. Dis-
turbances of co-ordination (ataxia) are very frequently observed,
and a peculiar, exceedingly characteristic tremor, which accom-
_panies voluntary movements and progressively increases, is
almost regularly present. These symptoms are accompanied by
a more or less extensive list of bulbar and cerebral symptoms,
the most prominent of which are a peculiar disturbance of speech
(Scanning, monotony of voice), noisy inspiration, impairments of
MULTIPLE SCLEROSIS. 475
sight, nystagmus, pronounced psychical disturbances of varying
degrees, and apoplectiform attacks.
We have to deal here with an affection that runs an exceed-
ingly chronic course—a course moreover which always goes on
progressively from bad to worse. Very considerable fluctuations
in the severity of the symptoms do occur, it is.true, but a per-
manent improvement is rarely observed.
For practical reasons we shall discuss together the multiple
scleroses of the cord and of the brain. The exclusively spinal
form of the affection is rare, and the characteristic morbid pic-
ture belongs essentially only to the cerebro-spinal form.
Etiology and Pathogenesis.
Hereditary influences may in many cases be regarded as pre-
disposing to multiple sclerosis. Duchenne observed hereditary
transmission of the disease in one case, and I have myself observed
the same thing. Frerichs saw a brother and sister who were
suffering from the disease, and a similar case has come under my
own observation. The general neuropathic tendency may per-
haps play its well-known réle here also, as hysteria and other
nervous disturbances sometimes, though relatively seldom, pre-
cede the affection: In other respects but little is known concern-
ing the influence of this diathesis.
According to Charcot’s statements, the female sex presents a
considerably greater predisposition to the disease than the male
sex. The fact that his observations were partly conducted at the
Salpetriére (Women’s Hospital), will explain the discrepancy
between his statements and those of other observers. Chvostek
observed sixteen cases, of which ten were men and six women.
Of the nine cases observed by myself, four were men and five
women. Hence there is no marked difference between the two
sexes in this respect.
It is certain, however, that the affection is prsbentoentt a dis-
ease of youth and middle age. It most frequently makes its
appearance during the second and third decades of life ; it rarely
or never appears after the forty-fifth year, and relatively few
476 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
cases have been known to occur in children under ten years of
age.
Among the direct causes, we must mention first, “‘catehing
cold,” the influence of which has been repeatedly demonstrated.
The disease has been known to develop after sudden and severe
exposure (¢. g., a fall into cold water or the like), as well as
after continued or repeated exposure to injurious influences,
especially to the prolonged action of damp cold. It is impossible
to conceal the fact, that the mode of action of these influences is
as yet enveloped in the greatest obscurity.
Excessive mental and bodily exertions are also asserted to be
exciting causes. It is possible, that they prove so only in already
predisposed individuals. In this category belongs also the action
of intense emotions, particularly of long-continued depressing
emotions, such as sorrow, care, etc. These are often advanced as
the causes of the disease.
In one of my cases, that of a young lady whose father in all probability died
from the same affection, the disease was brought on by fright combined with
fatigue and exposure, which were incidental to a fire that broke out suddenly.
Hence, in this case, there were a number of injurious agencies active at the same
time.
Traumatic influences (injury of the head, concussion of the
entire body, railroad injuries, etc.) seem to be decidedly poten-
tial. In the etiology of the observations recorded in medical
literature, the occurrence of such injuries, some of which, it is
true, were received years before the breaking out of the disease,
is so frequently mentioned, that it is impossible to assume a
purely accidental coincidence.
Pregnancy has also been adduced as an etiological agent
(Guérard). Molliére believes that the disease is often developed
as a sequel to long-continued and severe hysteria. There is no
doubt that disseminated sclerosis can be developed as a sequel
to acute diseases. Ebstein and Westphal saw it after typhus,
and Charcot after cholera. Westphal has described some cases
of disease following variola, which in all probability must be
classed as disseminated sclerosis, although some important fea-
tures of the disease were wanting in the clinical picture. This
MULTIPLE SCLEROSIS. 477
theory finds support in the fact, that he subsequently demon-
strated the existence of a disseminated myelitis in some similar
but more acute cases. Otto has described a similar case.
None of these isolated facts, however, have as yet furnished
the slightest information concerning the more delicate processes
in the pathogenesis of this remarkable affection.
Pathological Anatomy.
Multiple sclerosis is, as a rule, very readily recognized by the
naked eye. In a few isolated cases, however—Bourneville has
described one such—the cord and brain appear normal, and the
existence of nodules of sclerosis is only revealed by microscopic
examination.
The alteration appears in more or less numerous spots and
nodules, which are not confined to the cord, but are scattered in
greater or less numbers through the medulla oblongata, the
pons Varolii, the cerebrum, and the cerebellum.
The individual nodules are usually recognized easily by their
color and consistency. When they lie close to the surface, they
often glimmer distinctly through the pia, and in very intense
cases, the entire surface of the cord may appear to be studded
with grayish and usually sharply defined spots. These are often
slightly swollen and elevated above the level of the surface of
the cord; more rarely they are somewhat sunken and atrophic,
while frequently they are level with the surface, and have con-
sequently undergone no change in volume.
They are usually seen much more distinctly in the cross-sec-
tions. More or less extensive spots are seen in every section in
the white or in the gray substance, or in both together. These
spots are gray or grayish yellow, and when exposed to the air
often take on a light reddish tint (like salmon-flesh). They are
somewhat translucent, resembling jelly or cartilage, or perhaps
more opaque; fine white lines are often seen running through
them (vessels, fatty spots). They are more or less sharply cir-
cumscribed; as a rule, the edges age pretty sharply defined
against the surrounding healthy tissue, but sometimes they are
478 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
blurred, and the transition from the diseased to the healthy tis-
sue is more gradual. They are frequently very closely packed,
and sometimes become confluent. In form they are rounded,
elliptical or more or less irregular, so that it is impossible to de-
scribe them very accurately. |
The consistency of these nodules is, as a rule, considerably’
increased. They are tough, dense, leathery or cartilaginous,
oppose considerable resistance to the cutting instrument, and
can usually be recognized by the palpating finger as firm nodules
imbedded in the soft nervous mass. In rare instances the nod-
ules are soft, semifluid, gelatinous; these are probably nodules
of recent date. |
Their cut surface is smooth, and uniformly glossy, and gives
exit to a very small quantity of clear fluid. In size they vary,
greatly. They may be so minute that they are only revealed by,
the microscope, or they may be as large as a hemp-seed, a bean
or a hazel-nut, or even larger; between the two extremes every
possible intermediate stage may exist. In the brain the diseased.
spots are sometimes very large and diffuse; in the cord they are
sometimes greatly elongated (from two to ten centimetres or even
longer—three-quarters of an inch to four inches), though con-
fined to single white columns.
Their number varies within the widest limits j in le individual
cases. Sometimes only a few are found, and again they are so
numerous that they might be numbered by hundreds.
The distribution of the nodules in the spinal cord is very dis-
similar in different cases, and apparently depends entirely on
accident. They may be situated in the white as well as in the
gray substance. All the white columns may be attacked with-
out distinction; the furrows on the cord do not constitute bar-
riers to the pathological process. In one cross-section the nod-
ules will lie chiefly in the lateral column, in another more in the
posterior columns, and in still another perhaps more in the gray
substance ; in one they will take up the greater part of the sec-
tion, and in another only a very small part of it; here they will
be confined to one side, and there they will involve continuously
both sides of the cord, etc. (See Fig. 6.)
The opinion held by many authors, that the anterior col-
MULTIPLE SCLEROSIS,
479
umns are pre-eminently affected, holds true at all events only
for a small number of the cases. The more recent German
observations include, as it happens, several
cases in which the disease attacked chiefly the
posterior columns.
Furthermore, numerous nodules are usu-
ally found also in the various parts of the
caudex cerebri, in the medulla oblongata,
the floor of the fourth ventricle, the pons,
and the pedunculi cerebri. These parts, to-
gether with the walls of the lateral ventricles,
the white substance of the cerebral hemi-
spheres, and the white columns of the spinal
cord, seem to be the localities for which the
nodules show most predilection. The nod-
ules may be scattered throughout the entire
extent of the structures forming the caudex
cerebri; they are of varying sizes, and are
sometimes superficial and again deeply seated,
sometimes numerous and closely packed and
in other cases more isolated (see Fig. 7). It
is very rare for these parts to be found free
from disease.
The cerebrum usually contains a large
number of disseminated nodules, which are
very distinctly seen on every section through
the organ. The gray substance of the cortex
is, however, generally spared by the disease,
nodules being only exceptionally found in it.
In the central, white substance, the walls of
the ventricles, the corpus callosum, etc., they
are, on the other hand,exceedingly numerous.
As arule, some nodules are also found in the
corpora striata and the thalami optici.
In the cerebellum, on the contrary, the
nodules are usually few in number. Here,
Fic. 6. Semi-diagrammatic
representation of the changes
in multiple sclerosis, as seen
in sections made at different
levels of the cord, The dark
spots represent the sclerotic
nodules,
too, they are located by preference in the central white sub-
stance, the cortical layers being usually left exempt.
480 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The account just given applies almost solely to nodules of
old standing, such as are met with in the bodies of persons who
have suffered for many years from the disease. In these cases
we usually find the firm, dense, gray masses, on which the clas-
sical picture of multiple sclerosis is based. . For an accurate
description of the characteristics of the younger and youngest
nodules, we must look to'the future. Zenker found in one case
rounded translucent masses of a soft gelatinous consistency,
which presented a, homogeneous, structureless and colorless
matrix enclosing numerous cells, and which he held to be young
nodules of sclerosis. In general, most observers manifest a
tendency to regard. the
gray nodules, which pos-
sess a softer, and perhaps
semi-fluid consistency, as
the younger, and those
which are harder and den-
ser asthe older. This may
be on the whole correct,
but at the same time the
possibility of individual
differences cannot be en-
tirely excluded.
Furthermore, it must
also be mentioned, that the
sclerotic nodules are not
Pig Dictate of ecleota nodes on oe artes by any means limaibed aa
the central organs ; on the
contrary, they not unfrequently extend beyond them and estab-
lish themselves in the nerve-roots and nerve-trunks. This has
most frequently been observed in the cerebral nerves. Here,
just as in the central organ itself, gray translucent, circum-
scribed nodules, involving the entire thickness of the nerves,
are not unfrequently met with; sometimes several of them are
found on the same nérve. Such nodules have been found in
the optici, the olfactorii and the trigemini; also in the nerves
of the muscles of the eye, in the hypoglossi, etc. On the roots
of the spinal nerves, too, such nodules haye been repeatedly
MULTIPLE SCLEROSIS, 481
seen. On the peripheral nerves, however, their occurrence has
not yet been demonstrated with sufficient positiveness.
Finally, we have still to mention the fact, that in addition to
the disseminated sclerosis, a more diffuse sclerosis has also been
occasionally met with in the cord as well as in the brain (e. g.,
the cases of Schuele, Kelp, Buchwald). The individual, appar-
ently isolated nodules are then united with one another by a
more or less altered intermediate tissue. It is probable, that a
gradual transition to a truly diffuse sclerosis may take place in
this way.
With respect to the microscopical appearances of the sclero-
tic nodules, we may, for all the essential points, refer to the
description given of the microscopical changes in chronic myeli-
tis. In the opinion of almost all observers, multiple sclerosis
presents the type of interstitial chronic myelitis. We shall
confine ourselves here to a brief sketch of the histological ap-
pearances.
It may be premised, that the sharp line of division between
the healthy and diseased tissues, which is apparent when the
specimen is examined with the naked eye, cannot usually be
recognized under the microscope. On the contrary, a very grad-
ual transition from the normal into the morbid tissue can, as a
rule, be demonstrated.
In the nodules themselves we find: more or less marked
thickening of the trabeculee of the neuroglia, swelling and pro-
liferation of the nuclei, large and very sharply defined spider-
cells; gradual transition into a fibrillated and delicately fibrous
connective tissue; finally, nothing but parallel bundles of fibrils
placed close to one another; between them remains of the me-
dulla, fat- and granule-cells and masses of the same substance,
free fat.
In the nerve-fibres atrophy of the medullary sheath and
swelling of a few of the axis-cylinders, most of which, however,
remain unchanged ; disappearance of the medullary sheaths, per-
sistence of the naked axis-cylinders, which are closely embraced
by the small-meshed fibrillated tissue ; at last, the axis-cylinders
also may become sclerotic, glossy, brittle. Finally, these too
disappear in great part, and there remains only the dense fibril-
VOL. XIII.—31
482 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
lated connective tissue, which contains large and beautiful spider-
cells, a moderate abundance of nuclei and a varying number of
corpora amylacea ; free fat and drops of myeline are then usu-
ally wanting.
The remarkably long persistence of the axis-cylinder in the sclerotic tissue,
which was pointed out by Charcot and confirmed by Leyden, does not really
possess the importance ascribed to it, in the differential diagnosis from other forms
of chronic myelitis. At all events, even in advanced cases of sclerosis of the pos-
terior columns (tabes), we not unfrequently find very numerous well-preserved
nerve-fibres and axis-cylinders; hence I do not think that the persistence of the
axis-cylinders can be regarded as a radical point of difference or an essential char-
acteristic.
A considerable sclerosis of the walls of the vessels is regularly
observed. They are thickened, blended with the surrounding
fibrillated tissue, and very rich in nuclei; not unfrequently they
are in a state of pronounced fatty degeneration, and there is an
abundant infiltration of fat into the lymph-channels which en-
velop them. ‘The lumen of the vessel is thereby greatly dimin-
ished.
If the sclerotic process extends into the gray substance, the
ganglion-cells located therein generally become atrophied. They
frequently acquire a strikingly yellow color (yellow degenera-
tion), and are no longer stained perfectly by carmine; later on
they undergo colloid atrophy, lose their processes, and may
finally be completely destroyed.
Very little attention has hitherto been paid: in cases of mul-
tiple sclerosis, to the familiar secondary degenerations. I find
them hardly ever mentioned, and still, in view of the position
and extent of many sclerotic nodules, their absence would seem
decidedly remarkable. They seem at all events to occur rela-
tively very seldom; in many cases, however, it might be difficult,
without a very searching examination, to decide exactly what
belongs to the primary sclerotic nodule and what to the second-
ary degeneration. A closer study of this question would be de-
sirable.
Jolly’s case is the only one in which the descending degeneration of the lateral
columns is expressly mentioned. It is not positively certain, however, that the case
MULTIPLE SCLEROSIS. 483
belongs in the present category. The cord was free, and the changes in the brain
were of a more diffuse character.
In addition to the changes in the central organs themselves,
some other subordinate alterations take place, which require
only a brief mention. The skull-cap is frequently found abnor-
mal; it may be thickened or thinned, presenting sclerotic or
eroded spots. The membranes of the brain and cord are fre-
quently perfectly normal, but in other cases present more or less
pronounced evidences of hyperzemia and chronic inflammation.
The cerebro-spinal fluid is, as a rule, increased, frequently
cloudy, somewhat flocculent, etc.; the ventricles are considera-
bly dilated.
In the other organs of the body (muscles, peripheral nerves,
skin, bones, bladder, kidneys, lungs, etc.) the changes already
spoken of in connection with chronic myelitis are occasionally
observed. Some of them are direct consequences of the severe
spinal affection (such as bed-sores, vesical diphtheria, pyelone-
phritis, etc.), while others constitute more or less accidental com-
plications or terminal diseases (pneumonia, pleuritis, pneumo-
phthisis, typhus, etc., etc.). It is unnecessary to speak of them
here.
Pathology of Multiple Sclerosis,
Symptoms.
General clinical history.—In the majority of the cases the
disease develops gradually and insidiously. Sometimes, how-
ever, it commences abruptly: the scene is opened by an apoplec-
tiform attack, a sudden paralysis, severe headache and vertigo,
or the like.
In the cases which develop slowly the initial symptoms are
usually very obscure, vague and manifold. Sometimes they are
chiefly referable to the spine and sometimes to the brain. In one
case there may be slight disturbances of sensation, paresthesia,
weakness, paresis of the lower extremities, uncertainty of gait,
disturbances of co-ordination recalling those of ataxia, difficulty
in writing, cardialgic attacks (so-call@d crises gastriques) with
484 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
vomiting, etc. In another there may be vertigo, headache, stag-
gering gait, tremor of certain muscles or limbs, impairments of
speech, of sight and of particular cerebral nerves, psychical dis-
turbances, and a convulsive or apoplectiform attack. The com-
mencement of the disease is very frequently marked by head-
ache, dizziness, uncertain gaitand slight psychical depression.
It is evident, however, that the initial symptoms may occasion-
ally show themselves in all possible parts of the body.
The symptoms slowly become more severe, and new ones
are gradually or abruptly added. The disease continues for
years with slight fluctuations and occasional, deceptive improve-
‘ ment, but the practised eye can usually recognize a slow, progres-
sive aggravation. The forms in which the disease can present
itself are exceedingly numerous, and Charcot was right when he
called it par excellence a polymorphous affection.
In marked and typical cases the following morbid picture, or
something very like it, is developed after the lapse of a variable
period. The patients complain of sensory disturbances which
vary very greatly in intensity, quality and localization. Usu-
ally there are only parzesthesiz ; severe pains are less common,
but still they do occur. They assume the most manifold shapes,
and may present themselves in any part of the body ; they may
take the form of facial neuralgia, or of girdle-pains, or of lanci-
nating or diffuse pains in the extremities or the trunk, etc. To
these are added later, anzesthesiee of varying degree and location,
impairment of the muscular sense, etc. It is a striking fact,
however, that in a relatively large number of the cases, these
sensory disturbances are very slightly developed or even entirely
wanting ; at least the objective examination often fails entirely
to reveal any of them.
The motor disturbances, on the other hand, are generally
much more constant and more severe. The first to attract atten-
tion are usually pareses and paralyses, which almost always
begin in one leg, and extend subsequently to the other leg and
then to the arms; occasionally, however, they occur in some
other order of development, all imaginable variations from the
above sequence being possible. From a simple difficulty in walk-
ing, which is usually of a spastic character (see Part L., p. 97),
\
.
|
MULTIPLE SCLEROSIS. 485
the disease passes slowly through all the stages of development
up to complete paraplegia. Muscular contractions (Muskelspan-
nungen) usually make their appearance early, and in the later
stages very marked contractures of the lower extremities are the
rule; the legs are held as rigid as sticks in a position of exten-
sion and adduction. In the upper extremities the paralyses
rarely attain such a high grade as in the lower extremities, and
contractures are rarer; still both contractures and marked par-
alyses occur in them.
In a certain number of the cases, there is also true and pro-
nounced ataxia of the extremities. The most trustworthy ob-
servers report that they have seen exquisitely jerking move-
ments of the legs, setting down of the heels, etc., with the con-
sequent uncertainty in walking and standing ; also corresponding
ataxic disturbances of movement in the hands, etc.
A particularly striking, and in most cases exceedingly im-
portant and characteristic symptom, is an active, shaking tre-
mor, which occurs chiefly or exclusively during voluntary move-
ments (volitional trembling), and disappears or becomes scarcely
noticeable during rest. As long as the patient remains quietly
seated, there is either no tremor at all, or at most a slight shaking
movement of the head, or a slight oscillation of the trunk. As
soon, however, as he attempts to seize anything with the hand,
the tremor sets in; it is a forcible, rhythmical, shaking move-
ment, which increases in violence with the increase in the force
of will exerted, and which is very different in character from the
irregular, impulsive movements of ataxia, although it is occa-
sionally combined with them. The intended movement is gener-
ally carried out correctly, but it is attended by oscillatory
vibrations with more or less regular excursions. When the
patient attempts to raise a glass to his mouth, he cannot do it
without spilling the contents, which are often scattered widely
about him; if he succeed finally in the attempt, the tremor
makes the glass rattle against his teeth in a rhythmical manner.
The oscillations increase as the goal is approached, in a direct
ratio with the increasing intensity of the will-force, and the aug-
menting strain on the attention. The oscillations of the head and
the trunk also increase in intensity, when movements of the
486 ERB.—DISEASES OF THE SPINAL CORD AND ITS. ENVELOPES.
arms are attempted. When the patient rises and attempts to
walk, the tremor involves the entire body. He staggers on his
feet, and his entire body, head and arms are shaken by a violent }
tremor; in the severer grades of the affection he is often unable
even to stand, let alone to walk.
As soon as the effort of will is relaxed and the limbs are sup-
ported, the tremor ceases. While the patient is in the recumbent
posture with the head well supported, no trace of it can, as a
rule, be detected, but the slightest effort of the will, any strong
emotion, and any excitement will immediately call it forth in a
very marked degree. A continuous tremor, persisting also dur-
ing rest, and hence resembling somewhat the tremor of paralysis
agitans, has only been observed in a few isolated cases ; in some
of these it was a transitory and in others a persistent symptom.
In connection with all these motor disturbances, the condition
of the reflex activity may vary. Usually it remains unaffected
for a long time, sometimes it is diminished, but frequently, es-
pecially in the ordinary cases which present paraplegia and mus-
cular contractions, it is increased, the tendon-reflexes in par-
ticular being exquisitely developed.
The vesical disturbances are usually remarkably trivial, per-
haps on account of the relatively slight implication of the gray
substance of the cord. In some cases, however, all imaginable
disturbances of the vesical function, from the most trivial up to
the most severe, viz., retention and incontinence, have been ob-
served, just as in the other forms of chronic myelitis. Usually,
however, these symptoms belong to the latest stages. The same
statements may be made with respect to the rectal function and
the sexual powers. The latter often remain unaffected for a re-
markably long time, but towards the last they almost invariably
become impaired, and are finally extinguished.
Trophic disturbances are usually wanting for a long time.
As a rule, the blooming appearance of the patients presents a
striking contrast to the complete helplessness to which they are ~
condemned by the motor disturbances. Sooner or later, how-
ever, but in general only in the last stage, trophic disturbances
of various kinds are wont to occur. The muscles become atro-
phied and lose their electric excitability. Bed-sores are devel-
OO a ae
.
j
j
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MULTIPLE SCLEROSIS. | 487
oped, the state of the general nutrition sinks along with the di-
gestive powers, and fever hastens the advance of the cachexia.
The symptoms thus far enumerated are supplemented in most
cases by a series of phenomena, whose origin can positively be
referred to changes in the brain (cephalic or cerebral symptoms).
We must mention first certain bulbar symptons, which are
among the most important of the entire morbid picture ; first of
all, a remarkable alteration of speech and of the voice. The
speech is slow, hesitating, distinctly scanning, and later on more
or less indistinct. The voice is weak, monotonous, and has less
Staying power. The acts of laughing and crying are accom-
panied by peculiar, noisy inspirations. Later on the movements
of the tongue and lips are not unfrequently impaired, mastica-
tion and deglutition are accomplished with great difficulty, ete.
The disorders of the organ of vision are, as a rule, very signifi-
cant. ‘Temporary or permanent diplopia, due to pareses of the
ocular muscles, has been observed. A marked nystagmus,
which, according to the statements of different observers, is in-
creased by any exertion of the will or by any violent emotion, is
very common. Finally, amblyopia is not infrequent, but it is
only in a few cases that it increases to complete amaurosis, with ©
atrophy of the optic nerve as its basis.
Furthermore, psychical derangements are very generally
present. Often, these consist-only in slight irritability, changes
in disposition, a more active reaction to all sorts of impressions,
a great tendency to weep, or to laugh without motive, etc. Im-
pairment of the memory and the intelligence is common, as is
also the development of pronounced psychoses; melancholia,
monomania taking the form of persecution or of exaltation, final-
ly craziness and complete dementia.
The attacks of vertigo, the sleeplessness and violent head-
aches, which are not unfrequently observed, complete this pic-
ture ;and when we add that in some cases repeated apoplectiform
attacks, accompanied by high fever and followed by temporary
‘hemiplegia, are observed, we have therewith put the finishing
touch to the general description of the clinical history.
This description, however, applies only to the very pro-
nounced and typical cases of the diséase. It.cannot be denied
488 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
that the variations are exceedingly numerous; that, on the one
hand, this or that symptom may be wanting, while on the other
hand, symptoms may occupy the foreground, which will stamp
the clinical history with a great resemblance to that of other
known diseases. The accidental localization of the principal
nodules affords a ready explanation of the fact, that certain
cases present an unmistakable resemblance to sclerosis of the
posterior or of the lateral columns, or to myelitis transversalis,
etc. The inconstancy of often the most important symptoms,
the absence of some, the occurrence of others, and the great
changeableness of the clinical picture, also find a natural expla-
nation in the great differences in the number and localization of
the nodules in the different cases..
An attempt has been made to differentiate different forms of
the affection, according to the predominating localization of the
disease. The most frequent form has been accordingly desig-
nated as the cerebro-spinal, because in it the nodules are found
both in the brain and the cord ; in contrast to it, a purely spinal
form (with exclusive spinal localization) and a purely cerebral
form (with exclusive cerebral localization) have also been set up.
We shall return to this point in another place, and we shall see
that in practice this sharp differentiation is, as a rule, impos-
sible.
The course of the disease is usually exceeaingly slow and
sluggish. A very striking improvement sometimes occurs—an
actual remission that almost simulates a cure. It is wont to be
deceptive, however, and is rarely persistent. Usually the dis-
ease makes continuous, though often very slow progress. Its
duration must be reckoned by years, often by many years. As
time elapses, all the symptoms increase in intensity and extent ;
the paralysis, the contractures, and the psychical weakness
assume more and more the upper hand, and bring about an
exceedingly deplorable state of affairs. The speech becomes
more and more unintelligible, the pains augment, and the rest-
lessness of the limbs becomes unbearable ; affections of the blad- ~
der and bed-sores, with all their consequences, are superadded.
Those patients are most fortunate who are rapidly carried off by
some acute intercurrent disease (pneumonia, septicaemia, typhus,
MULTIPLE SCLEROSIS. 489
cholera, etc.), as they thereby escape a lingering death after un-
utterable sufferings, from the advancing general cachexia.
Analysis of the Individual Symptoms.
It is not necessary here to go into all the details, since a great
number of the phenomena met with are to be explained exactly
in the same way, as the same symptoms in chronic myelitis.
Hence, we can, for many of them, refer to the preceding chapter.
This applies especially to the disturbances of sensibility, the
paretic and paralytic phenomena, the state of the reflex activity,
the muscular contractions and contractures, the vesical symp-
toms, the occasional atrophy of the muscles, the bed-sores, ete.
Of course a part of these symptoms may be of cerebral origin,
€. g., the pareses and paralyses, which may be due to sclerotic
nodules situated in the thalami optici, the corpora striata, the
pedunculi, ete.
Many authors speak of the absence of marked, objective dis-
turbances of sensibility, which they claim to be especially charac-
teristic of the disease. This is, however, decidedly incorrect.
Berlin found disturbances of sensibility noted in fifteen of the
thirty-nine cases examined by him. In not a few cases all pos-
sible varieties and grades of sensory disturbance are found. In
Engesser’s case, there were distinct diminution of the cutaneous
sensibility and considerable impairment of the muscular sense,
with much staggering when the eyes were closed, but without
ataxia. Other cases have presented marked ataxia, without any
disturbance of sensibility, and also without any staggering when
the eyes were closed—a fresh proof that this last symptom has
a direct dependence solely on the sensory disturbance, and has
no connection with the ataxia as such. It is certainly remark-
able, that in many cases the disturbance of sensibility should be
so exceedingly trivial, or even entirely absent, in spite of wide-
spread multiple sclerosis involving also the posterior columns.
Schuele has investigated this question thoroughly, and found in
the immunity from the lesion of certain parts of the posterior
columns and the gray substance, the conditions which in all
probability secure the undisturbed conduction of the sensory
490 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
impressions, despite apparently large gaps in the normal sensory
tracks.
We must now devote some space to a special discussion of
that very important and characteristic symptom, the shaking
tremor during voluntary movements (the volitional trembling—
Intentionszittern—of F. Schultze). This presents a very peculiar
and easily recognized ensemble. While the patients remain
seated, we notice only a slight rhythmical trembling and oscilla-
tion of the trunk and the head, the extremities remaining quiet.
It must be borne in mind in this connection, that in the act of
sitting the muscles of the trunk are constantly in a state of
slight action, which is requisite for the retention of the equi-
poise. ‘¥
As soon as any movement is made with the upper extremities,
an active trembling and shaking becomes noticeable in them,
while at the same time the oscillations of the head increase in
intensity. All delicate and even all coarse manipulations are
thereby impeded or made impossible ; in writing, the letters are
very greatly distorted, and finally become entirely undecipher-
able, ete.
When the patients attempt to stand and walk, the entire body
is violently agitated, the legs being particularly affected. In the
highest grades of the affection, both walking and standing are
rendered impossible by this shaking ; in the slighter grades, it is
observed particularly in changing from one position to another,
in rising from a chair, at the commencement of a walk, etc.
On the other hand, when the patients are in a position of per-
fect rest, lying comfortably in bed, no trace of the tremor can be
noticed, at least in the majority of the cases. Strong emotion
(anger, irritation, embarrassment, shame) will, however, excite
the tremor in these cases even during the state of rest, just as
it will notably increase it during voluntary motion. In con-
trast to the above, it is recorded of isolated cases, that a shaking
movement of the extremities was present even during perfect
mental and bodily rest, and persisted more or less uninter-
ruptedly for days, weeks, or even longer. I have myself ob-
served one such case. The unfortunate patient was almost con-
stantly tormented in the most pitiable manner by tremor-like,
MULTIPLE SCLEROSIS. 491
twitching movements of the extremities ; there was but one way
in which the restless movements could be controlled even for a
few minutes, and that was by firmly holding the limbs.
It is very probable that in such severe and intense cases even the automatic
movements of voluntary muscles, ¢. g., the respiratory act, or the half involuntary
movements of the muscles of the eye, the muscles of facial expression, etc., are capa-
ble of exciting and keeping up the shaking tremor, while the body is apparently at
rest.
In the great majority of the cases, however, and in the first
stages of the disease, it is always a very essential and character-
istic point, that the tremor is ingrafted on the voluntary move-
ments, that it appears with every innervation of the muscles.
Even in the later stages, when the tremor has become more con-
tinuous, it is at all events certain that it is enormously increased
by every attempt at movement. As a rule, it is wanting during
absolute rest, and appears in connection with all voluntary or in-
voluntary movements, becoming more intense as they become
more forcible ; the more extensive the movement, the more forci-
bly it is performed, the more the attention is directed to it, so
much the more violent is the tremor.
Therein lies also the essential point of difference between the
tremor of multiple sclerosis and that of paralysis agitans, two
forms of tremor which were almost invariably confounded until
Charcot pointed out their exact differential characteristics. In
paralysis agitans the trembling is observed also during perfect
rest ; it is not increased by voluntary movement, but, on the con-
trary, the patients are able—at all events in the earlier stages of
the affection—to control it for a time at least by force of will ;
any voluntary movement, any change in the position of the limb,
is sufficient to still the tremor for a few minutes, but it gradually
begins again after the limb has lain quiet fora time. The char-
acter of the tremor also is essentially different in the two affec-
tions. In paralysis agitans the oscillations are much smaller
and more frequent ; they possess more of the character of a true
tremor, than do the wide oscillations of multiple sclerosis. In
the latter, moreover, the tremor of the hands frequently assumes
a peculiar and very characteristic type ; * it looks as if the patients
492 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
- were about to spin, or to mix pills, or the like. The head is sel-
dom or never involved in the tremor of paralysis agitans.
As far as I can judge from my own experience, the trembling
of paralysis agitans can in most cases be easily distinguished
from the shaking of multiple sclerosis. Any one who has once
observed closely and compared the two forms of tremor, will
never confound them together in pronounced cases. It would
be very wrong, however, to conceal the fact, that cases of multi-
ple sclerosis occur, in which the tremor resembles in character
very closely that of paralysis agitans, and in which the decision
as to the quality of this one symptom may be very difficult—cases
in which the two forms of tremor exist side by side. It isin my
opinion much more correct, to assume a combination and compli-
cation of two different clinical processes in such cases, than to
deduce from them, few in number as they certainly are, the con-
clusions that the two forms of tremor are not essentially different,
and that they can occur promiscuously in both diseases. The
former view is supported by the great majority of the observa-
tions, which speak plainly in favor of the essential difference of
the two forms of tremor. We must wait for more accurate ob-
servations, however, before passing finally on the correctness of
this view.
With actual choreic movements, the shaking tremor of mul-
tiple sclerosis cannot be easily confounded in ordinary cases.
The movements in chorea are very irregular, violent and impul-
sive, and not rhythmic or oscillating as those of multiple sclero-
sis. They occur also during rest very abruptly and without
apparent cause. In chorea the direction of an intended move-
ment is altogether distorted ; it is zigzag and irregular: in mul-
tiple sclerosis the general direction of the movement is preserved,
but the line of movement is wavy, oscillating about a central line.
This holds true, at all events, in the typical cases of the two dis-
eases ; here too, however, it seems to me that combinations and
undecided intermediate forms occasionally occur, in which doubt
may arise as to the proper classification of the existing motor
disturbance.
These remarks apply also to true ataxia, that disturbance of
co-ordination which is present in its typical form in the sclerosis
|
|
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MULTIPLE SCLEROSIS. 493
of the posterior columns. Here, too, the differentiation is very
easy in ordinary cases. The ataxic movements do not constitute
a regular, rhythmical trembling or shaking; on the contrary,
they are disorderly, immoderate, jerking movements, which make
their appearance at the moment a voluntary impulse is formed
and frustrate the intended movement. It is very difficult to de-
scribe them in detail, but when once seen and studied, they can
scarcely be confounded with anything else. Here too, however,
and much more frequently even than in the cases of paralysis
agitans and chorea, combinations and mixed forms occur, which
permit the development of both motor disturbances in one and
the same patient, and which lead uncritical observers to con-
found them together both in description and in pathogenesis. It
is, in my opinion, exactly in these cases, that it is most easy to
recognize the combination of the fwo motor disturbances, to de-
monstrate the simultaneous occurrence of ataxia and volitional
tremor ; in fact it has already been repeatedly demonstrated by
different observers. The pathogenetic explanation of this com-
bination is ready at hand, since the anatomical basis of the
ataxia is given in the location of sclerotic nodules in the posterior
columns. Other symptoms of sclerosis of the posterior columns
are usually present in such cases, viz., lancinating pains, anes-
thesia, impairment of the musenlar sense, staggering when the
eyes are closed, etc. With regard to the volitional tremor itself,
we are, it is true, not yet in an equally desirable position, for we
are unable to ascribe it even with probability to any specific
anatomical localization.
The tremor is one of the most constant, and unquestionably
one of the most characteristic symptoms of multiple sclerosis ;
whenever it is met with, it must direct the attention to that dis-
ease. It is not always present, however, not a few cases having
been recorded, in which it was absent throughout the entire course
of the disease (Leube, Ebstein, Engesser, Jolly, and others), cases,
moreover, to which Charcot’s suggestion, that it may perhaps
have existed during a time when the patients were not under ob-
servation, cannot wellapply. Itis certainly true, that the charac-
teristic tremor diminishes in the later gtages of the disease, and
finally disappears entirely. This diminution progresses in an
A494 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
inverse ratio to the increase in the prominence of the paralysis and
the contractures. Another form of tremor, however, frequently
appears at this time, namely, the clonic tremor on passive dorsal
flexion of the foot (the so-called epilepsie spinale of Brown-
Séquard and Charcot). We have already shown (Part I., p. 101)
that this is a reflex phenomenon, and that it is usually connected
with increased tendon-reflexes. Beyond the external form, it has
nothing in common with the volitional tremor, and only a super-
ficial observer would confound it with the tremor that accompa-
nies voluntary movements, and utilize it in the characterization
of multiple sclerosis.
The origin of the typical volitional tremor of multiple scle-
rosis is as yet exceedingly problematical. It is a variety of
derangement of co-ordination, which, however, when closely ex-
amined, differs very essentially from true ataxia, and hence must
certainly have another anatomical basis. Charcot’s theory, that
the relatively long persistence of the axis-cylinders in the sclero-
tic nodules might perhaps have something to do with it, because
the impulse of the will would be conducted through the naked
axis-cylinders only in a sort of jerking manner, will certainly not
find many adherents. It is open to too many objections. The
theory, that some specific localization of the sclerotic nodules is_
answerable for the production of the tremor, is certainly more
plausible, and it is maintained by many authors. Ordenstein .,
asserts, that it is principally the pons and the parts of the brain |
situated in front of it, that come into question here, and Ham-
mond says, that the tremor is wanting in the exclusively spinal
cases.
In point of fact, if we pass in review the recorded cases of
simple chronic myelitis, we do not find this characteristic tremor
enumerated among the symptoms, even when several centres of
disease exist in the cord. The matter becomes more difficult to
decide, when the individual cases of multiple sclerosis are under
examination, because in them the wide extension and great mul-
tiplicity of the nodules place almost unconquerable obstacles in
the way of every attempt to draw a simple and clear conclusion.
Still, a critical study of these cases reveals some facts that are
worthy of note. Thus Ebstein describes a case of purely spinal
=
ee Coe 94a a 7
.
~~” (eee =:
MULTIPLE SCLEROSIS. | 495
localization without tremor, but with ataxia; in Kelp’s case, on
the contrary, which belonged to the purely cerebral form, the
tremor was present. Engesser also describes a case without tre-
mor, in which the localization was predominantly spinal, and
Vulpian’s first case was of the same sort. From these facts it
seems to follow, that the localization of single nodules in the
brain is, in point of fact, necessary for the production of the tre-
mor. It is still more difficult to decide exactly what parts of
the brain must be affected, in order to produce the tremor. I
have examined twenty-two recent cases, with a special view to
the decision of this question. In all of them which had pre-
sented the tremor during life, the structures of the caudex (pons,
medulla oblongata, pedunculi, etc.), besides other portions of
the brain, were particularly involved in the sclerosis; on the
other hand, in the few cases in which the tremor was veins
during life, although nodules existed elsewhere in the brain,|
there were either none at all or at most only small ones in
the pons, the oblongata, the cerebellum, etc. (See the cases of
Jolly, Leube and Engesser). Uncertain and ambiguous as these.
facts may be, they at all events speak in favor of the opinion,
expressed by Ordenstein, that the localization of the nodules in
the pons and the parts of the brain situated anterior to it, is an
essential condition for the production of the tremor. This con-
clusion withal necessarily rests on very insecure foundations,
and numerous observations are requisite for its complete con-
firmation. At all events, the appearance of volitional tremor
furnishes even now valuable evidence that a pathological pro-
cess has been established in the brain itself, evidence which,
in doubtful cases, may prove of great diagnostic value.
Among the motor symptoms, the fonie contraction of the
paralyzed muscles, which appears in the later stages and may
subsequently increase to very marked contracture, also deserves
mention. It affects pre-eminently the lower extremities, which
are also, as a rule, more intensely affected by the paralysis. At
first isolated attacks of spasmodic extension, of tonic stiffness of
the legs, etc., occur, either spontaneously or when the patients
attempt to perform some movement; or they may be excited by
external cutaneous irritants, or probably also by violent emo-
496 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPEs.
tions. In a certain stage of the disease, movements, which
are otherwise still practicable, may be greatly interfered with
by these attacks of stiffness and rigidity. The attacks become
progressively more frequent and more prolonged, until finally
permanent contractures in the position of extension are devel-
oped; the legs are as rigid as sticks, and are held closely to-
gether by contracture of the abductors; the feet are in the
varo-equinus position. Sometimes, however, contractures in the
position of flexion are developed ata later period. These con-
tractures are almost always accompanied by a considerable aug-
mentation of the tendon-reflexes. The already repeatedly de-
scribed, clonic twitching of one or even of both legs excited by
passive dorsal flexion of the foot (called by Charcot tonic spinal
epilepsy), has been mentioned particularly by many observers.
This clonus can be excited by cutaneous irritation, as well as by
passive dorsal flexion of the foot; it is also excited occasionally
by voluntary movements and by the act of defecation or of mic-
turition. if
The upper extremities are rarely the seat of contractures.
Still, exceptions do occur, when the paralysis has extended to
the arms; the contractures have then been observed both in the
flexed and the extended positions. Schuele observed in one case
a temporary, cataleptic or tetanic rigidity of the muscles of the
upper extremities. |
The explanation of these phenomena is probably the same as
that of the analogous symptoms in simple chronic myelitis: in-
terruption of the tracks for controlling the reflex actions and
increase of the reflex activity on the one hand, and direct irrita-
tion of the motor tracks on the other. Their anatomical basis
must, in the present state of our knowledge, be assumed to be
the development of sclerotic nodules in the lateral columns and
the consecutive, descending secondary degeneration of the same
columns. |
Among the cerebral disturbances, the impairment of speech
deserves to be mentioned first; it is a frequent, a striking, and,
for the diagnosis, an important symptom. The so-called scan-
ning speech is the form of impairment which is most frequently
observed. The speech is slow, drawling, and hesitating; every
thin,
—
MULTIPLE SCLEROSIS. 497
syllable is pronounced separately and distinctly, the words being
as it were scanned. Later on, particular letters are pronounced
indistinctly and replaced by others, a peculiarity that was espe-
cially marked in Radlick’s case. Finally, in the more intense
degrees, the entire articulate expression becomes indistinct, lal-
ling, and even unintelligible. The impairment consequently is
not a true stuttering, and neither is it the form of impediment
which is so common in progressive cerebral paralysis. In paraly-
sis, the words tumble over one another, syllables and words are
left out entirely or are jumbled together in a confused mass, and
letters and syllables are inserted in the wrong places; in multiple
sclerosis, on the other hand, the words fall from the lips in a
hesitating, regular, scanning manner.
The mobility of the lips is often impaired, and they may
present slight twitching movements in speaking. In many cases
the tongue can only be put out in a slow and tremulous manner.
The monotony of the voice, which has been already spoken of,
is in most of the cases a striking peculiarity. The voice remains
in the same key, is weak and low, and often almost whispering ;
it breaks readily when forced efforts are made. Leube examined
one such case with the laryngoscope, and found that the vocal
cords could be brought together, but that their tension was
soon relaxed and frequently changed. In one case observed by
myself, the monotony alternated with the exactly opposite con-
dition; there was a constant, rhythmical, perfectly regular
change in the key at fixed musical intervals, e. g., a third, so
that the key was altered in the pronunciation of every syllable,
always observing, however, the same interval, just as if the
patient were constantly singing a-c, a-c, a-c, etc. The effect pro-
duced was very peculiar.
Leube’s observations show, that this peculiar disturbance of
the voice probably depends on a diminution in the innervation
and the capacity of the vocal cords. Whether the scanning is
due to the same cause is still questionable. Leube attempts to
explain it also by the exhaustion and weakness of the cords;
their capacity, according to him, is only equal to the production
of isolated syllables, and hence the syllables are enunciated in an
isolated manner. Under such circumstances, however, we should
VOL. XIII.-—32
498 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
rather expect to find the articulation confused and precipitate.
Persons who suffer from weakness of the vocal cords due to
other causes are not wont to scan. It seems to us, consequently,
that in order to account for the scanning, we must assume the
existence of disturbances in the nerve-tracks that preside over
articulation.
The entire disturbance of speech can in most cases be referred
to the presence of sclerotic nodules in the medulla oblongata and
the pons. Still we cannot exclude the possibility, that nodules
located further forward in the nerve-tracks for the organs of
speech may be answerable for this disturbance. Jolly’s case
certainly presented the impairment of speech, and still there
were absolutely no changes in the pons, and only doubtful altera-
tions in the medulla oblongata.
In connection with the above we must consider the manifesta-
tions of bulbar paralysis, which have been observed in several
cases (Joffroy, Leube, Schuele, Jolly, and others), and which give
us a distinct glimpse of the typical form of that affection. Im-
paired mobility of the lips and tongue, difficulty of swallowing,
paralysis of the velum palati, permanently open mouth, increased
secretion of saliva, etc., are the symptoms. In the majority of
the cases they are certainly due to the presence of nodules in the
bulb, but Jolly’s case proves that this is not invariably and neces-
sarily the case; in it the morbid process a wide-spread sclerosis,
was located more centrally.
The disturbances of respiration, which are often observed,
also belong here beyond a doubt. Especially characteristic are
the disturbances in the innervation of the larynx, which manifest
themselves on the one side by the already described monotony of
speech, and on the other by the stridulous inspirations, which
are frequently observed during laughing, weeping, ete. They
may probably be explained by a paresis of the crico-arytenoidei
postici.
The nystagmus is usually the most striking of all the eye
symptoms. It consists of short twitches, which have a horizontal
direction, and draw the eyes sometimes in an outward and some-
times in an inward direction; they are at times persistent, but
again may occur only during forced accommodation, or when
MULTIPLE SCLEROSIS. 499
movements are performed with the extremities. In the latter
case the eyes present nothing abnormal, when the body is ina
state of general rest. This symptom is pretty common ; accord-
ing to Charcot it is met with in about half of the cases. Whether,
and to what extent, this nystagmus differs from the ordinary
nystagmus of eye-patients; whether or not it is an essentially
different disturbance, are questions that must still be left open.
It is probable that, in many cases, we have to deal with the
‘‘ataxic nystagmus”’ (disturbance of co-ordination of the mus-
cles of the eye), recently differentiated and described by Fried-
reich ;* in other cases it may be analogous to the volitional
tremor.
Both physiological and pathological facts (compare the ac-
count given in the work of Friedreich just cited) warrant the
assumption, that the cerebellum, the corpora quadrigemina and
the medulla oblongata possess important functions relating to
the co-ordination of the movements of the eyes. Hence it is
probable, that the presence of sclerotic nodules in these struc-
tures may be the cause of the nystagmus in multiple sclerosis.
This still lacks positive demonstration, however.
The next symptom in point of frequency is amblyopia, a pro-
gressive weakness of sight, sometimes accompanied by color-
blindness and diminution of the field of vision, and, in rare cases,
increasing to complete amaurosis. Sometimes the development
of the amblyopia is preceded by photopsia, flashes of light, ete.
On ophthalmoscopic examination the papilla is sometimes found
perfectly normal or only partially diseased, while in other cases
it isin a state of pronounced white atrophy. All this is prob-
ably produced chiefly by sclerotic nodules in the tractus and.
the nervi optici. The fact that these nodules are essentially
of an interstitial character, affecting the nerve-fibres only at a
later stage, and in a secondary manner, is, according to Charcot,
the reason why the amblyopia is not very intense and complete ;
the axis-cylinders, being left intact for a long time, are still capa-
ble of performing their functions.’
1 Ueber Ataxie mit besonderer Beriicksichtigung der hereditiiren Formen. Virch.
Arch. Bd. 68. 1876. .
* See also Yoerster, Beziehung der Krankheiten des Nervensystems zum Sehorgan,
500 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Finally, diplopia is not unfrequently observed, sometimes as
an initial and transient symptom, sometimes in the later stages,
when it depends on complete and permanent paralysis of the
different muscles of the eye. There can be no doubt that these
later disturbances are to be ascribed sometimes to nodules in the
peripheral nerves of the ocular muscles, sometimes to nodules in
the intra-cerebral tracks for the innervation of these muscles.
Impairments of smell, taste, and hearing occur in isolated
cases, but they are rare, and hence possess no great importance.
Psychical disturbances, on the other hand, are common, and
belong essentially to the morbid picture. In the commencement
and in the milder cases, simple depression of spirits and impair-
ments of the memory, the intelligence, and the intellectual ca-
pacity, are observed. With these are combined attacks of yawn-
ing or sobbing, and a great tendency to laugh or weep without
motive. Later on the patients become stupid, the face acquiring
a correspondingly apathetic and varyingly stupid expression.
Sometimes, however, the mental disorder becomes very pro-
nounced; an intense melancholia, sometimes accompanied by
stupor, rejection of food, etc., or mania with delusions of perse-
cution or of grandeur, conditions of exaltation, etc., may be
developed. These disorders can run their usual course, termi-
nating finally in complete destruction of the intellectual life.
It is clear, that all these disturbances can be ascribed only to
the development of nodules of sclerosis in the hemispheres of the
cerebrum. It is scarcely necessary to add, however, that we
have not yet discovered the exact relations of the specific local-
izations of the nodules to the particular forms of the mental
disorder.
The same may be said with respect to an almost constant, or
at all events, in all stages of the disease, a frequent symptom,
viz., the vertigo. This often makes its appearance very early,
even in the prodromal stage. According to Charcot, the dizzi-
ness is usually of the turning variety ; the patients feel as if they
themselves were turning around, or it seems to them that all the
in the Grife-Siimisch Handbuch d. Angenheilk. VII. 1. p. 104; and Kiesselbach, Zar
Kenntniss der grauen Degener. der Sehneryen bei Erkrankungen des Cerebrospinalsys-
tems. Diss, Erlangen. 1875,
\
'
mee wer ae ih ~
ae ae eC nN
MULTIPLE SCLEROSIS. 501
surrounding objects are engaged in a gyratory movement. This
vertigo occurs in short, isolated attacks. Its mode of develop-
ment is entirely unknown. Occasionally an existing diplopia
may give rise to a visual vertigo (Gesichtsschwindel) which is
easily distinguished from the other form.
We have, last of all, to mention one other group of symptoms,
which also stands in direct connection with the brain, viz., the
apoplectiform attacks. These are apparently entirely analogous
to the apoplectiform attacks in progressive paralysis, in which
disease they have been long known and accurately studied.
It has not yet been satisfactorily demonstrated that the epileptiform attacks,
which are likewise not infrequent in paralysis, occur in multiple sclerosis as well.
Charcot has not yet met with them. On the other hand, they were observed in
Kelp’s case, and Leube reports one case (without an autopsy) in which an epilepti-
form attack was observed.
The apoplectiform attacks occur only in a comparatively
small proportion of the cases of multiple sclerosis—about one-
fifth of them, according to Charcot. They are characterized by
the abrupt development of severe cerebral symptoms, accompa-
nied by considerable elevation of temperature. After slight pro-
droma, such as a feeling of oppression in the head, an apathy
and an obscuration of consciousness appear, which in the course
of a few hours may increase to deep coma. The face is red and
hot, the pulse quick, and the temperature rises to 40° or 41° C.
(104°-1054° F.). Very soon the existence of hemiplegia can be
demonstrated by the complete relaxation of the extremities of
one side. After a shorter or longer interval (one or two days)
the consciousness reappears, the temperature falls, and the pa-
tient sinks into a deep sleep, from which he awakens relatively
well. The hemiplegia, however, persists for a few days longer,
and then disappears gradually. These attacks are nevertheless
invariably followed by a general aggravation of the disease.
Attacks of this sort may be repeated several times. They may
recur every few months, or even at intervals of a year. Some-
times death occurs during the attack, while the patient is in a
condition of deep coma.
The interpretation of these attacks js still very obscure. They
differ from true apoplexy particularly in the high temperature of
502 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the body, the, as a rule, gradual development of the coma, and
the rapid disappearance of the hemiplegia.
The autopsies in such cases reveal no signs of acute conges-
tion of the brain. Charcot could never discover in them either
cedema or hyperzemia, or, in fact, anything but old changes.
He draws attention, however, to the fact, that these attacks are
only met with in those cases of the disease, in which the pons
and the medulla oblongata are involved either primarily or sec-
ondarily. Weare, however, still ignorant of the actual cause of
these very transient but violent attacks. The suggestion, that
they perhaps indicate the acute development of new nodules of
sclerosis, has little to support it; they would in that case be
much more common. :
The above embraces all the chief symptoms of multiple scle-
rosis, but it still remains for us to mention briefly a few uncom-
mon symptoms, which are occasionally met with, although they
do not belong to the typical morbid picture. The first of these
to be mentioned is the muscular atrophy. This may attain a
very high grade, and may present itself in any part of the body—
in the upper or the lower extremities, in the neck, the face, or
even in the tongue (Kbstein). It is unquestionably to be ex-
plained by the localization of sclerotic nodules in the correspond-
ing parts of the gray substance.
With this atrophy the condition of the electric irritability
stands in the most intimate connection. The latter usually
remains intact for a long time, or presents at most only slight
quantitative changes. In the later stages, when there is increas-
ing atrophy, the electric irritability may diminish very consider-
ably ; at such times accurate examination will undoubtedly re-
veal also the reaction of degeneration. Thus, Leube observed
marked impairment of the electric irritability with indications
of the reaction of degeneration. In Engesser’s case the irrita-
bility was at first increased, and subsequently considerably
diminished. The customary conclusions with respect to the
nutritive state of the muscles and the condition of the gray sub-
MULTIPLE SCLEROSIS. 503
stance corresponding to them, are to be drawn from these facts.
The electrical examination has not, however, up to the present
time proved of any great practical value.
The disturbances of the vesical function are also variable and
inconstant. They are often wanting for a long time, and then
set in in various forms and degrees ; they are sometimes marked
by great fluctuations in intensity (Engesser’s case), but do not
present anything that is at all characteristic. The entire history
of the vesical complications is essentially the same as in chronic
myelitis. This may be said also of the affection of the sphincter
ani.
The disturbances of the sexual functions are also very incon-
stant. Sometimes the sexual power is retained for a long time,
and again it is lost at an early period. In some cases excessive
onanism gives evidence of unusual sexual excitement.
In a few cases the so-called tabic symptoms are developed in
avery pronounced manner; disturbances of the cutaneous sen-
sibility, impairment of the muscular sense, lancinating pains,
girdle-sensation, distinct ataxia, staggering when the eyes are
closed, etc., are observed in such cases. In most of these cases,
this may be explained by the development of a large sclerotic
nodule, or of several such nodules, in the posterior columns. A
combination of band-shaped sclerosis of the posterior columns
with insular sclerosis of the rest of the nervous system, is also
possible. Such cases may interpose grave difficulties in the way
of a diagnosis. Asa rule, however, the presence of other symp-
toms, which belong only to sclerosis, will clear up the matter. Ke dav
At all events, the cases of hereditary ataxia described by Fried-,_ ot Ib
reich (1. ¢.), which, as far as their clinical history is concerned,’ p/
occupy a sort of intermediate position between ordinary sclerosis
of the posterior columns and insular sclerosis, but still must
unquestionably be classed only under sclerosis of the posterior
columns, warn us to be very careful in making a diagnosis. We
shall return to this subject in another place.
In a similar manner, the symptoms of the so-called Zateral
sclerosis are not unfrequently found in the clinical history ;
paresis of the lower extremities, muscular contractions, increased
tendon-reflexes without disturbancéS of sensibility, etc. These
504 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
symptoms may even exist alone for a long time, and their true
significance may then only be cleared up by the development of
cerebral symptoms at a later period. A primary or secondary
sclerosis of the lateral columns accounts sufficiently for this state
of affairs, as has already been stated above.
But little progress has as yet been made in the differentiation
of different forms of multiple sclerosis. The French authors
distinguish a cerebro-spinal, a purely cerebral, and a purely spi-
nal form. The correctness of this division has not yet, however,
been demonstrated with satisfactory clearness, and it is even
positively rejected by some authorities (Buchwald eé al.). A
sharp separation, an unquestionable limitation of the affection
to the brain alone or to the cord alone, is in all probability
very rare. Still, there undoubtedly are cases, in which the locali-
zation is so predominantly in one or the other of these nervous
centres, that we are justified in speaking of a cerebral and a
spinal form in a somewhat wider sense.
The cerebro-spinal form has been described in the preceding
pages. The cerebral form seems to be relatively very rare. The
cases recorded by Kelp and Jolly should probably be classed
here. In this form only the cerebral symptoms are present; the
psychosis usually occupies the foreground in the clinical pic-
ture. The tremor is said to precede the paralytic manifestations.
In other respects the clinical picture cannot differ greatly from |
that of the cerebro-spinal form; it is difficult to exclude the
simultaneous implication of the spinal cord.
The limitation of the spinal form to the cord is usually more
easily recognized. Generally, it is sufficiently characterized by
the absence of the cerebral symptoms, particularly the nystag-
mus, the volitional tremor, the psychical disorders, the vertigo,
the apoplectiform attacks, etc. The disturbances of speech and
_of co-ordination may, however, be present. In Ebstein’s case,
for instance, there were no cerebral symptoms and no tremor,
but there were disturbances of speech and of co-ordination. In
Engesser’s case, which also presented an almost purely spinal
type, and formed a sort of transition to diffuse chronic myelitis,
the tremor, the disturbance of speech, the nystagmus, the vertigo
and the apoplectiform attacks were wanting. Vulpian also de-
MULTIPLE SCLEROSIS. 505
scribes a purely spinal form without tremor, with the exception
of the reflex clonus in the leg, which, of course, must not be con-
founded with the volitional tremor. In cases like these, the
purely spinal localization can be easily recognized. The great
difficulty, however, will be to determine the existence of mul-
tiple nodules. Usually, the clinical picture will present a hope-
less similarity to that of simple chronic myelitis, and we can
only regard it as a happy accident, when the localization of the
nodules is such, that we can recognize from the symptoms a
simultaneous affection of several isolated parts of the cord. A
close study of the symptoms will enable us to succeed in this in
some cases. It is unnecessary to enter into further details on
this point.
There still remains a certain number of cases, which I might
term unusual or anomalous, in which the autopsy reveals a
multiple cerebro-spinal sclerosis, although during life the charac-
teristic symptoms of the affection were absent, and a diagnosis
was consequently impracticable. An example of this is furnished
by the case published by Westphal, in the new Charité-Annalen ;
in this case the only symptoms were paraplegia with contractures
and coincident dementia. A very similar case was recently ob-
served in the hospital at Leyden, and was published by Killian
under the name of myelitis diffusa. The clinical history of the
case is very unsatisfactory (dementia, extensive paralysis with
contractures), but anatomically it was plainly nothing else than
a disseminated, cerebro-spinal sclerosis. Several cases similar to
these are to be found in medical literature. Here, as well as
elsewhere in the pathology of the central nervous system, we
must accustom ourselves to the facts, that processes apparently
similar in nature and extent do not always produce the same
symptoms, and that, asa natural consequence, we shall be unable
to make an accurate diagnosis during life in not a few cases.
Course—Duration— Terminations.
Charcot has very appropriately distinguished three stages,
into which the as a rule exceedingly slow and chronic course of
the disease can be divided. His jirst stage embraces the com-
506 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
mencement and development of the disease up to the appearance
of marked incapacity for motion, with contractures. This stage
may last from two to six years or even longer.
Development generally very slow; sometimes begins with
cephalic symptoms, headache, vertigo, uncertain gait, etc. ; more
frequently, however, with spinal symptoms—-paresis of the lower
extremities, etc. ; in the latter case the supervention of cerebral
symptoms, the appearance of tremor, etc., are necessary to com-
plete and clear up the clinical picture. In rare cases a more
rapid development with more violent manifestations is observed :
occurrence of an apoplectiform attack, gastralgic troubles, etc., to
which paralyses, disturbances of co-ordination, tremor, etc., are
superadded in rapid succession.
Very slowly and gradually the above described syndrome is
fully developed. Considerable ameliorations may occur, and
sometimes a very striking improvement, which persists for months
and years, is observed, but the progressive course of the disease
is only temporarily checked. Sometimes sooner, sometimes
later, the various characteristic symptoms appear, until finally
the complete morbid picture is developed. The patients become
more and more helpless, their intellectual powers more and more
impaired, complete paraplegia confines them to the bed, the
tremor deprives them of the use of their hands, and at last the
legs become rigid, contractured, and the seat of frequent spas-.
modic clonus.
The second stage, that of the completely developed disease,
is now attained. This stage too can last a number of years,
from four to six or even more. The disease remains in general
at the same point, without producing disturbances of the general
nutrition or other threatening symptoms. In spite of their help-
lessness and rigidity, in spite of the eternal trembling and the
constant confinement to bed, the patients often remain well
nourished, and present a tolerably fair appearance, the slow but
unceasing progress of the affection being often appreciable only
to the practised eye of the physician.
Gradually the third stage appears on the scene; it is charac-
terized by impairment of the vegetative functions, with simultane-
ous development of threatening nervous symptoms. Loss of
MULTIPLE SCLEROSIS. 507
appetite, digestive disturbances, and emaciation set in; the par-
alysis of the bladder leads to cystitis; bed-sores with consecu-
tive pyzemic or septiceemic fever are developed ; the increasing
bulbar symptoms impair the nutrition still more, and apoplec-
tiform attacks threaten life directly.
Under these circumstances death is no longer distant. The
patients may succumb before the augmenting difficulties of deg-
lutition and respiration, or in an apoplectiform attack (sometimes
with enormous increase of temperature during the agony), or the
general cachexia may lead to the gradual extinction of life. Not
unfrequently, however, death is brought about more rapidly by
some intercurrent disease, such as typhus, pneumonia, pleurisy,
pulmonary consumption, or the like. Pulmonary affections, in
particular, are among the most frequent complications of the
last stages.
The duration of the disease is very variable. There are cases
which terminate fatally in one or two years, but they are rare.
In other cases the disease drags along for ten, twelve, seventeen,
or twenty years. The usual duration is about five to ten years.
The termination of the disease seems to be invariably death.
It is true that marked fluctuations occur as it runs its course,
and ameliorations have been observed that seemed to border on
a cure, but they were not permanent. No well-authenticated
case of recovery has been reported up to the present time. Vul-
pian records a case of multiple sclerosis, that was influenced in a
remarkably favorable manner by an intercurrent varioloid ; the
symptoms disappeared entirely, but returned again after the
lapse of three years. While speaking of chronic myelitis (see p.
449) we mentioned the existence of similar experiences.
Diagnosis.
The recognition of multiple sclerosis may, under some circum-
stances, be a very easy matter, and under other circumstances be
very difficult, or even actually impossible. The purely cerebral
form does not properly come into question here ; it cannot, more-
over, be easily confounded with diseases of the cord. The purely
spinal form, as has already been stated, is frequently undistin-
508 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
guishable from simple chronic myelitis; when reduced to its
elements, moreover, it is really nothing more than this.
It only remains for us, consequently, to consider the cerebro-
spinal form, which is, however, by far the most frequent. In
pronounced cases it can be recognized with the greatest facility ;
in the rare, anomalous cases, on the other hand, the recognition
is very difficult, or even impossible. The symptoms may be so
trifling, so vague and undecided, and so ambiguous, that a diag-
nosis is either impossible, or can only be made with a certain
degree of probability.
When, however, all or the greater part of the following symp-
toms are present, the disease can be diagnosticated without diffi-
culty: commencement with vertigo and uncertainty of gait; more
or less marked paresis and paralysis of the extremities, combined
with the characteristic tremor and sometimes also with ataxia,
and later on with muscular contractions and contractures; im-
pairment of sight, nystagmus, and the characteristic disturbance
of speech ; disproportion between the intense disturbance of mo-
tility and the relatively slight disturbance of sensibility ; head-
ache, attacks of dizziness, psychical disorders; finally, bulbar
symptoms, disturbances of respiration, apoplectiform attacks.
There are only two affections with which the disease can really
be confounded, when it is at all pronounced. One of them is
paralysis agitans, with which it was formerly almost univer-
sally confounded, and for which it is even yet occasionally mis-
taken. Since the publication of Charcot’s excellent descriptions,
there is no longer any excuse for this mistake. No one who
has ever observed closely the two forms of disease will be liable
to confound them with one another; the differences are too strik-
ing and characteristic. In individual cases, the significance of
particular symptoms (é. g., the tremor) may, it is true, be some-
what obscure, but the combined clinical picture is, as a rule, so
distinctive that the diagnosis is easy.
The following are the most important points for the differen-
tial diagnosis. The most essential is the variety of the tremor.
In paralysis agitans it has the character of short, definite, com-
plicated movements, resembling oscillations ; it appears during
perfect rest, and may also persist during voluntary movement,
MULTIPLE SCLEROSIS. 509
but is, as a rule, temporarily controlled by volition ; it rarely
or never extends to the head. In multiple sclerosis the tremor
ceases entirely during rest; it is excited or aggravated by vol-
untary movements ; the head is invariably involved ; its form is
that of longer and more extensive oscillations, or regular to and
fro movements, which extend to the entire body when any volun-
tary exertion is made. Paralysis agitans is a disease of advanced
age; it may be said to never occur in persons under forty years
of age. Multiple sclerosis is a disease ef youth and middle age,
and is seldom or never developed after the fortieth year. In
paralysis agitans the paresis is not developed until long after the
tremor, perhaps not for a year or more; in multiple sclerosis the
paresis or paralysis, as a rule, precedes the tremor, or, at all
events, follows it in a relatively short time. In paralysis agitans
the cerebral and bulbar symptoms, the scanning speech, the im-
pairment of sight, the nystagmus, the vertigo, the ataxia, the dis-
turbances of sensibility and the paralysis of the sphincters, are
wanting, while all of these symptoms belong to the regular and
almost invariable phenomena of multiple sclerosis. In addition
to these symptoms—which are all-sufficient for most cases—we
can also deduce points for the differential diagnosis from other
phenomena, which cannot be enumerated in detail here. Above
all things, we must bear in mind, that paralysis agitans is a dis-
ease which positively is noé based on gross anatomical changes in
the central organ, while in multiple sclerosis, on the other hand,
we have to deal with severe anatomical lesions.
F. Schultze has quite recently reported a case of paralysis agitans, in which
small sclerotic nodules were found in the posterior columns and the left lateral
column of the cervical enlargement, together with much more extensive sclerotic
changes in the lumbar enlargement. One might be tempted to conclude from this
case, that multiple sclerosis may also be the anatomical basis of the syndrome of
paralysis agitans; in my opinion, however, this conclusion would be decidedly too
far-fetched. The concurrence in this case was in all probability purely accidental.
We can hardly assume the small nodules in the cervical medulla to be the cause of
the paralysis agitans, in the face of the numerous and well-authenticated antagonis-
tic facts. Moreover, the much larger nodules in the lumbar enlargement produced
no symptoms at all. The only certain conclusion that can be drawn from this case,
is that the existence of paralysis agitans does not exclude the possibility of the ex-
istence of sclerotic nodules in the brain and the cord, At all events, it is evident
510 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
from numerous facts that the anatomical basis of paralysis agitans is still entirely
unknown, and that in all probability it zs not to be found in sclerotic nodules in
the cord.
The other affection, with which the disease under considera-
tion may possibly be confounded, is sclerosis of the posterior
columns, tabes dorsalis (ataxie locomotrice). Here, too, the diffe-
rentiation in pronounced cases is usually very easy, even though
ataxia is not at all rare as a symptom of multiple sclerosis.
The points which indicate tabes are the lancinating pains,
the girdle-sensation, the disorders of sensation and of the blad-
der, the reeling when the eyes are closed, the ataxia without
marked impairment of the gross strength, the absence of the ten-
don-reflexes, of the nystagmus, of the impairment of speech, and
of the psychical disorders, the very tardy development of pare-
ses, etc. Tor multiple sclerosis speak: the attacks of dizziness,
the cerebral symptoms, the early appearance of pareses and
paralyses, the development of contractures, the augmentation
of the tendon-reflexes, the tremor (which can easily be distin-
guished from the ataxia), the nystagmus, the disturbance of
speech, the psychical disorders, the apoplectiform attacks, ete.
Even in those cases, in which symptoms of tabes accompany the
multiple sclerosis, we can, as a rule, recognize the presence of
multiple nodules from the paralyses, the contractures, the tre-
mor, the cerebral symptoms, the vertigo, etc.
In consequence of the presence of impairment of speech and
nystagmus, Friedreich’s cases of hereditary ataxia are, however, —
more liable to be mistaken for multiple sclerosis, and, in fact,
French authors have confounded the two affections together.
In this they are unquestionably wrong; in hereditary ataxia we
have undoubtedly to deal with a sclerosis of the posterior col-,
umns, though, itis true, of a special and not uncomplicated form.
It can be distinguished from multiple sclerosis by the fact that
the pareses and paralyses, the contractures and the tendon-re-
flexes, the disturbances of sensibility, the psychical and bulbar
symptoms, the vertiginous and anoplentiorn attacks, etc., are
all wanting.
In the diagnosis of the case reported by Leube (Jenaer Krankenhausbericht)
great caution is necessary. The clinical symptoms were those of multiple sclerosis,
MULTIPLE SCLEROSIS. 511
but at the autopsy gray degeneration of the posterior and lateral columns of the
cord was found, together with diffuse sclerosis and considerable meningeal changes
in the brain. It does not seem to me altogether certain, that the lesion in this case
consisted of ‘‘the usual changes of a gray degeneration of the posterior columns,”
but it evidently follows from it that the more or less diffuse affection of the brain
must ultimately give rise to the same symptoms as the multiple, insular affection.
The same centres are involved in both forms of the disease, and there can be no
doubt, that the most essential symptoms of multiple sclerosis are produced by those
nodules that are located in the brain.
Some other affections that are also accompanied by active
trembling (tremor senilis, mercurialis, saturninus, etc.) may pre-
sent certain points of resemblance to multiple sclerosis, but the
differential diagnosis can always be easily made from the anam-
nesis alone.
The differentiation from chorea minor is also, as a rule, easy,
since the volitional tremor differs very essentially from the cho-
reic movements. One case that came under my own observa-
tion, has, however, convinced me, that the choreic motor-disturb-
ance can, like ataxia, occasionally occur as a concomitant symp-
tom in multiple sclerosis. In such obscure cases, the true state
of affairs will only be recognized, when the existence of multiple
sclerosis is demonstrated by other and unequivocal symptoms.
In this connection, too, we must always bear in mind the facts,
that anomalous and obscure cases occur, and that, in conse-
quence of the entirely accidental and irregular localization of
the nodules in the nervous system, the most peculiar clinical
pictures are developed, which may give rise to all sorts of errors
in diagnosis.
It has already been stated that the prognosis of multiple scle-
rosis is, under all cireumstances, an unfavorable one. Up to the
present time no well-authenticated case of recovery has been
recorded. The ultimate termination of the affection is conse-
quently a question about which there can be no doubt, although
it may not be deemed advisable to inform the patients of the
fact. To encourage them stress may be laid on the fact, that
marked remissions and ameliorations which persist for a long
time, are often observed in the course of the disease. To most of
the patients the almost certain prospect of a long duration of the
512 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
disease, and of the consequent prolongation of life for years, will
prove a source of tolerable comfort.
The special prognosis depends of course upon the conditions
of each particular case. It is unnecessary to enter into details
concerning the manner in which the more or less rapid course
of the disease, and the development of particular threatening
symptoms, such as cystitis, bed-sores, bulbar symptoms, apo-
plectiform attacks, etc., can influence the prognosis. This is
sufficiently evident from the general principles on which the
prognosis of any affection must be based, as well as from the
description of the disease given in the preceding pages.
Treatment,
In all essential points, the treatment is the same as that laid
down for chronic myelitis. The indications and principles of
treatment are the same in both affections, but in multiple scle-
rosis we must expect the therapeutic effect to be still more lim-
ited. In fact, all authors who have written about the treatment of
multiple sclerosis agree in the statement, that its results are deci-
dedly discouraging. Charcot, whose experience with this disease
has perhaps been more extensive than that of any other man,
although his cases, it is true, were mostly advanced and hope-
less, has almost nothing but failures to report. Arsenic, bella-
donna, bromide of potassium, ergot, and strychnine, proved en-
tirely useless in his hands; chloride of gold and phosphate of
zinc aggravated rather than relieved; nitrate of silver, on the
contrary, had a distinctly favorable effect, which, however, was
only transitory ; hydropathy proved decidedly useful in one
case. He recommends that further investigations be made with
electricity. Hammond advises chloride of barium in doses of
0.05 grm. (three quarters of a grain) three timesa day. Schuele
saw a transitory improvement after the cold-water treatment, and
I have myself had a similar experience. On the other hand, sev-
eral cases have been recorded (Otto, Baerwinkel, Berlin), which
were aggravated by the use of the therme. In one case that was
treated in the hospital in this city, marked improvement set in
under the use of subcutaneous injections of arsenic; at a later
TABES DORSALIS, 513
period this case was distinctly benefited by the galvanic current.
As has already been stated, no authenticated case of recovery is
known.
These unsatisfactory results, however, must not lead us to
abandon all therapeutic efforts, especially in more recent cases ;
in these a favorable result may occasionally be obtained, just as
in simple chronic myelitis. In the first place, the treatment rec-
ommended for chronic myelitis must be steadily and patiently
followed out; the persistent employment of the galvanic cur-
rent, of hydropathy, and of nitrate of silver, is especially to be
commended. If these remedies prove useless, there will always
be time and opportunity for extended therapeutic trials of all
possible measures, and perhaps accident will lead to the discov-
ery of an efficient remedy for this, at present hopeless, disease.
12. Gray Degeneration of the Posterior Columns—Sclerosis of the
Posterior Columns—Tabes Dorsalis — Ataxie Locomotrice
_ Progressive (Duchenne)—Leukomyelitis Posterior Chronica.
Ollivier, 1. c. 8. 6d. Tom. IL. p. 454. Obs. 132 and 133.—Cruveilhier, Anat. patho-
log. Tom. II.—Romberg, Lehrbuch der Nervenkrankheiten. I. 8. Abth. 8. 184.
2. Aufl. 1851.— Wunderlich, Handbuch d. Pathol. u. Therapie. 2. Aufl. 1854,
Axenfeld, In the Dict. encyclop. des Sciences médic. T. VII. p. 56. 1867.—
Trousseau, Medic. Klin. des Hdtel-Dieu, Deutsch von Culmann, IL. p. 544.
1868.—Benedikt, Elektrotherapie. 8. 331. 1868.—Hasse, 1. c. 2. Aufl. 8. 713.
—Hammond, 1. c. 34 edit. p. 860.—Leyden, Klinik d. Rickenmarkskrankhei-
ten. II. 2, Abth. 8. 324. 1876.
W. Horn, De tabe dorsuali prelusio. Berol. 1827.—Decker, De tabe dorsuali. Diss.
Berolin, 1888.—Brach, Med. Zeitung des Vereins f. Heilk. in Preussen. 1840.
Nr. 45, und 1842. Nr. 8, 4.—Jacoby, Exempl. tabis dorsual. epicrisi ornatum.
Berolin, 1842.—Kuschel, De tab. dors. Berol. 1844.—Steinthal, Beitr. z. Ge-
schichte u. Pathol. d. Tab. dors. Hufeland’s Journ. Band 98, 1844.—Todd,
Cyclop. of Anat. and Physiol. III. 1847.—7Zuerck, Ueber primaire Degeneration
einzelner Riickenmarksstriinge. Sitzungsber. d. k. Akademie zu Wien. Mathem.
naturw. Classe. XXI. Jahrg. 1856. Heft I. u. IL. 8. 112.—Duchenne (de Bou-
logne), De Vataxie locomotr. progressive. Arch. génér. de Méd. 1858. Déc.
1859, Janv., Avril.—Electrisat. localis¢e. 2. 6d. 1861. 8. ¢d. 1872.—Harless,
Physiol. Vermittlungswege paralytischer und paret. Erscheinungen. Bayr. iirztl.
Intelligenzbl. 1858. Nr. 13.—Oppolzer, Krankh. des R.-M. Spitalszeit. 1859.
Nr. 21.—Trousseau, De Vatax. locomotm progress. Union méd. 1861. Nr. 12,
14, 20.—Bourdon, Cas d’atax. loc. Gaz. hebdom, 1861. Nr. 41.—Bourdon et
VOL, XIII.—383
514 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Luys, Etudes clin. et histol. etc. Arch. génér, Noy. 1861. Avril, 1862.—Teis-
sier, De l’ataxie musculaire. Gaz. méd. de Lyon.. 1861, Dec. 1862, Jany.—
Dumenil, Union méd. 1862. Nr. 17.— Oulmont et Luys, Union méd. 1862. Nr, 41.
—Charcot et Vulpian, Atrophie des cordons postér. etc. Gaz. hebdom. 1862. Nr.
16, 18.—Marotte et Luys, Union méd. 1862. Nr. 67.—Trousseau et Sapey, ibid.
Nr. 88, 89.—Duguet, Atax. locom. de forme hémiplég. Ibid. Nr. 122.—Marius
Carré, De Vatax. locom. Thése. Paris, 1862.—M. Carré, Gaz. méd. de Lyon.
1864. Nr. 15, 20; Nouv. recherches sur l’atax. loc. progr. Paris, 1865.
—Dujardin-Beaumetz, De Vatax. loc. Paris, 1862.—Hisenmann, Die Be-
wegungsataxie. Wien, 1863.—Friedreich, Ueber degenerative Atrophie der
spinalen Hinterstriinge. Virch. Arch. Bd. 26 u. 27. 1863.—Leyden, Die graue
Degeneration der Hinterstr. de R.-M. Berlin, 1863. Deutsche Klinik. 1863. Nr.
13. Virch. Arch. Bd. 40. 1867.—Ueber Muskelsinn und Ataxie. Ibid. Bd. 47.
1869.— Westphal, Tabes dorsual. u. Paralysis universal. progress. Zeitschr. f.
Psych. XX. 1863. u. XXL 8S. 361. 1864.— Westphal, Ueber Erkrankung des
R.-M. bei der allg. progress. Paralyse der Irren. Virch. Arch. Bd. 39 u. 40.
1867.—Charcot et Vulpian, Deux cas de Sclérose des cord. postér. etc. Gaz.
méd. 1863. Nr. 14.—Azenfeld, Des lésions atroph. de la moélle épin. Arch.
génér. 1863, Aug. Oct.—R. Remak, Ueb. Tabes dorsalis. Deutsche Klin. 1862.
Nr. 49. Berl. klin. Wochenschr. 1864. Nr. 30, 41.—Benedikt, Wien. med.
Wochenschr. 1862. No. 44-48, 1864. Nr. 23, 30, 37.—Teissier, De Vat. loc.
Gaz. méd. de Lyon. 1864. Nr. 19.—Cornil, Gaz. méd. de Par. 1864. Nr. 19.—
Duchenne, Rech. clin. sur état pathol. d. grand Sympath. ete. Gaz. hebd.
1864. Nr. 8, 10.—Diagnost. differ. des affect. cérébell. et de l’atax. loc. Gaz.
hebd. 1864. Nr. 29, 31.—Cel. Bernard, De Vat. loc. These. Strasbourg, 1864.
—Finkelnburg, Beobb. tib. d. paralyt. Bewegungsataxie. Berl. klin. Wochen-
schr. 1864. Nr. 538.—Topinard, De l’at. locom. Paris, 1864.—Jaccoud, Les para-
plégies et l’atax. du mouvement. Paris, 1864.—Fr. Vaneschi, De tabe dors.
Diss. Berol. 1864.—Remak, Allgem. med. Centralz. 1862, Dec. 1863, Dec.
1864. Nr. 83.—Spaeth, Zur Lehre von d. Tab. dors. Dis. Tiibingen, 1864.—
Nachtweyh, Kauert, Mette, De tabe dors. Diss. Berol. 1864.—Fr. Boening, Be-
obb. tiber progress. Bewegungyataxie. Deutsche Klinik. 1865. Nr. 1, 5, 8—
Bouchard, Des lésions anatom. de l’at. loc. progr. Lyon, 1865.—WNothnagel,
Berl. klin. Wochenschr. 1865. Nr. 17.—0. Frohwein, Diss. Erlangen, 1865.—
Oppolzer, Wien. med. Wochenschr. 1866. Nr. 26-28.—Charcot et Bouchard,
Douleurs fulgur. de l’ataxie sans incoordin. des mouv., Sclérose commengante
des cord. post. Gaz. méd. 1866. Nr. 7. Compt. rend. de la Sociét. de Biolog.
1866.—abre, Physiol. pathol. et diagn. de l’atax. etc. Gaz. des hop. 1866. Nr.
107, 108.—Althaus, On Epilepsy, Hysteria, and Ataxy. London, 1866.—Lock-
hart Clarke, On Locom. Ataxy. St. George’s Hosp. Rep. I. 1866. Brit. Med.
Journ. 1869. July 3, 31; Sept. 25; Dec. 11.—H. Fabricius, Diss. Berlin, 1867.
E. Cyon, Zur Lehre von der Tabes dors. Berlin, 1867. Virch. Arch. Bd. 41.
1867.—Frommann, Unters. tib. d. normale u. pathol. Anat. des R.-M. II. Jena,
1867.—Robitesch, Zwei ungewohnl. Fille von Tab. d. Diss. Berlin, 1867.—Z.
5 aay 7
TABES DORSALIS. 515
Schulze, Ucb. d. Aetiologie der Tab. dors. Diss. Berlin, 1867.—Vulpian, Etat
des nerfs sensit., des gangl. spinaux, etc. Arch. d. Physiol. norm. et pathol.
I. p. 128. 1868.—Vulpian, Retard des sensat. dans les cas de sclérose, ete.
Ibid. I. p. 463. 1868.—LZarroche, These. Montpellier, 1868.—Dubois, Etude
sur quelques points de l’at. loc. These. Paris, 1868,—Azel Jaederholm, Studien
iib. d. graue Degener. des R.-M. Nord. medic. Arkiv. I Nr. 2. 1869.—TA.
Laycock, Influence of Libid. Excess on the Causat. of Locom. Ataxy. Dubl.
Quart. Journ. May, 1869.—Bracht, Zur Symptomatol. d. Tab. d. Diss. Berlin,
1869.— Winsor, Case of Loc. At. Bost. Med. and Surg. Journ. 1870, Oct. 6.—
Meredith Clymer, Some Points in the Clinical History, etc. New York Med.
Record. 1870, Febr. 1.—Arndt, Mittheil. tib. die Histol. der grauen Degen. u.
s. w. Berl. klin. Woch. 1870. Nr. 11.—Pierret, Altérat. de la subst. grise dans
Yat. locom. progr. Arch. de Physiol. III. p. 599. 1870.—Pierret, Selérose des
cord. postér. dans l’ataxie. Ibid. IV. p. 864. 1871, 1872.—Cas de Sclér. pri-
mit. du faisceau médian des cord. postér. Ibid. V. p. 74. 1873.—Sam. Wilks,
Ataxia. Guy’s Hosp. Rep. III. Ser. Vol. XVII. p. 198. 1872.—Tigges, Ueb.
mit Tab. dors. complic. Psychose. Allg. Zeitschr. f. Psych. Bd. 28, 8, 245.
1872.—». Krafft-Ebing, Ueb. Tab. dors. mit finaler Geistesstérung. Ibid. 8.
578.—H. Leonhardt, Ueb. Tab. dors. Diss. Berlin, 1872.—-Vossius, Beitr. z.
Symptomat. d. Tabes. Diss. Berlin, 1873.—Charcot, Legons sur les malad. du
syst. nerveux. II. Sér. 1. fasc. 1873.—C. Lange, Nord. medic, Ark. IV. 1872.
8. Virchow-Hirsch, Jahresber. pro 1872. II. 8. 79.—Martin, De l’atax., loc. pr.
These. Paris, 1874.— Voisin, Progrés méd. 1875. Nr. 10.—Hayem, Atax. loc.
progr. Nécropsie. Gaz. méd. 1876. Nr. 19.—Zrdmann, Z. Beurtheilung des
Verlaufs tabet. Lihmungen. Jahresber. d. Gesellsch. f. Natur- u. Heilk. in
Dresden. Oct. 75. Juni, 760-8. 56. 1876.—Friedreich, Ueb. Ataxie mit beson-
derer Beriicksichtigung der hereditiren Formen. Virch. Arch. Bd. 68. 1876.
Bd. 70. 1877.—Kellogg, Two Cases of Loc. At. in Children. Arch. of Electrol.
and Neurolog. Vol. IL p. 182. 1875.—Du Castel, Sclérose primit. des cordons
de Goll. Gaz. méd. 1874. Nr. 3.—Fournier, L’ataxie locomotrice d’origine
syphilitique. Gaz. méd. 1876. Nr. 53.
Landois u. Mosler, Neuropathol. Studien. Berl. klin. Wochenschr. 1868. Nr. 41.
—E. Remak, jun., Ueb. zeitliche Incongruenz der Beriihrungs-und Schmerzemp-
findung bei Tab. dors. Arch. f. Psych. u. Nervenkrankh. IV. 8. 763. 1874.
—Naunyn, Ueb. eine eigenthiiml. Anomal. d. Schmerzempfindung. Ibid. 8.
760.— Osthoff, Verlangsamung d. Schmerzempfind. bei Tabes. Diss. Erlangen,
1874.—Hertzberg, Sensibilititsstérung bei Tabes dors, Diss. Jena, 1875.
Galezowsky, Des troubles oculaires dans l’atax. loc. progr. Gaz. des hép. 1874. Nr.
85.—Leber, Ueber graue Degener. d. Sehnerven. Arch. f. Ophthalm. XTY. 2. 8.
177. 1868.—Kiesselbach, Zur grauen Degen. der Sehnerven bei Erkrank. des
Cerebrospinalsyst. Diss. Erlangen, 1875.—Hempel, Ueb. Spinalmyosis Arch. f.
Ophthalm. XXIL 1. 1876.—Fverster, Im Handb. d. gesammt. Augenheilk.
von A. Graefe u. Saemisch. VII. 1. S131. 1876.—A. Pierret, Essai sur les
symptomes céphaliques du Tabes dorsalis. Paris, 1876.
516 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Delamarre, Troubles gastriques dans l'at. I. pr. Thése. Paris, 1866.—Fetitjean,
Crises gastriques dans l’ataxie. These, 1874.—@rainger Stewart, Peculiar Form
of Gastric Crisis in Loc. Ataxy. Medic. Tim. 1876. Oct. 7.—M. Raynaud, Crises
néphrétiques dans l’at. loc. Arch. génér. Oct. 1876.—¥Féréol, Sur quelques
sympt. visceraux-laryngo-bronchiques de l’atax. Gaz. hebdom. 1869. Nr. 7.—
Jean, Troubles atax. du coté du larynx et du phar. Gaz. hebdom. 1876. Nr.
27.—Chvostek, Tabes complic. mit Atrophie des linken Halssympath. u. s. w.
Allgem. Wien. med Zeit. 1874.—M. Cuffer, Hémiatrophie d. 1. langue surven.
d. 1. cours d’une ataxie. Union méd. 1875. Nr. 72.
Charcot, Sur quelques arthropathies, qui paraissent dépendre, etc. Arch. d. Physiol.
L p.161. 1868; u. IL p. 121. 1869.—Charcot et Joffroy, Lésion de 1. subst.
grise dans un cas d’arthropath. ataxique. Ibid. III. p. 306. 1870.—Ball, Ar-
thropathies, etc. Gaz. des. hép. 1868. Nr. 128 u. 1869. Nr. 58-62.—Hervey,
Arthrop. liée a l’at. Ibid. 1868. Nr. 33.—Blum, Des arthropathies d’origine
nerveuse. These. Paris, 1875. pp. 19-50.— Buzzard, Locomot. ataxy with
anomalous joint affections. Lancet, 1874, Aug. 22.—Charcot, Luxat. pathol. et
fractures spontanées multiples dans l’atax. Arch. d. Physiol. VI. p. 166. 1874.
—Forestier, Arthropathies, fractures et luxat. consécut. Paris, 1874.—Brochin,
Des lésions osseuses chez les atax. Gaz. des hop. 1875. Nr. 12.—Raymond,
Note sur les arthrop. de l’at. Gaz. méd. 1876. Nr. 8.
R. Remak, Ueb. d. Behandlung der Tab. d. mit d. const. galv. Strom Med. Cen-
tralz. 1858. Nr. 29. 1862. Dec. 3.— Wunderlich, Behandlung der Spinalparaly-
sen mit Silbersalpeter. Arch. d. Heilk. 1861 u. 1863.—Charcot et Vulpian,
Emploi du nitrat d’arg. etc. Bullet. d. Thérap. Juin, 1862.—Hulenburg, Erfolg
yv. Arg. nitr. Verh. d. Berl. med. Ges. 1866. Heft. 2. 8. 142.—Hitzig, Schiid-
liche Wirkung des Arg. nitr. bei Tabes dors. Berl. klin. Woch. 1867. Nr. 31.
Dujardin-Beaumetz, Emploi du phosphore, etc. Bull. génér. Thérap. 1868.—
Siredey, Action du bromure de potass. dans l’atax. 1. pr. Ibid. 1872. Aofit 30.
—Delmus, Six observat. d’atax. loc. Journ. de Méd. d. Bord. Mars, 1865. (cold-
water treatment).—v. Krafft-Ebing, Ueb. Heilung und Heilbarkeit der Tabes
durch den galy. Strom. Deutsch. Arch. f. klin. Medic. IX. 1872.—Karmin,
Fall von geheilter Tabes. Wien. med. Woch. 1868. Nr. 35.—Onimus, De
V’emploi des courants contin. dans le trait. de at. Gaz. des hép. 1868. Nr.
116-119.—Delmar, Trait. de l’at. loc. Rev. méd. 1874. Nr. 38. 39.— Wald-
mann, Behandlung d. Tabeskranken als Anhalt fiir Aerzte u. Kranke. Halle,
1872.— Mendel, Beh. der Tabes dors, Deutsch. Zeitschr. f. prakt. Medic. 1874.
Nr. 39.—F. Richter, Ibid. 1874. Nr. 48.—Ueb. Temperatur u. Mechanik der
Badeformen bei Tabes, etc. Ibid. 1875.—Caster, Oxide of Silver in Locom.
Ataxy. Philad. Med. and Surg. Rep. 1875. Dec.
Refer, furthermore, to the text-books on Electrotherapeutics, Balneotherapeutics,
and Hydrotherapeutics, also to the larger hand-books and encyclopedias of
Special Pathology and Therapeutics, all of which contain more or less detailed
accounts of the pathology and therapeutics of Tabes.
TABES DORSALIS. 517
History.
We begin the discussion of those affections of the spinal cord
which are limited to certain definite portions of the transverse
section of the cord, but which reach a very varied longitudinal
extent, with the consideration of that form thereof which is best
known and most studied, viz., gray degeneration or degenerative
atrophy (Friedreich) of the white posterior columns. ‘This is the
same affection which is now almost universally designated as
‘*tabes dorsalis,” in Germany, the term which was formerly used
for atrophy of the spinal cord in general being thus restricted to
this special form.’
This disease was undoubtedly known to the most ancient phy-
sicians, and frequently enough came under their observation.
Among the forms of spinal disease which are more or less defi-
nitely spoken of, under the name of tabes, or of phthisis ischia-
dica, by Hippocrates, Galen, Bonetus, and others, there were
undoubtedly also cases of sclerosis of the posterior columns.
But it is hardly worth the while to trace out the reports of the
older physicians on these forms of disease, for we shall nowhere
find anything like an accurate characterization of the same, or
a correct distinction between the different forms.
Neither would it prove any more profitable to follow up all
the descriptions of tabes dorsalis, phthisis of the spinal cord,
etc., which at the end of the last and the beginning of the present
century were ascribed to the influence of sexual excesses and
spermatorrheea, and which reached their climax in the extrava-
gancies of Lallemand.
It was not until the third and fourth decade of the present
century that occasional more exact observations appeared, which
are to be regarded as the first foundation stones of the doctrine
of tabes dorsalis. The anatomical observations of Hutin (1827)
and Monod (1882) undoubtedly belong to this disease, although
the latter were still cited by Ollivier as cases of hypertrophy of
the gray substance. Cruveilhier, in his celebrated atlas, besides
1 More generally known in English as progressive locomotor ataxy.—TRANS,
518 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
admirable anatomical representations, also gives a series of histo-
ries of the disease.
But it was principally German physicians who, in the next
two decades, occupied themselves in working up the subject of
tabes, presenting a more precise picture of the disease, and col-
lecting the results of post-mortem examinations belonging there-
to. The Dissertation of W. Horn (1827) may be regarded as the ©
starting-point of these labors. In the subsequent classical de-
scription given by Romberg all the principal symptoms of the
disease are enumerated, and he even draws the distinction be-
tween the peculiar form of motor disturbance that is present and
true paralysis. The anatomical changes were more accurately
made known through the investigations of Froriep, E. Horn,
Jacoby, and others, and the work of Steinthal (1844) gave a tol-
erably complete representation of the pathology of tabes, even
though it does include under that head a good deal that is for-
eign thereto. German physiologists (Joh. Mueller, Spiess) recog-
nized the peculiar form of motor disturbance which Bouillaud
(1845) and Todd (1847) correctly designated as a disturbance of
co-ordination, and not as paralysis. The description of the dis-
ease given by Wunderlich (1854) leaves but little more to be
desired. Rokitansky and Tuerck advanced our knowledge of —
the anatomical alterations by their microscopic examinations.
In Germany, therefore, as early as the beginning of the latter
half of this century, the history and pathological anatomy of
tabes dorsalis was firmly established in its main features, and
was sufficiently well known to the medical public.
It was therefore a somewhat peculiar and certainly an unjus-
tifiable undertaking on the part of Duchenne, in the year 1858,
to describe the disease as'an entirely new one and under a new
name (Ataxie locomotrice progressive). Entirely ignoring all
the labors of his predecessors, he seeks the seat of the disease,
on theoretical grounds, in the cerebellum, whereas it had long
since been found to lie in the spinal cord.
At the same time, we must certainly admit that Duchenne
gave a most admirable description of the disease, one more accu-
rate than had previously been furnished ; that he characterized
and emphasized the first stage of the disease, though, perhaps,
TABES DORSALIS. 519
in a somewhat one-sided manner; that he was the first more
accurately to establish the idea of a disturbance of co-ordination
(ataxy), and to demonstrate unequivocally, by means of the
dynamometer, the preservation of the gross muscular strength.
Duchenne’s work unquestionably excited an extraordinary
degree of interest in all directions, and gave occasion to such
numerous works on Tabes dorsalis that the literature of the sub-
ject has already swelled to dimensions which we can hardly com-
pass.
Numerous investigations and discussions first arose in France
over the ‘‘new”’ disease, which, under the powerful protection
of Trousseau, soon claimed general recognition. An extensive
amount of material was accumulated, partly in the form of com-
prehensive representations of the disease (Dujardin-Beaumetz,
Mar. Carré, and others), partly in the form of reports of cases
(Bourdon, Luys, Oulmont, Teissier, Dumenil, Charcot, Vulpian,
and others), thus clearing up the views held on the subject.
| Stimulated by a prize question proposed by the Academy, several
larger works on Ataxy appeared in 1864 and 1865, which treated
the question in an exhaustive and in part ina most admirable
manner (Topinard, Mar. Carré, Jaccoud).
But in Germany also numerous and admirable works ap-
peared. In the year 1863 three very noteworthy works, of great
value in the history of tabes, were put forth by Friedreich, Eisen-
mann and Leyden, to which were afterwards added many larger
and smaller communications and investigations (Westphal,
Frommann, Spaeth, Remak, Benedict, Finkelnburg, Boening,
and others).
Since then the production of works on tabes has hardly, as
yet, suffered any diminution; particularly in France and Ger-
many, each year brings a series of valuable contributions, while,
aside from the admirable labors of Lockhart-Clarke, English lite-
rature actually contains but very little on this subject.
The last few years have materially advanced and deepened
our knowledge of tabes, although we are doubtless still far from
having arrived at a final conclusion of the same. The anatomical
changes have been more accurately investigated in their finer
histological details, and in their more precise localization in a
520 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
transverse section of the cord; the picture of the disease has
been more sharply defined and relieved of unimportant and acci-
dental features ; the careful observation of details has taught us
to recognize a series of rarer but not less interesting symptoms ;
the theory of the disease and of its individual symptoms has
been elucidated by thorough and lively discussions, although if
has not yet been finally established ; the diagnosis has been ren-
dered easier and more delicate, the distinction between this dis-
ease and neighboring and kindred affections has been materi-
ally advanced; and the prognosis, too, which was formerly so
gloomy, has been essentially modified by noteworthy advances
in the therapeutics of the disease. The evidences of this are to
be found in the writings of the past ten years, as cited in the
above table of literature. |
It would carry us too far if we were to follow, even quite cur-
sorily, the historical development of the various scientific vic-
tories gained in connection with this subject of tabes; if we
were to attempt to show how the dnatomical views gradually
developed themselves up to the present standpoint; how the
theoretical views of the entire disease and of single symptoms
thereof (for example, the ataxy) slowly assumed form, amidst
the most lively disputations; what stages of development the
therapeutics of the disease itself has undergone, etc. The reader
who desires information on this subject must make his own spe-
cial studies thereon.
We desire only to be permitted a few remarks on the most
appropriate designation for the disease. None of the designa-
tions thus far in use can be regarded as entirely appropriate or
exhaustive. The term ‘‘tabes dorsalis’’ is hardly to be justified
by the history of the disease and not at all so by its anatomy,
although it at least has the advantage of antiquity. The term
“ progressive locomotor ataxy ” is still more unfortunately chosen,
as it is derived from one single symptom which often does not
appear until the disease has existed for years, and is sometimes
also present in other diseases. From an anatomical point of
view, to which we should endeavor, as far as possible, to adhere,
the term “‘ gray degeneration or degenerative atrophy of the pos- —
terior columns of the cord’? might the most readily be accepted.
ae LS
TABES DORSALIS. 521
Aside- from its length and awkwardness, however, it is open to
the objection that it only designates a comparatively late stage
of the anatomical alterations, and that, in all probability, it is
not even exhaustive, inasmuch as an extension of the process to
the gray substance and to neighboring portions of the lateral
columns probably constitutes the rule. The same objection ap-
plies to the name ‘‘ Leukomyelitis posterior chronica,’’ although
this in a happy manner emphasizes the chronic inflammatory
character of the process.
Still, in the end, it is all the same what we call a thing, the
main point being to know and to determine what we wish to
have understood under a certain designation. If we can unite
on the clinical and anatomical characterization of the disease—
and I think that at the present day there is no serious difficulty
about this with regard to the disease under consideration—we
shall also be able to come to an understanding as to an appro-
priate designation for the same. In my opinion—until something
better is found—it might be most appropriate to adhere to the
old name of tabes dorsalis, which was naturalized by Romberg
and has also of late been extensively used by the French, it being
distinctly understood that the term is to be limited to the desig-
nation of that form of disease described in the following pages.
‘‘ Sclerosis of the posterior celumns”’ (‘‘ Hinterstrangsklerose’’)
is another not very prejudicative designation which might recom-
mend itself, on account of its brevity, to those who favor a name
selected from an anatomical standpoint.
Definition.
Under the name of tabes dorsalis we understand a disease of
the spinal cord which runs a slow course, which arises princi-
pally during youth and middle age, and which in all probability
belongs to the group of chronic myelitis.
It is anatomically characterized by ribbon-like sclerosis of the
white posterior columns, leading to gray degeneration, and prob-
ably also by later participation on the part of the adjoining por-
tions of the white lateral columns ayd the gray posterior horns ;
still, nothing more accurate is established with regard to the
522 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
more or less regular and uniform participation of these parts in
the process. The affection generally begins in the lumbar region,
and may extend throughout the entire cord as far as the upper
cervical portion, and even into the medulla oblongata. .
Clinically the disease is characterized by a first stage, which
often stretches over many years, and which is marked by lanci-
nating pains, disturbances of certain cerebral nerves (the optic
and the nerves supplying the muscles of the eye), pareesthesias
in the legs, on the trunk, and in the domain of the ulnar nerve,
debility, a tendency to weariness and unsteadiness in the legs,
weakness of the bladder and of the generative organs.
The second stage is that of the fully-developed disease, in
which, aside from a more or less high degree of disturbance of
sensation (pain, anzesthesia, paresthesia, sensation of a tight
girdle, etc.), and aside from weakness of the bladder and the
genitals and the disturbance of certain cerebral nerves, a distinet
and characteristic disturbance in the co-ordination of motion be-
comes prominent, without the gross power of movement being, to
any considerable degree, diminished (ataxy). The cerebral func-
tions still remain intact.
Finally, there is the third stage, that of progressive spinal
paralysis, characterized by actual paralysis, muscular atrophy,
contractures, troubles of the bladder, bed-sores, and, at last,
general marasmus. |
It is a disease of a decidedly progressive character, although
it is not exactly rare for it to come to a standstill and improve,
and in some few instances actual recovery even takes place.
It is always a question of a disease of long duration, which is
to be counted by years, and not rarely by decades.
Etiology and Pathogenesis,
Tabes is one of the most frequent affections of the spinal cord.
The predisposition to the same must, therefore, be tolerably
wide-spread. _ |
In developing this predisposition, the newropathic tendency
of numerous individuals undoubtedly plays a very prominent
part. The increasing frequency of nervous diseases generally,
TABES DORSALIS. 523
and of tabes in particular, the large number of nervous and hys-
terical women, result in the birth of an ever-increasing number
of individuals with a tendency to nervous diseases. In the family
history of those affected with tabes it will not be rare to be able
to demonstrate the occurrence of hysteria, epilepsy, mental dis-
eases, migraine, or it may be only of violent fits of anger, drunken-
ness, or anomalies in the form of the skull, malformations of the
external ear, etc. Such instances have been narrated by Trous-
seau, Rosenthal, Topinard, and others. The condition of things
most rarely found is that of the direct hereditary transmission of
the disease ; the most striking instance of this is given by Carré,
who saw eighteen cases of the disease occur in one family, in
three generations. Asarule, parents transmit to their children
only the predisposition to tabes. This was also especially true
in the remarkable observations communicated by Friedreich. In
three different families several brothers and sisters were each
time attacked with the disease at almost the same age, without
the parents themselves having suffered from it. The only thing
we can suppose is that in such cases a certain weakness and irri-
tability of the nervous system, perhaps also a species of impedi-
ment to the development of certain portions of the same, is he-
reditarily transmitted, which renders the nervous system less
capable of resisting external injuries.
At the same time, according to my experience, there is a very
large number of cases of tabes in which there is decidedly no
hereditary neuropathic tendency, the patients coming from fami-
lies that were, nervously, perfectly well. |
Almost all observers concur in the statement that the male
sex shows a decidedly greater predisposition to tabes than the
female. I can fully confirm this from my own observation ;
among eighty-three cases of undoubted tabes seen by me, seventy-
four were men and only nine women. It is probable that this
greater predisposition is largely owing to the fact that men are
far more exposed than women to the strongest direct causes of
tabes—taking cold and sexual excesses. Still, this might not
entirely account for so striking a preponderance of males.
The statistics of different authors, althofgh without exception confirming the
fact of a marked preponderance of the disease in men, still show great differences
524 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
in the proportionate frequency of the disease in the two sexes. I here place together :
some of these statements:
Men, Women.
CS Ree See oe 42 18 — about in the proportion of 24: 1
PTMMMATC 343 6 02 sigces ne 21 4 & va = 5-33
Bteinthal:.. 0.22.2 ccc 42 6 - * a y air |
Eisenmann........... 46 20 - . = 24:1
Schulze iy .c6 ese sea 37 9 ad + ‘ 4°34;
Ovo. Zit<d tines 149 43 - - “ 34:1
Leonhardt ........... 12 11 4 - Sf 1. <4
BAtl . . 5 pce bagel 74 9 €: . " 8 :1
It is not permissible to add together these numbers, as they refer, in part, to
the same cases. Of course these depend very much on the accidental supply of
material, and it is only thus that the striking statement of Leonhardt can be ex-
plained, which, it is true, only relates to quite small numbers. At all events, the
preponderance of males is established beyond all doubt.
Tabes is a disease of youth and middle age; by far the ma-
jority of individuals are at the top of the hill of life when the
disease begins—between their thirtieth and fiftieth year. In the
third decade of life, too, cases of the disease are tolerably com-
mon; before the twentieth and after the fiftieth year, however,
they are very rare. This, too, might have some connection with
the above-named ¢ausal conditions.
Among sixty-eight observations of my own, in which the beginning of the dis-
ease could be determined with some certainty, it was found to occur as follows:
Between the ages of 11 and 20, three times.
¥ # 21 “ 30, thirteen se
i * 31 ‘* 40, thirty-one ‘“
= 5 41 ‘ 50,eighten ‘“
« . 51 ‘* 60, three
The statistics collected by other observers (Topinard, Carré, Cyon, etc.) corre-
spond pretty accurately with these,
No doubt it is owing to the greater influence of external
injurious causes that certain occupations furnish a larger pro-
portion than others to the number of those attacked with tabes.
This is said to be the case especially in those persons who, by
reason of their calling, are obliged frequently to expose them-
selves to all extremes of the weather, cold and wet—and who
are subjected to all sorts of bodily hardships, such, for instance,
TABES DORSALIS. 525
as commercial travellers, hunters, engineers, soldiers, firemen,
workers on ice, railroad conductors, fishermen, ete. At the same
time, all these are more subordinate and accidental causes.
Bodily and mental overexertion are certainly to be counted
among the injuries which may occasion an increased predisposi-
tion to tabes. The increased demands of the fight for existence,
the excitements and exertions of modern social life, are certainly
in no small degree responsible for the more frequent occurrence
of tabes at the present day. This explains the greater frequency
of the affection in large cities and in the higher walks of life, in
which mental overexertion, want, cares, anxiety, failures in life,
and the like, often play a very prominent réle. All these things
are to be regarded as weakening to the body, and especially to
the nervous system, and thereby as predisposing to disease.
The same predisposing influence may be exerted (E. Schulze)
by previous acute and chronic diseases (typhus, intermittent
fever, and the like), whether occurring but once or repeatedly. A
similar effect may also be claimed for syphilis; for the existence
of an actual, specific, syphilitic sclerosis of the posterior columns
may yet well be doubted. But in view of the comparative
frequency of both forms of disease, it is hard to exclude an acci-
dental concurrence of the same.
Sexual excesses and onanism are certainly of no slight signifi-
cance, at least in the development of a predisposition to tabes.
We have already previously expressed ourselves in detail on this
point (page 147), and what was said there holds especially good
with regard to tabes, the most frequent of all chronic diseases of
the spinal cord. We do not entertain the slightest doubt that
such sexual excesses, of the most varied kind, over-irritate and
weaken the spinal cord, and at all events make it more suscepti-
ble to the influence of direct injuries.
Among the direct causes of tabes the first that may be
mentioned is taking cold. It is regarded by some (Leyden, Leon-
hardt) as the most frequent, in fact as the almost exclusive cause
of tabes; but while fully recognizing the undeniable potency of
this injury, we must yet look upon this view as being extreme.
It is notorious that individuals who are otherwise quite well
and not burdened with any neuropathic tendency, vigorous
526 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
people from among the working classes, those working in water
and ice, foresters, soldiers, etc., frequently notice the first symp-
toms of tabes after they have been, once or repeatedly, exposed
to some serious injury in the way of taking cold. Instances are
not rare in literature going to prove that the disease has come to
an outbreak as the result of inundations, after a person’s falling
into the water or getting wet through, after a wet, cold bivouac,
after occupying damp living-rooms or workshops, and the like,
This holds particularly true for persons of a nervous tempera-
ment, or who are exhausted and reduced through exposure,
sexual excesses, mental disturbances, night-watching, and the
like; in such persons even the slighter causes for taking cold
may be effective, such as sleeping in a damp room, ete.
We possess no more plausible explanation of the modus
operandi of “ taking cold”’ in the production of tabes than in the
numerous other forms of disease which may likewise be brought
about by the same cause. It is true that various attempts at an
explanation cf the same have been set up, which are very well
meant, in themselves, but do not stand the test of severe criti-
cism. We consider it unnecessary to enter into any more de-
tailed consideration of this question, and content ourselves with
merely confirming the fact that, in many cases, ‘‘ taking cold”
can be shown to be the immediate exciting cause of tabes.
Bodily overexertion and the exhaustion induced thereby,.
hardships of all sorts, are often stated as being the direct occa-
sion of tabes. Their efficacy appears to be especially manifest
if, at the same time, an opportunity is given for taking cold, and
active mental disturbances likewise exist. I have twice seen
tabes break out in consequence of fatiguing and exciting busi-
ness journeys undertaken during severe cold winter weather.
The fact that severe marches and other hardships, combined with
mental activity and excitement, very readily lead to tabes, has
been most unequivocally proved by all the campaigns of this
century, after which the development of tabes has always been
observed to be especially frequent. To be sure, it is hard to
determine in such cases the share of responsibility to be assigned
to each of the injurious conditions. At the same time, I believe
that the mere overexertion of itself, especially in persons dis-
TABES DORSALIS. 527
posed that way, may prove effective to this end. (For an exam-
ple of the same see Waldmann, p. 74.)
All this holds good, to a still higher degree, with regard to
sexual over-excitement and excesses, which may also sometimes
become the direct causes of tabes. Formerly these were regarded
as the principal and almost the only causes of tabes, and every
poor victim of the disease lay under the suspicion of having led
a dissolute life. This was certainly wrong; it is but a limited
number of cases that are unquestionably caused in this way. But
it is at least equally wrong to deny this etiological connection
entirely, or in great part. Aside from the predisposing influences,
which doubtless constitute the main feature, cases are also not
rare in which the first manifestations of tabes immediately fol-
lowed great sexual excesses (for instance, in newly-married per-
sons). This view is even somewhat favored by the mere fact of
the far more frequent occurrence of tabes in men, and during the
period of their greatest sexual activity.
Onanism, carried to excess, acts in the same way as the exces-
sive natural gratification of the sexual appetite ; the same is true
of very frequent pollutions, pollutiones diurnz, spermatorrhea,
and the like. And yet, with regard to just these last processes, it
is often hard to determine what is the cause and what may perhaps
already be the effect of the disease beginning to be developed.
With regard to the method of operation of sexual excesses it
is also difficult to arrive at any plausible theory which shall have
more weight than that of a mere conjecture. We shall touch
briefly, below, upon the opinions expressed on this subject.
Extreme and lively emotional activity appears now and then
capable of being the starting-point of tabes; at least this is
asserted to be true of lively fright, terror, continued anxiety,
cares, repeated anger, etc. It is well known that these emotions
are often accompanied with serious disturbances of innervation
(trembling and weakness of the limbs, vaso-motor disturbances,
etc.). It is at least not inconceivable that an increase and repe-
tition of these disturbances might also finally lead to actual dis-
ease of the spinal cord. But nothing accurate can be said on this
point. f
It is hard to determine what relation certain acute diseases
a
528 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
bear to the tabes which follows them, whether they are merely
predisposing, or whether they directly light up the disturbances
of nutrition in the spinal cord. The fact is, however, that evi-
dences of tabes are often developed, sometimes more quickly and
sometimes less so, in the train of typhus, articular rheumatism,
acute pneumonia, etc. The same thing holds true of repeated
labors and abortions, of serious losses of blood, too long con-
tinued lactation, etc.
Ataxy has also been repeatedly observed among the nervous
disturbances which so often appear in the train of diphtheria ;
but it may appear doubtful whether we here have an actual
affection of the posterior columns of the cord, or perhaps another
form of ataxy; still, the observation reported by Jaccoud (1. ¢.,
p. 631) appears to me to speak positively for the first supposi-
tion. Iam myself at present observing an interesting case, in a
child nine years of age, which, after diphtheria of the fauces, at
first showed paralysis of the pendent palate, paresis of accommo-
dation, and insufficiency of the internal recti muscles, and now
presents well-marked ataxy of all four extremities, with slight
muscular weakness, with very slight disturbances of sensibility,
with swaying of the body on closing the eyes, and the failure of
reflex irritability of the tendons—therefore presenting an almost
complete picture of the symptoms of sclerosis of the posterior
columns. -
Among chronic diseases syphilis in particular has often been
credited with being the cause of tabes ; with what justice cannot
as yet be determined. E. Schulze, in his dissertation, cites quite
a series of cases in which no other cause but previously existing
syphilis could be brought into etiological connection with the
tabes. Judging by my own experience this connection seems
doubtful, although I have often enough seen the development of
other forms of myelitis in syphilitic patients. On the other
hand, Fournier most recently insists on this connection as being
comparatively frequent, which, if it should be confirmed, would
of course be a point of the utmost importance in the therapeutics
of the disease.
The connection between hemorrhoids and tabes is still more
obscure and doubtful. The same is true of the causation of tabes
by the suppression of sweating of the feet, as has been so often
claimed.
K. Schulze also, in some instances, assigns a causative agency
to traumatic injuries: fracture of the thigh, a fall upon the
belly, the shock of a gunshot wound, concussion of the spinal
cord, etc. This probably requires further confirmation.
Finally, various authors adduce excessive tobacco-smoking
among the causes of tabes. We are unable to support this in
itself not improbable assertion from our own experience, but
neither can we deny it.
Over against all these statements, however, it must also be
emphatically declared that, in no inconsiderable number of cases
of tabes, the most careful investigation is able to show no cause
whatever for the disease.
If the very existence of a causal connection between the con-
ditions above mentioned and tabes may often be called into
question, it must be admitted that we know still less with regard
to the method in which this causal connection proves effective in
the individual case; in what way sexual excesses or exposure,
taking cold, or mental impressions, induce the disturbances of
nutrition in the spinal cord lying at the foundation of the group
of symptoms which constitute tabes. Of course the most varied
opinions have been advanced on this subject, all of which, how-
ever, have been confined more or less to the domain of hypothe-
sis. This much seems certain, that all cases do not have the
same pathogenesis, but that those alterations which we designate
as sclerosis or gray degeneration may finally be developed from
various starting-points within the spinal cord. In view, however,
of the great difficulties which lie in the way of obtaining ana-
tomical material from the earliest stages of tabes, these points
cannot, at the present time, be positively decided.
The views with regard to the origin of tabes which seem to us
most plausible are those advanced by Remak, Sen., reproduced
by Cyon, and still further carried out by Waldmann. We lay
these before the reader, without, however, vouching for their cor-
rectness. According to Remak, the disease may arise in two
ways. In the one, the central nervous apparatuses are primarily
affected and disturbed in their nutrition by over-irritation and
VOL. XIII. —34
TABES DORSALIS. 529
i)
580 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
overexertion ; primary atrophy and degeneration of the same
take place, as a result of which, however, inflammation and
hypereemia may also afterwards be developed. Under this head
might be ranged those cases where tabes arises from hardships
and overexertion, from sexual excesses, from mental disturb-
ances, and the like.
The other way is by the primary development of an inflam-
matory process in the interstitial tissue of the posterior columns,
which only secondarily induces atrophy and degeneration of the
nervous elements. To this category belong those cases of tabes
which originate in taking cold, in traumatic injuries, the suppres-
sion of perspiration in the feet, acute and chronic diseases, and
especially syphilis.
In the second group of cases, the interstitial changes lying at
their foundation may either begin originally and principally in ©
the tissue of the posterior columns, thus constituting a primary,
chronic interstitial myelitis, or they may arise by extension from
a chronic spinal meningitis. The inflammation of the pia mater
is, in these cases, the primary step, the sclerosis of the posterior
columns only secondary, extending thither from the meninges.
This order of things has been especially noticed by Waldmann.
It is evident that before these views can be considered as
scientifically established, pathological anatomy must demon-
strate, first, that there is such a thing as a primary, non-inflam-
matory, degenerative atrophy of the posterior columns; second,
that in certain cases of tabes this alone exists at the beginning ;
third, that in other cases of tabes the interstitial changes are the
primary disturbance; and fourth, that the meningitic changes
occasionally found in the autopsies of those who have had tabes,
preceded the other changes in point of time. We shall presently
see, in looking at the pathological anatomy of the subject, how
far these postulates are or are not sustained.
However plausible these pathogenetic views may therefore be,
they must nevertheless, for the present, be regarded as merely
hypothetical.
(
TABES DORSALIS. 531
Pathological Anatomy.
In cases taken from the later stages, macroscopic inspec-
tion, as a rule, enables us to recognize an atrophy and wasting
of the spinal cord, especially in its lower divisions, and on care-
ful observation this is also found to be especially the case in the
region of the posterior columns, which appear somewhat sunken
and narrowed.
Even on looking at it through the pia mater, or, if this is
thickened and cloudy, after the removal of the same, we may
recognize a gray or grayish-yellow discoloration along the pos-
terior median fissure, at both sides of the same, extending almost
throughout the entire length of the spinal cord.
As a rule, the cord shows a distinct increase in its consist-
ency ; sometimes, however, this appears quite normal, very rarely
being diminished.
Generally, also, the posterior roots are discolored, gray, trans-
lucent, thin, atrophied, in great contrast to the normal white
anterior roots; this discoloration and atrophy are marked with
striking distinctness in the cauda equina in particular.
The pia mater usually appears cloudy and thickened, con-
nected by numerous adhesions to the dura mater, which is but
rarely thickened and roughened, the pia showing abundant bony
plates and sometimes stronger pigmentation. This change is
almost always confined to the posterior division of the spinal
cord, and corresponds in some degree to the area of extension of
the gray discoloration; more rarely the pia mater appears altered
over a larger area. The spinal fluid always appears increased
—sometimes to a large degree. The anterior and lateral divisions
of the spinal cord, like the anterior roots, usually appear, on
external inspection, to be quite intact.
More accurate information can only be obtained by the study
of numerous transverse sections of the cord.
In the most well-pronounced cases, the various transverse sec-
tions show the posterior columns entirely, or throughout their
greater extent, as gray, translucent, of firmer consistency, or
more gelatinous, and of a grayish-yellow color. They are often
wasted, sunken, evidently shrunken, so that the two posterior
532 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
columns appear more approximated to each other, and show
greater precipitousness in the direction of their course. This is
Fie. 8. Sclerosis of
the posterior columns,
Half diagrammatic.
The most marked de-
velopment is shown in
the upper lumbar and
the thoracic portion.
In the cervical portion
there is a less uniform
involvement of the
posterior columns,
often very marked, particularly in the dorsal
portion. (See Fig. 8.)
Generally the degeneration is not uniformly
distributed over the entire transverse section
of the posterior columns [Hinterstrange], the
middle portions and those peripheral portions
lying next to the pia mater being ordinarily
most intensely affected, and often still sepa-
rated from the posterior commissure and the
posterior horns of gray matter [Hintersaule] by
a narrow zone of white substance. As arule,
nevertheless, the external portions of the pos-
terior columns [‘‘die Keilstrange,”’ the ‘‘ Funi-
culi cuneati” of Burdach. — TRANs.] are the
parts, in particular, which are likewise affected,
thus affording a characteristic contrast to pure,
secondary degeneration which is confined to
Goll’s columns [‘‘ die zarten Strange,” ‘‘ Funi-
culi graciles’’ of Burdach.—TRANS. ].
It is also rare for the posterior columns to
be the subjects of gray degeneration throughout
their entire length. In the lowest lumbar divi- |
sion, we often see but a slight gray discoloration
in the external half of the columns; this in-
creases in width as we ascend, until finally, in
the upper half of the lumbar enlargement, the
entire transverse section of the posterior columns
appears discolored; this then generally con-
tinues upwards throughout the entire dorsal
portion, again to diminish in the cervical portion,
and finally to be limited to the columns of Goll.
In the majority of cases, therefore, the rule holds
good that the intensity and extent of the pro-
cess is greatest in the upper lumbar and the
dorsal portions, diminishing both upwards and
downwards from these points.
TABES DORSALIS. 538
At the same time the changes may also extend upward into
the medulla oblongata, into a portion of the restiform bodies,
but then they cease there without any definite boundaries.
Not rarely, however, even the unaided eye can recognize a
slight grayish discoloration of the neighboring posterior and
external divisions of the lateral columns, which may extend for-
ward as far as the anterior columns, in a gradually narrowing
seam, admitting of no sharp line of demarcation between itself
and the normal tissue.
In like manner the posterior horns of gray matter are, in
many cases, also not free ; they appear of a darker gray, shriv-
elled, distorted ; the pillars of Clarke have repeatedly been found
altered.
This is the picture of the fully developed, typical cases,
such as most frequently occur.
At the jirst beginning of the disease, however, if anything
at all is to be found, it is only a pair of narrow, scarcely recog-
nizable gray strips at each side of the median line, in those por-
tions of the posterior columns designated by French authors as
the ‘‘rubans externes’’ (Charcot, Pierret), But in some cases,
also, macroscopic inspection shows nothing abnormal and the
microscopic alone reveals the beginning sclerosis.
In the oldest and most severe cases, on the contrary, the spi-
nal cord, throughout long portions of the same, appears dwin-
dled, atrophied, and hardened in its entire thickness. On mak-
ing a transverse section it is found, almost throughout its entire
extent, transformed into a gray, translucent mass, in which the
usual picture of a transverse section is no longer distinctly to be
recognized.
But complete information with regard to the kind and the
extent of pathological change present can only be attained by
the microscopic examination of hardened preparations, treated
with various coloring matters.
Histologically, we may, in the earlier stages of the disease, at
first recognize a greater or less degree of thickening of the inter-
stitial tissue, a greater wealth of nuclei in the same, offen en-
larged and very much developed Deiters’ cells; in the nerve-
fibres there is generally not much to be seen that is abnormal,
534. ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
aside from simple emaciation, dwindling, and final disappearance
of the same; a slight thickening of the nerve-fibres is rare; there
is usually no breaking down of the medullary sheaths, nor fatty
degeneration of the same, nor swelling of the axis-cylinders ; it
is merely a question of simple atrophy and disappearance of the
fibres. Generally, especially in the more recent cases, numerous
granule cells are also to be found, and these are sometimes
particularly abundant in certain definite zones of the diseased
tissue and scanty in others. The vessels are commonly thick-
ened, their walls rich in nuclei. Corpora amylacea are scattered
throughout the tissue in greater or less number.
In the Zater stages the principal mass of the structure is com-
posed of a firm, fibrillar, often wavy connective tissue, which con-
tains numerous nuclei, and is usually disseminated with innume-
rable corpora amylacea. Most of the nerve-fibres have entirely
disappeared, ordinarily not even a trace of the axis-cylinders is
to be seen; but even in the oldest cases one will still find quite
a large number of single, isolated, but well-preserved nerve-
fibres scattered through the increased, firm connective tissue.
The vessels are sclerotic, the number of granule-cells is small,
but generally there is an increased number of admirably de-
veloped, large spider cells.
The posterior roots, so far as they run their course within the
cord in the posterior columns, endeavoring to reach the gray
posterior horns, usually take part in the degenerative process ;
their fibres are broken down, atrophied, have grown more sparse
and thinner, and are separated from one another by broader
bands of connective tissue.
The microscope also generally gives the best information with
regard to the more accurate localization of the process, with re-
gard to the degree of its extension through a transverse section
of the cord.
In the posterior columns, as a rule, the entire transverse sec-
tion is more or less attacked, although to a very varying degree
of intensity in different cases. Strictly speaking, however, this
only holds good with regard to the upper lumbar and thoracic
regions. In the lower lumbar region the middle and innermost
divisions are often tolerably free; in the cervical region, on the
ae er ae ee Se ae
—— ee eC
Ss
TABES DORSALIS. 535
contrary, the external divisions are generally free while the col-
umns of Goll are principally or exclusively attacked. These
then generally behave exactly as in simple secondary degenera-
tion. The bundles of roots lying within the posterior columns are
always affected likewise, and even within the posterior horns of
gray matter they show all the evidences of degenerative atrophy.
It is, of course, a matter of importance to find specimens
showing what part of the posterior columns is involved in the
lightest cases and is the earliest at-
tacked. The opportunity for this
is, naturally enough, but rarely
presented. In such cases Pierret
found the external ribbons of the
posterior columns (bandelettes
externes) exclusively or pre-emi-
nently attacked, the columns of
Goll, on the contrary, being free
(see Fig. 9, a, a).
In contrast and complement thereto,
Pierret, in one case, found the columns of
Goll exclusively involved in the sclerosis.
The symptoms observed during life were
quite different from those belonging to
tabes.
Fra. 9. Sclerosis of the posterior columns, con-
The microscope furthermore fined to the external ribbons of the saine, repre-
senting the first stage of sclerosis of the posterior
reveals a regular participation im columns in tabes. (4 a.) After Pierrot, Aroh. de
the disease on the part of the gray
posterior horns, manifested by disappearance of nerve-fibres,
thickening of the connective tissue, but very slight changes in
the ganglion-cells, which at most appear somewhat more pig-
mented. Clarke’s pillars also appear to be regularly involved,
even though their ganglion-cells frequently remain tolerably in-
tact. This involvement of the posterior horns is, according to
Lockhart Clarke, so constant that he raises the question whether,
after all, the posterior gray horns are not the first to be diseased,
or, at all events, are not very early,affected in all cases. This is
a point worthy of all consideration.
5386 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
In like manner there is also, almost always, especially in the
later stages, a well-defined extension of the disease to the lateral
Fia. 10.— Alterations
in a transverse section of
the spinal cord in a case
of tabes dorsalis (Fried-
Teich’s form): a high de-
gree of ataxy without dis-
turbance of cutaneous or
muscular sensibility. We
recognize a widespread
disease of the lateral col-
tumns and other portions
of the spinal cord in addi-
tion to sclerosis of the
Posterior columns,
columns, which is very variable and sometimes
quite considerable in extent. <A sclerotic stripe,
varying in width, and diminishing in width an-
teriorly, extends forward from the gray poste-
rior horns along the periphery of the lateral
columns, sometimes even extending far into the
anterior columns.
Sclerosis of the posterior columns is there-
fore, in the majority of cases (perhaps in all %),
mot the only condition found in tabes, but the
process extends beyond the posterior columns
to the lateral columns and the posterior horns,
often involving them to a very considerable ex-
tent. Such a case is given, for example, in the
accompanying Figure 10.
Sometimes, also, degeneration, sclerosis, and
atrophy of the ganglion-cells is met with in the
anterior gray horns, although this is a rare form
of change. According to Pierret this alteration
stands in connection with sclerosis of the poste-
rior inner root-bundles, and extends from these
along the bundles of fibres that radiate into the
anterior gray horns.
After this brief exposition of the principal and certainly
the most essential anatomical changes in tabes, various ques-
tions at once arise which are of the highest importance to the
pathology of the disease, whose solution falls chiefly within
the domain of pathological anatomy, but has, as yet, hardly
been undertaken. What is the true essence of the diseased
process? Is it inflammation? Is it simple degenerative atro-
phy ? Is it secondary degeneration? Is the sclerosis of the pos-
terior columns the only essential part of the process? Where
does it begin, in what portion? How does it advance? What
is primary and what secondary about the changes? Are not
certain portions of the gray substance and of the lateral col-
umns affected with equal regularity, and is not sclerosis of these
parts of equal importance with that of the posterior columns ?
TABES DORSALIS. 537
All these questions still await their solution. Many attempts have been made
to answer them, and with very varying results. Conclusive proofs could scarcely
be brought forward for any of the opinions advanced, and but too often the pref-
erence of a writer for a certain theory, or some preconceived opinion of his, has
been sufficient ground for causing him to group or to explain the facts in a certain
way.
The most recent views differ widely even with regard to the general patholo-
gical significance of the process. While Leyden treats of tabes under the head
of chronic myelitis he nevertheless denies the inflammatory character of the pro-
cess under consideration, and accounts for it rather as a peculiar chronic degener-
ation of the nerve-tracts, without any special participation on the part of the con-
nective tissue and without inflammatory manifestations. He considers the main
thing to be the atrophy of the nerve-fibres; that this constitutes the starting-point
of the process, which is probably first localized in the external portions of the
posterior columns.
Charcot, indeed, coincides with Leyden in so far as to locate the starting-point
of the process, in all probability, in the nerve-elements (parenchymatous sclerosis) ;
but he regards the process as a chronic inflammation, and gives prominence to the
hyperplasia and fibrillar transformation of the connective tissue at the expense of
the nerve-elements.
Friedreich, too, has long since declared himself of the opinion that sclerosis of
the posterior columns represents a chronic inflammatory process leading to second-
ary atrophy of the nerve-elements.
C. Lange, on the contrary, believes that so-called secondary degeneration plays
a prominent réle in sclerosis of the posterior columns, and is inclined to attribute it
to a primary affection of the roots caused by meningitis.
It certainly cannot be denied, on making an unprejudiced examination of the
anatomical conditions present, that secondary degeneration does indeed play an im-
portant rdle in sclerosis of the posterior columns. The gray degeneration so com-
monly present in the cervical portion, confined to the columns of Goll, is very cer-
tainly only of a secondary nature, and is always found present when the greater
part of a transverse section of the cord in the lumbar region is degenerated. But
how and where we are to establish the boundary between secondary and primary
degeneration cannot as yet be determined. Evidently, also, secondary degeneration
—such, for instance, as occurs in chronic transverse myelitis—has in many cases
been confounded with tabes; thus, for instance, in the two cases of Robitzsch.
At all events, most of the more recent observers are entirely agreed in the opin-
ion that the affection does not begin in the posterior roots, but within the spinal
cord itself. Vulpian speaks with all positiveness against the possibility of the
former; Charcot and Pierret locate the beginning of the process very positively in
the spinal cord itself, and Leyden is of the same opinion.
The French school has recently made the attempt, based on some fortunate post-
mortem discoveries, to locate more definitely fhe point of the first beginning of
sclerosis in the posterior columns, and to investigate the way and method of its
5388 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
further spread from this point of origin. The views of Charcot and Pierret, to
whom we are indebted for the investigation of this difficult and important question,
are essentially as follows: The sclerosis begins in the external bands of the posterior
columns, at the point where the inner root-bundles mix with the vertically ascend-
ing (probably commissural) fibres of the posterior columns; this sclerosis of the
lateral bands or ribbons (Keilstriinge) is the only essential anatomical change in
ataxy. The sclerosis of the columns of Goll (zarte Striinge) is to be regarded
principally as a secondary ascending degeneration. At the beginning of the disease
the posterior roots do not show the slightest change. In the lateral bands of the
posterior columns, the sclerosis now gradually spreads upwards from root to root;
from here it spreads to the columns of Goll, in part directly, and in part (and prin-
cipally) as secondary degeneration; it furthermore spreads from here to the pos-
terior gray horns, to the posterior roots, and to the external portions of the lateral
columns, and finally, in rare cases, to the anterior gray horns. (The only obserya-
tion which stands opposed to these statements is one published by Charcot himself,
in connection with Bouchard,' of a case which was regarded as the beginning of
tabes on account of the lancinating pains that were present, and in which the begin-
ning sclerosis was found in the ‘‘inner and posterior” portions of the posterior col-
umns, therefore, after all, in the columns of Goll.)
However plausible all these views may be, they can by no means as yet be
looked upon as firmly established. Much still remains to be confirmed by further
observation. After maturely weighing all the facts and opinions, we can probably
only say this much, viz. :
It is in the highest degree probable that in tabes we have to deal with a chronic
inflammatory process; that it therefore merely represents one form of chronic mye-
litis.
It is possible, and perhaps probable, that this chronic myelitis may take its origin
in two different ways: at one time from a primary irritation and degeneration of
the nerve-elements themselves (parenchymatous sclerosis), at another from a primary
irritation and proliferation of the interstitial tissue (interstitial sclerosis) — thus
giving a double method of origination of tabes, as was believed by Remak, Senior.
It is possible, and perhaps probable, that the sclerosis begins in the external
bands of the posterior columns, and spreads from here further, and that the scle-
rosis of the fasciculi graciles, or Goll’s columns, must, to a great degree, be regarded
as a secondary degeneration.
It is certain that the disease does not begin in the posterior roots.
It is, finally, probable that sclerosis of the posterior columns-is not the exclusive
and essential change in tabes, but that a simultaneous involvement of the posterior
gray horns and of certain portions of the lateral columns is constant, and, perhaps,
equally essential—a statement which, it is true, finds its support more in clinical
observation than in the anatomical facts now before us.
1 Gaz. méd. de Paris. 1866. No. 7%.
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TABES DORSALIS. 5389
After this digression, it remains for us to touch briefly on the
anatomical changes to be found outside of the spinal cord in tabes.
The posterior nerve-roots are generally found diseased in the
later stages; they are highly atrophied, flat, gray, translucent,
showing degenerative atrophy of the nerve-fibres, proliferation of
connective tissue, and abundant corpora amylacea. In the earlier
stages, however, they are also often found quite normal; the
posterior roots have never been found diseased alone (Vulpian).
In striking contrast thereto, the peripheral sensitive nerves
are always found entirely intact, even if the posterior roots
belonging to them (even to the spinal ganglia) are entirely the
subjects of gray degeneration.
The anterior nerve-roots are intact. The spinal ganglia are
likewise generally found entirely intact.
Some have attached great value to the examination of the
sympathetic and its ganglia, because they sought in this the
seat of the disease. This has, however, always been found intact
(Carré), and where gray degeneration of the main trunk of the
sympathetic and the like has been demonstrated, as in the case
of Chvostek, it has certainly always been on account of a rare
and accidental complication.
The peripheral spinal nerves have likewise generally been
found intact; Friedreich alone, in one case of his, found pro-
liferation of connective tissue, and emaciation of the nerve-fibres
in the sciatic nerve.
The muscles are generally quite normal; they are at most
simply emaciated in the later stages; degenerative atrophy of
the same has been found, as a very rare complication, in individ-
ual instances.
Certain of the cranial nerves, on the contrary, are more fre-
quently the seat of changes. This occurs oftenest in the optic
nerves, which show gray degeneration—essentially the same
change that takes place in the posterior columns—proliferation
of connective tissue, rapid and complete disappearance of nerve-
fibres, and numerous corpora amylacea. The trunks of the optic
nerves are generally most intensely attacked; still, the affection
may also extend throughout the entiré length of the optic tract as
far as to the corpora geniculata. Thus far it has proved impossible
540 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
to find any anatomically demonstrable continuity of the gray
degeneration between the optic nerves and the posterior columns.
In quite rare cases, alterations belonging to the class of atro-
phy and gray degeneration have also been found in some other
cranial nerves (oculomotorius, abducens, hypoglossus).
The nuclei of these nerves, on the floor of the fourth ventricle,
also appear sometimes to be affected.
Among the pathologico-anatomical changes found in other
parts of the body those of the joints claim special interest. In
those cases in which disease of the joints belongs to the symp-
toms of tabes dorsalis we find a disappearance of the articular
cartilages, a grinding off of the articular head and of the cavity
for its reception, the surfaces of which are hollowed out and
rough, or ground off and flattened ; a peculiar characteristic of
this condition is that with the rapid disappearance of bone there
is so insignificant a tendency to exostosis. In more recent cases
the amount of articular fluid is materially increased, points of
thickening and fungosities are found on the synovial membrane,
the surrounding soft parts are more or less strongly and exten-
sively swelled and suffused with fluid.
The changes in the skin (bed-sores, etc.), in the bladder (cys-
titis, ulceration, diphtheria, etc.), in the kidneys (pyelonephritis,
interstitial abscesses, etc.), in the respiratory apparatus, the di-
gestive apparatus, etc., are the same as in chronic myelitis.
They belong to the very latest stages of tabes or are more acci-
dental complications.
Pathology of Tabes Dorsalis.
Synuptoms.
I give first the general picture of the disease in the ordinary
typical form of tabes, which includes by far the greater number
of cases, and which, in my opinion, must constitute the starting-
point for all further investigations and observations. The remain-
ing rarer forms I shall endeavor to characterize briefly farther on.
In view of the importance of the malady, and the wealth and
|
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e- FE eee oe - we eo
I Te a
I
TABES DORSALIS. 541
manifold character of its symptoms, this delineation must be
allowed a somewhat wide sweep.
The disease almost always begins with an introductory stage
(also designated as a precursory, prodromal or neuralgic stage),
which may last for a very variable period of time, generally
extending over many months or a few years—sometimes, how-
ever, over a longer period of years.
The most characteristic and almost constant signs of this
stage are the lancinating neuralgiform pains ; lively, stabbing,
boring pains, shooting through a part like lightning, lasting for
single days or nights, or often merely for hours; pains which
may be of furious severity, generally occurring in paroxysms,
and consisting of an aggregation of numerous single, often merely
momentary impressions of pain; pains which often remain con-
fined for a long time to one or both lower extremities, often
changing their position within these, but which also extend far-
ther to the trunk (very generally), and to the upper extremities
(more rarely).
These pains, occurring in paroxysms, are generally regarded
as rheumatic in character and treated accordingly, and are often
but little regarded for years. At first they recur but rarely, at
intervals of months—for instance, in the spring and fall; gradu-
ally they become more frequent and more tormenting, occur with
every change of weather, especially with every considerable vari-
ation of the barometer, with rain, wind, snow, and the like, after
bodily overexertion, and after mental disturbances.
They may last for years without any further symptoms being
developed.
Sooner or later, however, in many cases—by no means in all
—symptoms appear on the part of certain cranial nerves; above
all things, diplopia, caused by paresis or paralysis of various
muscles of the eye, especially those supplied by the oculomoto-
rius. This diplopia may be transitory and may change its place,
or it may persist for a longer time, for some months ; it is but
rarely that such paralyses are permanent.
Quite the contrary is true with regard to the amblyopia,
which is of almost equal frequency, ngt rarely arising in the in-
troductory stage of tabes, and which more or less rapidly de-
542 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
velops to complete amaurosis, being dependent on a degenerative
atrophy of the optic nerve, which is hardly ever capable of re-
covery.
More frequent, however, than these disturbances of the high-
est sense, during the introductory stage, are disturbances of the
sensibility and mobility of the lower extremities, which, after a
longer or shorter time, become constantly associated with the
lancinating pains, sometimes even preceding these, or at least
arising simultaneously with them. |
The first disturbances are usually those of a sensory charac-
ter, appearing in the form of various kinds of paresthesia ; such
as a feeling of numbness, the sense of having wool or felt on the
soles of one’s feet, formication in the feet, the legs, and thighs,
also on the trunk, and—what is tolerably frequent and charac-
teristic—in the ulnar domain of one or the other hand; in other
cases the sense of a tight girdle at various heights on the trunk,
or also on the extremities, about the knee- or ankle-joint. An@s-
thesia which can be objectively demonstrated is very rare at this
time.
On the other hand, the sensations of motor weakness and
insecurity, of growing more easily fatigued on standing or
walking for any length of time, belong to the most constant
symptoms. These may also, in part, be regarded as belonging
to the class of sensory disturbances. That striking sense of fa-
tigue, in particular, of which the patient is often aware even
before he has left his bed in the morning, or which becomes quite
oppressive on the slightest exertion, especially on standing, and
which is followed by an uncomfortable disquiet in the limbs,
might be regarded, in part, as an irritation or paresthesia of the
Sensitive nerves of the muscles. |
Undoubtedly, however, true motor disturbances are also asso-
ciated with this condition ; patients decidedly lose the strength
of their limbs; exertions which were formerly borne with ease
become a severe effort; their powers of endurance, in walking
and standing, diminish materially. Patients find the perform-
ance of these acts increasingly difficult and disagreeable; they
feel themselves unsteady on their legs, believe that they sway to
and fro, or actually do so to a slight degree, and yet sufficiently
» ay
a” ba
A EE ae Se Se
TABES DORSALIS. 5438
so to be capable of objective demonstration. In many patients
all these manifestations increase materially when it grows dark,
and in such persons we can also always recognize a higher de-
gree of disturbance when they close their eyes. All these mani-
festations may require a variable length of time for their devel-
opment. !
In many instances disturbances of the bladder appear sooner
or later (difficulty of micturition, dribbling of urine thereafter,
etc.), and almost more frequently there is weakness and irrita-
bility of the sexual functions (various grades of impotence,
insufficient erections, premature ejaculations, nocturnal or diur-
nal pollutions, increased excitability on coming in contact with
women, etc.).
Among the much rarer disturbances at this period of the dis-
ease are severe attacks of gastralgia (crises gastriques), which
doubtless stand in close relation to the lancinating pains; pecu-
liar affections of the joints (arthropathies des ataxiques) ; head
symptoms of various kinds, as a sense of confusion, headache,
pain in the neck, evidences of an oversupply of blood to the
head, dizziness, great psychical irritability or slight psychical
aberration, etc.
There is usually, at this period, but a very slight sense of ill-
ness ; nutrition is good; there is never, or but very rarely, any
fever. Finkelnburg and M. Rosenthal claim to have seen slight
febrile disturbances in the initial stage.
While all the manifestations hitherto described increase, the
stage of the fully developed disease then approaches, generally
very slowly and gradually. This may, with some propriety, be
called the ataxic stage, on account of the symptom which most
forcibly strikes the eye. Of course it is impossible to establish
a sharp boundary between the stages.
The unsteadiness of the gait increases more and more, until
distinct disturbance of co-ordination (ataxy) is developed, and
the patients clearly show the atazic gait ; their legs are moved
unsteadily, irregularly, and with a flinging motion, the toes are
pointed outwards and thrown into the air, the heels are brought
to the ground with a stamp; the gait becomes insecure, swaying,
staggering ; the majority of such patients anxiously follow their
544 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
steps with the eye, and can only walk with difficulty, or tone
not at all if they turn away or close their eyes.
At the same time their powers of endurance diminish more
and more; the promenades grow shorter and shorter; finally,
every little trip throws the patient into a profuse perspiration ;
there is no longer any question of his standing on his feet con-
tinuously.
In remarkable contrast hereto, it appears, on examination in
the lying posture, that the gross strength of the legs is not at
all, or but very little, reduced; that single movements can be
executed with almost normal strength and certainty. Still, on
more careful examination, in the majority of cases, slight local
pareses may be recognized. ‘Tension of muscles is, however, en-
tirely lacking.
Soon, however, well-developed ataxy of the legs shows itself,
even in the lying posture. Somewhat more complicated move-
ments (movement in a circle, the touching of an object held be-
fore them, etc.) are accomplished with increasing uncertainty,
with many zigzag motions, etc., in spite of the anxious assistance
given by the eye. This is frequently still more the case if the
patients close their eyes, the movements then becoming quite
uncontrolled, irregular, unmeasured.
In the further course of the disease the ataxy keeps increasing ;
patients are obliged to avail themselves of one, and afterwards
of two canes; eventually they have to be led; then they can no
longer walk under any circumstances, and finally they can no
longer stand. On attempting to do so, swaying and staggering at
once begin, or the patients fall to the ground outright.
Sooner or later the ataxy also extends to the upper extremi-
ties ; this occurs with very variable rapidity in different cases,
and sometimes does not occur at all, even where the disease has
existed for years. The more delicate and complicated move-
ments—writing, piano-playing, handiwork, etc.—are the first to
become difficult or impossible; the attempt to take hold of
things is accomplished with singular, jerking, irregular move-
ments; the acts of dressing, eating, and the like become visibly
more difficult, and the patients are thereby rendered to a great
degree helpless.
TABES DORSALIS. 545
At the same time the disturbances of sensation are liable to
increase ; the lancinating pains continue with varying intensity
and frequency, the sense of a tight girdle is generally very con-
siderable and sometimes increases to a feeling of oppression and
constriction. The diminution of sensibility in the legs is now
likely to be distinctly and objectively demonstrable, though to a
very variable degree ; sometimes it can hardly be demonstrated,
even on the most careful examination, at other times itis of a high
degree and well pronounced. Partial paralysis of sensation is
also very common—analgesia, as well as partial paralysis of the
sense of touch and the perception of temperature. Retardation
of sensitiveness to pain is not rare, as well as the long continu-
ance of sensations, or hyperalgesia with diminished sense of
touch. Almost always corresponding anomalies in museular
sensibility can also be demonstrated, such as a diminished
perception of the position and attitude of the extremities or of
passive movements, greater difficulty in performing movements
with closed eyes, etc.
The reflex action of the skin acts variously ; sometimes it is
increased, generally normal, often lowered or extinguished. On
the other hand—and this seems to be a very noteworthy symp-
tom —the reflex action of the tendons is always completely
extinguished, and this seems to stand in no regular relation to
the reflex action of the skin.
The disturbances in function of the bladder and sexual
organs already referred to increase in intensity. The nutrition
of the muscles generally remains intact for a very long time ; the
same is true of the nutrition of the skin ; at this period bed-sores
are very rare. | |
- In some instances vdrious rarer symptoms are added to the
disturbances already named, whereby the picture of the disease
may be rendered very manifold, but which must yet be looked .
upon as subordinate and by no means regular manifestations.
Among these are disturbances of hearing, nystagmus, slight
derangements of speech, troubles with the joints, muscular
twitchings, muscular atrophy, attacks of suffocation, difficulty
of swallowing, etc. | -
Aside from the previously described disturbances of motility,
VOL. XIII.—35
546 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
of sensation, of reflex action, etc., an objective examination
reveals but very little. The spinal column is generally quite
normal, nowhere sensitive. It is but very seldom that points
which are painful on pressure can be demonstrated thereon.
The urine usually remains normal for a long time. The internal
organs are healthy. The general nutrition ordinarily remains
good for a long time; sleep, appetite and digestion are apt to be
good, notwithstanding that patients suffer from more or less
obstinate constipation. Many patients are strikingly well nour-
ished, of blooming appearance, corpulent ; some, to be sure, pre-
sent a pale, sickly, faded appearance. :
The psychical functions, intelligence, memory, disposition, etc.,
generally remain intact for a long time—often permanently. The
observation of Steinthal that patients sick with tabes rejoice in a
striking degree of cheerfulness and contentment, and bear their
pitiable troubles with wonderful good humor, can often be con-
firmed. Of course, this is by no means always true, and but
too many patients experience the burden of their tortured exis-
tence with double weight.
Thus matters may remain in this stage for many years (5, 10,
15, or 20 years), slowly and gradually changing for the worse,
and this does not exclude the existence of periods of standing
still and fluctuations towards improvement. The helplessness of
the patients constantly increases, their discomforts augment, the
pains do not abate, and the whole misery of their condition is
made more insupportable by the amaurosis, the incontinence of
urine, the slowly developing vesical catarrh, etc.
And thus the jinal stage gradually approaches—the stage of —
true paralysis and of increasing cachexia (stadium paralyticum,
paraplegic stage). The motor power diminishes sooner or later,
faster or slower, finally reaching the point of complete paraple-
gia; the legs grow stiff, contractions set in, and deformities
caused thereby, the muscles become more and more emaciated,
the extremities grow thin and skeleton-like. |
Distinct disturbances of digestion now set in, the appetite
diminishes, the bowels grow increasingly sluggish, and when a
movement of the bowels is about to take place it can no longer
be held back. The prolonged paralysis of the bladder leads to
TABES DORSALIS. 547
cystitis with its results; finally bed-sores set in, accompanied
with fever, and if an earlier end is not put to the sufferings of the
patient by some intercurrent disease (typhus, pneumonia, pul-
monary phthisis, dysentery, or the like), death finally occurs
through general, exhaustion.
This is the way it goes in the worst cases. Sometimes, how-
ever, we see the disease, in its earliest stages, turn towards a
cure; it is true this is seldom enough the case—still it does
occur.
Or the disease may come to a stand-still for a longer time,
the patients remain for decades of years in the same situation,
without any material fluctuations, until finally the terminal stage
brings about the end in a comparatively short space of time, or
the unfortunate victim is carried off by some intercurrent dis-
ease.
The analysis of the individual symptoms of tabes brings us
in contact with numerous interesting problems in the pathology
and physiology of the spinal cord, which may be conducted
toward their solution by the accurate clinical analysis of this
disease and through careful histological examinations.
Disturbances of Sensibility.
Among these, pain stands largely in the foreground, partly
on account of its early occurrence as regards time, partly on
account of its great severity and frequent recurrence.
This is very particularly true of the so-called lancinating
pains (boring, darting like lightning) which belong to the most
regular manifestations of the initial stage, but also not rarely
accompany the disease throughout its entire course.
These are the excessively severe boring or piercing pains—
darting through like lightning, or sometimes raging in one spot
for some seconds, and occasionally conveying the sense of a tight
cord—which have already been graphically described by so many
548 ERB.—-DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
authors, and which we have also already previously attempted
to characterize (p. 79).
They usually occur in paroxysms, which are repeated with
varying frequency, and which themselves, again, are composed
of a larger number of single painful sensations. They are at
times confined to a small, circumscribed region of the skin, and
are then not rarely accompanied with a high degree of circum-
scribed hyperesthesia at the same spot, causing a light touch to
be uncommonly painful, while, on the contrary, stronger -pres-
sure appears to be grateful, Or these pains may be situated
deep within the soft parts or in the bones, and one sees the
patient every moment or two twitching in body and his face dis-
torted with pain, sometimes even moaning and whimpering. Or
the pains may follow certain definite nerve-tracts, in the form of
neuralgia, as darting pains through the limbs, generally desig-
nated as ‘‘rheumatic.’’ Then during the paroxysms the nerve-
trunks are likely to be sensitive to pressure.
The intensity of the pain is very variable in different cases.
Some patients are so little troubled with it that it requires care-
ful questioning to determine the existence of the pain. Others
are obliged to endure the most fearful tortures during the at-
tacks, which equal in intensity the worst neuralgic paroxysms.
Almost every patient gives a somewhat different description of
the pain; but its momentary, boring, paroxysmal character, like
a streak of lightning, almost always stands forth so prominently
that it can readily be recognized.
The duration of the individual attacks is very variable: often
but single darts of pain arise; at other times an attack of half an
hour is all that is experienced for one or several days; but fre-
quently the attacks last for hours and days, and generally attain
their greatest intensity during the night. The intermissions may
be quite free from pain, or may present only moderately painful
Sensations.
The frequency of the attacks is extremely variable: some-
times they are repeated in the course of days or weeks; at others
the individual attacks are separated by intervals of months, and
even of years.
It is not to be denied that external impressions are of the
TABES DORSALIS. 549
greatest influence on the occurrence of the attacks. This is
undoubtedly true with regard to the influence of the weather.
Although this influence may not be capable of being demon-
strated with certainty in all patients, yet it certainly exists in
many, and [I have often been surprised at the unanimity with
which my tabes patients complained of attacks of pain on cer-
tain days. In our climate, patients have the most reason to fear
wind, a low barometer, rain and snow, also fog; hence, doubt-
less, the often observed greater frequency of the attacks in the
spring and autumn. In the height of summer those days are
especially to be feared on which there are thunder-storms.
Aside from the influence of weather, the attacks are also
sometimes brought about by bodily exertion, emotional disturb-
ances, the act of coition, and the like. |
The lancinating pains undoubtedly belong to the most con-
stant symptoms of tabes; Topinard states that they were want-
ing 22 times in 104 cases; in 60 of my own observations, in
which a statement is made with regard to them, they were ab-
sent only 8 times; on paying more particular attention thereto,
they may perhaps be found still more frequently. Quite lately it
happened that one of my patients, on being repeatedly ques-
tioned, stated that he had never had any pain; and then, when he
happened to have a characteristic attack of pain, declared that
that was his old ‘‘rheumatism,’’ from which he had suffered for
many years. Generally the pains precede all other symptoms
for a longer or shorter time ; sometimes, however, they occur at
the same time with other symptoms, or follow them. Whenever
the characteristic attacks of pain are met with, we may seriously
suspect the presence of tabes; at the same time, it would be a
matter of interest to determine more positively whether similar
pains may not also occur here and there without any reference
to sclerosis of the posterior columns, or whether they are, as it
almost appears, well-nigh pathognomonic of tabes.
With regard to the actual pathogenesis of these lancinating
pains, we have as yet only conjectures, the most probable of
which is that they are caused by irritation of the posterior root-
fibres within the posterior columns. * Charcot, with all positive-
ness, places the anatomical location of the same in the external
550 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
bands of the posterior columns which contain the internal root-
fibres, claiming that the lancinating pains are entirely character-
istic of sclerosis of these bands.
According to this, they might probably also occur in other diseases of the spinal
cord as soon as these involved the above-named bands—for instance, in multiple
sclerosis.
Analogous perhaps to the lancinating pains are the visceral neuralgias described
of late by a number of writers: the urethral and rectal colics, the gastralgic attacks
(Delamarre, Charcot), the attacks of renal colic (Raynaud), etc., to which we shall
refer again farther on.
Pain in the back belongs decidedly to the rare symptoms of
tabes. In many cases patients do not complain of the least ab-
normal sensation along the vertebral column ; this is nowhere
sensitive to pressure or on motion. Sometimes complaint is
made of circumscribed or more diffuse pain in the vertebree, be-
tween the shoulder-blades or in the small of the back. But
these are manifestations of only slight severity. In some cases,
points which are painful on pressure may be found on the spi-
nous or transverse processes of single vertebree—a fact to which
Mor. Meyer has recently again called attention '—which furnish
an important basis for treatment, but which are, unfortunately,
only too rare. Whenever there is prolonged and severe pain in
the back, when this pain is materially increased by movements
of the body or of the extremities, by riding over a rough road,
by pressure on the spinal column, we may suspect the immediate
cause to lie in meningitic complications, as has also been plainly
shown by the descriptions of Waldmann.
Among the varieties of paresthesia, which rarely fail in the
picture of tabes, the most prominent is the sense of a tight girdle.
It is apt to be extremely annoying to the patient ; sometimes it
appears as a very troublesome sense of being tightly laced around
the thorax or the abdomen, combined with a more or less severe
sense of oppression, or it appears to the patient as if he were
enclosed in a tight coat of mail. But it also not rarely occurs on
the extremities, at the knee- or ankle-joint, or like a garter below
the knee. The intensity of the sensation is very variable, fluctu-
Berl. klin, Wochenschr, 1875. No, 51.
TABES DORSALIS. 551
ating from one day to the next, but rarely rising to the point of
severe pain. The most probable views with regard to its patho-
genesis have already been given on page 75.
The statements of patients with regard to the presence of
other varieties of paresthesia, which so often occur, especially .
in the lower extremities, are exceedingly manifold. The most
common are the feelings of formication, of numbness, and of in-
sensibility. One patient says that he feels as if he were walking
on felt soles or on wool, another as if he were walking on blad-
ders filled with water, etc. A sensation of burning in the skin,
or of cold, is also not rare. The feeling of formication is not
rarely confined to circumscribed spots in the skin or to the do-
main of single nerves, as to the thigh, the perineum, or anus, etc.
This or a similar abnormal sensation is also especially frequent
in the ulnar region of the upper extremities, and I must, accord-
ing to my experience, agree with Erdmann when he ascribes a
certain significance to this symptom, which so often occurs in the
initial stage of the disease. |
These forms of paresthesia belong to the most common man-
ifestations of tabes, and we shall rarely find a case in which
the one or the other cannot be demonstrated. They usually
appear in the earliest stages, and may then change their seat and
the area of their extension with the progress of the disease. At
the same time there is not much that is characteristic about
them, as they occur in so many diseases of the spinal cord. We
have already expressed ourselves with regard to their pathogene-
sis on page 74.
. The appearance of hyperesthesia of the skin is much more
rare in tabes. Still, it occasionally takes place to a high degree,
entirely irrespective of the quite circumscribed hyperzsthesias
which sometimes accompany the lancinating pains. Then large
regions of skin may possess a special sensitiveness over against
certain kinds or all kinds of irritation. I have seen a man who
showed a high degree of hyperzesthesia towards impressions of
temperature, over the entire back, while at. the same time there
was anesthesia towards impressions of touch. It is also not rare
to see a moderate paralysis of the,sense of touch accompanied
by a high degree of hyperesthesia towards impressions of pain.
552 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The statements of physiologists with regard to the occurrence
of hypereesthesia in lesions of the posterior columns would suffi-
ciently explain this manifestation; only one would then expect
hypereesthesia to be much more common in tabes. (Compare
page 73.) .
Anesthesia of the skin certainly iy to the most regular
manifestations, and to those most carefully studied with refer-
ence to the theory of the ataxy. The possibilities with regard to
the occurrence, the intensity and the extent of this disturbance,
are positively innumerable. Almost every case behaves differ-
ently in this respect, | |
The patients themselves are often unconscious of the anes-
thesia which objective examination demonstrates in them. Gen-
erally, however, they are informed on the subject by means of
various little discoveries which they have made on themselves:
they no longer feel the floor distinetly ; articles which they touch
seem to them to be covered with velvet; they cannot judge with
certainty of the temperature of a foot-bath; they cannot hold on
to small objects with their fingers if they turn their eyes away ;
they can no longer button their clothes, or tie a cravat, without
the looking-glass; they cannot readily handle things in their
pockets ; and more of the same sort. If there is a higher degree
of anesthesia, the patient is in great doubt, when in the dark, as
to the existence and position of his legs, and he knows that the
anesthetic parts must be taken hold of vigorously before —
recognize any sensation.
A more accurate picture of the kind and the degree of anes-
thesia can, however, only be obtained by an objective examina-
tion, With regard to the methods to be employed in carrying
this out we have expressed ourselves in detail elsewhere,’ and
would refer the reader to what is there said. By these means we
ean, first, recognize the most varied grades of dulness of sensi-
bility, often such insignificant and circumscribed disturbances
especially on the soles of the feet, the toes, and back of
the feet that they can only be demonstrated by the most
— 3 - aaah eed
1 Hrd, Diseases of the Peripheral Nerves. This Cyclopedia, Vol. XI. p. 212 and
following. )
eS
TABES DORSALIS. | 553
careful examination. Generally, however, we find distinct and
easily demonstrable diminution of sensation, most marked in the
feet and legs, but also not rarely extending over the thighs, the
trunk, and even portions of the upper extremities. The higher
degrees of cutaneous anzesthesia—such as occur, for instance, so
frequently in transverse myelitis, in slow compression of the
cord, etc.—are but seldom observed in tabes; even in the latest
stages such severe anzsthesia is an exception, and in the earlier
stages, even though extending over many years, it may be stated
as a rule that the cutaneous anesthesia only reaches a moderate
grade. ,
On the other hand, especially in the later stages, more careful
examination very often reveals the existence of partial paralyses
of sensation. It would carry us too far to describe in detail
all the individual possibilities of these interesting disturbances,
almost every case behaving differently in this respect. Suffice it
to say that all possible combinations of partial paralysis of sen-
sation, such as we have characterized on page 199 of Vol. XL,
occasionally appear—for, is not tabes the very richest field of
observation for these disturbances? Perhaps analgesia occurs
the most frequently—toss of the sensibility to pain with retained
sensibility to touch ; but the reverse is also not rare: retention
or even increase in the sensibility to pain, with diminution of
sensibility to all or to some varieties of touch; partial paralysis
of the sense of touch may be combined with analgesia or hyper-
algesia, or with hyperesthesia towards impressions of tempera-
ture, and the like. According to Topinard, sensibility to tem-
perature is, in many cases, retained an unusually long time; in
short, the individual cases present an inexhaustible variety of
manifestations.
Ata later period it is not rare to find a distinct retardation
of the conduction of sensations, especially of impressions of pain,
as we have already more explicitly set forth at page 70. This
manifestation, which has long been known, has recently been more
accurately studied (E. Remak, Osthoff, Naunyn, Hertzberg) ; it
is not rare in the typical cases, as taught in the schools, and
may even be found present in the early stages of the affection.
According to the most recent observations, it at first seemed as
554 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
though this retardation extended only to the sensation of pain,
a fact which would stand in admirable accord with physiological
conditions discovered by Schiff; indeed, this is by far the most
frequent state of things. And the statement of patients with re-
gard to the double sensation produced, for instance, by the prick
of a needle, on account of the normal rapidity with which the
sense of touch is conveyed, and the retardation of the sense of
pain, is often very striking, being the most so in typical cases of
tabes, and being more frequently found, on careful examination,
than was hitherto supposed. But this retardation is by no means
always limited to the sensation of pain ; in fact, Hertzberg has
demonstrated that in some cases the sensations of touch and of
temperature are also retarded, although to a far less degree than
those of pain.
Usually, in such cases, a corresponding retardation of reflex
action can also be demonstrated; likewise, as a rule, a strikingly
long duration of, not rarely a supplementary increase in, the
sensation of pain, so that patients declare the highest degree of
pain not to be reached until several seconds after it has begun.
Intimately connected with this is the inability to separate with
certainty and to count several tactile impressions rapidly follow-
ing one another. These manifestations, too, have previously been
spoken of.
Not less frequent than the disturbances of cutaneous sensi-
bility in tabes, are the anomalies of muscular sensibility, which,
long since known and acknowledged, have recently been brought
more into the foreground by Leyden. Here, too, the conditions
may vary much.
First of all, it may be said that the extreme feeling of fatigue,
which is so frequent and so annoying at the beginning of the dis-
ease, may perhaps be nothing else than a perverse condition of
muscular sensibility, a pareesthesia of the sensitive nerves of the
muscles. Spaeth has endeavored to establish this view ; I must
confess that it appears to me quite plausible, notwithstanding
that it is thus far incapable of direct proof. In the same cate-
gory with this sensation we might probably also rank the annoy-
ing feeling of disquiet in the limbs which arises on sitting or
lying still for any length of time.
TABES DORSALIS. 555
But a much more frequent and important manifestation is
that of diminution of muscular sensibility which can, by means
of the proper examination, be shown to exist in persons suffer-
ing from tabes. .
It is here less a question concerning so-called muscular sensi-
bility, or electro-muscular sensibility’ (though this may like-
wise be diminished), or concerning the so-called sense of power
[Kraftsinn}, which, as Leyden has shown, does not figure so
prominently here, being an essentially psychical act, than it is
a question of the diminution of what is called muscular sense
{Muskelsinn], which can very often be demonstrated in patients
with tabes. Such patients more or less entirely lose the sense of
the position or attitude of their lower extremities ; in the dark
or with closed eyes they do not know where their legs are, how
they lie, whether they are crossed, or how far apart from one
another they are. If one leg is passively placed in a certain po-
sition and the patient is asked to put the other in the same po-
sition, he cannot succeed in doing this at all, or but very imper-
fectly, while a well person can do it with the greatest precision.
These patients have likewise lost control over the extent and the
direction of the movements required of them, if they are to exe-
cute these in the dark or with closed eyes. Their movements are
thus rendered uncontrolled, excessive, shooting far over the mark
or wide of it. This is generally mistaken for an increase in the
ataxy which is commonly present. On careful observation, how-
ever, it is easy to recognize that the true ataxic disturbances of
motion are not essentially changed, that it is not the uncertainty
of movement that is increased, not the zigzag character of the
gait when the eyes are closed, but merely that the patient is
uncertain with regard to the direction of the motion to be under-
taken, and does not know when he has reached the Zimit of the
required movement. These two things are to be sharply dis-
tinguished from one another.
Finally, such patients have more or less completely lost the
sensation which judges of passive movements of the limbs. If
the appropriate tests are made, according to the method given
7
1 Compare Vol. XI.
556 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
on page 67, it will be found that much more extensive move-
ments are required than in a well person in order to produce any
sensation thereof, and that patients are very much mistaken
with regard to the direction and the degree of the movements.
In fact, it will be found, in the severer cases, that in certain joints
such passive movements cannot be felt at all, and that, when
their eyes are closed, patients are in absolute uncertainty as to
the position in which their limbs have been placed. |
All these disturbances sometimes, though much more pe
occur in the upper extremities as well.
It does not need to be specially insisted on, that it is not the
sensitive nerves of the muscles alone which are to be held re-
sponsible for these disturbances, but that the sensitive nerves of
the joints, the tendons, ligaments, fasci#, and in part of the
skin also, must take part, if the group of disturbances anOve
described is to be brought about.
So far as concerns the occurrence of anesthesia in tabes, the -
statements of different authors widely disagree. While Leyden
regards aneesthesia (cutaneous and muscular) as a very constant
symptom, and is even inclined to believe in ifs existence where
good and reliable observers have been unable to demonstrate if,
a large proportion of other authors are of the opinion that while
cutaneous and muscular anesthesia belong to the very frequent,
they are by no means among the constant symptoms of tabes.
Topinard, for instance, in 109 cases, found cutaneous anesthesia
76 times distinctly, 15 times very lightly, and 18 times not at
all; and among 50 cases that contained statements on the
subject, muscular anesthesia 20 times to a high degree, 8 times
slightly, and 22 times not at all. Friedreich has repeatedly and
quite recently described cases of intense sclerosis of the posterior
columns in which the most accurate and exhaustive tests of sen-
sibility, in all directions, have failed to show the slightest trace
of cutaneous or muscular anesthesia, at least during very long
periods of the well-developed disease. I too must express the con-
viction, founded on my own experience and special investigation
directed to this point, that—though they may be rare—there aré
cases of well-pronounced tabes in which every sort of disturb-
ance of cutaneous or muscular sensibility is lacking, or, at all
—
Ee
TABES DORSALIS. 557
events, cannot be recognized on the most careful investigation,
while in such cases the highest degree of ataxy may be present.
In the remaining, much more frequent cases, which certainly
constitute the rule, the anzesthesia appears at very variable peri-
ods in the course of the disease. It is rare for a distinct, objec-
tively demonstrable anesthesia to be present in the initial stage ;
it generally does not appear till the beginning of the second
stage. Topinard asserts outright that the cutaneous anesthesia
always appears simultaneously with or after the ataxy, never
before it—a declaration which we cannot entirely subscribe to.
During the further progress of the disease the anesthesia may
gradually increase in intensity and extent, so that, during the
later periods, at least the feet and legs below the knee may be-
come almost completely anesthetic. Still, this is subject to the
greatest variation in individual cases.
Notwithstanding the assertion of Leyden that, on careful
examination, a dulness of cutaneous or muscular sensibility, or
of both, can regularly be demonstrated, corresponding to the de-
gree of ataxy present, I must, on the strength of my own obser-
vations, subscribe to the opinion of numerous other observers:
that, in patients who have tabes, there is not even an approxima-
tively constant relation between the degree of ataxy and the
degree of cutaneous or museular anesthesia. In the typical
and more frequent cases, it is true, both forms of disturbance are
usually very well marked ; but, aside from these there are numer-
ous other cases of tabes in which there is a high degree of ataxy
and only a very slight disturbance of sensibility, and still others
with well-pronounced disturbances of sensibility and but very
slight ataxy.
The question of the pathogenesis of all these disturbances of
sensibility, as regards the anatomical basis of the same, is gen-
erally answered on the supposition that the gray degeneration
of the posterior columns and posterior roots is abundantly suffi-
cient to explain the disturbances of sensibility here found. But
the proof of this is not adduced. Serious doubts on the subject
are aroused by the not unfrequent cases in which the highest de-
gree of gray degeneration of the posterior columns has been
found, without any considerable disturbance of sensibility ; by
558 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the experience of secondary ascending degeneration of the poste-
rior columns; by the physiological facts, which indicate with all
certainty that a lesion of the gray matter of the cord always lies
at the foundation of retardation in the conduction of sensations ;
by the investigations of Woroschiloff, which show that the late-
ral columns take an essential part in the conduction of sensory
impressions. This is not the proper place further to enlarge
upon and to defend these doubts; but it does appear proper to
state that gray degeneration of the posterior cord does not seem
to us to furnish, with certainty, sufficient ground for the disturb-
ances of sensibility in tabes. We are more disposed to conjec-
ture that wherever there are profounder disturbances of sensi-
bility, retardation of conduction, etc., the gray substance (posterior
horns) prominently participates in the anatomical changes. This
point, however, as well as the degree of possible participation of
the lateral columns in the causation of sensitive disturbances,
must be left to be determined by further careful investigations.
It may be permissible here to treat at once of a symptom
which seems to us to stand in intimate relations to the disturb-
ances of sensibility, and which, by the frequency of its occur-
rence, and through the authority of Romberg, has acquired great
importanee in the clinical history of tabes, viz., the patients
swaying and falling to the ground on closing his eyes. This
belongs to the most constant and regular symptoms of tabes.
Still, there are exceptions even to this; cases in which, with the
highest degree of ataxy, there is no swaying on closing the eyes,
or at least the swaying which does exist is not aggravated
thereby ; there are always cases in which there is an entire ab-
sence of any disturbances of sensibility. We have already spo-
ken of this manifestation in detail previously (page 93), and
endeavored to demonstrate its intimate connection with the dis-
turbances of sensibility. This symptom will never be found
lacking where there are distinct disturbances of sensibility in the
lower extremities. To be sure it also occurs, at least in its light-
est forms, in not a few cases in which, as yet, no disturbance of
sensibility can be objectively demonstrated. We are therefore
disposed to regard swaying on closing the eyes as the first and
lightest symptom of a diminution in the so-called muscular sen-
a -.
TABES DORSALIS. 559
sibility, which is not, as yet, otherwise objectively demonstrable.
Inasmuch as constant sensory impressions coming from the
periphery are necessary for the maintenance of the equilibrium
and the position of the body in space, it is just in this very dis-
turbance of equilibrium (in swaying) that the least disturbance
of these centripetal currents is noticed the soonest. Atall events,
we must adhere to the opinion that this symptom does not stand
in closer relation to the symptom of ataxy.
Disturbances of Motility.
The most important among the symptoms belonging here, and
the one most thoroughly discussed, is unquestionably the atlazy,
the disturbance of co-ordination, of tabes.
The characteristics of this disturbance of motility are that the
certainty and precision of movements, especially of all combined
and complicated movements, is naturally diminished, while the
strength of individual movements and the certainty of the simplest
movements is not at all, or but very slightly diminished. What
we have here is a disturbance in the co-ordination of movements,
and not a true paralysis. Notwithstanding the frequency with
which an unmistakable diminution even of gross motor power,
and especially of endurance, can be demonstrated in tabes, still
this paresis is by no means the typical feature in the picture of
the disease. In all typical cases the true disturbance of co-ordi-
nation certainly stands very much in the foreground as compared
to the paresis, and the amount of the disturbance of co-ordina-
tion is out of all proportion greater than that of any paralysis
that may be present. Ataxy, and not paralysis, is the essential
and characteristic disturbance of motion in tabes.
The method of appearance of the ataxy is, in the great ma-
jority of instances, the same. The disturbance almost always
begins in the lower extremities. In the lightest grades the ex-
perienced eye notices a certain unsteadiness and irregularity in
the gait; the steps grow somewhat uneven, the position of the
feet somewhat irregular; more difficult movements betray a
higher degree of insecurity; rapid swerving to the right or left,
quick turning around, are accompanied with distinct swaying ;
560 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the patient finds greater difficulty in running and hopping, climb-
ing stairs, stepping upon a stool, walking on a crack, walking
on a waxed floor, etc.; not unfrequently they complain of an
ageravation of all these troubles at evening, in the dark, or when
they shut theireyes. No material disturbance is as yet noticeable
in standing ;. only in standing with closed: eyes is there a slight
degree of swaying, the patient quickly grows uncomfortable, or
slight twitching movements of the anterior muscles of the leg may
set in. Standing on one foot grows very uncertain, and soon im-
possible. On lying down, however, all movements generally seem
as yet altogether quiet and secure, and are commonly also per-
formed without any material diminution in gross strength.
Soon, however, the disturbance reaches a higher grade; now
the movements of walking grow quite unsteady, excessive, and
are executed with a flinging motion; the toe of the foot is flung
forward and outward with a brisk motion, the heel is brought to
the ground with a stamp, the knee is held. as stiff as possible,
and generally the patient is seen to follow the movements of his
feet sharply with his eyes, his glance directed to the ground.
The gait is thereby rendered to a high degree shaky, insecure,
reeling, the steps quite uneven and jerky; the line pursued in
walking is irregularly zigzag.
The disturbance now also makes itself more distinctly notice-
able in standing; patients sway and: oscillate to and fro, espe-
cially if they are made to stand with their feet together; back-
ward movements of the legs and trunk disturb the equilibrium ;
that form of ataxy has been reached which Friedreich has of late
very appropriately designated as statie atazy, and has set up
over against locomotor ataxy. The former is made manifest dur-
ing the quiet fixation of the extremities or the trunk, such as is
required for the quiet stretching out of an arm, the quiet holding
up of a leg, or in sitting and standing ; the latter occurs during
the execution of movements of the trunk or extremities, and
represents a lighter grade of ataxy ; static ataxy appears only in
the later stages and in advanced disturbances.
But now, even movements performed when lying down, and
which are comparatively simple, also become distinctly ataxic,
and it is precisely the study of these movements which I consider
TABES DORSALIS. 561
as especially calculated to insure a correct insight into the true
essence of ataxic disturbances of motion. The patients are un-
able to touch an object held before them by means of a quiet and
uniform movement of the tip of the foot, but the line of motion
executed is an irregular, zigzag line; simple raising of the leg oc-
curs in a similar line, rendered irregular by brisk side movements ;
the leg which has been lifted falls back upon the bed at a point
more or less remote from its former position; instead of describing
a circle with the tip of the foot, as the patient intends to do, he de-
scribes quite an irregular figure with a zigzag outline; it thereby
becomes evident that the direction of movement in general is
retained, but that a straight or uniformly curved line has become
an irregular and zigzag line. Patients are unable to execute any
quiet and steady movements, and even the simplest motions are
executed in a jerky and abrupt manner. In many cases this
becomes much more distinct if the same movements are required
to be made with closed eyes; but this is only true when there is
a simultaneous disturbance of sensibility, especially when there
is muscular anesthesia; to the ataxy there is then added un-
certainty with regard to the direction and the degree of motion
required, which thereby becomes quite excessive and uncon-
trolled. In those cases, however, in which sensibility is entirely
intact, it is easy to demonstrate that the ataxy is either not at all
influenced by closing the eyes, or but very slightly increased.
And in all cases that are at all extreme it can be shown that the
most careful control on the part of the eyes is not capable of
doing away with the actual ataxy of motion.
In the highest grades of ataxy, finally, it becomes entirely
impossible for patients to stand or walk. The legs find no sup-
port, slip out in every direction ; left to themselves such persons
at once fall to the ground ; if they are allowed to make attempts
at standing or walking, supported on either side, their legs fly
around in the air, widely and confusedly, are thrown in this and
that direction by all kinds of irregular, paroxysmal movements
not subject to the control of the will, and are incapable of giving
the least support to the body. In wonderful contrast hereto,
even in these cases, is sometimes the strength with which certain
movements can be executed, and the energy with which limbs,
VOL. XIII.—36
Wi
562 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
which are utterly useless for standing or walking, can offer re-
sistance to attempts at passive motion. In spite of this, such
patients are utterly helpless and are condemned to a permanent
sitting or lying posture.
The ataxy is liable to appear much later in the upper extrem-
ities than in the lower ; it seldom attains such a high grade here,
and—on account of the different method of using the upper ex-
tremities—appears in a somewhat modified form. In the more
frequent typical cases of tabes, ataxy of the upper extremities
belongs to the more rare and certainly to the very late manifes-
tations ; just the contrary appears in those cases belonging to
the group described by Friedreich; in these, ataxy of the upper
extremities appears very soon after that of the lower, or almost
simultaneously therewith.
It manifests itself earliest in the innumerable more delicate
acts in which we use our hands: in writing, playing the piano, ty-
ing a cravat, buttoning clothing, drawing, cutting, etc. All these
movements become more and more uncertain, difficult, irregular,
the more so if they have to be carried out without the guidance
of the eyes. Ata later stage the simpler movements also become
impeded, irregular, ataxic; here, too, it again appears that the
disturbance consists essentially in the transformation of rectili-
near directions of movement into movement in irregular, zigzag
lines. If these patients are asked to touch an object held before
them, with the tip of one of their fingers, they will shoot past the
mark, and only reach it after repeated, irregular swaying to and
froin front of it. This is particularly marked if they are required
to hold their two forefingers at a considerable distance apart and
then bring them together with tolerable rapidity so that the two
tips shall touch one another; here the ataxy stands forth ina
striking manner. Not less characteristic is the disturbance of
co-ordination in reaching for an object held before them ; this is
only reached by a roundabout way and with jerky interruptions ;
at the moment when the fingers are about to reach it they are
Spread out again, and the whole act of grasping is performed in
an uncertain, blind sort of way; finally, in attempts to draw
figures in the air with the forefinger, a circle, numbers, a cross,
etc., the ataxy also stands forth very prominently—all the out-
TABES DORSALIS. 563
lines are irregular and zigzag. This, too, becomes more so on
closing the eyes, but only when disturbances of sensibility are |
present at the same time.
At a later period there may also be static ataxy in the upper
extremities, as it has been strikingly depicted by Friedreich.
Patients can no longer hold their arms still when stretched out
horizontally, without the occurrence of slight backward move-
ments of the same and of the hand; they can no longer exert
uniform pressure with their hands, etc.
In the highest grades, finally, the hands become entirely use-
less for all the acts of daily life; patients can no longer dress
themselves, can no longer carry a spoon or glass to their lips, they
can hold nothing—in short, they are as good as completely de-
prived of the use of their upper extremities, although here too,
as a rule, the muscles are still for a long time capable of a sur-
prising development of strength.
But the ataxy does not always confine itself to the extremi-
ties. Occasionally that harmonious working together of the mus-
cles of the trunk is also disturbed which is requisite for main-
taining the balance in standing and sitting, and the body makes
irregular swaying movements; ataxy of the muscles of the neck
disturbs the quiet position of the head, which falls into irregular
shaking and swaying. Thus inthe cases described by Friedreich.
The same observer has formerly, as well as recently again,
described disturbances of speech and of the movements of the
eyes which may, without forcing things at all, be regarded as
ataxic, and the existence of which has been established by Fried-
reich in a whole series of cases. The disturbance of speech be-
trays itself first as a somewhat indistinct pronunciation of
words ; afterwards in the form of an irregular, stuttering inter-
ruption of speech. It decidedly does not take the form of delib-
erate measured speech, for often whole sentences are uttered
rapidly and then there is a slight stuttering, and this is repeated
in quite an irregular manner, while at the same time the volun-
tary movements of the tongue and lips are apparently quite
undisturbed. In the highest grades this disturbance may be-
come so extreme that speech is almogt incomprehensible on ac-
count of the bad articulation.
564 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Ataxy shows itself in the movements of the eyes as a form of
nystagmus, which appears on attempting to fix the eye on an
object held at rest, or to follow a moving object; a nystagmus
which is independent of disturbances of vision and affections of
the refracting media, and which is entirely absent when the eye
is at rest and no attempt is made to fix it upon an object. The
greater and more numerous the movements requisite for fixing
the eye on and following an object of vision, the more distinct
and pronounced will be the appearance of the nystagmus, in the
form of twitching movements of the eyeball, which do not fol-
low one another with the rapidity of these movements in ordi-
nary nystagmus, and which take place principally in the trans-
verse direction, but occasionally also in every other direction.
We cannot but concur entirely in Friedreich’s designation of
these movements as being ataxic; they differ from the move-
ments of ordinary nystagmus partly by their being independent
of diseases of the eye, partly by the fact of their following one
another with less rapidity, and partly in their occurrence exclu-
sively during movements of fixation.
The occurrence of these ataxic disturbances in the cranial
nerves certainly constitutes one of the greatest rarities in the
clinical picture of tabes; as far as our knowledge goes, thus far,
it appears to be confined to the peculiar cases of sclerosis of the
posterior columns described by Friedreich, and which will be
given more fully farther on. In the typical forms of tabes these
disturbances seem to occur rarely or never, in characteristic con-
trast to the conditions obtaining in multiple sclerosis, as set forth
in a previous section.
But little is known with regard to ataxy in the domain of the
other cranial nerves, especially the facial nerve, in tabes. In
some few cases grimacing movements of the face have been ob-
served. But at all events these are amongst the greatest rarities.
After the description given above, and if one has once care-
fully observed a series of tabes cases, it will not be easy to con-
found ataxy with any other disturbance of motion. Nevertheless
in some instances difficulties may arise. Some cases of chorea,
in particular, may easily be mistaken therefor, and yet this is
only because superficial observation sometimes reveals a remote
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TABES DORSALIS. 565
similarity between the two forms of motor disturbance. For
more accurate observation at once shows striking differences
between them. Let any one read the admirable description of
choreic movements given by von Ziemssen (this Cyclopedia, V ol.
XII.), and he will not doubt for a moment that it is here by no
means a question of ataxy, but true cramp. Friedreich has
again recently drawn a sharp line of distinction between the two
forms of motor disturbance: ataxy appears only during volun-
tary movements, and ceases during rest ; choreic twitchings con-
tinue also during complete rest of the body, and they only
incidentally disturb the otherwise quite well co-ordinated volun-
tary movements; choreic twitchings almost always affect also
the face and the tongue, ataxic disturbance does this but seldom,
and then only in a subordinate manner. We would add that in
ataxy a certain definite movement (taking hold of things, walk-
ing, etc.), whenever it is repeated, is always disturbed in about
the same way, while choreic twitchings have something entirely
accidental and irregular about them, and form a picture of motor
disturbance of a constantly and strikingly changeable type. Of
course, the other accompanying manifestations would also not
readily permit us to confound ataxy with chorea.
Nor will ataxy be easily mistaken for the tremor of multiple
sclerosis to which we have already explicitly referred (page 100).
In this tremor there are regular oscillations in the line of move-
ment ; in ataxy there are quite irregular zigzag movements, which
by no means make the impression of a tremor. Still, it must not
be forgotten that both disturbances may occur alongside of one
another, as is, indeed, not rarely the case in multiple sclerosis.
Less likely yet is ataxy to be confounded with the tremor of
paralysis agitans. The very manner of this tremor, which
moves in very small oscillations, positively forbids this mistake.
Added to this is the fact that the patient afflicted with paralysis
agitans can, for a very long time, still execute voluntary move-
ments with great precision and without trembling, while ataxy
only arises during voluntary movements, and is absent during
rest.
The appearance of ataxy almost always occurs at a period of
time more or less removed from the beginning of the disease,
566 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
after having been preceded by the symptoms of the initial period
for months and years, sometimes many years. Indeed, we are
ordinarily accustomed to reckon the beginning of the second
stage from the time of the appearance of ataxy. Still, this varies
in different cases; the disturbance arises with very varying rapid-
ity, and ataxy may even figure among the earliest symptoms, or
even be the first and for a long time the only symptom of the
disease, as in several cases described by Friedreich. But for the
ordinary typical cases the rule holds good that ataxy does not
appear until after various initial symptoms have existed for
months or even for years. It must still be regarded as question-
able whether the cases of ‘‘acute ataxy,” described by a num-
ber of observers, or those ataxic disturbances observed after acute
diseases (diphtheria, typhus, variola, etc.), and which are gener-
ally developed with striking rapidity, are really to be accounted
as true tabes.
Great difficulty has for a long time been experienced in arriy-
ing at a pathogenetic explanation of the symptom of ataxy.
Innumerable attempts at an explanation have been set up, the
most various hypotheses have been defended with more or less
of spirit and of good fortune, and discussions with regard to the
**theory of tabes”’ have hinged only too much on the theory of
the symptom, ‘‘ataxy.’ It would lead us much too far to enter
into a full discussion and explanation of these interesting points
of dispute.
We have already at a previous place (p. 83 et seq.) entered
somewhat minutely into this question, and have endeavored
to make clear the method of origin of spinal ataxy. After ma-
turely weighing the various views, we came to the conclusion,
based upon the facts thus far ascertained and supported by nu-
merous investigations of our own, that the ataxy, in tabes, can by
no means be made dependent upon the disturbance of sensibility
which may happen to coexist, but that it must rather depend
upon a disturbance of co-ordinatory tracts lying within the
spinal cord ; that it is therefore a ‘‘motor”’ ataxy.
To-day we have but little to add to the explanations there
given, and we have nothing to take back of the views there ex-
pressed, in spite of the explicit defence which has, in the mean-
TABES DORSALIS. 567
time, been put forth by Leyden, whereby he endeavors to uphold
his former theory. On the contrary, we are only confirmed in
our opinion by renewed study of the literature of the subject and
accurate observation of new cases, so that we have no doubt that
the ataxy in tabes is not at all, or at least in but a very unim-
portant manner, influenced by the disturbance of sensibility.
In the meantime Friedreich has also opened up the question
anew in a thorough and admirable work, has refuted Leyden’s
view, and has thoroughly fortified his own opinion, which is to the
effect that the immediate cause of ataxy does not lie in a disturb-
ance of sensibility, but that it must rest upon a disturbance of
co-ordinatory tracts within the spinal cord.
It only remains for us here to introduce to the reader a few of
the most prominent advocates of different views, so as briefly to
render him familiar with the various attempts a: the explanation
of ataxy. In so doing, we can only permit ourselves a very brief
criticism of the same.
A whole group of authors, being led thereto by the anatomical conditions found,
which in the main show disease of the posterior roots and the posterior columns,
and by the physiological investigations which assign to these parts only sensitive
functions, or at least only the function of:centripetal conduction, seek the causes of
ataxy in a disturbance of the sensitive functions, or at least in a disturbance of the
centripetal excitation which is conducted through the posterior roots.
A part of these authors seek the causes of ataxy, independently of the disturb-
ances of conscious sensation, in a disturbance of the reflex activity within the spinal
cord. Thus, according to Jaccoud, the ataxy depends in part upon a disturbance
of the cutaneous and muscular sensibility, and represents an anomaly of spinal
motor irradiation and of spinal reflex action.
According to Carré, ataxy is independent of conscious sensibility, but depend-
ent upon disturbances of reflex activity, upon conscious sensibility.
Cyon regards co-ordination as taking place through a reflex process within the
spinal cord; disturbances of this reflex process call forth ataxy. The diminution
in the excitation which is conducted through the posterior roots causes a sinking
in the excitability of the motor nerves, and thus calls forth irregular, flinging, ex-
cessive movements, because the patient applies too strong impulses of the will.
Benedict set up a theory of his own, on the basis of certain experiments of Har-
less, the correctness of which has with justice been challenged. MHarless found,
namely, that section of the posterior roots lowered the excitability of the mixed
nerves belonging thereto, as he believes through the loss of a centripetal excitation,
which is conducted through the posterior roots. According to Benedict, the ataxy
now takes place through the failure of the regulating influence of the spinal cord,
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568 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
which is exercised upon the periphery through the medium of the posterior roots.
He considers the ataxy as independent of the perception of peripheral sensitive ex-
citation.
Great doubt is thrown upon all these views, first, by the opinion established by
Goltz and others, that the centres for the co-ordination of movements, for the main-
tenance of the equilibrium and the locomotion of the body, do not lie in the spinal
cord at all, but higher up. To be sure it may be conceded that the proof of this
opinion, at least with regard to the human spinal cord, is not entirely conclusive ;
at the same time it is to a high degree probable that the actual processes of co-
ordination, which regulate voluntary activity, do not take place in the spinal cord
at all. If the spinal cord were really possessed of the co-ordinatory functions
ascribed to it, then—as was correctly urged against the views of Jaccoud--a de-
capitated animal ought to be able to stand, or, having once been started in walking,
ought to be able to walk further.
The experiments of Cyon, however, are out and out irreconcilable with the
reflex theory, and thus this author has himself refuted his own views. He has
shown that section of the posterior roots (which are supposed to have caused these
reflex manifestations) causes no interference with ordinary movements (jumping,
hopping, swimming, etc.), or at most interferes only with the most complicated
movements, for the explanation of which the simultaneous disturbance of sensi-
bility undoubtedly suffices. But we must certainly agree with the authors here
cited in the opinion that conscious sensation, or the disturbance of its tracts, cannot
possibly have anything to do with the ataxy. But the recently discovered fact of
the apparently almost constant failure of+the reflex action of the tendons in ataxy —
at least leaves the remote possibility open that disturbances of certain reflex tracts
in the spinal cord, which act in an entirely unknown way in the co-ordination of
movements, may have a relation to the ataxic disturbances of motion. This might
be more carefully investigated in the future.
The view advanced by Leyden originally regarded the disturbances of conscious
sensibility as the essential cause of the disturbance of co-ordination, and Leyden
has taken much pains to demonstrate the disturbances of conscious sensibility in
all patients, and asserts that these always exist to a degree about corresponding to
the degree of ataxy. He therefore also attaches the greatest value to the careful |
examination of conscious sensibility. Almost all other authors have expressed
themselves as opposed to this significance of conscious sensibility, and so of late
Leyden himself also admits that it is not conscious sensibility that lies at the foun-
dation of these co-ordinatory functions, but that probably these unconscious cen-
tripetal excitations within the spinal cord are conducted through the same tracts
as the conscious sensations.
Leyden has most recently defended his theory over against the exceptions taken
thereto, and expresses himself to the effect that, even though the question of the
origin of ataxy through disease of the posterior columns be not satisfactorily re-
solved, the cause of ataxy is to be sought in the loss of the connections leading in a
centripetal direction between the periphery and the centre of co-ordination.
eae
TABES DORSALIS. 569
We must admit that Leyden’s view has something seductive about it, and that
the way in which he has sought to refer the ataxic disturbance of locomotion back
to a disturbance of the muscular sense appears to us quite plausible. We would
also accept this theory without hesitation if a whole series of well-established facts
did not exist which make this doctrine a logical impossibility. We have already
adduced these facts at another point, and have drawn the conclusions resulting
from them. We can furthermore refer to the new work of Friedreich, which
brings forward such facts in still greater completeness, and radically refutes the
deductions of Leyden. We may here perhaps add the cases of Trousseau and
Bourdon, in which there was distinct ataxy with no anesthesia of the skin or
muscles; then a case of Ebstein’s’ in which there was sclerosis of the posterior
columns accompanied by a high degree of ataxy without any disturbances of sensi-
bility ; finally a case of Engesser’s,? from Kussmaul’s clinic, in which muscular
feeling was extinguished, cutaneous sensibility diminished, and Romberg’s symp-
tom present, without any trace of ataxy.
We must attach special value to the newer cases of Friedreich (which we were
able, in part, to examine ourselves) in which exhaustive tests of sensibility, applied
in all directions, showed no trace of disturbance of cutaneous or muscular sensi-
bility, although a high degree of ataxy existed. When Leyden seeks to weaken
the force of these cases by saying that they appear to him to deviate from the usual
type of tabes, and are, therefore, ‘‘ not directly to be credited to his theory,” we
can only reply that, from the standpoint of scientific logic, it appears to us, in such
a dilemma, where well-established and undoubted facts will not fit a theory, much
more correct to let the theory fall, than, for the sake of the theory, te reject the
facts as inapplicable.
In like manner we cannot accept the rejection, proposed by Leyden, of the case
of Spaeth and Schueppel (page 89). We do not see why “the turning to any
theoretical account of so exceptional a case” should be “impossible.” When
such a case has been so accurately and repeatedly investigated, and that with special
reference to Leyden’s theory, it can surely be turned to account, even if it should
throw the highest degree of doubt upon that theory. And when Leyden adduces,
as the main argument against this case, that we might just as well conclude there-
from that disease of the posterior columns has nothing to do with ataxy, we must
confess that this conclusion does not appear to us by any means so absurd, and that
this very case of Spaeth and Schueppel furnishes one of the grounds on which we
advocate the possibility, and perhaps probability, that the co-ordinatory tracts may
not lie in the posterior columns themselves, but only in their neighborhood.
At all events, it would require new, well-confirmed, and unequivocal facts to
make the theory of Leyden tenable; it can, in our opinion, simply not be main-
tained on the basis of the facts and observations now known. The disturbance of
sensibility, as far as it has been possible thus far to investigate and confirm it, can-
1 Deutsches Archiv f. klin, Med. X. p. 595.
?Ibidem. XVII. p. 577.
570 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
not have anything essential to do with the ataxy; it may perhaps have some influ.
ence in determining the form of the ataxic manifestations, but probably has none in
producing them. The ataxic movements, in walking, for instance, may indeed be
somewhat modified in their method of appearance, and perhaps increased, by the
disturbance of sensibility, but they cannot be called forth by this alone.
It is possible that the testing of ‘‘ unconscious” sensibility, of reflex action, and
especially the more careful following up of the reflex action of the tendons, may
afford some new fixed points for this theory. This remains to be seen. ButI can
already state, on the ground of some cases quite recently observed, that the failure
of reflex action of the tendons probably also does not stand in any constant causal
relation to ataxy. I have seen two cases in which there was undoubted ataxy with
distinct increase in the reflex action of tendons, and one case of ataxy with fail-
ure of the reflex action of tendons (after diphtheria) ; this latter symptom persisted
after the ataxy had long since disappeared.
For the present we consider those theories admissible which make the ataxy de-
pendent on a disturbance of the apparatuses of co-ordination themselves.
It is out of the question to suppose that we are dealing with a disturbance of
centres of co-ordination lying outside of the spinal cord, as was taught by the theo-
ries of Duchenne and Eisenmann. In tabes we have undoubtedly to deal with an
affection of the spinal cord ; the ataxy can, therefore, hardly be made to depend on
a disturbance of the cerebellum—if, indeed, the centre of co-ordination lies there.
Finkelnburg considers the explanation of ataxy by a disturbance of sensibility
as entirely untenable; according to him, it is a question of an immediate disturb-
ance of the power properly to co-ordinate muscular movements.
Topinard likewise denies that motor weakness or cutaneous or muscular anes-
thesia has any influence on ataxy; he considers the rather that this takes place by
a disturbance of the co-ordinating function of the spinal cord, which he looks upon
as a reflex power. His opinion is open to the same objection as all reflex theories. ©
Spaeth says: Ataxy can only be explained by the disturbance of some definite
apparatus which, under normal conditions, presides over the function of the co-or-
dination of motion. This apparatus would seem to have to be sought in part in the
gray substance of the spinal cord. Spaeth, like Topinard, wrote at a time when
the situation of the centres of co-ordination outside of the spinal cord was not yet
demonstrated.
Friedreich’s opinion is to the effect that ataxy is caused by a disturbance of
those tracts in the spinal cord which conduct the influence of the centre of co-ordina-
tion (which is to be sought outside of the cord) to the motor nerves. These tracts
lie in the posterior columns.
Our own view, already expressed above, is also to the effect that ataxy depends
on a disturbance of co-ordinatory tracts lying within the spinal cord, and leading
in a centrifugal direction.
We are therefore forced to the conclusion that there must be
co-ordinating tracts in the spinal cord, tracts which maintain the
— 7
SO
TABES DORSALIS. 571
communication between the centres of co-ordination and the
peripheral motor nerves, and that ataxy can be explained only
through a disturbance of these tracts. The question of where
these tracts lie naturally obtrudes itself. Naturally, we first
think of the posterior columns. But there are some objections
to this view. One is, that cases of extensive degeneration of the
posterior columns have been observed without any ataxy ; an-
other argument against it is the Spaeth and Schueppel case ;
another is perhaps the so frequent involvement of the gray mat-
ter and of the lateral columns in the later stages of tabes. We
would therefore not regard the question as decided with entire
certainty ; we have already previously expressed ourselves on
this question (page 95), and have scarcely anything to add to
what was said there. Ought not, in the future, more attention,
perhaps, to be given to the ‘‘direct tracts from the cerebellum
to the lateral columns” which have been studied by Flechsig ?
At all events, many questions here remain to be solved by future
investigation.
The fact of swaying on closing the eyes, previously referred —
to, has been regarded as having various different relations to
ataxy, and as being a sign that ataxy was increased by closing
the eyes. We have already previously shown that this is not
correct. In fact, there are numerous instances where the sway-
ing is present long before ataxy arises; and others in which,
while the ataxy is great, closing the eyes causes no increase in
the swaying ; in these latter there are no disturbances of sensi-
bility. Therefore this symptom, which, it is true, is seldom
absent, remains chiefly as the sign of the existence of disturb-
ances of sensibility, especially of the disturbance of muscular
sense. If, nevertheless, in some patients suffering from tabes,
there is a slight increase of ataxy on closing their eyes, this only
proves that a moderating and directing influence can be exer-
cised over the disturbance through the sense of sight, after the
withdrawal of which the disturbance stands forth in its true
magnitude.
Among the remaining motor disturbances the first that de-
serves notice is the motor weakness,which may afterwards in-
crease to complete paralysis. Asarule, the ‘‘complete retention
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572 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
of gross motor power’’ does not go very far. There are, indeed,
individual instances, in which the ataxy is also liable to be espe-
cially well marked, in which the patients are capable of an ap-
parently quite normal and even unusual development of strength,
offering exceedingly energetic resistance to passive movements,
and executing all single movements with great power. But
these cases do not constitute the rule, and in many of them there
will at least be found a distinct diminution in the power of en-
durance (Ausdauer) of motor efforts. Just this very diminution
in the power of endurance of movements belongs to the earliest
and most marked symptoms of tabes; and the lively feeling of
fatigue in such patients appears to stand in some relation thereto.
But in the great majority of tabes patients, and especially in
the typical ones, a distinct diminution of motor power can early
be demonstrated. Topinard already observed this, and Cyon
claims to have found this motor weakness in almost all tabes
patients. My own observations agree therewith in so far as that
very distinct motor paresis is to be demonstrated in at least one-
half of all cases. Here and there I have also observed transitory
paralysis in the domain of single nerves—for instance, the pero-
neal—but this is very rare. Pierret most recently pronounces
these partial and temporary paralyses in the extremities as a
very common appearance in tabes, and seeks, by these alone, to
explain the disturbance of co-ordination. But we must await a
more accurate confirmation of this theory of ataxy.
In the later and latest stages, however, true paralysis seldom
fails ; the legs grow heavier and heavier, finally, more or less com-
pletely paralyzed, they emaciate, contractures set in, etc. With
the appearance of paralytic symptoms the ataxic manifestations
naturally fall more and more into the background, and finally
disappear altogether.
It is in the highest degree probable that these last symptoms
—paralysis, with contractures—are to be referred to a final spread
of the anatomical process to the lateral columns. Whether the
earliest symptoms of motor weakness and exhaustion can also be
explained in the same manner, may still be a matter of doubt ;
at the same time, in the present state of our knowledge, we are
quite inclined to the idea that, wherever distinct manifestations
TABES DORSALIS. 573
of motor weakness are present, there is some, even though but
slight, involvement of the lateral columns or the gray substance.
This, however, can only be decided by further investigations.
In tabes there is but very little to be seen in the way of mani-
Sestations of motor irritation. Here and there, particularly in
the earlier stages of the disease, slight jerking contractions may
be observed, spasms of single muscles, occasionally also fibrillar
contractions. Not unfrequently there are also stronger twitch-
ings of entire extremities, and the like; but these occur almost
always only in connection with lancinating pains, and, therefore,
are doubtless to be regarded as reflex.
There is an entire absence of only so-called muscular tension
in all genuine and typical cases; the limbs are limp, easily mova-
ble, and do not offer the slightest resistance to passive move-
ments.
On the other hand, in the later stages, muscular tension and
contractures may also arise, with the true paralysis, and may
finally reach so high a grade that the limbs remain immovable in
the position of extension or flexion, as they do in the later stages
of multiple sclerosis or of chronic myelitis.
The statements of authors differ much with regard to the re-
lations of electrical excitability in tabes. This is sometimes
said to be heightened, sometimes normal, sometimes lowered.
The truth probably is, in other words, that the conditions of
electrical excitability vary in different stages of the disease.
In my own examinations—and I pay no regard to any that
are not made by my own method, which alone is applicable in
such cases—I found the faradic and galvanic excitability, ina
whole series of cases, to be quite normal in respect both to
quality and to quantity. |
In another series of cases I found a distinct, even though but
slight increase in the faradic and galvanic excitability in the
domain of the peroneal nerves, without any qualitative altera-
tions.
And finally, in still another group of cases, I found a more
or less distinct diminution of electrical excitability in the domain’
of the peroneal nerves, likewise withdut qualitative changes.
On the whole, I have received the impression that in the
574 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
earlier stages of tabes there is rather an increase, in the later
stages rather a diminution, of electrical excitability to be demon-
strated. In one case I observed this directly, finding the electri-
cal excitability at first materially increased, and afterwards di-
minished. Still, in view of the small amount of material before
us, and the very variable intensity in the course of the disease,
it is difficult to arrive at a definite conclusion with regard to
these relations.
I have thus far not found any qualitative changes of the gal-
vanic excitability in the domain of the peroneal (anomalies of
the law of twitching [Zuckungsgesetz]); in particular have I
never been able, in spite of careful search, to confirm what is
claimed with regard to the existence of a greater tendency to
twitchings at the opening of the circuit. Only in one case was
I able to demonstrate, in the region of the ulnar, the occurrence
of the AnSZ before the KaSZ, and a preponderance of the former
over the latter, with low powers of the current.
Certainly, in the present situation of affairs, there is no great
advantage to be gained, in the diagnosis or prognosis of tabes,
from electrical examinations; we will therefore give no further
time to the subject.
Disturbances of Reflex Action.
These have hitherto, it appears to us, received perhaps too
little attention; in most histories of cases statements on this
subject are very incomplete or are altogether wanting.
So far as the reflex action of the skin is concerned, it presents
no sort of constant or essential anomalies. According .to my
own observations it appears to present no considerable deviations
from the normal ; that is to say, reflex action is generally present,
more or less well marked, sometimes very active, sometimes hard
to call forth. Ihave but very rarely found it absent; still it is
known that this may be the case, even in health. In future these
conditions should be more carefully observed, and it might per-
haps be desirable in all cases more accurately to test the reflex
action originating in the sole of the foot, that of the cremaster
TABES DORSALIS. 575
muscle originating from the inner surface of the thigh, and that
originating from the skin of the abdomen.
Since writing the above I have carefully tested the reflex action of the skin, in
this respect, in eight typical cases of tabes. In all of them the reflex action of the
tendons was completely extinguished. Reflex action of the skin was retained in all
of them, though in a very varying degree in different individuals. Sometimes the
plantar reflex was very active, sometimes the cremaster and the abdominal reflexes
were more marked, but in no case was there an absence of all the skin reflexes at
once. No definite relation was found to exist between the reflex action of the skin
and the degree of ataxy present, nor did the former bear any relation to the degree
of disturbance of sensibility present. I have thus far merely received the impression
that the reflex action of the skin behaves the same in persons with tabes as in those
who are well, the latter also reacting with very variable degrees of intensity to
cutaneous irritants capable of producing reflex action. Further investigations on
this point are to be desired.
The condition of reflex action of the tendons, on the con-
trary, is very remarkable in tabes, and probably also very im-
portant. Westphal’ first called attention to the entire absence
of the reflex action of tendons in tabes. Since then I have
always paid attention to this symptom, and can fully confirm
Westphal’s statements. In all typical and well-developed cases
of tabes the reflex action of the tendons is entirely wanting, even
though reflex action of the skin may be present and even in-
creased. In only one case which I count as tabes, but in which
there was, as yet, no ataxy, but only some initial symptoms,
could the presence of reflex action of the tendons of the patella
be demonstrated. Wherever the case had advanced to the de-
velopment of ataxy, or even to slight indications of the same,
reflex action of the tendons was entirely lost.
It would, of course, be in the highest degree interesting to
know more accurately when reflex action of the tendons is ex-
tinguished—whether it disappears before or after the occurrence
of ataxy, whether it disappears in the initial stage already, and
thus to be able to establish the early diagnosis of tabes and the
like. I have thus far labored in vain to clear up these questions.
They require years of observation of single cases, or very favor-
1 Arch. f, Psych. u. Nervenkrankheiten. V. p. 819.
>
576 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
able accidental circumstances. This matter is therefore com-
mended to the study of our professional brethren.
At all events, the great constancy of this symptom lends it a
high diagnostic significance. It certainly stands in no demon-
strable relation to cutaneous or muscular sensibility, nor to the
reflex action of the skin. I have seen the reflex action of tendons
fail when the cutaneous and muscular sensibility were entirely
intact and when they were greatly diminished, when the reflex
action of the skin was normal, raised, or lowered. This symp-
tom, therefore, seems to be entitled to a certain isolation in the
symptom-picture of tabes. At the same time there are compli-
cated cases—and we shall return to this again under the head of
Spasmodic Spinal Paralysis—in which, together with ataxy and
other symptoms of tabes, an increase in the reflex action of ten-
dons shows itself, together with other manifestations of spas-
modic spinal paralysis. These are certainly not typical cases of
tabes, and they constitute well-characterized exceptions.
Disturbances of the Organs of Special Sense.
We would mention, first, the paralyses of the muscles of the
eye, which play a not unimportant rdéle in the clinical picture of
tabes. |
They most frequently affect the motor oculi and abducens,
far less frequently the trochlear nerve, and manifest themselves
by the corresponding disturbances of binocular vision, diplopia,
strabismus, dizziness, etc. von Graefe calls attention to the fact
that tabes patients who are suffering from diplopia show a strik-
ingly small tendency to the blending of images in binocular
vision, which is supposed to point towards a central origin of the
affection.
These paralyses may arise quite transitorily, lasting, with
varying intensity, for a couple of days, weeks, or months, then
disappearing, and returning again after a longer or shorter time ;
in the later stages of the disease, however, permanent paralyses
of the muscles of the eye doubtless also occur.
Not infrequently disturbances of accommodation also take
place, pareses of the same, and alterations in the pupils. The
TABES DORSALIS. 577
latter are sometimes contracted or dilated on one side; but more
frequently there is a bilateral, uniform, generally pretty con-
siderable contraction of the pupils, which presents the characters
of spinal myosis; that is, the pupils do noé react to the stimulus
of light, but do still react distinctly to accommodative impulses
(Arg. Robertson, Knapp, Leber, Hempel). This condition is gen-
erally permanent.
The occurrence of all these changes in the muscles of the eye
is by no means rare in tabes. If we embrace them all in our
estimate, including the slight and. transitory disturbances, the
differences in the pupils, the spinal myosis, then we shall be
able to establish the existence of such changes in more than one-
half of all cases. The more prolonged and permanent disturb-
ances, on the contrary, may probably not arise in more than
one-third to one-fifth of all cases.
The transitory disturbances occur with special frequency in
the initial stage of tabes, and are to some degree characteristic of
the same, although by no means as constant as Duchenne at first
stated. But paresis of the ocular muscles may arise in every
stage of tabes, and it is just the severer forms of the same which
generally appear only in the well-pronounced disease.
In a pathogenetic point of view, the most important item, as
influencing these changes, is doubtless the disease of those fibres
of the ocular nerves which run together in the medulla oblon-
gata. Probably slight diseases of the nerve-tracts here situated,
and of their nuclei, are to be looked upon as the causes of paresis.
Still, such diseases have not hitherto been anatomically demon-
strated ; neither has any direct connection with the degeneration
of the posterior columns been thus far established, either ana-
tomically or physiologically. Pierret declares these paretic dis-
turbances of the muscles of the eye (as well as of the muscles
of the face and of mastication, which sometimes occur) to be
dependent on primary irritation or disturbance in the tract of
the trigeminus, which participates in the disease in a manner
quite analogous to that of the posterior spinal nerve-roots, and’
he regards them, therefore, as paralyses of sensitive origin (reflex:
paralysis, etc.). The idea that, particularly in prodromal diplo-
pia, it is a question of rheumatic paralysis of the muscles of the
VOL. XIII.—87
578 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
eye, consequent on taking cold, will find but little support. The
changes in the pupils would, first of all, suggest the involvement
of the cilio-spinal centre and the oculo-pupillar tracts emanating
therefrom and lying within the cervical portion of the cord ; but
here, too, we are thus far without the support of any anatomical
proof.
The nystagmus observed by Friedreich in a series of cases,
and more accurately described by him, is a peculiar, but, on the
whole, a very rare disturbance of the muscles of the eye. This
is always a bilateral nystagmus, which follows partly a horizon-
tal, partly a vertical, or probably also a diagonal direction,
which does not occur during rest, but does occur at every
attempt to fix the eye. If an object is moved in various direc-
tions in the field of vision, irregular, jerky twitching of the ball
of the eye takes place, being all the more prominent the more
the object is approximated to the outer limits of the field of
vision. In the higher grades of the trouble, nystagmus also
occurs when the eyes are fixed upon an object held at rest, but —
even then it is absent when the glance is quiet and not fixed.
The movements are slower and less regular than in the ordinary
nystagmus, dependent only upon disease of the eye, and are
principally to be distinguished from the latter by the fact that
they only arise on voluntarily moving the eye or fixing the
glance. Friedreich is undoubtedly right in considering this
nystagmus as a form of ataxy of the movements of the eye, and
in setting it up as ataxic nystagmus, over against the ordinary
form of the disease.
Friedreich seeks the cause of this nystagmus in a disturbance
of the co-ordinatory tracts which lead from the centres of co-or-
dination to the nuclei of the nerves of the ocular muscles lying
on the floor of the fourth ventricle, and declares himself to be
of the opinion that nystagmus does not arise in spinal disease
until the medulla oblongata is involved. This proposition also
still lacks anatomical proof in tabes. Pierret explains these
phenomena also on the ground of the primary disease of the
sensitive root-tracts of the trigeminus in the medulla oblongata.
The occurrence of ataxic nystagmus is rare in tabes, and has
thus far only been observed by Friedreich in five of the nine
TABES DORSALIS. 579
peculiar cases described by him. It belongs to the later symp-
toms, and becomes associated with the other ataxic manifesta-
tions only after the disease has existed for a number of years
(five to twenty-one).
But the atrophy of the optic nerve, which is unfortunately
very frequent in tabes, is of much more importance than the dis-
turbances of the visual apparatus thus far considered, and is
much harder for the patient toendure. It belongs to the saddest
complications of this already melancholy disease ; the helpless-
ness caused by the ataxy is aggravated beyond all measure by
the blindness added thereto, and the sources from which the
patients can obtain comfort and oblivion amid their suffering
are materially diminished.
The trouble begins with slowly or rapidly advancing diminu-
tion in the sharpness of vision, which soon increases to amblyo-
pia, and finally to amaurosis. The field of vision, which is at
first slightly veiled and cloudy, becomes increasingly narrowed,
generally from without inward, sometimes from without and
above, sometimes more from below. Examination shows that
this narrowing of the field of vision does not take place.in a
uniform manner, but with entering angles. Finally, the blind
area involves all but a spot towards the inside, which allows the
patient but a limited and insufficient amount of vision.
Color blindness can usually be demonstrated in. patients be-
fore any limitation in the field of vision. Generally the percep-
tion of green is lost first, then that of red, finally that of yellow
and blue; still, deviations from this order are not excluded.
In such cases the pupils are frequently contracted rather than
dilated ; their reaction to light entirely suspended. In the ear-
lier stage many patients show an increased sensitiveness to
bright light, and therefore see somewhat better in the wee
than in bright daylight.
Ophthalmoscopic examination reveals the signs of so- called
white atrophy of the optic nerve. At first there is a slight gray-
ish discoloration of the papilla, which gradually grows paler
and finally appears quite white and sharply outlined. The arte-
ries at the same time show a progressive narrowing, but other-
wise the retina remains quite unaltered. These changes are
580 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
easily to be distinguished from the ophthalmoscopic picture of
neuritis optica and congested papilla, and according to French
authors they are so characteristic that the existence or the ap-
proach of tabes can be recognized from them alone.
Atrophy. of the optic nerve in tabes is always—with quite
rare exceptions—a decidedly progressive malady, and leads with-
out interruption to complete amaurosis. In different cases, it is
true, this occurs with very variable rapidity ; sometimes it re-
quires only weeks, sometimes months, or even years, for its ac-
complishment. Occasionally the malady comes to a stand-still,
even after it has lasted for a comparatively long time. Some-
times the trouble is limited for a considerable time to one eye,
but it is far more common for both to be attacked and to become
blind simultaneously or within a short time. Modifications be-
tween these two extremes are of course manifold.
Atrophy of the optic nerve belongs to the more frequent of
the complications of tabes, but we have no accurate statistics as
to its frequency. The statements of ophthalmologists are per-
haps generally too high. I myself have seen it but eight times
among about seventy cases. Topinard, on the contrary, gives
‘*¢ disturbances of vision’’ in 49 cases out of 102. Cyon, in 203
cases, finds 60 of amblyopia and amaurosis. More accurate
statistics on this subject are to be desired.
Very commonly atrophy of the optic nerve arises in the initial
stage of tabes; it may even be the first manifestation of the
disease, and may, for a longer or shorter period, precede the
lancinating pains and the other symptoms. The amaurosis
caused thereby may even exist for years (up to ten years, Char-
cot) before other symptoms of tabes are added thereto.
The immediate cause of the amaurosis of tabes is, of course,
the gray degeneration of the optic nerves, a typical gray degen-
eration entirely analogous to the changes in the spinal cord, and
one which we have learned to know more accurately through the
labors of Leber. The disease begins at the periphery of the
trunk of the optic nerve and attacks the most central fibres of the
same last. It always begins on the trunk of the optic nerve itself,
in the divisions nearest to the eye, and spreads from here to--
wards the centre to the optic tract, in rare cases also to the
TABES DORSALIS. 581
tubercula quadrigemina. The narrowing of the field of vision
and the method of its development would alone enable us to
decide with certainty that the change always begins in the trunk
of the nerve and not in the tractus opticus (Foerster.)
What connection is there between this degeneration of the
optic nerve and the sclerosis of the posterior columns? Probably
there is no direct connection, for no anatomical continuity can in
any way be demonstrated between the process in the optic nerve
and that in the posterior columns. The idea which naturally sug-
gests itself, that the disease in the posterior columns of the cord
might interfere with trophic influences exerted on the optic nerves
and thus cause their gray degeneration, can also hardly be main-
tained in the face of the fact that atrophy of the optic nerve often
for a long time precedes all manifestations of the spinal disease,
Consequently for the present there is not much of anything
better left for us than the conclusion that gray degeneration ‘‘ is
developed simultaneously or successively at various points in
the central nervous system especially predisposed thereto”’ (Foer-
ster.)
Disturbances of hearing very rarely arise in tabes. Imper-
fect hearing has indeed been observed here and there (Leyden,
Remak, Vossius), but in the majority of instances it was doubt-
less due to an accidental concurrence of two diseases, each
frequent enough in itself. This accidental character of the deaf-
ness in tabes has been especially demonstrated by Lucae’ in two
cases. But it seems probable, from a case observed by me, that
tabes may also be accompanied by purely or principally nervous
deafness, which probably depends on atrophy of the auditory
nerve and is thus analogous to atrophy of the optic.
The case was that of a Russian naval officer, who for some years had suffered
from the manifestations of a somewhat complicated tabes. During the initial stage
of the same, besides psychical disturbances, occasional headaches and deaj‘ness had
arisen, the latter gradually increasing. When I first saw him the patient was suf-
fering with moderate ataxy of the legs, with swaying on closing his eyes, was very
easily fatigued, had a sense of numbness in his feet, slight weakness of the bladder,
etc. My colleague, Prof. Moos, had the goodness to examine the organ of hearing
1 Tucae, Ueber Schwerhirigkeit bei grauer Degeneration des R.-M. Verh. d. Berl.
med. Gesellsch. Bd. I. 8. 127, 1866, *
582 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
more accurately, and to communicate to me the following results: July 2ist, 1873.
‘‘On both sides hyperemia of the handle of the malleus, and slight cloudiness of
the mucous membrane. Right ear: the tuning-fork could not be heard, either in
the air or by conduction through the bones; hearing of Appeg null, A watch of
_thirty feet hearing distance heard only on pressure. Left ear: C' and C" [tuning-
forks] not heard at all through the cranial bones, and but feebly through the air;
from a upward | the vibrations are heard both through the cranial bones and by
way of the air. High tones can be heard through the air at a distance of seven
paces. With the watch, H. D. = two inches; conduction through cranial bones
very good; spoken words understood at a distance of four feet.” There was,
therefore, probably atrophy of certain fibres of the auditory nerve. On the 7th of
August, 1873, Prof. Moos reports: “‘ Right ear: C’ not heard; C” heard; a also
heard through the air; no conduction through cranial bones; watch heard a dis-
tance of two inches; words distinguished at a distance of one foot. Left ear:
tuning-forks of a low pitch are now heard through the cranial bones, as well as
through the air; high tones are heard through the air at a distance of ten or twelve
paces; watch, eight inches; spoken words, six paces.”
Appreciable improvement had therefore followed the treatment employed
(galvanism). .
But, at all events, the question of the occurrence of affections
of the auditory nerve in tabes requires more accurate inves-
tigation.
Disturbances of taste and smell have indeed been observed
here and there in tabes, sometimes with simultaneous anesthe-
sia of the mucous membrane of the tongue and mouth ; they are,
however, of very subordinate significance.
Disturbances of the Action of the Brain.
These are comparatively rare in tabes. In the typical form
of the disease, intelligence, memory, and disposition are likely
to remain entirely intact. The state of mind of the patients is
often even remarkably cheerful and contented, and they often
endure their serious troubles with wonderful good humor. At
other times, it is true, one also finds these patients depressed,
unhappy, very irritable and moody, tormented with sleepless-
ness, quarrelling with their fate.
More serious psychical disturbances, through complication
of the tabes with an affection of the brain, are but seldom ob-
TABES DORSALIS. 583
served. These may precede the tabes for many years, or may
become associated with it after it has existed for years, or,
finally, may not arise until the terminal stage.
Since the admirable labors of Westphal special attention has
been directed to the connection between tabes (that is, gray de-
generation of the posterior columns) and the progressive paraly-
sis of the insane. We can here only briefly touch on this inter-
esting and far-reaching subject, and must refer our readers, for
further information, to the original works on this subject, espe-
cially those of Westphal. According to this author, all, or at
least the majority of the patients who present the picture of ordi-
nary progressive paralysis, and, in so far as they present motor
disturbances of the extremities, seem to have an anatomically
demonstrable disease of the spinal ‘cord (chiefly degeneration of
the posterior columns). In these cases, therefore, the tabes is one
of the manifestations of a more or less diffuse process of disease,
extending over a great part of the central nervous system ; the
tabes, at its very beginning, is combined with a psychopathic
group of symptoms.
In another set of cases, however, the paralytic insanity is
added to the spinal affection of tabes only after the latter has
existed for years. Naturally, in all such cases, the importance
of the spinal becomes subordinate to that of the cerebral disease.
The frequency with which the true cranial nerves are involved
in tabes is very variable. We have already seen that the motor
nerves of the eye and the optic nerves themselves are very often
diseased. On the other hand, the involvement of the remaining
cranial nerves not yet mentioned is among the greatest rarities in
tabes. The trigeminus shows signs of irritation here and there
(pain, pareesthesia, etc.), or it may be paretic conditions (anes-
thesia, sense of numbness, disturbance of taste, etc.) which have
been thoroughly established by Pierret, and referred to sclerosis
in the region of the lower nucleus of the trigeminus in the me-
dulla oblongata. Pierret attributes very great importance to this
disturbance in the development of various ‘‘cephalic’’? symptoms
of tabes. The facial nerve is but very rarely found implicated,
and then it is principally the branches serving for the mimetic
movements of the mouth. The Aypoglossal has occasionally
584 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
been found affected (Friedreich). The pneumogastric and spinal
accessory, aS well as the glossopharyngeal, appear to be impli-
cated comparatively seldom ; difficulty of swallowing is rare in
tabes; palpitation of the heart, attacks of difficult breathing,
gastralgic troubles, and the like, do, indeed, occur, but it is not
certainly decided whether they are caused by an affection of the
nerves above named.
Disturbances of the Functions of the Bladder and Rectum.
These are among the most common symptoms of tabes.
Sometimes evidences of irritation are to be observed in these
parts; spasmodic dysuria, hypereesthesia of the neck of the
bladder, neuralgic (lancinating) pains in the depth of the pelvis,
in the perineum or the neck of the bladder, on urinating, on coi-
tion, or on defecating, have repeatedly been observed.
But signs of paresis are far more common, especially on the
part of the bladder, more rarely on that of the rectum. All those
various disturbances in the evacuation of the bladder occur
which we have previously depicted (p. 131 et seq.), and have
endeavored to refer to their physiological causes. It is particu-
larly the lighter difficulties with which tabes patients are af-
flicted ; severe and complete paralysis of the bladder does not
occur at all, or only in the latest stages of the disease.
Patients either complain of slight retention, so that emptying
the bladder takes a longer time, and is only accomplished by
stronger pressure and with some subsequent dribbling, or there
is a moderate degree of incontinence, so that when patients feel a
desire to urinate, they must do so at once, or the evacuations
of the bladder occur more frequently, and sometimes take place
into the clothes or bed. Itis but rarely that patients are obliged
to have recourse to the catheter or to make provision against the
constant involuntary flow of urine and its ill effects. |
After a longer or shorter time evidences of vesical catarrh
almost always show themselves, but this likewise remains re-
Stricted within moderate limits, and but seldom calls for direct
interference.
For an explanation of all these disturbances we refer to the
~
TABES DORSALIS. 585
discussion of the subject at a previous place; still, we must not
fail to call attention to the fact that the sclerosis of the posterior
columns in itself probably does not afford sufficient ground for
these disturbances, but that, in order to explain them, we must
probably assume a simultaneous disease of the gray substance.
But these are all matters calling for still further examination.
The disturbance of the functions of the rectum is also likely
to be but insignificant in tabes. The most frequent is anesthesia
of the anus, whereby patients lose the feeling of approaching or
actual evacuations of the bowels, so that they not infrequently
dirty themselves. True paralysis of the sphincter probably
occurs only in the latest stages of the disease.
Disturbances of the Sexual Functions.
These are scarcely ever absent in tabes. Weakness is the
most frequent and common evidence of this disturbance ; still,
evidences of abnormal irritation are not always wanting. At the
beginning of the disease, in particular, these evidences of in-
creased excitement are not rare. Trousseau and Hammond have
observed increased sexual power at the beginning of the disease ;
Charcot, in one case, saw satyriasis. Not infrequently patients
are possessed of a high degree of sexual excitability, so that
their passions are at once aroused by the sight or the innocent
touch of a woman. But this increased excitability is almost
always already associated with signs of sexual weakness; if
patients are still able to perform the act of coition, they still
have premature ejaculation; discomfort, a sense of weakness
and pain follow the act ; such patients suffer from frequent pol-
lutions, and cases are not infrequent in which a lascivious
thought or word, or the mere sight of a woman, is enough to
excite an escape of semen, which then takes place without an
erection and without any libidinous sensation.
More frequently, however, there is ¢mpotence, beginning early
and increasing rapidly. At first such patients can still perform
the act of coition, but more rarely, with less power and pleasure.
It is very common for patients with tabes to beget children even
586 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
after the disease has lasted for several years. But gradually
this power is more and more extinguished, erections become
rarer and weaker, and finally fail altogether. As a rule, sexual
desire is at the same time more or less completely extinguished ;
still, there are cases in which frequent pollutions and increased
sexual excitability exist together with complete impotence.
It must finally be mentioned that some tabes patients may
also retain perfectly undiminished sexual power for a very long
time.
We have already previously intimated (p. 137) how imperfect
our knowledge is as yet with regard to the more exact localiza-
tion of these disturbances within the spinal cord.
In women with tabes, disturbances of the sexual functions
are, as arule, not observed. Menstruation, pregnancy, and the
puerperal condition may run their course quite normally.
Vaso-motor Disturbances.
These fall very much into the background in tabes, and are
but little studied. In many cases cold feet are very common;
the occurrence of blue spots on the skin, increased or diminished
secretion of sweat, especially suppression and disappearance of
sweating of the feet; sometimes also a great tendency to the
occurrence of ‘* goose-flesh”’ (cutis anserina). 'The more accu-
rate relation of all these disturbances to sclerosis of the posterior
columns is not yet determined.
Trophic Disturbances.
These likewise belong to the infrequent symptoms ; in fact, it
is quite striking how admirable the general nutrition—the nutri-
tion of the muscles and the skin—is in many tabes patients. It
is not until the final stages of the disease that trophic disturb-
ances are frequent, and only in single cases that they occur in
the earlier and even in the initial stage.
On the skin, eruptions of herpes, of lichen, and of something
like pemphigus are to be observed here and there. Bed-sores
belong only in the last stage to the ordinary and almost constant
TABES DORSALIS. 587
manifestations, and then they present all the characteristics of
chronic bed-sores, as previously depicted (p. 122), and are amena-
ble to the same attempts at an explanation.
In the ordinary and typical cases the nutrition of the muscles
remains for a long time entirely intact ; there are tabes patients
enough with splendidly developed, hard, and powerful muscles.
Not until the latest stages, when there is already complete
paralysis, do we often see a high grade of muscular atrophy set
in, which, however, only represents simple emaciation of the
muscles, and is not to be regarded as degenerative atrophy.
In occasional, rare cases, however, this complication appears
earlier, with a high degree of atrophy of single muscles or of
groups of muscles (atrophy of the ball of the thumb, hemi-atro-
phy of the tongue, atrophy of the calves of the legs or the
thighs, etc.). These atrophies are doubtless, in the majority of
cases, to be regarded as degenerative atrophy ; they cannot pos-
sibly depend upon the sclerosis of the posterior columns, and
their appearance points with all certainty to the fact that the
pathological process in the spinal cord has extended further, to
motor and trophic tracts. It is in the highest degree probable
(Charcot, Voisin) that in such cases there is gray degeneration of
the corresponding portions of the anterior horns of gray matter.
The few cases of this kind which have thus far been more care-
fully examined with the naked eye argue in favor of this.
Those disturbances of nutrition of the joints—‘ arthropa-
thies des ataxiques’’—of which we have also previously spoken
(p. 126), and which occur quite often in tabes, certainly belong
to the most remarkable manifestations met with.
This joint affection generally develops itself in the initial
stage, even before the ataxy is manifest. If any joint trouble
appears later, it is usually in the upper ‘extremities, when the
disease spreads to them; therefore when the initial stage has
been reached for these extremities. ‘The joint most frequently
attacked is the knee-joint ; descending in the order of frequency,
after that are the shoulder, the elbow, the hip-joint, and the
wrist.
In describing this very charactefistic affection we can be
brief.
588 ERB.—-DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
The scene opens with a sudden and high degree of swelling of
the joint, caused by an accumulation of fluid, without pain,
without redness and heat, and generally also without fever;
associated with this there is a great and often widespread doughy
swelling of the surrounding parts, so that the whole extremity
may be extensively swollen; what is particularly striking is the
non-sensitiveness even of joints that are greatly altered on active
or passive motion.
If the joint affection is of a benign form all these manifesta-
tions may disappear again in the course of a few weeks,
Generally, however, the affection is of a character very disas-
trous to the joint; it results in progressive destruction of the
articular extremities, sub-luxations or spontaneous luxations of
the joints, causing notable deformities; thus at the knee-joint,
in particular, an exceedingly striking hyper-extension of the leg
is produced. |
As a rule, it is easy to distinguish this joint affection of tabes
from rheumatic inflammation of the joints or from arthritis sicca.
Probably the abnormal friability of the bones now and then
observed belongs in the same category of disturbances. In one
case Charcot saw numerous spontaneous fractures arise, and
Blum found these to be occasioned by a rarefying ostitis.
It is in the highest degree probable that these trophic disturb-
ances in the joints and bones are of neurotic origin ; still we
have as yet no positive demonstration of their dependence on
disease of definite portions of the spinal cord. Probably disease
of the gray matter of the anterior horns is to be held responsible
for it. Charcot and Joffroy at least found disease thereof in a
case of arthropathy; and in A. Pick’ I find the notice of an
observation of Westphal’s, in which, together with alterations of
the joints, atrophy of the large ganglion-cells of the anterior
horns was found. In another case Charcot, on the contrary,
found no changes whatever in the gray substance, though there
was swelling of the spinal ganglia, which may, therefore, also
possibly have an influence on these processes.
We must finally notice still another series of rare symptoms
1 Arch. f. Psych. u. Nervenkrankh. VI. p. 695. 1876.
yi en ees
TABES DORSALIS. 589
of tabes which we enumerate more for the sake of completeness
than because they contribute particularly to the characterization
of the disease.
First of all an increased frequency of the pulse may be men-
tioned, which is considered by some authors as a tolerably con-
stant manifestation in tabes; the pulse is said to beat over a
hundred and even up to a hundred and fifty to the minute. I
have no personal experience in this.
Friedreich, in one of his cases, observed profuse sweating,
diabetes insipidus and salivation. Bouchard claims once to
have found acid saliva.
More importance attaches to the gastralgic attacks, the so-
called ‘‘crises gastriques,’’ which are by no means rarely to be
observed, and the existence of which was first thoroughly estab-
lished by Delamarre and Charcot. These are extremely severe
cardialgic pains, arising in paroxysms, associated with nausea,
retching, vomiting, dizziness, sometimes with diarrhea, but gen-
erally with constipation, etc. In the severest forms there is
swelling of the abdomen, rigors amounting to convulsive trem-
bling, vomiting of watery mucus with bile and blood, very fre-
quent heart’s action, etc. These attacks may last one day or
several, and may return every couple of weeks, thus greatly re-
ducing the patient. They may arise at any period of the dis-
ease, in the initial or the ataxic stage, and evidently bear the
greatest analogy to the severe attacks of lancinating pains. They
may, doubtless, also be referred to the same anatomical causes
as the latter.
The ‘‘crises néphrétiques’’ recently described by Raynaud,
which present the most exquisite picture of severe renal colic
and may cause the patient fearful torture, evidently show great
analogy to the above. They are to be distinguished from true
renal colic by the longer duration and more frequent return of
the attacks, and especially by the absence of all disturbances in
the urine (admixture of blood, gravel, renal calculi, etc.). The
‘‘rectal and urethral colics,’’ described repeatedly, doubtless
also belong in the same category of disturbances.
The ‘‘ bronchial crises’’ first described by Féréol, attacks of
spasmodic cough, difficulty of breathing and of swallowing, are
590 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
at least doubtful, as yet, so far as their connection with tabes is
concerned (Bracht). Martin has recently described a case which
perhaps belongs here, in which cough, dyspnoea, and convulsions
were observed. In a case of tabes in which there were attacks
of suffocative cough (arising spontaneously or on eating), con-
nected with noisy inspiration and expiration, with tickling in the
fauces, and difficulty of swallowing, Jean found atrophy of the
left pneumogastric and recurrent laryngeal.
Finally, it may be mentioned that in some of Friedreich’s
cases dizziness was also observed, in part to a very marked
degree.
Individual Clinical Forms of Tabes.
For the present we must depend upon clinical observation to
teach us the different forms of tabes, and how to distinguish
between them ; to demonstrate which forms are the most frequent
and common—the typical forms, as it were; what other forms
and varieties stand next to them, and what relation they all bear
to allied forms of disease. Pathological anatomy is as yet un-
able to perform this task, in part because the pathological anat-
omist principally sees the latest stages of the disease, in part
because he is not yet able with certainty to recognize the earliest
and lightest grades of change and its spread within the spinal
cord.
The more abundant the amount of material furnished for
clinical observation in any department of medicine, and the more
sharply and completely we are able to recognize and to fix the
symptom-picture of individual forms of disease, the easier will
it become for us to draw the line of demarcation between differ-
ent symptom-pictures, and the more readily shall we be enabled,
in the frequently confusing multiformity of manifestations, to
distinguish between the essential and the non-essential, the pis
lar and typical, and the irregular and non-typical.
This has also been particularly true with regard to tabes. No
nerve-pathologist of the present day would think of regarding
everything as tabes which was so regarded even ten years ago.
We have, through many conflicts and difficulties, it is true, ob-
TABES DORSALIS. 591
tained a keener eye for the symptom-picture of tabes; we are
able, with greater certainty, to distinguish between the clean
typical cases and the irregular, the complicated, mixed, and
transition forms. We have progressed far enough to obtain a
quite definite, sharply-outlined idea of tabes, so to speak, an
ideal picture of the same, which we regard as the regular and
normal one, even though it may arise in numerous varieties, the
connection of which with the typical form is, however, easily
recognizable. Any considerable deviation from this type always
at once indicates an unusual manifestation of the disease, a com-
plication of the same, a combination with other allied forms of
‘disease. And these deviations occur but comparatively seldom.
Regarded from this point of view the sifting of the numerous
individual cases of tabes appears tolerably simple. As far as we
can see, there is, first of all, a large group, comprising by far the
greater number of cases of tabes, and which we may, therefore,
regard as the regular and typical form of the same. This has
been depicted in the preceding pages.
Next to this comes a far smaller group, containing fewer
cases, but likewise well characterized and distinctly deviating
from the typical form. This group comprises the cases of ‘‘ he-
reditary ataxy’’ described by_Friedreich, which agree among
themselves in a remarkable manner.
All other forms may probably be best regarded as merely
varieties of these two types; as cases in which single symptoms
attain peculiarly prominent significance, or new and unusual
symptoms appear, or the signs of other diseases of the spinal
cord (or probably also of diseases of the brain) are mixed with
the symptoms of tabes.
We may here be permitted a brief characterization of these
different forms.
The regular, typical form of tabes.—Special regard has been
had to this in the preceding pages, and it therefore only requires
to be sketched in very brief outlines.
* The beginning of the disease, which usually attacks men dur-
ing middle age, is with lancinating pains ; with disturbances
in the muscles of the eyes and the optic nerves ; with disturb-
ances in the sensibility and motion of the lower, much more
592 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
rarely of the upper extremities, such as paresthesias, the sense
of a tight girdle, slight anesthesias, swaying on closing the
eyes, a great feeling of fatigue, and the fact of getting tired
soon, lowering of the motor power and endurance ; and gener-
ally also weakness of the bladder and sexual weakness.
During a second stage of the disease, while the symptoms of
the first stage gradually increase, disturbance of the co-ordina-
tion of motion—atary—is added. This spreads slowly from
above downward. Patients grow increasingly helpless; there are
well-marked disturbances of sensibility, partial paralysis of sen-
sation, retardation of the sense of pain, though rarely complete
anesthesia. Reflex action of the tendons extinguished. Vesical
and sexual weakness increased. Motor weakness more distinct.
General nutrition still good ; psychical functions remain intact.
Finally, in the last stage, there is a transition to trwe paraly-
sis, paraplegia, contractures, muscular atrophy, bed-sores, pro-
gressive cachexia, which finally induces death with or without
intercurrent diseases. |
Naturally there are numerous deviations from this general
picture of disease (although a strikingly large number of cases
show a uniformity extending even to the smallest minutis). Of
course, in many individual instances, the picture of the disease
will assume a somewhat different form, according as the one or
the other symptom predominates, or arises earlier or later, ac-
cording to the slower or more rapid progress of the disease from
the lower to the upper extremities, according to the complica-
tions or rare symptoms that arise earlier or later. But the
typical picture of the disease will still always be recognizable in
its most essential features.
But in our opinion it has not yet been possible, on the ground
of these differences in the symptom-picture of tabes, to establish
different forms of the same, among which all the individual cases
could be classified. Nor is it as yet possible, on the ground of
the symptom-picture, to determine whether we are dealing with
an inflammatory or a simply degenerative form of sclerosis of the
posterior columns, nor to classify the cases according to their
anatomical seat at different heights within the spinal cord. To
be sure, with our present knowledge, it will be easy to distin-
TABES DORSALIS. 593
guish in each individual case about how high the anatomical
process extends in the spinal cord, whether the lumbar portion
alone is involved, or the dorsal and cervical portions as well ;
furthermore, whether the cranial nerves are implicated, whether
the bulb of the medulla oblongata is likewise affected, etc. After
our repeated explanation of these points no one need remain in
doubt about them.
On the other hand, one may be justified in doubting whether
it is a possible thing to determine the seat of the disease, not
only by the localization, but also by the quality of the symp-
toms, and whether one is justified in accepting this accidental
seat of the disease as a sufficient ground for distinguishing dif-
ferent forms of the same.
Remak, in this way, distinguished not less than six forms of tabes, all of which
he thought he could recognize by certain symptoms: a tabes lumbalis, lumbo-dor-
salis, dorsalis ascendens, cervicalis, basalis, and cerebellaris. Cyon has tried to
simplify this division so far as to accept only three forms, which he characterizes
as follows: 1. Basal form—Begins with disturbances in the muscles of the eye; pro-
gressive atrophy of the optic nerve; pupils not contracted; ataxy always present;
anesthesia frequent, especially in the upper extremities; psychical alterations may
arise. 2. Cervical form—Contracted pupils; severe, boring pains in the extremities ;
ataxy rare; the eye affected only later, never any paralysis of the muscles of the
eye; always irritability of the genitals, and impotence. 8. Dorsal form—Anes-
thesia rarely absent ; bladder troubleand difficult defecation frequent; pains not
as severe as in the first two forms; paresthesia and the sense of a tight girdle com-
mon; never any eye trouble, only sometimes dilatation of the pupils.
This indefinite characterization of itself shows that all possible transitions of
the individual forms amongst themselves must take place, and if one takes the
trouble to test a large number of cases with reference to their belonging to one of
the three groups, he will find that but very few of them fit into the corresponding
mould, but that most of them directly represent transitions between the different
forms. We therefore regard it as a hitherto unsatisfactory task to attempt such a.
division; it will suffice to content ourselves with recognizing tabes as such, and,.
in certain cases, also with determining approximatively its more exact seat at
different heights within the spinal cord.
The Friedreich form of tabes.—The disease is developed on:
the basis of a hereditary or family predisposition. The cases.
thus far known are distributed among three families, in each of.
which several brothers and sisters were attacked, especially the:
Semale members of the families. It begins at avery early period
VOL. XIII.—33
594 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
of life—between the twelfth and eighteenth years—perhaps in
connection with the development of puberty (or with a congenital
imperfect development of the spinal cord ?). Lancinating pains
are very rare at the beginning ; motor disturbances, on the con-
trary, occur very early, quite at the beginning, in the form of
well-marked ataxy, which spreads rapidly to the upper extremi-
ties, even arising simultaneously in the lower and upper ex-
tremities. Co-ordinatory disturbance of speech ; ataxic nystag-
mus. Vo disturbances of sensibility, or but very late and
insignificant ones; the sensibility of the skin and muscles re-
mains quite intact for many years. No swaying on closure of
the eyes. Reflex action of the tendons extinguished. No dis-
turbance of the bladder nor bed-sores. No psychical disturb-
ance, no tremor,no amaurosis. Paresis and contractures, atrophy
of the muscles, weakness of the bladder, appear only in the
latest stages. Remarkably long duration of the affection (reach-
ing to over thirty-two years).
The cases recently described by Kellogg—unfortunately in an extremely imper-
fect manner—probably belong here. The disease was developed in two brothers,
in each at the age of six years; there were several similar cases in other branches
of the same family.
In addition to these well-marked types of the disease there are
numerous cases, in practice, which deviate more or less from the
type without having to be thrown out of the general group of
tabes. We have already above called attention to the fact that
the different forms of chronic myelitis, in which we also include
tabes, are by no means always sharply separable, but that they
not infrequently extend beyond a certain definite domain in the
transverse section of the cord, and even beyond the cord itself,
and thus produce combined and complicated symptom-pictures,
the true significance of which can only be attained through an
accurate knowledge of the typical forms. These remarks also
hold good, to the fullest degree, for tabes ; here, too, there are
numerous complicated and transition forms, which, however, do
not possess regularity enough to justify their being set up as a
well-characterized form of the disease. A comprehensive and
expert judgment will very often be able to recognize the typical
germ in the abnormal symptom-picture, ‘and will correctly grasp
— a
TABES DORSALIS. 595
the significance and the pathogenetic basis of each unusual and
complicating symptom. These remarks may suffice to call at-
tention to these irregular forms, to only a few of which we can
cursorily allude. Sometimes it will be simply impossible to
establish a clear-cut diagnosis of any customary form of the dis-
ease, but we shall have to content ourselves with establishing the
existence of a more or less irregularly localized and extended
chronic myelitis.
In a certain number of cases manifestations of motor weakness
and paresis come into prominence very early, while the ataxy is
less pronounced, but the other symptoms are as usual; in this
way symptom-pictures may be reached which suggest paraplegia
—emaciation and atrophy of the legs may become associated
with it. In such cases one doubtless has a right to suppose an
early involvement of the lateral columns and the anterior gray
substance, both of which conditions, indeed, have been anatomi-
cally demonstrated repeatedly.
In other cases the lancinating pains stand forth with strik-
ing prominence in the picture of the disease ; they are for a long
time the only and afterwards certainly the most tormenting mani-
festation, and arise during the whole course of the disease, some-
times in rarer, sometimes in more frequent paroxysms, which, by
their intensity and duration and the other symptoms associated
with them, may become an excessive torment to the patients.
The attempt has been made to organize these cases into a separate
form, ‘‘ tabes dolorosa,’’? and Remak especially claims this char-
acter for his ‘‘ cervical form’’ of tabes.. We have not yet been
able to satisfy ourselves that this is justifiable; we have ob-
served such severe and repeated attacks of pain occasionally in
most of the forms of tabes.
In other instances, again, manifestations of pain in the back,
spinal sensitiveness, circumscribed or diffuse cutaneous hyper-
esthesia, and the like, are extremely prominent, and in such
cases one is doubtless justified in thinking of a meningitic com-
plication of tabes. The relations of sclerosis of the posterior
columns to the accompanying spinal meningitis may be very
varied, and thus a great variability may appear in the individual
cases belonging under this head. ~
596 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Finally, it is not rare for tabes to be complicated with psychi-
cal disturbances, as has already previously been intimated ;
here, too, the most varied combinations may arise. We may not
make special forms of tabes out of these, but must simply con-
clude that the occurrence of the psychical disturbance signifies
nothing more than a disturbance in the brain, which is added to
the disease in the spinal cord.
We might give many more similar hints with regard to ir-
regular forms of tabes, but it would be superfluous. We only
wish once more to emphasize the fact that these irregular, com-
plicated cases of tabes constitute decidedly the minority over
against the regular, typical forms of the disease. |
Course—Duration— Terminations.
With regard to the method of development and course of
tabes, we have but little to add to what appears from the general
description of the disease.
Tabes is a disease of a remarkably chronic course, and it seems
to us extremely questionable whether what has of late repeatedly
been described as ‘‘acute ataxy’’ has any relation whatever to
tabes and to sclerosis of the posterior columns.
The development of the trouble is accordingly slow, chronic,
extending over months, not rarely over a whole series of years.
Only in rare cases has the disease hithérto been seen to develop
itself so far within a few weeks or months as that a positive
diagnosis could be made. Generally, however, we observe the
slow development described above, the rise of single symptoms
which remain isolated for a long time, to which others are grad-
ually associated, until in the course of months and years the pic-
ture of the disease is complete. This development usually begins
in the lower extremities; still, single cases have also been ob-
served in which the upper extremities were first and prominently
attacked with the symptoms of tabes (Vossius). In not alto-
gether rare instances a unilateral development may also be ob-
served, and the existence for a longer period of exclusively or
mainly unilateral manifestations.
When the disease has once become developed, its further
*
TABES DORSALIS. 597
course usually leads slowly from bad to worse. More or less
rapidly the intensity of the individual symptoms increases, new
symptoms arise, and the condition of the patient grows ever
more deplorable.
This does not exclude the possibility of more or less consider-
able fluctuations: slight or even considerable improvement may
go on for months and years, then again to give place to an unfa-
vorable change; during the summer patients feel better and more
comfortable, while the winter always makes them worse again.
Generally, however, the evil influence of winter outweighs the
good of summer ; it is but very rarely that the tendency to im-
prove gains the upper hand, and the patients then advance grad-
ually towards recovery.
A prolonged arrest of the disease is quite common in tabes;
when it has reached a certain point of development, when it
has, perhaps, progressed so far as to compel the patient to use a
rolling-chair, he will be seen remaining in about the same con-
dition for years, and even for decades, dragging out a miserable
existence, often with tolerable cheerfulness and resignation.
These arrests may then occasionally be interrupted by exter-
nal influences and injuries (by taking cold, by an emotional dis-
turbance, a disastrous attempt at a bath-cnre, mistaken thera-
peutic measures, or the like), and the occasion be given for
renewed and more rapid progress of the disease. This, of course,
varies exceedingly in different cases.
The duration of the disease is generally very considerable,
and is always to be counted by years, and sometimes by de-
cades. Even the initial stage may last for twenty years, and
there are single cases in literature where patients have lived over
thirty and thirty-two years after the first beginning of the dis-
ease. With regard to many such cases, it may be said that the
duration of the disease cannot be determined ; that the malady,
having once become stationary, only reaches its end with the
natural termination of life, brought about by some intercurrent
disease or the weakness of age. This, however, only holds good
for a minority of the cases; in the majority of typical cases of
tabes, it may be said that the disease puts a limit to the life ot
the patient in the course of a few years (about six to ten or
598 ERB.—DISEASES OF TIIE SPINAL CORD AND ITS ENVELOPES.
twelve years), either because its progress within the spinal cord
directly threatens life, through bed-sores, cystitis, troubles of
respiration, bulbar symptoms, and the like, or because the dis-
ease causes a diminished resistance of the individual to intercur-
rent illnesses (infectious diseases, pneumonia, dysentery, etc.),
which bring about death.
Among the terminations of tabes, that in recovery is certainly
the most rare. In quite recent and light cases, in particular,
under appropriate treatment, one may sometimes see things
change for the better and recovery set in. I have repeatedly
seen this take place in the initial stage ; to be sure, the doubt
may then always arise whether it really was a case of beginning
tabes, as long as there was no ataxy yet present. Still, 1 am in
possession of two such cases, which I was obliged with great
positiveness to regard as beginning tabes, because the initial
symptoms were very distinctly present (lancinating pains, parees-
thesiz, swaying on closing the eyes, weariness and diminished
endurance, vesical and sexual weakness, etc.), and which have
now been entirely cured for a number of years. But even where
the disease is fully developed, we may, although very rarely,
see recovery take place, or an improvement bordering on recov-
ery. I am likewise in possession of two cases which demonstrate
this. In the one there were lancinating pains, unsteadiness,
weariness and distinct ataxy of the legs, paresthesia in the
domain of the ulnar nerve, and vesical weakness. After the
malady had lasted for several years, the patient recovered com-
pletely, with the exception of slight vesical weakness, and for
the past few years has attended to his duties as a civil function-
ary, without suffering any inconvenience. The other case was
that of a naval officer, in whom the disease was farther advanced.
He suffered from paresthesia and slight anzesthesia of the legs,
diplopia, distinct ataxy and weariness of the legs; could not
walk without being led; had a high degree of vesical weakness
(incontinence, with cystitis), ete. After systematic treatment for
two years, he was so far restored that he marched for three or
four hours, could retain his urine for five or six hours, showed
no disturbance of sensibility, got married, and has now for two
years served as commander of an iron-clad frigate.
TABES DORSALIS. 599
I could make still further reports of similar, if not as well-
marked instances of improvement. Since Remak’s celebrated
case, other observers also have now and then been able to report
cures of actual tabes.
There cannot, therefore, be the slightest doubt that in a cer-
tain, though very small per cent. of all cases of tabes, recovery
actually follows.
Far more frequently patients must content themselves with a
slight and moderate improvement, or an arrest of the malady ;
and this, too, is a result which does not constitute the rule, but
is, likewise, only reached in a certain number of cases.
As a rule, however, this trouble is of a decidedly progressive
character, its tendency being slowly to grow worse. The final
Jatal termination may then be brought about in various ways,
as follows :
The disease in its progress may lead to paraplegia, to cystitis
and bed-sores, with their results, and the patient then dies from
increasing cachexia under the picture of severe spinal paralysis.
In that case we usually see a very protracted death-struggle,
and not rarely, during the last days, severe cerebral symptoms,
coma, delirium, etc., under which life is extinguished.
Or, in its progress upward, the disease leads to symptoms
which directly threaten life, to disturbances of respiration, suf-
focative attacks, difficulty of swallowing, etc., and thus causes
death. |
Or, finally, some intercurrent disease (typhus, pneumonia,
diphtheria, cholera, pulmonary phthisis, etc.) brings about the
end. It is remarkable that so many tabes patients succumb to
typhus ; still this might in part be explained by the fact that
their long sojourn in hospitals more frequently exposes such
patients to the danger of infection.
Theory of the Disease.
We have here but little to say on this point. By the theory
of tabes we understand not merely the theory of ataxy, which is
but a single symptom of the same, but the reference of the whole
symptom-picture to definite anatomigal changes in the spinal
cord—the demonstration that a certain definite method of devel-
600 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
opment and form of symptoms stand in a causal relation to a
certain definite kind and localization of anatomical changes.
We have been obliged in a number of places to point out the
fact that we are, as yet, still far from having reached this goal ;
we still lack the positive evidence of a whole array of single
facts which belong to a theory of the disease. We may there-
fore here only briefly touch upon those views which are now cur-
rent, and upon the most satisfactory hypothesis of tabes, at the
same time indicating the gaps which they contain and the objec-
tions which, as yet, may be urged against them.
The view of some authors, which was advocated with special
zeal by Trousseau, that tabes is merely a functional disease—a
pure neurosis, and that the anatomical changes are merely sec-
ondary results of this neurosis and not necessary causes of the
same, is absolutely no longer tenable in view of the entire una-
nimity of all more recent anatomical discoveries. Tabes is with-
out doubt an organic disease of the spinal cord.
The general opinion at present is undoubtedly to the effect
that the sclerosis of the white posterior columns is the only
essential, and in many cases also the exclusive alteration of the
spinal cord in tabes, and that it is abundantly sufficient to ac-
count for all, or at least for the most essential symptoms; and
that only a part of the symptoms is brought about through a
simultaneous localization of the disease in certain cerebral nerves
and districts of the brain. |
The advocates of this doctrine explain the lancinating pains
by the irritation of the sensitive root-fibres and their virtual pro-
longations within the posterior columns; the-parzesthesias and
aneesthesias by disease of the ascending sensitive fibres in the
posterior columns ; the disturbances of co-ordination by affection
of the co-ordinatory tracts presumed to lie within the posterior
columns; and they only concede the gradual extension of the
process to the neighboring portions of the lateral columns to
explain the motor paresis and paralysis which arise late. Va-
rious other symptoms, the vesical weakness, the sexual weak-
ness, the trophic disturbances, etc., thus remain silently unex-
plained ; and, altogether, the certainty with which the disease
of the posterior columns is made responsible for so many differ-
i i ll a i a ie —
:
\
t
4
7
|
TABES DORSALIS. 601
ent kinds of symptoms is in remarkable contrast to the perfect
uncertainty in which physiologists find themselves, in spite of
numerous experiments, with regard to the function of these very
posterior columns.
There are not a few serious doubts in the way of accepting
this exclusive reference of the tabes symptoms to the disease of
the posterior columns. In the most extensive degeneration of
Goll’s columns the specific tabes symptoms are liable to be regu-
larly wanting; very extensive degeneration of the posterior col-
umns has been observed without the symptom-picture of tabes;
and although the symptom-pictures of the few hitherto known
cases of primary sclerosis of the columns of Goll do not seem to
agree among themselves, still they also differ from the symptom-
picture of tabes. (Pierret found paresthesia and slight anes-
thesia, difficulty of walking, the impulse to run forward, a high
degree of weariness, swaying on closing the eyes, no ataxy. Du
Castel, on the contrary, paraparesis, trembling, and amblyopia,
but no anesthesia and no ataxy.)
It has, therefore, been found necessary to admit that Goll’s
columns have nothing immediately to do with the actual tabes
symptoms, but that other portions of the transverse section of
the posterior columns must be diseased if the symptom-picture
of tabes is to arise. Charcot-and Pierret have endeavored accu-
rately to establish the fact that in tabes the disease always first
attacks the lateral ribbons of the posterior columns, and that the
lancinating pains and the pareesthesias are the expression of this
initial disease. If the affection extends from here outward and
inwards, then there is ataxy (according to Charcot, the co-ordina-
tory fibres are supposed to lie in the external halves of the pos-
terior columns, between the inner root-bundles) ; if the affection
extends to the gray posterior horns and the posterior roots, a
high degree of anesthesia is produced; its extension to the
lateral columns causes manifestations of motor weakness and
paralysis, while its extension to Goll’s columns is betrayed by
no new symptoms.
This view has something very seductive about it, and is also
materially supported by a number vot beautiful observations.
Perhaps it could be opposed by but one remarkable observation
602 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
recently reported by F. Schultze.’ Here there was (probably
secondary) degeneration of the external ribbons of the posterior
columns, which, it is true, manifested itself only by disappear-
ance of the axis-cylinders, not by proliferation of connective tis-
sue simultaneously with a sarcoma of the corpus callosum ;
during life there were no symptoms of tabes, especially no ataxy.
It will be seen that, for the explanation of important symp-
toms of tabes, Charcot himself admits a more or less extensive
participation on the part of the gray substance and of the lateral
columns. Indeed, according to all that we know of the func-
tions of the spinal cord, the theory of an exclusive disease of the
posterior columns can hardly be maintained. Thus, for instance,
the retardation of the sensation of pain, which is so frequent,
and the partial paralysis of sensation, argue with great proba-
bility in favor of a disease of the gray substance. C. Lange
believes that the excentric pains are also produced through irri-
tation of the sensitive tracts within the gray substance; the
vesical and sexual weakness, the articular troubles and other tro-
phic disturbances, likewise point to a lesion of the gray substance.
The motor paresis and paralysis can hardly be explained other-
wise than through disease of the lateral columns or of the ante-
rior gray horn, and the oft-cited case of Spaeth-Schueppel only
admits of the conclusion that the co-ordinatory tracts of the
spinal cord also do not lie in the posterior columns.
All these facts favor the view that the typical form of tabes
does not depend exclusively upon disease of the posterior col-
umns of the spinal cord, but that other parts in the vicinity
of the. posterior columns must also be involved in the disease.
We would announce the following as for the present the most
probable theoretical view of the disease of the spinal cord in tabes,
a view which is still to be tested by further investigations. The
affection begins in the posterior columns, and probably always in
the external portions of the same (régions des bandelettes ex-
ternes), and thus causes the symptoms of the initial stage; it
spreads from here longitudinally and transversely ; its extension
longitudinally is caused by the advance of the disease from below
1 Centralbl. f. d. med. Wissensch. 1876. No. 10.
OO a ES ee
ee
een eae
Cal eee ed
nee peng
‘ _—
ERT i me
TABES DORSALIS. . 603
upward ; its extension laterally is at first caused by the fact
that a secondary degeneration of Goll’s columns is gradually
added to the primary affection of the fasciculi cuneati [Keil-
strange], whereby the peculiar and charateristic gross anatomical
picture of tabesis caused. The direct transverse extension of the
disease to the neighboring gray posterior horns and the contigu-
ous portions of the lateral columns may explain the later, more
severe disturbances of sensibility, the disturbance of codrdination,
the motor paresis and paralysis, the vesical and sexual weakness.
This leaves it still to be more accurately determined to what part,
in particular, the lesion must extend in order to produce the
single disturbances of function named.
We believe that a hopeful field for further investigations and
observations is here presented ; probably much may still be arrived
at by careful attention. We must not be satisfied with the con-
ditions found in the posterior columns, and which readily strike
the eye, but must above all things cultivate the methods for the
examination of the gray substance, which as yet are very crude ;
at all events, it is not until then that we shall be able to say, with
greater confidence, whether the lesion is confined to the posterior
columns or not, and how far it regularly extends beyond this.
The determination of the extent of the lesion, as to space, will
be the easier task. Then, however, the more difficult question
still remains for solution as to the essential character of the
pathological process; whether it is an inflammation or not,
whether parenchymatous or interstitial inflammation, etc. We
need not travel over this ground again. But it is evident that
the theory of tabes cannot be complete until these questions also
have been answered.
For the present we can only designate this as a peculiar form
of disease with a special tendency to localization in definite por-
tions of the nervous system (posterior columns, certain cranial
nerves), and to extension chiefly in certain tracts which, anatomi-
cally and physiologically, to a certain degree belong together.
Diagnosis.
If, under the name of tabes, we ynderstand only that form of
disease defined and explicitly described in the foregoing pages,
604 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
then its diagnostic recognition, as a rule, offers no serious dif-
ficulties, The typical cases, in particular, are very easy to
recognize, gnd are distinguished, in quite a characteristic man-
ner, from the remaining chronic spinal affections. Whenin such
a case of disease, disturbances in sensitive domains (lancinating
pains, pareesthesize in the extremities, sense of a tight girdle,
sense of weariness, etc.) and symptoms on the part of certain
cranial nerves have gone before, when diminished endurance and
precision of motor efforts appear, when vesical and sexual weak-
ness are noticed, when objective examination shows a distinct dis-
turbance in the co-ordination of movements, while there is but
very slight motor paresis or none at all, when the different kinds
of sensation seem to be more or less disturbed, when swaying or
closure of the eyes appears, when the reflex action of tendons
fails, etc., then the typical form of tabes can be easily and posi-
tively recognized.
Nor will it be any less easy to diagnosticate with certainty
the Friedreich form of tabes, after the description already given
above (page 593).
To be sure, such a clear and significant symptom-picture does
not exist in all cases, and one will often meet with serious diag-
nostic difficulties in those obscure, complicated cases which occur
not rarely, in which the affection extends a greater or less dis-
tance beyond its usual limits, in cases which are complicated
with meningitis, with affections of the gray substance, the ante-
rior and lateral columns. We have already stated repeatedly
that transition-forms between the different classes of chronic
myelitis are not rare; and we here once more declare that it is
of less consequence to force an individual case of disease into a
definite diagnostic scheme than to conceive as clear a picture as
possible of the anatomical changes actually before one, as to
their seat and extent, even though these may not exactly fit
into the typical mould of tabes, or of any other form of chronic
myelitis. If one holds to this, he will find himself in a com-
paratively safe position, even over against the irregular, compli-
cated forms of tabes which are difficult to classify.
One of the most difficult matters, and at the same time one of
the highest practical importance, is the recognition of tabes at
TABES DORSALIS. 605
its commencement, in the earliest stages of its development. We
will here merely emphasize the fact’ that, in this stage, attention
is especially to be directed to the lancinating pains—often too
little regarded by the patient,—to any symptoms that may be
present on the part of certain cranial nerves, to pareesthesias of
various kinds, é. g., the sense of a tight girdle, and especially
paresthesia in the domain of the ulnar nerve. It should also be
borne in mind that slight swaying on closing the eyes—the only
disturbance of sensibility recognizable on careful examination,—
that a great sense of weariness and a certain unsteadiness in per-
forming the most difficult and complicated movements, as well
as the failure of the reflex action of tendons, that slight weak-
ness of the bladder, dribbling of urine after micturition, and dis-
turbances of the sexual organs, are often, at an early period,
noteworthy indications of the severity of the disease which is
just beginning. The greater the number of these symptoms that
exist at once, the more distinctly, in particular, disturbances
of motility and sensibility can be objectively demonstrated, the
more probable is the diagnosis of tabes. In this way, also, the
distinction is easy between this disease and neurasthenia spinalis,
which bears some resemblance to the earliest stages of tabes
(compare page 379). At the same time, in not a few such cases
of beginning tabes the patient will have to be observed for some
time before even a probable diagnosis can be made.
Among the other chronic spinal diseases which may come
into question in the diagnosis of tabes, we may speak of the fol-
lowing:
Common chronic myelitis (transverse, etc.) will, as a rule, be
easily distinguished. Here the picture of the disease is essen-
tially characterized by paralysis of all the spinal functions,
motor and sensitive paralysis, which generally shows a sharp line
of demarcation at its upper limit; no ataxy; on the other hand,
quite commonly spasms, muscular tension, contractures, greatly
heightened reflex action of the skin and tendons; furthermore,
actual paralysis of the bladder, often with cystitis; a tendency
to the early formation of bed-sores. And even the initial stage
of chronic myelitis will generally be easy to distinguish from the
beginning of tabes, by the absence of fancinating pains and of the
606 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
cranial nerve symptoms, and by the early appearance of paretic
symptoms.
There may occasionally be some trouble in distinguishing this
affection from multiple sclerosis, inasmuch as, when the foci are
situated in the posterior columns, tabes symptoms may also
arise. On careful observation, however, the diagnosis can gener-
ally be easily made, as cerebro-spinal sclerosis presents a picture
of disease much richer in symptoms and much more complicated
than tabes. The following symptoms may be regarded as par-
ticularly significant of multiple sclerosis, and should, there-
fore, engage our attention: great dizziness, headache, psychical
disturbances, early nystagmus, scanning speech (which can be
distinguished from the ataxic disturbance of speech of the Fried-
reich patients) ; the characteristic tremor on voluntary movement,
the pareses, paralyses, muscular tensions, contractures, increased
reflex action of tendons, etc., in the lower extremities, which are
always present, and the apoplectic attacks.
The Friedreich form of tabes, too, which bears a certain re-
semblance to multiple sclerosis, on account of the nystagmus, the
disturbance of speech, and the static ataxy of the muscles of the
trunk, can generally be distinguished from the latter disease on
the ground of the symptoms named.
The differential diagnosis between tabes and spasmodic spinal
paralysis (lateral sclerosis), the aggregation of spinal symptoms
described by me (compare the following section, No. 13), is very
easy ; the latter is characterized by paresis and paralysis, with
muscular tension and contractures, with greatly increased reflex
action of the tendons, and by the absence of ataxy, of disturb-
ances of sensibility and of the bladder, of lancinating pains, of
cranial nerve lesions, etc.
The question of distinguishing tabes from affections of the
cerebellum has greatly occupied authors, and sometimes offers no
little difficulty. The evidences of cerebellar trouble are: frequent
and severe headache, especially in the back of the head, occa-
sional vomiting, and general convulsions, a staggering gait, like
that of a drunken man, reminding one of ataxy, but not identi-
cal with it, sometimes a straddling gait, or an impulse to walk
backward, diplopia, and amaurosis. On the other hand, in cere-
TABES DORSALIS. 607
bellar affections there are, as a rule, no lancinating pains, no
disturbances of sensibility, no vesical or sexual weakness. By
these means a diagnosis can be made in most cases.
As a rule, tabes can be easily distinguished from chronic
spinal meningitis; in some few cases, however, this cannot be
done, because the latter is occasionally complicated with tabes.
The evidences in favor of meningitis are the pains in the back
which may exist, and the stiffness of the back, the sensitiveness
of the spinous processes to pressure, the more or less uniform
but not very extreme sensitive and motor paresis, the absence of
ataxy, etc.
The difference between progressive cerebral paralysis and
tabes will be apparent by the absence, in the latter, of the dis-
turbances of speech and psychical changes which are character-
istic of the former. Those cases in which the two forms of dis-
ease are combined, whether the psychosis is added to the latter
history of tabes, or whether symptoms of tabes arise during the
course of progressive paralysis, will call for a special exercise of
judgment, and will, as a rule, not be hard to interpret aright.
Prognosis.
Tabes dorsalis is, under all circumstances, a very serious dis-
ease, although, indeed, its prognosis is not quite so hopeless as
it was once thought to be by Romberg. It is certainly not quite
as unfavorable as the prognosis of multiple sclerosis, or even as
that of simple transverse chronic myelitis.
Although in the great majority of cases the disease is more
or less continuously progressive, advancing to an unfavorable
termination, still a certain number, even though it be but a small
number, of cases end in recovery. In many instances at least
a certain degree of improvement takes place, and the malady
remains at a stand-still for years. If the disease is at all well de-
veloped, it is hardly to be supposed that the anatomical changes
can recede.
It is always a question of a disease of long duration—and this
is at least a comfort to many patients; however variable it may
608 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
be in individual cases, a number of years always elapse, often
many, very many years before the fatal termination. The slower
the development of the disease, the better the general condition,
the slighter the disturbance of sensibility, the less there is of a
neuropathic predisposition, the longer, as a rule, will be the
duration of the disease.
The judgment of each individual case, with regard to the
prognosis, is generally very difficult; even one who has a rich
experience in such matters will be able to give but an uncertain
verdict. The prognosis is favorably influenced by the absence
of a neuropathic predisposition and hereditary causes, by the
absence of previous sexual excesses, by a very slow development
and moderate intensity of the symptoms, by but slight disturb-
ances of sensibility, rare and moderate lancinating pains, by the
favorable effect of certain therapeutic measures, by favorable
external circumstances which enable the patient to do every-
thing requisite for his health, ete. On the other hand, it is wn-
Javorably influenced by hereditary predisposition, sexual over-
stimulus, by the rapid progress of the manifestations, severe
paroxysms of pain, rapid emaciation and loss of strength, by
affections of the special senses and of the brain, great general
irritability, serious irritation of the genitals, a tendency to bed-
sores, vesical catarrh, by the uselessness of all therapeutic inter-
ference, by unfavorable circumstances in life, forcing one to labor
for his daily bread, ete. 3
The prognosis of individual symptoms is very various.
While the disturbances of sensibility, the pareesthesias and
aneesthesias, are generally very easily improved or removed, the
prognosis of the ataxy is ordinarily quite unfavorable ; it gener-
ally remains unimproved, even though the motor power as a
whole improves. The lancinating pains, as a rule, are extremely
obstinate ; the vesical weakness may disappear, the sexual weak-
ness usually remains unimproved. Paralysis of the muscles of
the eye generally admits of a favorable prognosis, while the
amaurosis due to atrophy of the optic nerve is almost absolutely ~
hopeless ; it is almost always incurable, and but rarely can even
any ‘slight improvement be observed.
TABES DORSALIS. 609
Therapeutics,
With regard to the prophylazis of tabes, which ought perhaps
to be considered oftener than it is now, we may refer to what was
said above on the therapeutics of chronic myelitis. The points
to be specially noted in this connection are the combating of the
neuropathic tendency by appropriate diet and habits of life, and
the prevention, by every means in our power, of things notoriously
injurious, especially the combating of onanism and avoidance of
sexual excesses. In not a few families will one find fitting objects
for the exercise of this sort of household medical supervision.
In most cases it will be found impossible to fulfil a causal
indication, as one is dealing with quite chronic conditions, the
causes of which have long since passed away. We shall, there-
fore, but rarely find ourselves in a position to do anything in this
direction, and whatever is to be done will appear from the indi-
vidual circumstances of the case. Where there are signs of syph-
ilis, we should not fail to carry out the appropriate treatment.
As arule, the physician will find that he has to deal with the
disease after it has arrived at a certain degree of development,
and he will have, before all else, to satisfy the indicatio morbi.
What we have said more specifically above, under the therapeu-
_ tics of chronic myelitis, is here especially applicable. At the
same time, we must not fail just here especially to emphasize
some facts, and again to subject to closer inspection the effects of
certain remedies in tabes particularly. Of all forms of chronic
spinal affection, tabes is certainly the one that has been subjected
to the most extensive and manifold therapeutic experiments.
As a rule, nothing at all is to be expected from actual anéi-
philogistic treatment. This could at most be thought of in quite
recent cases, with well-marked evidences of irritation and a more
inflammatory character ; and here, according to the observations
of Frerichs, it does sometimes seem to be useful. But in all later
stages, and during the well-marked chronic course of the disease,
antiphlogistic treatment has always proved useless. As a rule,
therefore, it is to be ignored. But the application of dry cups
may often be permitted for the relief of pain.
In just this form of chronic myelitis derivatives also seem to
VOL. XIII.—39
610 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
accomplish the least possible good. This is especially true of
the actual cautery, which was formerly very often used, but is to
be discarded as entirely useless. I have likewise never seen any
distinct benefit from the milder derivations (blisters, salves that
raise pustules, irritating inunctions, etc.). |
Among the means of treatment still discussed for tabes, sim-
ple thermal baths formerly headed the list. If anything is plain
in the therapeutics of tabes, it is the fact, confirmed almost unani-
mously by all recent experience, that thermal baths are injurious
rather than beneficial in tabes, that in this form of chronic my-
elitis they should either be entirely avoided or only employed
with the utmost care. Benedict says, outright: ‘‘ Thermal baths
belong to the essentially injurious agencies in tabes;’’? and M.
Rosenthal, Erdmann, von Krafft-Ebing, Richter, and others, have
expressed themselves quite to the same effect ; and my own ex-
perience likewise quite agrees therewith. Leyden is the only one ~
among recent writers who expresses himself as ‘‘ unequivocally ”’
in favor of the value of thermal baths. In opposition to this
view, we would maintain what was said generally above (page 460)
on the subject of thermal baths, under the head of Chronic My-
elitis, as being especially applicable to tabes. We would advise
the trial of thermal baths in tabes patients only under quite
peculiar conditions, when all other methods of treatment have |
failed. The cases which are generally declared to be especially
adapted to the use of thermal baths are those with prominent
evidences of irritation, lancinating pains, with great general ex-
citability, sleeplessness, ete. It is very much to be wished that
these indications might be made more exact.
At all events, one should be extremely cautious in the appli-
cation of thermal baths. Only a moderately warm temperature
is allowed ; all above 90° F. may be injurious; most of the
natural thermal waters therefore must be cooled. The duration
of the baths must not be too long (not over fifteen to twenty
minutes); they are not to be employed daily, but only every
two or three days. Only when thus carefully used do thermal
baths sometimes seem to be of use in tabes.
The sulphur baths which have been used with special fre-
quency in France have probably no other effect than that of
TABES DORSALIS. 611
simple thermal baths ; what has just been said, therefore, applies
equally to them.
Saline thermal baths can certainly show better results, and
Rehme, in particular, has long enjoyed a well-founded reputa-
tion in the treatment of tabes. From my own experience I can
likewise make a report in the main favorable to these baths
(Nauheim). But here, too, it is greatly to be desired that more
accurate indications and contra-indications should be established.
The rules of caution given above (p. 461) might be especially
applicable to tabes; the baths should not be given too often
(Waldmann considers three baths a week as sufficient for most
cases), they should not be of too long duration nor too warm,
and the more exciting forms of baths should be especially
avoided, as they only too often interfere with the good results to
be expected from such a course of baths.
No conclusive experience is at hand with regard to the effects
of chalybeate-baths or mud-baths in tabes. The latter seem to
act favorably in some cases, though we cannot as yet say pre-
cisely in what class of cases.
But a cold-water cure, carefully conducted, must be very
especially recommended for the treatment of tabes. The results
thereof are extraordinarily favorable, especially in comparison
with the other curative measures at ourcommand. Aside from
the hydropaths, whose judgment might be impugned as not alto-
gether unbiassed, Benedict, M. Rosenthal, and others, express
themselves decidedly in favor of the beneficial action of hydro-
therapeutics. Waldmann ascribes a strikingly favorable effect
to mild, cool sponging of the body. Here also Leyden alone sets
himself in opposition to all other authors, and claims that tabes
patients, as a rule, bear cold water badly. According to my own
experience, I must directly contradict this statement. Among
nineteen of my tabes patients who went through with the cold-
water cure, sixteen experienced more or less benefit, two saw no
improvement, and only one grew slightly worse. Most of my
patients bear cold-water treatment so well that I almost always
have them use the cold sponge-bath at home all winter, and have
never yet seen any harm come from it
Here of course everything depends on the method and the
612 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
manner of application, which must be determined and regulated
with the greatest caution.
The method of action of the water-cure on tabes may be two-
fold. In the first place, it contributes to the hardening of the
skin and thereby to the diminution of injurious effects ; it causes
general strengthening and improvement of nutrition, which then,
secondarily, also effects an improvement of the spinal trouble;
One almost always sees patients leave water-cure institutions with
a blooming appearance, increased weight, and a feeling of greater
well-being and increased capacity for work ; and all this is cer-
tainly not to be lightly esteemed.
But, secondly, the water-cure seems also to exert a direct and
beneficial influence on the affection of the spinal cord, and thus
to contribute more directly to the improvement and cure of the
disease.
From the statements of various specialists with regard to the
methods to be selected, it first of all appears very decidedly that
all low temperatures as well as all more exciting forms of bath
are injurious and to be avoided, that, on the contrary, moderate
degrees of temperature—not below 68° F.!—and the milder,
more quieting, or only slightly exciting forms of bath alone are
permissible. While, therefore, actual cold water, cold full-baths,
shower-baths, cold slappings, etc., are decidedly forbidden, it is
admissible to use simple wet rubbings (beginning with 77° F.
and going down to 68°, or at the utmost to 59°), half-baths (of
about 86° to 70° F.) with simultaneous washing of the back and
sprinkling of the back; furthermore, also mere washings of the
back, of the feet, wrapping the feet and the abdomen with cold
compresses which warm themselves, and here and there a hip-
bath. The wet pack should be used with extreme caution,
beginning with a temperature of 88° F. ; it is seldom borne at a
temperature below 77° F. (F. Richter). Czerwinsky recommends
only tub-baths to be used in tabes, with a temperature of 813° F
which is to be lowered only very gradually. At the same time,
some patients bear lower temperatures very well. Very much
reduced, anemic, irritable patients, who are very sensitive to
cold, are the least fitted for this treatment; at all events, in
such cases it may only be tried with the utmost caution.
TABES DORSALIS, 613
The choice of the institution to which tabes patients are to be
entrusted is of the greatest importance. It is not in all water-
cures that the requisite understanding and the necessary indi-
vidualization are to be found. Care must therefore be exercised
in this respect.
If possible, let those institutions be selected which lie in a
good mountain region, are provided with convenient walks, are
well conducted as to attendance, and are not too noisy. The
best plan is to send patients there at the beginning of summer
with instructions to remain till autumn. I have thus far not
found winter-cures in actual cold-water institutions as especially
to be recommended.
Since the pioneer labors of Remak, the galvanic current has
earned for itself a secure and honored place in the treatment of
tabes, as well as in that of other diseases. Electro-therapeutic
literature abounds in reports of cases which establish, beyond
all question, the value of the galvanic current in tabes. My
own experience also speaks sufficiently in favor of this good
effect, although it is certainly calculated to put me on my
guard against too great illusions in regard to the value of the
method. Among 66 cases treated by me, 25 received no benefit ;
41, on the contrary, were more or less improved. This improve-
ment, in most cases, it is true, did not amount to very much;
in but comparatively few was it very considerable, and only in
rare instances was there complete recovery.
Various authors differ somewhat among themselves with re-
gard to the methods which are to be employed, but almost all
agree in this, that they regard the main point as consisting in
the direct treatment of the back, with moderately strong, chiefly
stabile, more rarely labile currents, and recommend only short
sessions.
Von Krafft-Ebing advises simple stabile currents through the
spinal column, of from four to six minutes’ duration ; in addi-
tion, he recommends the labile action of the cathode on the nerve-
trunks. I cannot coincide with his opinion, that usually the
first six or eight sessions determine the result ; the improvement
often does not appear until very mugh later. Mendel has like-
wise applied stabile and labile currents to the spinal cord with
614 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
advantage. Mor. Meyer has found the action of the anode use-
ful in some cases, on points in the spinal column that were pain-
ful on pressure.
I myself for some years past have almost exclusively em-
ployed the method described on p. 183, and believe that I have
thereby attained comparatively the best results. Naturally this
will have to be variously modified in different individuals, so
far as the duration, intensity, and localization of the currents
are concerned. In very irritable persons, in particular, with
severe pains, it is well to apply very weak currents. I generally
combine with the galvanic treatment of the spine peripheral
galvanization of the nerves of the lower extremities (cathode
labile), which is to be used about two or three times a week.
In the same manner, any complications that may exist (paralysis
of the muscles of the eyes, atrophy of the optic nerve, lanci-
nating pains, vesical weakness, aneesthesia, etc.) are at the same
time to be treated symptomatically.
The sessions last about three to six minutes ; strong currents
are positively avoided; treatment usually takes place daily,
commonly for months together. We should not allow ourselves
to be prevented from continuing the treatment by temporary
fluctuations in the course of the disease.
Only if patients feel more tired and poorly after each gal-
vanization; if their condition, as a whole, grows gradually
worse ; if their pains increase, sleeplessness sets in, or the like,—
must we give up the galvanic treatment as inappropriate. |
Among the internal remedies for tabes, nitrate of silver
undoubtedly stands first, as it can show quite undoubted results.
The observations of Wunderlich, Charcot, Vulpian, Eulenburg,
Griesinger, von Graefe, and others, speak decidedly in its favor,
and lately Friedreich has also again expressed himself favorable
thereto, at the same time pointing out the danger of albuminuria
connected with its use; but this danger may no doubt be easily
avoided by cautious dosing.
Although we cannot, as yet, accurately designate the cases in
which nitrate of silver proves beneficial, still the fact that it
really has done good in a considerable number of cases, and that,
as a rule, and if used with some caution, its employment is
TABES DORSALIS. 615
without any danger or discomfort, is of itself enough to justify
its administration in most cases. The dose is 0.01 to 0.02 gramme
(one-sixth to one-third of a grain) several times a day, so that at
most 0.06 to 0.10 gramme (one to one-and-a-half grains) is used in
the course of a day; the remedy may be continued until about
8 to 10 grammes (two to two-and-a-half drachms) have been used ;
and its use may also be repeated again later.
Caster found material improvement under the oxide of silver in two cases where
the nitrate had been employed without effect.
Lodide of potassium, which is recommended by some on theo-
retical grounds, cannot show any results worth mentioning.
Leyden considers it effective against any meningitic complica-
tions that may exist; it is also said to moderate symptoms of
irritation.
According to Siredey, bromide of potassiwm is said to im-
prove the disturbances of co-ordination and to mitigate the pains
in doses of from 3 to 10 grammes (gr. xlv. to 3 iiss.) daily.
The systematic use of belladonna and ergot has, as a rule,
only resulted in failure. Ergot has lately found a eulogist in
Waldmann, who tried it on himself (he suffers, however, princi-
pally from spinal meningitis), and who urgently recommends it
for chronic meningitis and for tabes ‘‘caused by dilatation of
the vessels.” One to two grammes (fifteen to thirty grains) is to
be given daily, in the form of powder, and continued for a con-
siderable time.
There is not much to be said in praise of arsenic, chloride of
gold and sodium or chloride of bariwm (recommended by Ham-
mond in doses of 0.05 gramme [three-fourths of a grain] three
times a day) ; all these remedies generally leave one in the lurch.
Strychnine is decidedly objectionable in tabes.
Phosphorus, which has repeatedly been recommended. by
Dujardin-Beaumetz, appears to produce no effect in most cases,
and will but rarely be used on account of the danger connected
with it.
Quite recently, in a Russian periodical, Lesch has reported favorable results from
phosphorus treatment in tabes, from the clinic ofProf. Eck. The remedy is said to
act first on the sensibility, afterwards on motility also. Five centigrammes (three-
616 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
fourths of a grain) of phosphorus is to be dissolved in sulphuric ether, and this is to
be made into fifty pills, with breadcrumbs; three to six pills are to be given daily,
until about 0.15 to 0.25 gramme (two and a half to four grains) of phosphorus haye
been consumed, I tried the remedy in one case, without any result; it was well
borne. Further trials are to be desired.
Cod-liver oil is praised by many. It appears, besides its gen-
eral nourishing qualities, also to have a favorable effect on the
nutrition of the nervous system, and therefore deserves to be
used where it is well borne.
Very particular attention is, in all cases, to be given to the
matter of regulating the diet and the method of life of tabes
patients. On this subject we may refer to what was said under
Chronic Myelitis (see above, p. 464) and also to the admirable
remarks of Waldmann on this point. We have nothing to add
to what we have said above with regard to diet, mental labor,
digestion, sleep, sexual intercourse, etc. We would again recom-
mend the utmost possible indulgence in fresh air, especially
mountain-air, sea-air, and the air of the forests. As a feeble
substitute for a winter spent in the south, which is impracticable
for many patients, the daily inhalations of oxygen, lauded by
Waldmann, might be tried.
With reference to bodily movements, we may, according to
our best convictions, dissuade patients from too much walking.
The diseased spinal cord must be spared ; patients quickly grow
tired in walking, and may, therefore, only continue this exercise
until the beginning of fatigue; every overexertion or extreme
fatigue may be of the greatest detriment. Topinard likewise
recommends rest, especially for those people who otherwise work
hard and beyond their strength; on the other hand, he thinks
that light muscular exertion, though never to the point of over-
exertion, is the rather indicated for others, especially patients
from the higher walks of life, who have a poor appetite and
lowered nutrition. The proposition to cure commencing tabes by
quiet rest in bed for several months has not met with any en-
dorsement. As a matter of course, tabes patients must guard
themselves against wet, dampness, cold, and taking cold; for
many of them it is therefore well to wear flannel underclothing.
After having thus passed in review the different means and
ee ee
TABES DORSALIS. 617
methods recommended against tabes, it may be well to offer a
few suggestions with regard to the general plan of treatment
which should be carried out in individual cases.
In cases Just commencing, with light, initial symptoms, we
should first search for any causes of the disease which may be
present and still acting, and remove these. Then the diet and
method of life of the patient should be regulated in the most
careful manner, his activity in his business, his recreations, etc.,
and the patient should early have his attention called to the fact
that only the most methodical and persistent carrying-out of the
regulations prescribed for him may preserve him from a subse-
quent grievous malady. Of course, we should at the same time
strive to quicken his hope and courage. Much must still be left
to the tact of the physician, after careful weighing of the indi-
vidual characteristics of the case. Direct treatment in summer
may be limited to having the patient take up his abode for a few
_ weeks at some appropriate place in the mountains, in good forest
air, or at the sea-side, to having him use a regular cold-water
cure, or a cure at the baths of Rehme or Nauheim. We may
generally reserve for the autumn and winter the regular carry-
ing-out of systematic galvanic treatment, the administration of
nitrate of silver, or any other medicine called for by circum-
stances, as well as the regular use of cold rubbings, washing of
the feet, of the back, etc. In this way different therapeutic
measures may be carried on for months and years, interrupted
from time to time by pauses. If improvement or recovery takes
place, patients must still take good care of themselves for a very
long time, avoid all overexertion, and endeavor permanently to
establish their health and strength by subsequent treatment
(mountain-air, water-cures, sea-baths, etc.).
In quite recent cases, with very prominent signs of irritation, Frerichs (compare
the dissertations of Fabricius, Kauert, Mette, Nachtweyh) recommends the copious
abstraction of blood along the spinal column, and derivation to the skin and bowels
by flying blisters, irritating salves, and colocynth. This method may only be
employed with the greatest caution, and is, of course, entirely to be rejected in the
later stages of the disease.
In more advanced and completely developed cases we shall
not be able to build any too great hopes on therapeutics, how-
618 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
ever much it may be our duty to support the hopes of the
patient. There will be plenty of chance here for the systematic
trial of various means of cure. For the summer months a
course of baths at Nauheim or Rehme may be recommended ;
afterwards also at some one of the thermal springs, with subse-
quent residence in the mountains, or a cold-water cure. In the
intervals the patient should be allowed a couple of weeks of rest
at a pleasant place that suits him, and without any special treat-
ment, except perhaps cool rubbings. For the winter and spring
months the use of the galvanic current especially commends
itself, simultaneously with internal means and cautious hydro-
pathic treatment. If the use of nitrate of silver has been con-
tinued long enough, we may try, one after another, the internal
remedies mentioned above, giving tonics, cod-liver oil, and the
like, in the intervals. The method of life must be regulated ;
care must be taken that patients remain in the open air as much
as possible; they should use a good perambulating chair, and
we must seek by all sorts of external means, by rubbing with
liniments and spirituous washes, by symptomatic treatment, to
act favorably upon the state of mind of the patient. All this is
a very difficult task for the physician, and patients only too
readily lose courage and turn from one physician to another,
expecting help from each one, and dismissed by each with the
same lack of result. se
In quite old, incurable cases, finally, we should seek, so far
as possible, to restrain patients from all useless attempts at
curative treatment. Romberg’s utterances, which have become
celebrated, and were dictated by true humanity, apply to these
cases. If patients possess enough strength of character, they
should be cautiously. informed of the uselessness of further
‘‘cures ;”? if not, we may endeavor to keep them encouraged,
which is generally very easy, with the hopes of improving at a
better time of year, and conduct them through their long period
of suffering with harmless treatment. We should then confine
ourselves to regulating the method of life and the external rela-
tions as far as possible, seeking to secure to the patient as com-
fortable an existence as may be, giving him careful symptomatic
treatment, and letting him spend much time in the open air, at
————————
TABES DORSALIS. 619
the same time improving the general strength by cold rubbing
and sponging. Long journeys to bathing-places are decidedly
.to be avoided ; still we may advise well-to-do patients, who can
accomplish it with all comfort to themselves, to spend the sum-
mer where they can have good mountain or forest air.
In so tedious and severe a malady, running its course in part
with very tormenting symptoms, the symptomatic indications
often urge themselves upon the physician. One must be very care-
ful and ingenious in order to satisfy the desires of the patients.
First on the list are the pains, especially the lancinating
pains, the paroxysms of pain, by which patients are often terri-
bly tormented. Only too often we shall find ourselves helpless
over against them, endeavoring in vain to combat them with
every possible means. I here mention a list of remedies, all of
which help sometimes, but quite as often leave us in the lurch:
sinapisms, blisters, warmth (in the form of hot compresses, sand-
bags, etc.), Priessnitz’s cold-water compresses, opium or bella-
donna plasters, rnbbing with chloroform, veratrine, or oil of hy-
oscyamus ; faradization or galvanization (stabile cathode) of the
particularly painful and hyperesthetic points of the skin ; but,
above all, subcutaneous injections of morphine, which only too
readily become a necessity; among other internal remedies,
quinine and bromide of potassium in large doses, or the hydro-
bromide of quinia, recently recommended by Erlenmeyer (0.50
to 2.0 at a dose, gr. viiss. to gr. xxx.); iodide of potassium
(Leyden) in moderate doses, etc.
Against cutaneous anesthesia, motor weakness, and atrophy
of the muscles, electricity is the only rational means to be
employed.
In weakness of the bladder, faradization of the bladder,
either from without or with the aid of the bladder electrode, is
often useful.
Cystitis and threatening or existing bed-sores are to be
treated in the manner explicitly laid down before (p. 194).
For the amaurosis, strychnine has always thus far been
tried in vain; the galvanic current, also, is extremely seldom of
use. We may deem ourselves fortunate if we accomplish the
arrest of the evil while still in progress of development.
620 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The muscular twitchings that are sometimes present demand
the same means as were indicated for the pains.
The constipation, which almost always exists, is an especially
troublesome symptom. We must proceed against this carefully,
and only with the mildest purgatives. If we can succeed in
attaining our end by appropriate diet (much fruit, Graham
bread, etc.) and simple enemas, so much the better. In specially
obstinate cases the regular faradization of the intestines (one
pole to the sacrum or in the rectum, the other passed over the
entire abdomen, with a strong current) often yields good results.
Attacks of oppression must be combated by the customary
means. Paroxysms of gastralgia are best met with a strictly
limited diet and morphine injections.
The best remedy for the pollutions and increased sexwal
excitability is bromide of potassium (gr. xxx. to gr. xc.). Lupu-
lin and camphor have also often proved useful. Cool hip-baths,
the avoidance of any considerable filling of the bladder, and of
lying on one’s back at night, are also of benefit.
13. Paralysis Spinalis Spastica.—Tabes Dorsal Spasmodique
(Charcot).—Sclerosis of the Lateral Columns ?—Primary
Lateral Sclerosis ?
Tuerck, Ueber primiire Degenerat. einzelner Riickenmarksstringe. Sitzungsber. d.
k. Akad. d. Wissensch. zu Wien. Math. naturw. Classe. Bd. XXI. Jahrg. 1856.
8. 112.—Charcot, Sclérose des cordons latér. d. 1. moelle ép. chez. une femme
hystér. atteinte de contracture perman. des quatre membres. Gaz. hebdom.
1865. Nr. 7.—Charcot et Joffroy, Deux cas d’atrophie muscul. progress. avec
lésions de la subst. grise et des faisc. antéro-lat¢éraux de la moelle ép. Arch. d.
Physiol. II. pp. 854, 629, 744. 1869.—A. Voisin, Meningo-myélite suraigue,
Sclérose des cordons latéraux, etc. Gaz. méd. de Par. 1869. Nr. 40. p. 583.—
Gombault, Sclérose symmetr. des cord. latér., etc. Arch. d. Physiol. IV. p. 509.
1871-72.— Charcot, Sclérose primit. de la part. postérieure des cordons antéro-
lat. Gaz. méd. de Par. 1874. Nr. 3. pp. 88-89.—Charcot, Lecons sur les mal.
du syst. nerveux. II. Sér. fase. 3. Sclerose latérale amyotrophique. Paris,
1874.— W. Erb, Ueb. einen wenig bekannten spinalen Symptomencomplex. Vorl.
Mitth. Berl. klin. Woch. 1875. Nr. 26; und Bericht iib. d. 8. Versamml. stid-
westdeutsch. Irrenirzte zu Heppenheim. Zeitschr. f. Psych. Bd. 32. 1875.—
Fy. Richter, Zur Sklerose der Seitenstr. des R.-M. Deutsch. Arch. f. klin. Medic.
XVII. 8. 365. 1876.—0O. Berger, Die primire Sklerose der Seitenstriinge des
R.-M. Deutsche Zeitschr. f. prakt. Medic. 1876, Nr. 16-19.—Seeligmueller, Skle-
OS ee a eee eee
SPASMODIC SPINAL- PARALYSIS. 621
rose d. Seitenstr. d. R.-M. bei versch. Kindern derselben Familie. Deutsche
med. Woch. 1876. Nr. 16-17.—Leyden, Klinik der Riickenmarkskr. Bd. II, §,
434, 1876,—0. Berger, Ein Fall von Sclerosis later. amyotroph. Deutsche
Zeitschr. f. prakt. Med. 1876. Nr. 29, 80.—Bétous, Etude sur le tabes dorsal
spasmodique. Paris, 1876.—Charcot, Du tabes dorsal spasmodique. Progrts
médic. 1876. Nov. Nr. 45-47.—2Zrb, Ueber Lateralsklerose und ihre Beziehung-
en zur Tabes dorsalis. Arch. f. Psych. und Nervenkr, Bd. VII. 8. 238. 1876.—
Berger, Zur Lehre von der primiiren Lateralsklerose des R.-M. Deutsche Zeitschr.
f. prakt. Medic. 1877. Nr. 3, 5, u. 6.—Rich, Schulz, Mehrere Fille yon “‘ Lateral-
sklerose.” Arch, d. Heilk. XVIII. 8. 352. 1877.— W. Erb, Ueber spastische Spi-
nalparalyse (Tabes dorsal spasmodique, Charcot), Virch. Arch. Bd. 70. 1877.
Introduction and History.
It should be stated, in advance, that in this section we shall
consider that form of disease exclusively, the picture of which I
first gave fully and in detail (Berliner klin. Woch., 1875, No. 26),
and which Charcot has also recently described in detail under
the name of ‘‘ tabes dorsal spasmodique.’’ This was after that
author had for a number of years made short and suggestive
reports with regard to quite similar manifestations of disease,
and had spoken of them as being related to sclerosis of the spinal
lateral columns.
In the meantime, the opinion, that sclerosis of the lateral col-
umns is the anatomical basis of the disease described by Charcot
and myself, has been gaining more and more advocates ; indeed,
it is held by some authors as quite firmly established, although
this is without sufficient grounds, that is, without conclusive
anatomical investigation.
It is only on the supposition that this opinion, which we our-
selves regard as extremely probable, is correct, and will be con-
firmed by subsequent investigations, that we also discuss sclerosis
of the lateral columns in this section, that in the historical
review we allude to those works which treat of primary degen-
eration of the same, and that we shall depict its anatomical
characteristics. If, contrary to our expectation, this opinion
should prove to be false, the disease here to be described would
nevertheless remain as an independent, well-characterized form
of disease, and we should still have go search for the symptom-
picture of sclerosis of the lateral columns.
622 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Tuerck was doubtless the first who recognized a primary
sclerosis of the lateral columns; he expresses himself only briefly
and unsatisfactorily with regard to its symptomatology.
_. All other communications up to 1875 actually originate with
Charcot alone. The manifold investigations into secondary de-
generation of the lateral columns, which fall within this period, at
most furnished a few fixed points in symptomatology; and these
are capable of but very limited application, on account of the
primary disease of the brain or spinal cord.
Charcot first published a case of hysterical contracture which
had lasted continuously for nine years, and had before arisen re-
peatedly ; the autopsy showed symmetrical sclerosis of the poste-
rior sections of the lateral columns throughout the greatest por-
tion of their length. Subsequently, Charcot set up a peculiar form
of lateral sclerosis, which is complicated with muscular atrophy,
and which he afterwards designated as ‘‘sclérose latérale amyo-
trophique;” in giving the description of two cases belonging under
this head, he briefly defined the essential symptoms of sclerosis
of the lateral columns. His subsequent communications always
brought merely brief references of essentially the same import.
The matter then stood thus: The principal symptoms of
sclerosis of the lateral columns had little by little been recog-
nized, being taken from various complicated cases (secondary
degenerations, amyotrophic lateral sclerosis, etc.) ; and from these
the picture of ‘‘ primary lateral sclerosis’’ had been constructed,
with great probability of correctness—this being also said to have
been found present in some of the cases observed by Charcot.
These cases, however, were never published ; no detailed disease-
picture of lateral sclerosis was anywhere delineated ; the disease
figured in no text-book ; and, at least with us in Germany, it did
not occur to anybody to recognize and diagnosticate this as a
very frequent and well-characterized form of disease.
My introductory communication gave the delineation—con-
taining all that was essential—of a disease-picture which bore
the greatest resemblance to the symptom-picture of lateral scle-
rosis indicated in outline by Charcot, which may probably be
regarded as identical with the latter, and actually is so regarded
by most authors.
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SPASMODIC SPINAL PARALYSIS. 623
Charcot himself, then, in 1876, both had this disease described
by his pupil Bétous, under the name of ‘‘tabes dorsal spasmo-
dique,’’ and also himself published an essay thereon. He like-
wise, as yet, expresses himself very guardedly concerning the
anatomical basis of the disease, which can only be finally deter-
mined by renewed anatomical investigations. He says that the
cases formerly observed by him are too old and partake too de-
cidedly of the character of ‘‘somewhat confused memories’’ to
serve as evidence.
During the past year several works have also appeared in
Germany on so-called lateral sclerosis, and O. Berger, in particu-
lar, has handled the subject in several essays. I have myself
recently published my more detailed communications on this
disease.
Definition.
The disease is clinically characterized by a gradually increas-
ing paresis and paralysis, generally advancing slowly from
below upwards, with muscular tension, reflex contractions and
contractures, with strikingly increased reflex actions of tendons,
while at the same time there is entire or almost entire absence of
all disturbances of sensibility or trophic disturbances, of all
vesical or sexual weakness, and of all cerebral disturbances.
The disease, as a rule, is extraordinarily slow in its develop-
ment, insidious and very chronic in its course; it may occur in
various combinations, but in its typical cases is very easily to
be distinguished from all other forms of chronic spinal disease
(from chronic myelitis, myelitis transversa, tabes dorsalis, multi-
ple sclerosis, etc.).
The anatomical characteristics of the disease cannot as yet
be given with certainty ; if everything does not deceive us, the
anatomical basis of the group of symptoms consists in a sym-
metrical sclerosis of the lateral columns, especially of their pos-
terior divisions, advancing gradually from below upwards. It
would constitute a complete analogue to sclerosis of the poste-
rior columns. The correctness of thig presumption can only be
definitely decided by post-mortem examination.
624 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The designation of the disease would naturally be best selected on an anatomical
basis, and ‘‘sclerosis of the lateral columns” or “lateral sclerosis” would therefore
be most appropriate. As long, however, as we are not certain in this matter, it
would be better to select a symptomatic designation. Charcot has chosen the term
“‘tabes dorsalis spasmodica.” I cannot consider this choice very fortunate, and it
is hardly to be accepted for us in Germany. For us the term “‘tabes dorsalis” now
signifies exclusively sclerosis of the posterior columns, and it is doubtless best for
us to abide by it. But if by the term tabes we are again to designate all atro-
phic and sclerotic processes in the spinal cord, we should thereby still be in advance
of our anatomical knowledge of the disease. Furthermore, in Charcot’s designation
the spasmodic element of the disease is the only one that receives due prominence.
But the main symptoms of the disease are manifestly paralysis (paresis) and
spasm (muscular tension and contractures); these should, therefore, receive special
prominence in the designation. After various other trials—following the analogy
of atrophic spinal paralysis—I have chosen the name “ spasmodic spinal paralysis,”
‘‘ paralysis spinalis spastica,” as a provisional clinical designation, and hope that,
in spite of its lack of euphony, it will suffice as a somewhat suggestive name for
the disease, until satisfactory results of post-mortem examinations shall render pos-
sible the choice of a definitive anatomical designation.
Etiology and Pathogenesis.
There is thus far very little to be said on this point. The
disease is a tolerably frequent one, although by no means so fre- |
quent as sclerosis of the posterior columns. But little is known
of any definite predisposition thereto. Only in the smallest
number of cases can the neuropathic tendency be assumed as an
auxiliary cause. The disease seems to attack the male sex some-
what oftener than the female; still the difference is decidedly not
so great as in tabes.
The disease is developed almost exclusively during the age of
maturity ; by far the larger number of cases begin between the
ages of thirty and fifty. But from various observations which I
have reported (1. c.), it would appear that the disease may also
develop itself even in earliest childhood, and we might then
imagine the possible congenital defective development of certain
divisions of the spinal cord. Part of the cases described under
the name of spasmodic infantile paralysis may well belong here.
The remarkable observation communicated by Seeligmueller,
where four children of the same family were taken sick with
amyotrophic lateral sclerosis, should also be placed here.
SPASMODIC SPINAL PARALYSIS. 625
But most frequently it is just the robust, strong people, who
are subject to no neuropathic influences, that are attacked by the
disease, and in the majority of them the most careful interrogation
does not discover any sort of predisposing cause for the disease.
In fact, even the exciting causes of spasmodic spinal paraly-
sis are as good as unknown. Naturally enough, here, too, taking
cold is not rarely assigned as a cause, although not so often, nor
with as much certainty, as it is in some other things. At the
same time, the astonishing many-sidedness of this source of in-
jury may occasionally show itself in this malady too.
Bétous thought that he could demonstrate lead-poisoning as
a cause in one of his cases. Berger believes in the possibility of
its being produced after trawmatic influences. In my cases I
could never prove anything with regard to the influence of sexual
excesses or previous syphilis.
The etiological relations of the disease, therefore, certainly
still remain to be discovered.
Pathological Anatomy,
Going on the supposition announced above, and which is to
be still further established. below, that the disease is identical
with primary sclerosis of the lateral columns, we have here
briefly to depict the anatomical conditions in this affection.
Macroscopically we encounter the usual appearance of gray
degeneration, though here limited in a symmetrical manner to
the two lateral columns, and, indeed, especially to the posterior
divisions of the same. The gray discoloration here occupies the
entire posterior half of the lateral column in the form of a triane
gle, extending inwards to the posterior gray horn, outwards to
the pia mater, and being somewhat indistinctly shaded off for-
wards into the healthy tissue of the lateral column (Fig. 11, @),
According to Charcot and Bouchard, this very form of the: gray
wedge alone should enable one to distinguish primary lateral
sclerosis from secondary degeneration in most of the sections of
the cord. Secondary degeneration of the lateral columns, as a
result of disease of the spinal cord,“is characterized by the fact
VOL. XIII —40
626 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
that the inner posterior contour of the gray spot
does not reach the posterior horns, but remains
separated from it by a narrow zone of normal
white substance, while the gray discoloration, it
is true, here also extends to the pia mater (Fig.
11, 6). Secondary degeneration, the result of
brain trouble, in addition to its usually appearing
only on one side, is said to be distinguished by
the fact that the gray discoloration has a more
roundish form, standing out from the surround-
ing substance in sharp outlines, and never reaches
close to the pia mater (Fig. 11, c). Still these
characteristics are probably not absolutely uni-
versal, though they may, perhaps, apply to most
cases, and to the greater part of the spinal cord.
It must be left to future observations to deter-.
mine positively whether, in primary sclerosis of
Fie. 11,—Half dia-
grammatic representa-
tion of the various forms
of sclerosis of the late-
ral columns (from about
the upper part of the
dorsal region), a, Form
of gray discoloration in
primary sclerosis of the
lateral columns. 06. In
secondary degeneration
asthe result of disease
of the spinal cord. ec,
In secondary degenera-
tion as the result of dis-
ease of the brain.
the lateral columns, the innermost divisions of
the anterior columns, which, according to Flech-
sig, are likewise to be reckoned as part of the
pyramidal tracts, are also diseased.
The degeneration may extend over the greater portion of the
length of the cord, from the lumbar region up into the medulla
oblongata, and even beyond that, showing a somewhat different
configuration and intensity of the process in the different trans-
verse sections.
Microscopically we encounter the ordinary picture of oray
degeneration. In view of the incompleteness of the investiga-
tions thus far made, it is not yet possible to establish a positive
histological distinction between primary lateral sclerosis and
secondary degeneration of the lateral columns.
Among the possible complications of lateral sclerosis, we
must mention sclerosis of the posterior columns (a combination
which was seen repeatedly by Westphal, and is also very com-
mon in the later stages of tabes); furthermore, a more or less
diffuse sclerosis of the anterior columns ; and, finally, a lesion of
the anterior gray horns, which constitutes the rule in that form
of disease described under the name of sclérose latérale amyo-
SPASMODIC SPINAL PARALYSIS. 627
trophique. This degeneration of the anterior gray horns estab-
lishes itself by preference in the cervical enlargement of the cord,
where it involves greater or less areas, and, in addition to the
interstitial changes, especially induces degeneration, atrophy, and
disappearance of the large ganglion-cells in the anterior horns.
All these statements await further anatomical investigations,
to render them more precise.
Pathology of Spasmodic Spinal Paralysis,
Symptoms.
The general picture of the disease is that of motor paraplegia,
generally developing itself very slowly, and gradually advancing
upwards, to which symptoms of motor irritation early ally
themselves—muscular twitchings, muscular tension, rigidity,
and contractures, which lend to the disease-picture a peculiarly
fertile character. To this is added a very striking increase of
the reflex activity of the tendons, much more rarely also of the
reflex action of the skin, while there is an entire absence, at least
for a long time, of any serious disturbances of sensibility, of the
vesical or sexual functions, and of nutrition, and cephalic symp-
toms likewise never arise.
The disease often begins at once, without any further precur-
sors, with the manifestations of motor weakness in one or both
lower extremities.
In other, not rare cases, however, this is preceded, for a
longer or shorter time, by evidences of sensitive irritation—
pain in the back, dragging and tearing pains in the legs, formica-
tion and other pareesthesias, etc. But these are rarely severe,
and are generally of a transitory nature and easily subdued.
The motor disturbance, which sometimes begins in both lower
extremities at once, sometimes in one alone, and very rarely in
the upper extremities, consists at first only in weakness, in being
more easily fatigued, and in a certain heaviness of the limbs.
This gradually becomes actual paresis; the legs grow quite
heavy, the gait becomes dragging, difficult, unsteady. Only in
rare cases, and usually not until the later stages, does this paresis
628 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
increase to complete paralysis. No ataxy appears during the
entire course.
But distinct manifestations of motor irritation early ally
themselves to the paretic symptoms. At first single lighter
twitchings, or jerking of the legs, arise, which occur when sitting
or lying down, often appear at night, and are very frequent
when fatigued; or there may be a certain spasmodic stiffness,
which arises on the execution of certain movements and lasts for
a few moments. This gradually increases to more continuous
stiffness, to regular tension of the muscles, which appears on
active, and still more on passive motion, and affects the patient's
gait ; and finally it comes to permanent and severe contractures,
which fix the limbs in a position of extension. é
From all this, as long as the patients are still able to walk,
there results a very characteristic method of walking, the spas-
tic gait, which we have already previously described in brief
_(p. 97). At first but slight indications of it are to be observed ;
later the disturbance grows more distinct; the dragging and
trailing of the legs, the drooping of the toes on the ground, the
shuffling, the disposition to raise oneself on the toes, keep grow-
ing more marked, and in especially well-pronounced cases a hop-
ping sort of raising of the body takes place with each step, and
a tendency to fall over forward.
On merely placing the point of the foot on the floor, while
sitting, a tremor very generally sets in, evidently in no respect
different from the clonic trembling on passive dorsal flexion of
the foot. And this is caused by the ever-present high degree of
increase in the reflex action of the tendons, which can generally
be demonstrated very early. Not only does the normal reflex
action of tendons show a very abnormal increase, but this also
appears quite actively in many tendons which under normal re-
lations show no trace thereof. |
Objective examination reveals no disturbance of sensibility.
The sensibility of the skin and muscles, tested with the greatest
care and in all directions, appears entirely normal. Not the
slightest swaying appears on closing the eyes, nor any trace of
unsteadiness in the twilight. In part of the cases the reflex
action of the skin appears increased ; generally, however, it is
Rie pce enna Sera ae ale
TL eee WP ere ee |
eos
SPASMODIC SPINAL PARALYSIS. 629
normal, sometimes rather diminished. There is no atrophy of
the muscles. The functions of the bladder and rectum are en-
tirely normal, as are also the sexwal functions. But little is gen-
erally to be seen of vaso-motor disturbances, neither are there bed-
sores nor any other trophic disturbances of the skin. The func-
tions of the brain and the cranial nerves are entirely undisturbed.
During the further progress of the disease the disturbances
gradually continue to advance upward. The muscles of the
back and abdomen become paretic and rigid, the movements of
the trunk grow difficult, sitting up and holding oneself erect be-
come difficult or quite impossible.
Then the affection extends to the arms; this often occurs
tolerably early, but generally not till the later stages of the dis-
ease. Paresis, heaviness, and stiffness of the arms sets in; exam-
ination shows here also an increase in the reflex action of tendons,
but no disturbance of sensibility, no ataxy ; finally, rigidity and
contractures also occur, but rarely full paralysis.
This method of development is not the only and invariable
one. Sometimes the affection passes from one lower extremity
first to the upper extremity of the same side, and the affection
may persist for a long time (even for several years) in this hemi-
plegic form before the other lower extremity is attacked. Some-
times, too, the disease begins-in the upper extremities, and, rwn-
ning its course downward, does not involve the lower extremi-
ties until later.
When the disease has reached a certain point of development,
it may then remain stationary for a variable length of time,
often for many years, or show but a scarcely perceptible advance.
Generally, however, the paralysis eventually becomes com-
plete, the contractures increase in intensity, and the patients,
grown stiff and immovable, are doomed to permanent lying still.
At the same time, there may be an entire absence of pain and of
other disturbances of sensibility, the vegetative functions may
take their regular course.
The disease in itself does not appear directly to threaten life,
and patients generally die of some intercurrent disease.
Now and then, however, death is doubtless induced by the
extension of the processes within the spinal cord to structures of
630 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the same, which are more important to life. The complications
of the disease—always rare—which betray such an extension of
the same, are muscular atrophy, bulbar symptoms, disturbances
of sensibility, vesical weakness, cystitis, bed-sores, etc.
In estimating the importance of individual symptoms, “we
must principally direct our attention to the paresis and paraly-
sis, the spasms, rigidity, and contractions, to the peculiarities of
the gait resulting therefrom, and to the heightened reflex action
of tendons.
The manifestations of motor paralysis generally begin with
some fatigue, insecurity, weakness, and stiffness of the lower
extremities, sometimes of both at once, but not rarely of one leg
somewhat earlier than the other.
The legs feel as heavy as lead; every prolonged exertion
fatigues the patients extremely; finally, longer marches and
walks become impossible ; the gait grows distinctly dragging.
Gradually it comes to distinct paresis ; patients are no longer
able to raise themselves on their toes, much less to maintain them-
selves thereon ; it becomes difficult or impossible for themto raise
their legs, if extended, while lying down; the leg, extended at
the knee, offers less resistance to attempts at passive motion.
At the same time all movements are quiet and uniform, only
sometimes rather uncertain on account of the paresis. No sign of
ataxy is to be noticed. All movements called for can be exe-
cuted just as quietly and certainly with closed as with open eyes.
Finally, complete paralysis may be developed; it is generally
confined to the domain of single nerves and muscles, but may
gradually extend further. The paralysis seldom becomes quite
complete ; that entire immobility of the limbs, so characteristic
of many cases of myelitis, does not readily occur here.
This is the usual picture. But sometimes it happens that the
disease begins unilaterally, and retains its hemiplegic form for
quite a while, a point to which Berger called attention in his ©
first work ; the paresis then extends from one leg first to the arm
of the same side, and may exist in this way for a long time (as
much as several years) before the weakness invades the other
Jeg, and finally the other arm. In all these cases the leg is more
paralyzed than the arm.
a i i a a
. _
ee
SPASMODIC SPINAL PARALYSIS. 631
But now and then the affection also begins in one or both
upper extremities, and the legs are not invaded by the paralysis
until later. In these cases, however, the paralysis of the legs is
liable soon to become quite as intense as that of the arms.
Very soon after the signs of paralysis, occasionally almost
simultaneously with these, manifestations of motor irritation
also show themselves.
At first they are merely single jerkings, which arise under
the most varied circumstances while sitting, lying in bed, etc.,
and often appear to the patient like a sort of starting from
fright. The foot is suddenly raised, or the leg thrown some-
what into the air, or, on making voluntary movements, a species
of cramp sets in, single:muscles or the entire leg growing tem-
porarily stiff. . Often the familiar trembling on setting down
the toe of the foot occurs, especially if the patients are some-
what fatigued.
Then distinct muscular tension is developed. At first, on
performing passive motion, there is a doughy, gradually increas-
ing resistance, which can be overcome by increasing pressure
and somewhat lessened by repeated movements, but which again
appears distinctly, especially on brisk attempts at movement.
Soon the tension also shows itself in active movements, renders
them difficult, makes them uncertain, and thus causes the paresis
to appear greater than it is in reality.
Finally it comes to a permanent greater rigidity of the mus-
cles, which gradually goes on developing to a regular and high
degree of permanent contracture. This generally appears in the
lower extremities in the form of a contracture with extension.
The legs are held in the position of rigid extension, the feet in
the extreme position of talipes varo-equinus, the toes sometimes
flexed on the dorsum, and furthermore the legs are rigidly held
together by the extreme contracture of their adductors. The
rigid immobility of the legs is now and then interrupted by a
clonic trembling of the feet, which may extend to the entire legs,
which apparently often arises spontaneously, but is probably
to be referred to a dorsal flexion of the foot produced in a reflex
manner or called forth by touching the point of the foot, and
which may probably now and then also be referred to a volun-
632 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
tary effort. Contractures with flexion rarely occur in the lower
extremities, and then only in the latest stages.
The upper extremities are visited with contractures much less
frequently and intensely ; the arm is then drawn to the trunk,
the forearm is in half flexion and in pronation, wrist and fingers
in a high degree of flexion. All these contractures naturally in-
crease the helplessness of the patient,and are a greater hindrance
to the use of the limbs than the paresis.
As long as patients can still walk, these paralytic and spas-
modic manifestations result in an extremely peculiar and thor-
oughly characteristic gait, which we have already designated
as the ‘‘spastic gait’’ (p. 97).
The first thing noticeable is a certain dragging of the limbs;
the feet are drawn forward with difficulty ; they seem to cling to
the ground, and, as they slide forward, produce a characteristic
scraping noise; the tip of the foot catches on every little inequal-
ity of the ground, and patients readily stumble and fall. The
gait is thereby rendered uncertain and swaying; at every step
the patient changes his centre of gravity from one side to the
other. The shoes mainly wear off at the toes and outer border.
In the higher grades of the disturbance, patients show a dis-
tinct tendency to raise themselves on their toes; the friction
that takes place between the ground and the feet causes a cer-
tain disturbance of equilibrium in the upper portion of the body
which is tending forwards, and thus the disposition arises to fall
over forwards and in walking to adopt an increasingly rapid
step. In some instances this is further associated with a peculiar
hopping movement, a raising oneself up on the toes with every
step, which produces a very remarkable effect.
At the same time the legs are carried ina stiff and constrained
manner; they are locked closely to one another and somewhat
sunken at the knees ; the steps are small and hesitating.
It is evident at the first glance how sharply this variety of
gait is distinguished from the ataxic. There is no trace of the
flinging motion of the legs, of throwing forward or turning out-
ward the tip of the foot, of stamping the heels, of holding the
knee stiff to a degree bordering on hyper-extension, as in ataxy ;
we see, rather, the opposite of all this.
|
SPASMODIC SPINAL PARALYSIS. 633
The peculiarities of the spastic gait are very easily explained
—in part by the paresis, which causes the dragging and the catch-
ing of the toes; in part by the muscular tension, which brings
about the stiffness of the movements, the closed position of the
legs, the short steps, the scraping with the tip of the foot, the
walking on the toes ; and in part by the heightened reflex action
of the tendons, which probably explains the hopping movement
with every step.
At last, of course, all walking ceases, and patients are able,
at most, to drag themselves around on crutches, or, with the
help of their hands, to move about by holding on to chairs and
furniture, dragging their legs after them like two sticks, and
only now and then using them as props. Finally, patients are
doomed to continuous lying in bed, as sitting up often becomes
downright impossible, on account of the stiffness of their legs.
We have already, at various places in this work; referred to
another important, and, as it would appear, absolutely constant
symptom of the disease—the great increase in the reflex action
of tendons. This may be observed to a very intense degree in
spasmodic spinal paralysis, inasmuch as not only those tendon-
reflexes which normally exist in the majority of people show a
greatly increased intensity, but many other tendons likewise
(and even other aponeurotic structures) may be excited to active
reflex twitching through mechanical irritation.
The reflex action of the tendon of the patella is most con-
stantly increased—not rarely to such an extent that it can be
maintained in a clonic form by the sudden, forcible fixation of
the patella with a blow downwards. Not less constant is the
increase in the reflex action of the tendo Achillis, which can
generally be maintained in the clonic form on passive dorsal
flexion of the foot. The reflex activity of the tendons of the
adductors generally behaves in the same way. I have repeatedly
been able to excite this by tapping over the region of the lum-
bar vertebrxe. Tendon-reflexes, furthermore, occur in the lower
extremities in the tibialis anticus and posticus, in the biceps
femoris, the semi-tendinosus, etc. Reflexes in the quadriceps
also sometimes originate in the upper broad end of the tibia.
The reflex action of the tendons is generally no less well
634 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
developed in the upper extremities. It is to be found in the
biceps and triceps humeri. Quite remarkable reflexes can be
aroused from the lower end of the radius, as well as from the
ulna, by tapping—the first in the biceps, the latter in the triceps
and. the posterior portion of the deltoid. The flexors of the
fingers and the extensors of the wrist, as well as the supinator
longus, can be excited in a reflex manner by their tendons;
also sometimes the interossei by tapping on the metacarpal
bones, the deltoid from the spine of the scapula, the pertonaus
major from the sternum, etc.
It hardly requires demonstration that in all these cases we
have to deal with nothing else than a heightening of the reflex
processes. This appears as an absolute necessity, from some of
the facts heretofore communicated, entirely aside from the cir-
cumstance that all authors who, since the appearance of West-
phal’s works and my own, have occupied themselves particularly
with this circumstance, have come to the conclusion that the
physiological phenomena mentioned could only represent reflex
processes. We must therefore refer the increase in the tendon-
reflexes which arise in spasmodic spinal paralysis to an increase
in the reflex activity of the spinal cord.
The singular part of it is that this increase is almost always
confined to this one class of reflexes ; for the skin reflexes by no
means constantly show any similar relations. I found them dis-
tinctly increased in hardly one-third of my cases; in the rest
generally normal—often not at all distinctly present, but also
often tolerably lively, even if not exactly abnormally heightened.
At all events, however, the reflex activity of the skin by no
means bore any relation to that of the tendons, and the increase
of the former certainly does not constitute an essential symptom
of spasmodic spinal paral ysis.
The electrical excitability of the motor nerves never shows
any qualitative, but always merely insignificant quantitative
changes; in all the cases more carefully examined, I found a dis-
tinct, though slight, Zowering of the faradic and galvanic excita-
bility. Ihave never yet found an increase of the same. —
All the other symptoms that remain to be noticed areofan
essentially negative quality ; but this very fact contributes not a -
oS ee
SPASMODIC SPINAL PARALYSIS. 635
little to characterize the disease. The entire absence of every
disturbance of sensibility, even on the most careful testing of
the sensibility of the skin and muscles; the absence of vesical
and sexual weakness ; the absence of muscular atrophy and of
bed-sores ; the entire absence of disturbances of the brain and
cranial nerves,—are at least as significant and as important for
the characterization of the disease as the presence of paresis,
muscular tension, and increased reflex action of tendons.
Other isolated symptoms—and indeed of the most varied
kind—do occasionally arise, but appear as more or less acciden-
tal features in the disease, and will be more appropriately dis-
cussed under the head of Complications.
Course, Duration, Terminations.
The course of the disease, in the majority of cases, is very
slow, insinuating, and chronic. Months and years may pass
before the manifestations have so far developed that the disease
can be recognized with certainty. And then the trouble often
remains stationary for years. In some cases, however, the mani-
festations develop more rapidly, and may within a few months
assume the form of the typical disease-picture.
The duration of the disease is always of many years, and is
generally to be reckoned by decades. Complicated cases only—
of which we shall speak below—are sometimes of short dura-
tion, and run their course to a fatal termination within a few
years.
Among the terminations of the disease, that in recovery is
probably the rarest, although not quite as uncommon in this
form as in other forms of chronic spinal paralysis. Already in
two cases I have seen complete or almost complete recovery set
in. Several cases have been materially improved.
Generally, however, the disease remains stationary for an
indefinite length of time, or makes extraordinarily slow progress.
It does not seem, of itself, to threaten life directly ; in most cases
death occurs through accidental, intercurrent diseases.
If complications arise, these may cause death; thus, for in-
stance, bulbar symptoms, or the manifestations of severe spinal
636 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
paralysis, such as cystitis, bed-sores, etc., with their evil conse-
quences, which produce gradual exhaustion of the patient.
Theory of the Disease.
The theory of spasmodic spinal paralysis cannot as yet be
firmly established, on account of the lack of reports of post-mor-
tems. But some isolated conclusions may still be drawn from
our present physiological and pathological knowledge, and these
will here be given in brief. |
The essential features in the symptom-picture of spasmodic
spinal paralysis are, on the one hand, the presence of paresis and
paralysis, muscular tension and contractures, and the heighten-
ing of some kinds of reflex action (that of the tendons), and, on
the other hand, the absence of disturbances of sensibility, of
vesical and sexual weakness, of trophic disturbances of the skin
and muscles, of ataxy, and of all brain symptoms.
From these latter negative symptoms we may, with consider-
able certainty, exclude certain divisions of the spinal cord from
participation in the disease, viz.: the posterior columns, the pos-
terior gray horns, the central gray substance, and probably also
a great part of the anterior gray horns; of course, also the brain.
We therefore only have the so-called motor portions of the
spinal cord left for the localization of the disease, that is, the
antero-lateral columns, and perhaps also a portion of the gray
substance. |
More recent physiological investigations unanimously indicate
that the lateral columns at least quite certainly contain motor
tracts, while we are still uncertain with regard to the functions
of the greater part of the anterior columns proper. An irrita-
tion and paralysis of these motor tracts in the lateral columns,
caused perhaps by an inflammatory affection, might accordingly
very well explain the muscular tensions and pareses present in
our disease. The entire absence of atrophy probably justifies us
in excluding, with some certainty, disease of the motor tracts
within the gray substance; the same evidence, as well as the
failure of the reflexes, positively excludes disease of the anterior
roots—therefore probably also disease of those portions of the
et RN a EP AR We ke ee Seer ae = — = 3
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SPASMODIC SPINAL PARALYSIS. 637
anterior columns traversed by these roots. If, on the basis of
our present physiological knowledge, we are to refer the existing
manifestations of motor irritation and paralysis without atrophy
of the muscles to any lesion of the spinal cord, we are thus
pointed to the lateral columns, especially to the posterior divi-
sions of the same, which contain the so-called pyramidal tracts
of the lateral columns [Pyramidenseitenstrangbahnen] (Flechsig).
Then the increase of reflex action would still remain to be ex-
plained. This can hardly be referred to disease or increased
irritability of the gray substance, as all other symptoms of dis-
ease of the gray substance are wanting. The only explanation
then lies in a lesion of the tracts which control reflex action ;
according to the investigations of Woroschiloff, these also lie in
part within the lateral columns ; consequently we may with pro-
priety refer the symptom of increased reflex action of the ten-
dons also to a disease of the lateral columns.
Pathological experiences coincide with this in a significant
manner. Ifa unilateral paralysis, caused by cerebral apoplexy,
has contractures and increased reflex action of tendons associated
with it, anatomical investigation uniformly demonstrates the
familiar signs of descending secondary degeneration of the lateral
columns of that side. In the numerous affections of the spinal
cord, which present as one of their manifestations secondary de-
generation of the lateral columns (transverse myelitis, myelitis
from compression, hematomyelia, multiple sclerosis, etc.), mus-
cular tension, contractures, and increased reflex action of the ten-
dons, are found in addition to the symptoms of the fundamental
affection. In amyotrophic lateral sclerosis Charcot has several
times anatomically demonstrated sclerosis of the lateral columns
as a very probable cause of paralysis, contractures, and increased
reflex action of the tendons. In a case of combined sclerosis
of the posterior columns and the lateral columns, Westphal,’
in addition to disturbances of sensibility, found paralysis
with muscular twitchings and muscular tension, and increased
reflex action of tendons. As these symptoms never occur in
consequence of sclerosis of the posterior columns, they cannot
>
1 Archiv f. Psych. u. Nervenkrankh. Bd. V. p. 822. 1875.
-— ae
-
638 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
well be referred to anything else than the sclerosis of the lateral
columns.
Physiological and pathological experiences, therefore, with a
unanimity that is worthy of consideration, point to the lateral
columns as the seat of disease; and we shall probably not go
amiss if, as Charcot did long ago, we accept a chronic inflam-
matory process, a sclerosis of the posterior divisions of the
lateral columns, as the highly probable anatomical basis of
spasmodic spinal paralysis.
But, unfortunately, we thus far lack conclusive reports of
post-mortems. Until we have such, this assumption remains only
a very probable one; and, in view of the exceedingly vacillating
character which still attaches to our ‘‘ physiological and patho-
logical experiences’’ concerning the spinal cord, we shall do well
to await the definitive confirmation of this view before exchang-
ing our clinical designation for an anatomical one.
- *
’ ee a a
Complications.
The disease-picture of spasmodic spinal paralysis does not
always appear in its clear, typical form. Quite apart from those
cases in which this constitutes only one of the features in the
symptom-picture of other diseases, and is probably to be re-
garded as the expression of the secondary degeneration of the
lateral columns, we also encounter in this form of disease, as
well as in numerous other spinal diseases, single cases in which, |
while the symptom-picture of spasmodic spinal paralysis decid-
edly dominates, it still appears complicated with single symp-
toms or with whole series of symptoms, which give evidence of
the extension of the disease to neighboring or remote portions of
the spinal cord.
In my detailed work alluded to above, I have touched some-
what more specifically on these relations, and have pointed out
the fact that there are two series of symptoms in particular
which complicate the disease-picture of spasmodic spinal paral-
ysis in this way, and may render the diagnosis more difficult.
On the one hand there are the symptoms of sclerosis of the pos-
terior columns, of actual tabes (slight disturbances of sensibility,
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SPASMODIC SPINAL PARALYSIS. 639
swaying on closing the eyes, slight vesical weakness, lancinating
pains, distinct ataxy, etc.) ; on the other hand, the symptoms of
a more or less extensive, more or less progressive atrophy of the
muscles, which arises by preference in the upper extremities.
So far as complicated cases of the first variety are concerned,
to which Berger already drew attention, all possible gradations
of tabes symptoms occasionally take place in them, sometimes
only slight subjective disturbances of sensibility, combined with
some vesical weakness, sometimes lancinating pains, pareesthe-
sias, and the sense of a tight girdle, combined with indications
of ataxy, swaying on closing the eyes, etc.; sometimes the tabes
symptoms (anesthesia, ataxy, vesical and sexual weakness) may
even stand in the foreground, and only the simultaneous pres-
ence of paresis, muscular tension, and especially of increased
reflex action of tendons, gives evidence of the existence of spas-
modic spinal paralysis likewise. There are also cases in which
the diametrically opposite of the typical forms of spasmodic
spinal paralysis and tabes are more or less mingled, and in which
one may be in doubt whether to credit them more to the one or
to the other form of disease.
The doubt in such cases may be most easily solved on the
assumption—which seems the most natural and the most appli-
cable—that we here have to deal with a combination of sclerosis
of the posterior columns with sclerosis of the lateral columns.
Such cases have frequently been seen—their existence in the last
stages of tabes is well enough known,—and Westphal, in the
work cited above, especially pointed out their occurrence. But
this question, too, can only be cleared up by conclusive results
of post-mortem examinations.
In the complicated cases of the second variety, likewise, there
are all possible gradations of muscular atrophy to be observed.
Sometimes one sees merely a simple, not very high grade of ema-
ciation of the paralyzed extremities, with or without scanty
fibrillar contf&ctions, or there are more distinct atrophic condi-
tions, which may remind one of beginning progressive muscular
atrophy. This is seen particularly in the upper extremities, and
is sufficiently designated by the atrophy of the small muscles of
the hand, the sinking of the inter-metacarpal spaces, the charac-
640 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
teristic claw-shape of the hands, etc. But recently two cases
have fallen under my observation in which the typical manifes-
tations of spasmodic spinal paralysis were supplemented by this
atrophy of the muscles of the hand on paretic upper extremities.
To explain this complication, we must suppose that the scle-
rotic process, which we believe to exist in the spinal cord, extends
to the gray anterior horn—with special ease and frequency in
the cervical enlargement—and from here produces the muscular
atrophy by lesion of the large ganglion-cells.
But the highest degree of this combination of spasmodic spi-
nal paralysis with muscular atrophy is presented by those cases
in which the atrophy of the upper extremities shows a rapidly
progressive character, in which bulbar symptoms associate them-
selves with it sooner or later, and within a few years the disease
leads to a fatal termination.
These cases, which were formerly generally counted in with
actual ‘‘ progressive muscular atrophy,’’ but which may be
sharply distinguished from the typical form of the same, have of
late been more carefully investigated, anatomically and clinic-
ally, by Charcot, who has drawn a disease-picture of the same in
his customary masterly manner, and given it the name of
Sclérose Latérale Amyotrophique.
We will here devote a little space to the discussion of this
disease, as it appears to us to bear an undoubted relationship to
spasmodic spinal paralysis, although it differs from the latter in
some not unimportant points. As we do this in a manner that
implies no prejudgment of the case, we reserve the right, in case
further investigation of this interesting disease should justify it,
to assign to it another more appropriate place.
According to Charcot, amyotrophic lateral sclerosis is char-
acterized as follows: .
The disease generally begins in the upper ea@emities with
motor weakness, to which a more diffuse muscifar atrophy is
soon added, with fibrillar twitchings, etc. Then mwscular ten-
sion and contractures are developed, which bring the arms into
a permanently deformed position: the upper arm is pressed fast
|
{
|
}
SPASMODIC SPINAL PARALYSIS. 641
to the trunk, the forearm half flexed and pronated, hand and
fingers strongly flexed. Whatever movements can still be exe-
cuted are weak and tremulous. The muscular atrophy progresses
rapidly ; sometimes there is lipomatous hypertrophy of the same.
In a case, evidently belonging here, and which is furthermore of interest, because
the disease is developed on a young man who carries about him the sequels of an
attack of the “spinal paralysis of childhood,” galvanic examination shows the
most pronounced reaction of degeneration in the extremely atrophied muscles of
the upper extremities, while the excitability of the nerve-trunks is nevertheless
preserved. In a very marked case, Berger found normal qualitative and quantita-
tive electrical excitability in the nerve-trunks.
After a longer or shorter time, usually after from six to nine
months, the lower extremities are also attacked ; sometimes formi-
cation and numbness set in, always paresis, advancing to final
paralysis ; to these are added muscular tension, permanent con-
tractures, generally contractures in the position of extension, in-
creased reflex action of tendons. At first there is no atrophy in
the lower extremities ; the muscles are tense and firm ; no anes-
thesia, no paralysis of the sphincters, no bed-sores. It is not till
very late that fibrillar contractions take place, and gradually
diffuse atrophy of the legs ; then the contractures diminish.
Finally, in a third stage, the manifestations of bulbar paral-
ysis are added to the preceding: paralysis and atrophy of the
tongue and lips, paresis of the pharynx and larynx, finally dis-
turbances of respiration, which before very long induce death.
The malady develops itself rapidly, and is said always to
induce death in from one to three years.
The characteristics of the disease then are: the paralysis and
contracture, with rapid, diffuse muscular atrophy in the upper
extremities ; the paralysis, with contracture and afterwards atro-
phy in the lower extremities ; the final manifestations of bulbar
paralysis.
In a number of post-mortems, Charcot, Joffroy, Gombault,
and others, found symmetrical sclerosis of the lateral columns
and degenerative atrophy of the anterior gray horns, with loss
of the large ganglion-cells.
Charcot refers the paresis and contracture to the sclerosis of
the lateral columns ; the muscular atrophy to the degeneration of
VOL. XIII.—41
642 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the gray substance; the bulbar paralysis to the extension of this
degeneration to the nerve-nuclei in the medulla oblongata.
The lateral sclerosis is said to be the primary step; from the
lateral columns the process passes over to the anterior gray
horns, perhaps by conduction along the physiological tracts
which lead from the lateral columns to the large ganglion-cells
of the anterior horns.
The distinction between amyotrophic lateral sclerosis and the
typical form of spasmodic spinal paralysis is evident from the
earlier involvement of the upper extremities, from the superven-
tion of muscular atrophy and of bulbar paralysis, and, finally,
from the rapid course of the former. It differs from progressive
muscular atrophy in the fact that, in amyotrophic lateral scle-
rosis, the atrophy is preceded by paralysis, and that there are con-
tractures in the uniform atrophy which extends over whole mus-
cular masses, and in its decidedly more rapid pernicious course.
According to the experiences thus far before us, which are of
course by no means final, the prognosis of amyotrophic lateral
sclerosis seems to be absolutely unfavorable.
Further investigations with regard to this interesting form of
disease are greatly to be desired. |
Diagnosis.
The disease-picture of spasmodic spinal paralysis is so charac-
teristic that it can always be recognized with the greatest ease,
especially when it is uncomplicated. The sum of the positive
symptoms (paresis, paralysis, muscular tension, contractures,
increased reflex action of tendons, a development which is slowly
and, as a rule, systematically progressive from below upwards,
etc.), and of the negative symptoms (absence of anzesthesia, of
vesical and sexual weakness, of atrophy, of bed-sores, of cerebral
symptoms), usually establish the prognosis with certainty.
We must remember to distinguish it from the following forms
of disease: |
First, from myelitis transversa (myelitis from compression,
hematomyelia, etc.). In this we regularly find, besides the
motor, also sensitive paralysis of various degrees, vesical weak-
SPASMODIC SPINAL PARALYSIS. 643
ness, bed-sores; the paraplegia is developed more rapidly and
completely, but the upper boundary of the paralytic manifesta-
tions remains stationary. Reflex action of the skin, as a rule, is
materially heightened. To this are usually added extreme evi-
dences of sensitive irritation, at the beginning; furthermore,
those manifestations of the disease which indicate the existence
of compression, etc. 7
In fairly well-marked cases, spasmodic spinal paralysis is
very easily to be distinguished from tabes dorsalis. In tabes
there are lancinating pains, the sense of a tight girdle, sensitive
disturbances, the lowering of muscular sense, swaying on closing
the eyes, disturbance of certain cranial nerves, ataxy, a flinging,
stamping gait, vesical and sexual weakness, no paresis or paraly-
sis, no muscular tension and contractures, the entire absence of
all tendon reflexes. In spasmodic spinal paralysis we have the
opposite of all this. In all typical cases, therefore, the distinc-
tion will be easily made. In those cases, however, in which a
combination of the two classes of symptoms is recognizable, we
shall be enabled, according to the hints given above, to recog-
nize the greater or less participation on the part of each disease
by the preponderance of one or the other set of symptoms.
This disease is to be distinguished with certainty from polio-
myelitis anterior chronica (chronic atrophic spinal paralysis; see
farther on) by the fact that,in the latter, a high degree of atrophy
of the paralyzed muscles is very rapidly developed, with loss of
faradic excitability and with the reaction of degeneration ; that
there is an entire loss of the reflex action of tendons; and that
contractures, if they do occur, at first only attack the antago-
nists of the paralyzed muscles. The development of the paraly-
sis is furthermore very much more rapid.
In most cases the distinction between this disease and malti-
ple sclerosis is easy, except when the latter, at the beginning,
makes its first and only localization in the lateral columns, and
then presents itself quite under the typical picture of spasmodic
spinal paralysis. In that case a diagnostic distinction between
the two is simply impossible. Not until the moment when the
multiple sclerosis makes further localizations, and causes these
to be noticed by further more or less*characteristic symptoms
644 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
(sensitive disturbances, psychical changes, disturbances of cer-
tain cranial nerves, nystagmus, ataxy, trembling, disturbances
of speech, etc.), shall we be able to settle the diagnosis, with i in-
creasing certainty, in favor of multiple sclerosis.
In distinguishing between paralysis from lesions of the
cauda equina and other peripheral paralyses, the following
may be considered as decisive symptoms: the absence of disturb-
ances of sensibility and muscular atrophy, the retention of elec-
trical excitability and the increase of the reflex action of tendons.
The proper significance of those cases of spasmodic spinal
paralysis which assume a hemiplegic form will easily be recog-
nized on giving them a little attention. They are readily to be
distinguished from Brown-Séquard’s unilateral lesion of the spi-
nal cord, which we shall describe in the following section, by the
absence of crossed anesthesia and other symptoms to be de-
scribed in that section. Over against cerebral hemiplegia we
must remember that spasmodic spinal paralysis, as a rule, begins
in the lower extremities, and advances but very slowly to the
upper; that the upper extremities are usually much more lightly
attacked ; that muscular tension and contractures are developed
early ; that disturbances of sensibility, as well as all symptoms
on the part of the head and cranial nerves, are entirely wanting.
In view of these signs, it will not be easy to be mistaken.
The presence of the symptom-picture of spasmodic spinal
paralysis in mixed and complicated forms of disease (transverse
myelitis, myelitis from compression, multiple sclerosis, amyo-
trophic lateral sclerosis in connection with sclerosis of the poste-
rior columns, etc.) will generally be easily recognized by its
characteristic signs. |
Prognosis.
According to the experience thus far before us, spasmodic
spinal paralysis seems to run a less pernicious course than the
forms of chronic spinal disease thus far studied. On the one
hand, it seems to be compatible with an unlimited duration of
life (if very decided complications do not exist), and this doubt-
less depends on the absence of those disturbances of the bladder
SPASMODIOC SPINAL PARALYSIS. 645
—cystitis, bed-sores, etc.—which so often bring a fatal termina-
tion. On the other hand, the disease is capable of improvement,
and, in a few cases, also of recovery. I have thus far seen as
good as complete recovery in two cases, and material improve-
ment in three; though it is true that most cases receive no bene-
fit from treatment. The prognosis, as regards life, is therefore,
in general, very favorable ; as regards recovery, it is at least more
favorable than in the other forms of chronic myelitis.
If complete paralysis and extreme contractures have once set
in, we can hardly expect any improvement.
Certain complications, especially muscular atrophy, bulbar
symptoms, etc., of course vitiate the prognosis to a greater or
less degree. Furthermore, this is naturally also dependent on
the general and special circumstances of the individual case.
Therapeutics,
All that we have said above with regard to the treatment of
chronic myelitis, and that of tabes, might also be applied to the
therapeutics of spasmodic spinal paralysis, as this disease is
doubtless most intimately related to those just mentioned.
As one of the means which has thus far, in my own hands and
those of others, afforded the best results, may be mentioned the
galvanic current ; its application is to be conducted entirely
according to the general principles repeatedly laid down.
Aside from this, the use of a reasonably conducted cold-water
cure deserves the greatest confidence; gaseous saline thermal
springs may also be used; simple thermal waters, unless most
carefully managed, are objectionable.
Internally we may first try the nitrate of silver, and then the
other remedies mentioned above. Strychnine is, under all cir-
cumstances, contraindicated.
With reference to diet, method of life, exercise, living in the
open air, the regulating of sleep, of sexual intercourse, etc., I
refer my reader to the discussion of these points as cited above.
ee
ort 4
7
646 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
14. Unilateral Lesion of the Spinal Cord—Brown-Séquard s
Spinal Paralysis—Hemiplegia et Hemiparaplegia Spinalis.
Brown-Séquard, Course of Lectures on the Physiol. and Pathol. of the Central Nery.
Syst. Philad. 1860.—Recherches sur la transmission des impressions de tact,
de chatouillement, de douleur, etc., dans la mo#lle ép. Journ. d. 1. Physiol. de
Vhomme et des animaux. VI. pp. 124, 232, 581. 1863. (Also contains most of
the older cases.)—On spinal hemiplegia. Lancet. 1868. Vol. II. pp. 598, 659,
755, 821.—Recherches sur le trajet des diverses esp?ces de conducteurs d’im-
pressions sensit. dans la moélle ép. Arch. de Physiol. I. p. 610 u. 716. IL p.
236 u. 693. 1868 u. 1869.—Vigués, Plaie de la moélle ép. dans la région dor-
sale. Monit. des hdp. 1855. p. 838.—Bland Radcliffe, Lancet. 1865. May 27.
—Bazire, Lancet. 1865, July. p. 116.—Uspensky, Zur Pathologie des R.-M.
Virch. Arch. Bd. 35. 8S. 301. 1866.—Jaccoud, Lecons de clin. méd. Paris, 1867.
p. 451,—Perroud, Journ. de médec. de Lyon. Vol. X. p. 385. 1868.—Charcot,
Hémiparaplégie déterminée par une tumeur, etc. Arch. de Physiol. IL p. 291.
1869.—C. J. F. Richter, Fall’ von einseitiger Riickenmarksverletzung. Diss.
Berlin, 1868.—M. Rosenthal, Ueber spinale Halbseitenlahmungen. O6esterr.
Zeitschr. f. pr. Heilk. 1867. Nr. 47-52.—Klin. d. Nervenkrankh. 2. Aufl. §.
395. 1875.—Paoluzzi (Cantani), Affez. di una meta laterale del midoll. spin.
etc. Morgagni. Disp. XI. 1870.—Vieber, Klin. Stud. iib. d. Brown-Séquard’sche
Spinallahmung. Wien. med. Zeitung. 1871. Nr. 21-23.—W. Mueller, Beitr.
zur pathol. Anat. und Phys. des R.-M. Fall 1. Leipzig, 1871.—Joffroy et Sol-
mon, Plaie d. 1. moélle ép. dans, la rég. dorsale. Gaz. méd. de Par. 1872. Nr.
6-8.— Charcot et Gombault, Lés. dissém. des centres nervy. chez une femme
syphil. Arch. d. Phys. V. p. 143. 1873.—Riegel, Halbseitige Riickenmarksver-
letzung. Berl. klin. Woch. 1873. Nr. 18.—TZvoisier, Deux cas de lésions
scléreuses, etc. Obs. II. Arch. d. Physiol. V. p. 709. 1873.—Lanzoni, Sifiloma
sulla porzione infer. etc, Il Morgagni, 1874. Marzo.—M. Bernhardt, Halb-
seitige Riickenmarksverletzung. Arch. f. Psych. u. Nervenkrankh. IV. S. 227.
1874.— Viz, Einseitige Verletzung des verl. Marks u. s. w. Correspondenzbl. d.
iirztl. Ver. im Rheinland. 1874. Nr. 14. (Centralbl. 1875. Nr. 22.)—Burresi,
Lo Sperimentale. 1871. Gennajo. 1875. Noy. (s. Virchow-Hirsch Jahresber.
1871 u. 1875.)—G. ». Dall? Armi, Halbseitige Verletzung des R.-M. Diss. :
Wiirzb. 1875.—Feder. Alessandrini, Ferita della meta destra del mid. cervic. :
infer. Annal. univers. Oct. 1876.—H. Koebner, Die Lehre von der spinalen ;
Hemiplegie. Deutsches Arch. f. klin. Medic. Bd. XTX. 8. 169. 1877.
Introduction and History.
This section treats, not of a single, definite form of disease,
but of various different diseases of the spinal cord (such as
HEMIPLEGIA ET HEMIPARAPLEGIA SPINALIS. 647
traumatic injuries, inflammation, compression, sclerosis, tumors,
syphilis, etc.), all of which, however, by reason of their definite
localization, acquire such characteristic features that they may
be treated of under one common head. The very peculiar pic-
ture of disease here presented depends on the localization of the
trouble in one lateral half of the spinal cord—the more or less
complete destruction of one entire lateral half of a transverse sec-
tion of the cord, while the longitudinal extent of the diseased
process may vary exceedingly.
To Brown-Séquard, in particular, belongs the credit of having
exhaustively studied this group of symptoms, both by means of
clinical observations on the human subject and by numberless
experiments on the lower animals, and of having established,
beyond all doubt, the fact of its frequent occurrence. He was
the first who asserted, with all positiveness, that the sensory
fibres decussated in the spinal cord already, and who thereupon
demonstrated that section of one-half of the spinal cord produced
quite a peculiar group of symptoms, the chief characteristic of
which consists in the crossed sensory and motor paralysis. This
assertion gave rise to a long and vigorous war among physiolo-
gists, which may now be considered as virtually settled in favor
of Brown-Séquard.
In his great work, which appeared in 1863, this author also
endeavored to establish these physiological facts as applying to
man, and for this purpose collected and critically worked up
such clinical material as could be obtained. In so doing he
created the pathology of unilateral lesions. |
It is true that, before Brown-Séquard’s labors, a number of
cases belonging under this head had been described in literature
(for example, by Monod, Charles Bell, Gintrac, and others), but
generally without any comprehension of the pathogeny of the
same. These cases were first caused to be understood through
the labors of Brown-Séquard.
Since the accomplishment of this fundamental work, numer-
ous observations have been published under this head. In some
few, immaterial points, they have served to extend and render
more precise the doctrines of Brown-Séquard, but in all essential
points they have served only to confiem and establish those doc-
648 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
trines. Quite recently Koebner has put forth an ample treatise
on this affection, based on a collection of most of the known
cases.
Definition.
What we propose to do here is to present a brief and essen-
tially symptomatic picture of those forms of spinal disease
which, anatomically speaking, have only this much in common
—that they are more or less sharply and more or less completely
localized on one-half of the spinal cord, while they may vary as
to their longitudinal extent, or as to the height at which they are
situated. |
These cases are clinically characterized by unilateral motor
paralysis—either hemiparaplegia or hemiplegia—on the side of
the lesion; by crossed anesthesia on the opposite side of the
body ; by symptoms referable to the roots of the nerves, and cor-
responding exactly with the height at which the lesion is situa-
ted; and by a series of other manifestations which may vary very
much, according to the seat and extent of the process, but which
are also severally very characteristic of the different portions of
the spinal cord which may be affected.
Etiology and Pathological Anatomy.
As we have in this connection to deal with various kinds of
lesions of the spinal cord, we cannot very well speak of any spe-
cial etiology. The causes which respectively give rise to these
various lesions may also serve as causes of the unilateral par-
alysis. |
It is only necessary here to enumerate those pathological pro-
cesses in the spinal cord which occasionally affect one-half of
the cord ; if any one so chooses, he may regard these as the im-
mediate causes of the ‘‘ unilateral lesion.”
By far the most frequent cause is to be found in trawmatic
injuries which happen to involve only one-half of the spinal
cord, and thus, as it were, perform the experiment of cutting one
lateral half of the cord in man. Instances of wounding of the
EO ce
HEMIPLEGIA ET HEMIPARAPLEGIA SPINALIS. 649
spinal cord by blows with a knife or dagger are especially fre-
quent in literature (see the cases of Brown-Séquard, Vigués, W.
Mueller, Riegel, Joffroy, Vix, and others). Such pointed instru-
ments may very easily reach the spinal cord through a wound at
the side of the spinal column, may penetrate the cord more or
less deeply, and more or less completely divide one-half of the
same. The position of the intervertebral fissures readily ex-
plains why, in -the majority of such instances, only one-half of
the cord is wounded.
Compression of the spinal cord from without is the next
cause which not infrequently affects one-half of the cord mainly
or exclusively, thus giving rise to the manifestations of a unilat-
eral lesion. This may arise from meningeal tumors (cases of
Charcot, Gintrac, Oré), or from fracture or dislocation of the ver-
tebree (cases of Brown-Séquard), or doubtless, also, through intra-
meningeal effusion of blood. It is probably in this category that
we should place those cases in which the manifestations of a
unilateral lesion are developed after falling headlong or falling
upon one’s back.
But the same array of symptoms may likewise be called forth
by processes developed within the spinal cord itself in one of its
lateral halves. This has been seen to occur as the result of
hemorrhage in one lateral half of the cord (Monod’s case); as
the result of a unilateral cirewmscribed sclerosis (Troisier’s case) ;
as the result of chronic myelitis, developed in consequence of
taking cold or of concussion of the spine, or spontaneously and
gradually (Uspensky, Radcliffe, Paoluzzi, etc.) ; as the result of
an intramedullary twmor (Gendrin) ; and finally, as the result of
syphilitic affections (Charcot et Gombault, Lanzoni). In short,
all possible acute or chronic affections of the spinal cord may
produce the features of unilateral lesion whenever they extend
over the greater part of one lateral half of the cord.
Symptoms.
The characteristic group of symptoms belonging to a unilat-
eral lesion may either be developed very gradually and insid-
iously or quite suddenly. This, of tourse, depends altogether
650 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
upon the nature of the fundamental lesion: the stab of a knife
calls the entire group of symptoms into being at one blow; a
circumscribed sclerosis induces but a very gradual development
of these symptoms.
The peculiar signs of this affection are as follows: On the side
of the lesion there is motor paralysis, which is confined to this
side, therefore is wntlateral, which may merely involve one leg
(hemiparaplegia), or, if the lesion is situated higher up, may also
attack the arm of the same side (spinal hemiplegia). A marked
contrast is presented by the other side, the one opposite to the
seat of the lesion, which is either entirely free from all motor
paralysis, or is affected only to a slight and subordinate degree.
Evidences of vaso-motor paralysis are also generally found
on the side of the lesion, especially if the affection has been
rapidly developed (as in traumatism, hemorrhage, etc.). The
temperature of the paralyzed limbs appears more or less ele-
vated, to the extent of 1.8° Fahrenheit and more.
Muscular sensibility and muscular sense are diminished on
the affected side, according to the evidence of various observers
(Brown-Séquard, Burresi, Vix). Lanzoni also found electro-
muscular sensibility lowered on the affected side; while in one
case, in which, it is true, the paralysis was but incomplete, Bern-
hardt found the so-called sense of power [Kraftsinn] retained.
The sensibility of the skin, on the other hand, acts very
remarkably. The entire paralyzed side shows more or less con-
siderable hyperesthesia for all qualities of sensation. Impres-
sions of touch, of temperature, or of pain are recognized with
extraordinary and even with painful acuteness; sensitiveness to —
tickling is exceedingly marked and disagreeable; the test by
means of Weber’s compasses usually demonstrates greater acute-
ness in the power of localizing sensations of touch. Sometimes,
however, this hypereesthesia is limited to certain single varieties
of sensibility.
The hypereesthetic region of skin is, in many instances,
bounded above by an anesthetic belt, generally narrow, though
sometimes wider, which corresponds exactly with the height and
longitudinal extent of the lesion in the spinal cord. In some
instances another narrow hyperesthetic zone may be demon-
HEMIPLEGIA ET HEMIPARAPLEGIA SPINALIS. 651
strated above the anesthetic belt, the former extending, although
with less distinctness, to the opposite side, and surrounding this
likewise as with a girdle.
The conditions of reflex action on this, the paralyzed side,
are variously reported in different instances: Paoluzzi, Riegel,
and others have found reflex action increased ; Bazire, Brown-
Séquard, and others have found it diminished. Very special
interest might here be attached to the state of reflex irritability
of the tendons, and yet, up to the present time, this has, to all
intents and purposes, not been tested at all. In one case of uni-
lateral lesion caused by an intramedullary tumor, I found the
reflex irritability of the tendons materially increased. In a case
of traumatic unilateral lesion Joffroy and Solmon report the
existence—though not until several weeks after a traumatic uni-
lateral lesion—of clonic spasm of the dorsum of the paralyzed
foot. (Secondary degeneration of the lateral column 7)
On the side of the body opposite to the seat of lesion the fol-
lowing conditions are found :
There are no motor disturbances, or they are, at most, ex-
tremely insignificant; all movements can be executed easily,
safely, and powerfully. The sensitiveness of the muscles, as
well as electro-muscular sensibility (Lanzoni), is retained.
On the other hand, more or less complete anesthesia of the
skin exists to a height corresponding with that of the lesion.
All varieties of sensibility—that to touch, temperature, pain, and
tickling—are, as a rule, equally affected, though sometimes one
may be somewhat more, another somewhat less so. There may
even be very well-defined partial paralysis of sensation, as in a
case reported by Koebner. The anzesthesia extends exactly to
the median line of the body, as may be distinctly demonstrated
on the trunk, the scrotum, etc.
Now and then a narrow, slightly hyperesthetic zone may be
found at the upper limit of the anesthetic region, the former
corresponding with the similar zone of the other side. |
Reflex action generally seems to be retained and normal on
this side, although in some cases it has been found to be in-
creased (Brown-Séquard, Bazire). In the case above referred to
I found it normal.
652 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
On this side, too, there is no vaso-motor paralysis—at least,
in recent cases. The temperature is normal, and therefore lower
than that of the paralyzed side. Sometimes, however, and this
: e
“ye
ff)
My it GEA
Hal vill . Cp?
Fia. 12. Diagrammatic representation of the
skin symptoms in unilateral lesion of the dorsal
portion of the spinal cord on the left side. The
diagonal shading signifies motor and vaso-motor
paralysis; the vertical shading signifies anzs-
thesia of the skin; the dotted shading indicates
hypereesthesia of the skin.
seems to be especially true where
the affection has existed for a long-
er time, the reverse is found to
be the case: the anesthetized is
warmer than the paralyzed side,
which latter then shows an abnor-
mally low temperature.
In the accompanying diagram the char-
acteristic difference in the two sides is rep-
resented, so far as it relates to the skin symp-
toms. It is assumed that there is a unilateral
lesion of but slight longitudinal extent about
the middle of the dorsal region, in the left
half of the spinal cord. The left lower
extremity and left lower half of the trunk
show motor and vaso-motor paralysis, as
well as hypereesthesia of the skin (a); above
this there is a narrow anesthetic zone, cor-
responding to the longitudinal extent of the
lesion (0); and above this again a narrow
hypereesthetic zone, which likewise extends,
like a girdle, over the right side (c). The
right side shows complete anesthesia (d).
This diagram would be modified accord-
ing to the seat and extent of the lesion. If
the lesion is situated higher up, the upper
extremity may fall within the domain of the
anesthetic zone (6); or, if the lesion were
seated still higher, this zone would fall in
the region of the throat and neck, and the
upper extremity would become hypereesthetic
and paralyzed. If the longitudinal extent
of the lesion increases, the width of the
anesthetic zone (6) also increases; it may, for instance, extend over the entire
length of the trunk, and then the characteristic differences of sensibility between
the two sides would appear only on the lower extremities.
Aside from these main symptoms of a unilateral lesion,
HEMIPLEGIA ET HEMIPARAPLEGIA SPINALIS, 653
other less constant and less characteriste manifestations may
be observed in individual instances.
It is not uncommon to meet with a painful feeling of con-
striction at the height of the lesion; also with all sorts of
painful sensations (burning, darting, boring pain, etc.), which
sometimes occur most prominently on the anesthetic side, some-
times on that which is paralyzed and hyperesthetic, and some-
times on both sides.
Distinet disturbances in the evacuation of the bladder and
bowels are almost always present. In the acute traumatic cases
it is especially common to find severe paralytic symptoms at
the beginning of the attack (complete retention or complete in-
continence, involuntary stools, etc.), which, however, generally
soon recede and give place to lighter, more permanent troubles
(weakness of the bladder, weakness of the sphincters). Some-
times these disturbances are very insignificant.
The sexual powers act in the same way; generally are more
or less diminished, though sometimes they remain unchanged.
Decided emaciation of the paralyzed side generally sets in
quite early, sometimes making remarkably rapid progress. This
symptom is also present in quite chronic cases.
Corresponding to this, the paralyzed side has, in a number
of instances, shown a notable lowering of faradic irritability
(W. Mueller, Joffroy, and Solmon). This is a point, however, on
which further observation is much needed. In a very chronic
case of mine, which had arisen spontaneously, there was moder-
ate emaciation and but slight diminution of electrical irritability.
Everything probably depends upon the seat and the nature of
the lesion.
Among the more rare, although not less interesting symptoms,
we may mention the occurrence of gangrenous bed-sores on the
anesthetized side (Vigués, Charcot, Joffroy et Solmon), and the
development of an inflammatory knee-joint affection in the para-
lyzed leg (Vigués, Joffroy et Solmon).
Finally, we must not fail to mention that the two last named
observers, with the return of motility in their case, witnessed the
occurrence of well-marked afaxy,.
654 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Pathological Physiology of the Disease.
Physiologists have instituted numberless experiments on the
course of the motor, vaso-motor, and sensitive tracts, from the
brain through the cord to the roots of the spinal nerves, and have
especially and thoroughly ventilated the question of the crossing
of the various tracts.
The course of the motor tracts was soon made clear, and there
are no longer any serious differences of opinion with regard to
this. There is no doubt that for the most part they decussate
high up in the spinal cord and the medulla oblongata, in the
pyramids, and the motor tracts for each side of the body run in
that same side of the cord. Section of the right side of the cord,
therefore, causes motor paralysis of the right extremities and the
right half of the trunk.
The interesting results of Flechsig’s researches! have shown even this relation to
be only partly correct. It appears that the pyramidal tracts only in part pursue a
crossed course (in the posterior lateral columns), and in part run their course
uncrossed (at the inner portion of the anterior columns of the same side—[Hiil-
senvorderstrangband]). A vicarious relation exists between these two portions;
sometimes the greater part of the tracts runs in the lateral columns and is crossed,
sometimes in the anterior columns and is uncrossed. Consequently, very variable
symptoms may arise on unilateral section of the spinal cord: complete paralysis on
the side of section, or complete paralysis on the opposite side, or incomplete bila-
teral paralysis. The first of these conditions, according to pathological experience,
is by far the most frequent.
What has been said of motor tracts is also true of vaso-motor
tracts, at least to a great degree ; indeed, more recent investiga-
tions have again proved that the principal mass of these tracts
run their course in the lateral columns, and are uncrossed. A
lesion of these tracts would therefore manifest itself upon the
same side of the body. At the same time, their relations are
somewhat complicated by the existence of the nerve-centres lying
within the spinal cord itself, which have recently been demon-
strated by Goltz and others.
1 Paul Flechsig, Die Leitungsbahnen im Gehirn und Riickenmark des Menschen.
Leipzig, 1876. S. 291.
HEMIPLEGIA ET HEMIPARAPLEGIA SPINALIS. 655
On the other hand, a difference of opinion long existed with
regard to the point of crossing of the sensitive tracts. Brown-
Séquard was probably the most positive in his assertion, based
upon his numerous experiments, of their complete crossing with-
in the spinal cord.’ He stated that the sensitive tracts, conduct-
ing the sensations of touch, temperature, pain, and tickling, de-
cussated with those of the other side very near their point of
entrance into the spinal cord, and then ran to the brain in the
opposite half of the cord. The only tracts which did not take
part in this crossing, but ran through the cord on their own side
of the body, like the motor tracts, were said to be those concerned
in the phenomena of muscular sense (which enter the cord with
the anterior roots). Brown-Séquard also gave other details which
have thus far not proved of so much practical importance. <Ac-
cording to him, the four different conducting tracts cross at dif-
ferent heights ; those concerned in the sensation of temperature
crossing somewhat earlier than the rest. During their farther
course they lie separated from one another within certain definite
segments of the cord, the sensitive tracts of the lower extremities
being said to lie behind those of the upper extremities in the cer-
vical portion of the cord.
These teachings were long combated by many. But in more
recent times they have won universal recognition, especially on
the basis of numerous pathological observations made on man.
Even Schiff? has recently admitted their correctness for man,
and it appears that part of the opposition to these teachings was
due to the fact that the relations of these tracts is not the same
in all classes of animals, but that incomplete decussations fre-
quently occur. It has likewise been proved that centripetal
fibres concerned in the production of reflex action also have a
crossed course within the cord (Miescher, Nawrocki).
Section of one-half of the spinal cord would therefore cause
anesthesia of the opposite side for sensations of touch, pain,
temperature, and tickling, while on the side of section these sen-
1 Comptes rendus de la Soc. de Biolog. 1849. Gaz. hebdom. 1855. Nos. 31 and 36.
Journ de la Physiol. de homme, etc. 1858. Vol. I. i 176.
* Centralblatt f. d. medic. Wissensch, 1872. No. 49.
656 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
sations would be retained, but that of muscular sensibility would
be lost, which, in its turn again, would be retained on the oppo-
site side. ~~
The accompanying diagram gives a representation of the course of the principal
conducting tracts within the spinal cord. The motor and vaso-motor tracts (1 and
1’), which make their entrance, or
rather their exit, through the anterior
3° 217 ° .
t 4 | root (v), remain on the same side of
the spinal cord. The same thing is
es El cat
true of the tracts concerned with mus-
cular sensibility (2 and 2’). The sen-
sitive tracts concerned in the sensa-
tions of touch, temperature, pain, and
N tickling (3 and 38’), which enter
a
\
Ya
through the posterior roots (h), at
once cross to the other side of the
spinal cord, and pursue their course
upward on that side. Section through
the right half of the spinal cord at the
height of a would then affect the mo-
tor, vaso-motor, and musculo-sensitive
tracts of the right side (1 and 2) and
the cutaneous sensitive tracts of the
left side (3’). 3
Physiologists have fur-
thermore discovered the fact
that section of one-half of the
prindgal irate within the splat cont belogging to one SPinal cord causes a high de-
Bi er ae Team pty ete of cudanaous lyporaathe
Aig gerielorin poor borne pc gaging’ Say gee
ing to all varieties of sensa-
tion. This fact has not yet been satisfactorily explained. It
is in part referred to the secondary inflammation of the cord
following the wound, and the greater irritability of the sensitive
tracts caused by this inflammation; and in part to the with-
drawal of certain controlling influences which hold the irritabil-
ity of the sensitive nerves within bounds, and whose tracts re-
main on the same side of the cord.
The conditions of reflex action, on unilateral section of the
HEMIPLEGIA ET IEMIPARAPLEGIA SPINALIS. 657
cord, do not seem to have received sufficient study at the hands
of physiologists ; we still lack definite teachings on this subject.
The conditions seem to vary somewhat in different animals; at
all events, the relations of reflex action to unilateral section of
the spinal cord are not established with sufficient certainty to
admit of our deducing a law therefrom. Nor do pathological
observations on man lead to satisfactory conclusions on this sub-
ject. According to Woroschiloff’s experiments it would appear
that the fibres which control or check reflex action in a given
lower extremity run their course principally in the same half of
the cord, those which call forth reflex action principally in the
opposite half of the cord.
At the same time we have a sufficient number of well-authen-
ticated facts entirely to explain the most important manifesta-
tions of unilateral lesions. In case of simple unilateral section
(for instance, at @ in Fig. 13), we find motor and vaso-motor
paralysis of the same side, together with a diminution of muscu-
lar sense, and a high degree of cutaneous hyperesthesia. On
the opposite side there is complete anesthesia of the skin, while
mobility and muscular sense are retained, and the fulness of the
blood-vessels is normal. In fact, the correspondence of such
cases with the results obtained in physiological experiments is
quite complete.
If the unilateral lesion, however, is of somewhat greater lon-
gitudinal extent, if if extends over the domain of several enter-
ing roots, then another characteristic symptom arises in the form
of an anesthetic zone on the paralyzed side, lying above the hy-
pereesthetic region, and corresponding with the latter in width.
The origin of this anesthetic zone is easily explained. It is due
to the implication of root-fibres of the same side before their
crossing ; the more of these implicated, the wider will be the an-
zesthetic zone ; in progressive cases it may gradually extend over
the entire trunk.
This relation may also be made clear by a simple diagram. Fig. 14 represents
the course and the crossing of the sensitive nerve-tracts of five successive pairs of
posterior nerve-roots. If we now suppose a lesion of the right half of the cord, ex-
tending over the shaded space, this will involve the sensitive tracts of the nerve-
roots 1’, 2’, and 3’ of the left side as well as the Sensitive tracts of all roots on the
VOL. XIII.—42
658 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
left side coming from still further back, thus causing a crossed, left-sided ansesthe-
sia as high as the root 3’. It will, however, at the same time involve the sensitive
tracts of the roots 2, 3, and 4 on the right side, and will cause anesthesia within
the domain of these nerves; this anzsthesia
16-5 5’— 07 will therefore be zone-like, occurring on the
[ side of the lesion, while all sensitive tracts
entering behind the roots involved cross over
to the left side unscathed, and continue their
course undisturbed to the brain.
&
Ss
hee The narrow hyperesthetic zone
ee 4 in some cases observed above the
anesthetic belt—and, indeed, to a
more marked degree on the side
of lesion than on the opposite side
—is explained by Brown-Séquard
z onthe ground that the descending
fibres of the posterior roots fall
SS within the range of the lesion. It
is a matter of no practical signifi-
NY cance. :
ies Se We have thus seen the charac-
: teristic manifestations of a unilate-
E19. 14, Diagrammatic representation of ya] lesion satisfactorily accounted
the lesion of sensitive tracts in unilateral le-
ni f the right side, to the extent of the 5 ;
shaded space, All sensitive tracts of corre. 1OF by known physiological facts.
di heigh ll thos i f ° s ° a
further back, on the left aide, are interrupted, ‘THIS is, likewise, none the less true.
On the right side only those are interrupted > ° e
which enter by the roots from 1 to 3. with regard to certain manifesta-
of the right 2 etapa we with jhe, yaseetion tions which supervene when the
roots ; 0’ to 5’ the same on the left side.
seat of the lesion is very high, in
the cervical portion of the cord. These manifestations consist,
for example, of vaso-motor disturbances in the face, on the side
of lesion, and the corresponding half of the head ; in evidences
of paralysis of the sympathetic in the neck, on the same side
(contraction of the pupil, narrowing of the palpebral fissure,
sinking of the eye in the orbit), etc.
S
WW W Wh WW
A=:
=
&
ill
4
Certain differences in the symptoms will occur according to
the height, within the spinal cord, at which the lesion is situated.
OE ——<«_ ~~ =
JIEMIPLEGIA ET MNEMIPARAPLEGIA SPINALIS. 659
We must not fail briefly to notice these, although, in fact, they
follow, as a matter of course, from our knowledge of the physi-
ology of the different divisions of the spinal cord.
In a unilateral lesion of the lumbar enlargement of the cord,
in addition to the characteristic symptoms (paralysis and hyper-
westhesia of the lower extremity of the same side, anesthesia of
that of the opposite side, etc.), an aneesthetic zone may be found
on the paralyzed side, corresponding to the area of distribution
of one or more lumbar nerves, being situated on the pelvis, the
abdomen, the region of the groin, the anterior surface of the
thigh, etc., thus constituting a zone which need not be exactly
belt-like. By this means the anssthesia may appear to be dif-
fused over both lower extremities, but on careful examination it
will be easy to recognize the true condition.
A unilateral lesion of the dorsal portion of the cord presents
the most characteristic picture of symptoms, inasmuch as the
sharp distinction between the two lower extremities, as regards
their motor and sensory disturbances, stands forth with the
greatest prominence, The hyperesthesia and paralysis of the
one, the ansesthesia and complete mobility of the other, appear
in glaring contrast; the difference extends, in similar manner, to
the trunk, ascending to a variable height; the belt-like anzsthe-
sia of the paralyzed side becomes prominent, sometimes bounded
by a narrow hyperesthetic zone above (see Fig. 12).
In unilateral lesions of the cervical portion of the cord the:
relations are much more complicated, and often indistinct, espe-
cially if the lesion is just at the cervical enlargement. Aside
from the manifestations in the face, the eyes, and certain cranial
nerves, which, in this case, may complicate the picture of disease
in an interesting manner, numerous varieties of the picture may
be due to the higher or lower seat, and to the greater or less
longitudinal extent of the lesion within the cervical enlargement.:
A little consideration shows how varied the motor paralysis in:
the upper extremity may be, according as the lesion involves the:
domain of the upper or lower roots of the brachial plexus, and
how manifold the relations of hyperesthesia to anesthesia in
the upper extremity of the same side may and must be accord-
ing to the kind and the number of areas presided over by indi-
660 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
vidual nerve-roots which are directly involved. The possible
combinations that may here arise cannot all be cited, but if one
has formed a clear conception of these relations, and mastered
them in a simple case, he will also solve the problem in more
complicated and difficult cases. |
The symptoms presented in sucha case are as follows: In the
lower extremities and on the trunk the same conditions as ina
lesion of the dorsal portion (paralysis, loss of muscular sense,
elevated temperature, and hypereesthesia on the side of the
lesion; anzesthesia, normal temperature of the skin, no motor
disturbances, normal muscular sense on the opposite side). In
the woper extremities, on the side of the lesion, we find more or
less muscles and nerve-domains paralyzed, hyperesthesia in
some or in all parts, mingled with anesthesia of certain regions of
skin or for certain varieties of sensation ; on the opposite side no
paralysis, more or less complete anesthesia in all or in individual
parts. ?
The neck and head, on the side of the lesion, sometimes show
anesthesia and hyperesthesia of individual portions of the neck,
manifestations of paralysis of the vaso-motor and oculo-pupillary
fibres (higher temperature of that side of the head and body,
heightened sensibility, narrowing of the palpebral fissure, con-
traction of the pupil, etc.); on the opposite side, sometimes
anesthesia of the neck (and a narrow zone of hypereesthesia), a
normal condition of the face and eye.
Naturally enough, this complicated group of symptoms-is_
liable to manifold variations in individual instances.
As a matter of course, but little that is of general applica-
bility can be said with regard to the course, duration, and ter-
mination of this malady, on account of the varying character of
the anatomical changes which lie at the foundation thereof, and
we must therefore refer the reader mainly to what has been
stated in previous sections concerning wounds of the spinal cord,
compression, chronic myelitis, sclerosis, etc.
The development of the characteristic group of symptoms
HEMIPLEGIA ET HEMIPARAPLEGIA SPINALIS, 661
may either occur quite suddenly, or may but slowly and gradu-
ally advance to a certain degree of completeness.
It then but rarely remains stationary and unchanged for any
considerable length of time. The lesion generally extends fur-
ther, in part through the transverse diameter of the cord, and in
part longitudinally.
In most traumatic lesions the former change usually takes
place early, the traumatic inflammation quickly spreading over
the entire transverse diameter of the cord. Paraplegia at once
follows, and we have before us the picture of transverse myelitis,
which may end in death: Not rarely, however, the paraplegia
again recedes, and we recur to the symptomatic picture of a uni-
lateral lesion, which may then continue unchanged for many
years. In not a few instances complete recovery has been seen
to follow such traumatic unilateral lesions. . It is singular that,
according to Brown-Séquard, the disturbances of motion disap-
pear earlier and more completely than those of sensation, the
reverse of which holds good in case of peripheral injury of the
nerves.
In the more chronic cases a similar course is maintained ; the
sclerosis or the tumor extends gradually over the entire trans-
verse diameter of the cord; paraplegia occurs, followed by its
resulting evils, and the further progress of the affection is deter-
mined by the fundamental process upon which it is based.
The lesion may, however, also extend longitudinally, gradu-
ally advancing upwards. The sclerosis or tumor may thus
slowly creep upwards, and this does not usually occur without
serious modification of the typical symptomatic picture, inas-
much as lateral extension usually goes hand in hand therewith.
The final result is then likewise determined by the fundamental
affection.
Diagnosis.
In view of the characteristic symptoms presented, the diagno-
sis of a unilateral spinal lesion is usually extremely easy.
The distinction between this and other forms of hemiplegia
or hemiparaplegia is very simple. |
662 ERB.—DISEASES OF THE SPINAL CORD: AND ITS ENVELOPES.
'Hemiparaplegia from lesion of one side of the cauda equina
may be recognized by the fact that here the paralysis and anes-
thesia are to be found on the same side, and also that they gen-
erally affect only certain individual nerve-domains of the lower
extremities.
The hemiplegic form of spasmodic spinal paralysis is easily
to be recognized by the absence of all disturbances of sensation,
therefore, also, of crossed anesthesia, the absence of any disturb-
ance of the bladder, etc. .
The unilateral spinal lesion may at all times be readily dis-
tinguished from any form of cerebral hemiplegia by the fact
that in the latter there is either no disturbance of sensation, or
it is to be found on the same side as the paralysis; that there is
one-sided paralysis of the face and of the tongue; that there are
disturbances of various cranial nerves and other head-symptoms,
etc.
With regard to the kind of lesion that exists, it will some-
times be difficult in non-traumatic cases to arrive at a diagnosis.
We can only attempt to overcome this difficulty by the help of
general pathological and diagnostic principles.
Prognosis.
The prognosis of unilateral lesions is governed entirely by the
form of disease lying at the foundation of the lesion. It may be ©
remarked of traumatic cases that they justify a comparatively
favorable prognosis, as with proper handling the majority of
them end in recovery. Aside from these, the prognosis in indi-
vidual cases, is the same with that of other similar affections of
the spinal cord, which are not localized on one side of the cord.
Therapeutics,
Of course, there is no distinctive treatment for the unilateral
spinal lesion. What concerns us is merely the proper treatment
of those spinal affections which are sometimes localized in one
dJateral half of the cord.
The principles and methods which are applicable in the treat-
a eS
POLIOMYELITIS ANTERIOR ACUTA. 663
ment of wounds of the spinal cord, of compression of the cord,
of chronic myelitis and sclerosis, of hemorrhages and new forma-
tions in the substance of the cord, of spinal syphilis, etc., may
also be brought into play in corresponding cases of unilateral
lesions,
16.
Acute Inflammation of the Gray Anterior Columns [Ante-
rior Horns|.—Poliomyelitis Anterior Acuta (Kussmaul).—
Spinal Infantile Paralysis (von Heine).— Acute Spinal
Paralysis of Adulis—Acute Atrophic Spinal Paralysis.—
Paralysie Atrophique de Vl Enfance (Duchenne).
. Heine, Beobb. tiber Liihmungszustiinde der unteren Extremitiiten und deren
Behandlung. 1840.—Ueber spinale Kinderlihmung. 2. Aufl. 1860.—Badham,
Lond. Med. Gaz. 1836.—Rilliet, Gaz. méd. de Paris, 1851. p. 681.—Rilliet et
Barthez, Traité clin. et prat. des malad. des enfants. Paris. 1853. Tom. =
Duchenne (de Boulogne), de l’électrisation localisée. 1855. 2. éd. 1861. 3. éd.
1872.—Paralysie atroph. graisseuse de l’enfance. Gaz. hebdom. 1855.— Vogt,
Ueb. d. essentielle Lihmung der Kinder. Bern. 1858.—Bierbaum, Die Paralyse
der Kinder. Journ. f. Kinderkrankh. 1859. Heft 1 u. 2.—Briinniche, Ueb. die
sog. essent. Lihmung bei kleinen Kindern. Journ. f. Kinderkrankh. 1861. Bd.
36. 8. 366.—Cornil, Compt. rend. de la Soc. d. Biolog. 1863. p. 187.—Duchenne
fils, Atroph. graiss. de l’enfance. Arch. génér. 1864.—Laborde, De 1. paralys.
dite essentielle de l’enfance, Thése. Paris. 1864.—Roger, Paralysie infantile.
Annal, de l’Eléctric. 1865.—Prévost, Compt. rend. d. la Soc. d. Biol. 1865.
XVII. p. 215.—Mor. Meyer, Die Elektricit. in ihrer Anwendung u. s. w. 3. Aufl.
1868. 8. 209.—G. Salomon, Zur Diagn. u. Therapie einiger Lihmungsformen
im kindl. Alter. Jahrb. f, Kinderheilk. N. Folge I. 8. 370.—Bouchut, Nature
et trait. des paral. essent. de l’enf. Union méd. 1867.—Johnson and Lockhart
Clarke, Extreme Muscul. Atrophy, etc. Med.-chir. Transact. LI. p. 249. 1868.
—Charcot et Joffroy, Cas de paralys. infant. spin. avec lésions des corn. antér.
etc. Arch. de Physiol. norm. et path. III. p. 184. 1370.—Parrot et Joffroy,
Note sur un cas de paral. infant. Ibid. III. p. 309.— Vulpian, Cas d’atroph.
muse. graiss. etc. Ibid. III. p. 316. 1870.—Volkmann, Ueb. Kinderlihmung
und paralyt. Contracturen. Samml. klin. Vortr. Nr. 1. 1870.—Duchenne et Jof-
Sroy, De l’atroph. aigué et chron. des cellules nerveuses, etc. Arch. d. Physiol.
III. p. 499. 1870.—Roger et Damaschino, Rech. anat.-pathol. sur la paral. spin.
de l’enf. Gaz. méd. de Par. 1871. Nr. 41 ff.— W. Mueller, Beitr. zur pathol.
Anat. u. Phys. des menschl. R.-M. Beob. 2. 1871.—A. Hulenburg, Lehrb. der
function. Nervenkrankh. 1871. 8 607.—Dujardin-Beaumetz, De la myélite
aigué. 1872. p. 103.—Hitzig und Juergensen, Zur Therapie der Kinderlahmung. ~
Deutsch. Arch. f. klin, Med. IX. S. 330. 1872,.—Petit/ils, Considérat. sur
664 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Yatroph. aigué des cellul. motrices. Paris. 1873.—G@ombault, Note sur un cas de
paral. spin. de l’adulte suivi d’autopsie. Arch. de Phys. V.: p. 80. 1873.—Bern-
hardt, Ueb. eine d. spinal. Kinderlihm. fdhnl. Affect. Erwachsener, Arch. f.
Psych. u. Nervenhrankh. IV. 8. 370. 1873.—Beitr.. zur Lehre y. d. acut.
atroph. Spinallihm. Erwachs. Ibid. VIL. §. 313. 1877.—M. Roth, Anat. Befund
bei spin. Kinderlihmung. Virch, Arch. Bd. 58. 8. 263. 1873.—Bernheim, Dic-
tion. encycl. des scienc. méd. 2, Sér. Tom. VIII. 1874.—Mary Putnam Jacobi,
Americ. Journ. of Obstetr. June. 1874.—C. Lange, Hosp. Tid. 2. R. L Aarg.
1874 (Virchow-Hirsch, Jahresber. pro. 1874. IL. 8. 164).—Frey, Ueb. tempo-
rire Lihm. Erwachsener tu. s. w. Berl. klin. Wochenschr. 1874. Nr. 1-3.—
Charcot, Lecgons sur les mal. du syst. nerv. II Sér. 3. fascic. 1874.—Prévost et
David, Note sur un cas d’atroph. des muscles de ]’émin. thenar, etc. Arch. de
Phys. VI. p. 595. 1874.—Seguin, Spinal Paralysis of the Adult. Transact.
New York Acad. of Medic. 1874. Nov.—#rb, Ueber acute Spinallihmung bei
Erwachsenen u. s. w. Arch. f. Psych. u. Nervenkrankh. V. 8S. 758. 1875.—
Leyden, Beitr. zur. pathol. Anat. d. atroph. Lihm. d. Kinder u. d. Erwachs.
Ibid. VI. 8. 271. 1875.—Klinik der Riickenmarkskrankh. II. 8. 552. 1876.—
Weiss, Ein Fall von acut. Spinallihm. bei Erwachs. Diss. Breslau. 1875.—G@.
Burckhardt, Physiol. Diagnost. d. Nervenkrankh. 8. 174. 1875.—F. T. Miles,
Case of Acute Spin. Paral. Transact. Americ. Neurolog. Assoc. for 1875. p.
217.—M. Rosenthal, Klin. d. Nervenkrankh. 2. Aufl. 8. 409. 1875.—Déjerine,
Note sur l’état de 1. moélle ép. ete. Arch. d. Physiol. VII. p. 253. 2875.—Ray-
mond, Observ. de myél. centrale, Gaz. méd. de Paris. 1875. Nr. 18.—Deux cas
de paralys. essent. de l’enfance. Ibid. Nr. 19.— Wharton Sinkler, Palsies of
Children. Americ. Journ. of Med. Sc. April. 1875. p. 348.— W. Sander, Ueb.
Rickwirkung d. spin. Kinderlihm. auf. die motor. Gebiete der Hirnrinde.
Centralbl. f. d. med. Wiss. 1875. Nr. 15.—Hammond, Diseases of the Nerv.
System. 6. edit. 1876. p. 451.—# Schultze, Zur Lehre von d. spin. Kinder-.
lihm. u. d. analog. Lihm. Erwachsener. Virch. Arch. Bd. 68. 1876.—Hisen-
lohr, Mittheilung tib. anatom. Befunde bei spinaler Kinderlahmung. Tagebl.
der 49. Naturforschervers. in Hamburg. Beibl. 8. 146. 1876.— Couty, Note sur
un cas de myélite aigué des cornes antérieures. Gaz. méd. de Paris. 1876. Nr.
18 u. 23.—H. C. Seguin, Myelitis of the Anterior Horns or Spinal Paralysis of
the Adult and Child. New York. 1877.
Historical Sketch.
Jacob von Heine is doubtless entitled to be considered as the
actual founder of the doctrine of acute spinal paralysis in chil-
dren. In 1840 he wrote a monograph on the disease, and gave
an exhaustive clinical representatien of the same, especially with
reference to the atrophy and the deformities of the second
POLIOMYELITIS ANTERIOR ACUTA., 665
period. It is true that some individual cases had been described
before his time (by Underwood, 1784; Shaw, 1822; Badham,
1835; and others), but the knowledge of the disease had re-
mained very limited, and its separation from other forms of paral-
ysis during the age of childhood was not yet established.
This work of Heine’s, marking an epoch, as it did, was fol-
lowed by numerous discussions, and during the succeeding
decades a succession of works was published on this disease
(Rilliet and Barthez, Kennedy, Vogt, Bierbaum, and others),
prominent among which are the manifold and extensive investi-
gations of Duchenne (de Boulogne). They furnished an exhaus-
tive clinical picture of the disease.
But the pathological anatomy of the affection remained ob-
scure, and the strife as to whether this disease represented an
‘*essential’’ or a spinal or peripheral paralysis was carried on
more by theoretical arguments than by positive observations.
In the second edition of his work, in 1860, which is based
upon a largely increased amount of material for observation,
Heine declared very positively in favor of the spinal seat of the
disease, which has ever since been universally designated as
** spinal infantile paralysis.’’ He thought it extremely probable
that there was an alteration in the gray matter. Duchenne,
though partly on other grounds than those of Heine, had like-
wise declared the spinal origin of the disease as in the highest
degree probable. But at that time this view was not, as yet,
supported by any positive evidence from the cadaver.
Indeed, such evidence remained lacking for some time yet,
and, as we know now, could not be obtained until better methods
for the microscopic examination of the spinal cord had secured
general acceptance.
At the beginning of the previous decade workers in this dis-
ease, therefore, confined themselves almost entirely to clinical
observations. The number of cases actually belonging to this
disease was more accurately defined and limited, numerous
details were more closely investigated, etc.
Cornil (1863) was the first to recognize distinct alterations in
the spinal cord itself in this disease; but Prévost and Vulpian
(1865) were the first to make the positive observation that the
666 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
anatomical lesion was essentially situated in the gray anterior
horns. This was confirmed by the observation of Lockhart
Clarke in 1868. A very carefully investigated case of Charcot
and Joffroy (1870) then stands at the beginning of a series of ob-
servations which, in all cases of spinal infantile paralysis, have,
with perfect uniformity, demonstrated a disease of the spinal
cord, and especially of the anterior gray horns. The existence
of this lesion was established beyond all doubt by the cases of
Parrot and Joffroy, Roger and Damaschino, Roth, Leyden, F.
Schultze, Vulpian, W. Mueller, Déjerine, and others, and of late
years no post-mortem has been made in this disease without the
discovery of a similar lesion... It is true that there is not entire
unity amongst observers as to the significance or the origin of
the process, and that some apparently conflicting conditions
have been discovered, but the fact is certainly established beyond
all controversy that in this disease there is an acute lesion of the
spinal cord, and principally of the anterior horns of gray matter.
It was not until about the time when the anatomical basis of
the disease had been established that it was proved noé to be
exclusively an affection of early childhood, but one which might
occur, in its typical form, during the later years of childhood or
during adult life. This fact was first pointed out by Mor. Meyer,
and was also confirmed by Duchenne, with a series of cases.
Quite recently reports have accumulated establishing the oceur-
rence of acute atrophic spinal paralysis in adults (Hallopeau,
Gombault, Bernhardt, Frey, Charcot, Seguin, Erb, Weiss, F.
Schultze, and others).
It is true that some cases have also crept into these reports
with reference to which we may doubt whether they actually
were Poliomyelitis anterior acuta. The line of distinction be-
tween this form of disease in adults and other forms of spinal
disease, especially acute ascending paralysis, acute central mye-
litis, hematomyelitis, etc., can only be completed by further
observations.
Definition.
-
This disease has very sharply defined clinical characteristics,
as follows: It begins suddenly, usually with fever, with severe
POLIOMYELITIS ANTERIOR ACUTA, 667
cerebral symptoms (deafness, coma, delirium, general convul-
sions); there is very rapidly developed and complete paralysis
,With entire relaxation of the muscles, this paralysis being of very
variable distribution over the trunk and extremities, but gene-
rally in the form of paraplegia ; there is an absence of any severe
disturbances of sensation, no paralysis of the sphincters nor
bed-sores,
A rapid improvement of the general condition soon follows ;
the paralysis proves not to be of a progressive character—indeed,
gradual improvement of the same begins, although the restitu-
tion of movement is not uniform and remains in part lost forever.
In some of the muscles there is extreme and rapidly progressing
atrophy with degeneration of tissue; the development of the
bones is retarded ; the extremities are cold and cyanotic. Dur-
ing the further course of the affection considerable deformities of
the limbs and trunk arise (club-foot, curvatures of the spine,
paralytic contractures, etc.). The general condition of the indi-
vidual is admirable, in spite of the permanent defects in the
motor apparatus which almost invariably remain.
The disease may occur at all periods of life, though it is by
far the most frequent in children between the ages of one and
four years. It is susceptible of an unusually large number of
grades of severity. |
The anatomical lesion, although not yet quite certainly de-
termined for all cases, may be regarded as most probably consist-
ing in an acute myelitis of the gray anterior columns (anterior
horns), which may extend more or less over the greater part of
their entire length, but is disposed to be most heavily localized
in the cervical and lumbar enlargements.
Etiology and Pathogeny.
There is undoubtedly a striking predisposition to this disease
in the age of childhood, children between one and four years of
age being by far the most frequently attacked by it. Duchenne,
jils, even reports one case in a child twelve days old, and one in
a child a month old, and the number of instances of the disease
increases in the second half of the first year of life.
668 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
Various explanations have been given of this predisposition
of the age of childhood. Probably the least satisfactory doctrine
is to the effect that the physiological condition of the central
nervous system in such young children of itself causes greater
irritability and liability to disease of the same. C. Lange be-
lieves that the beginning of the exercise of voluntary move-
ments at this age, especially those of walking, not unfrequently
causes overexertion of the spinal cord,.and thus induces a
susceptibility to disease of the same. Dentition, however, has
been more frequently invoked than anything else in explana-
tion of this fact, and Heine in particular has emphasized the
not rare occurrence of the symptoms of difficult dentition in
his observations. At the same time, it is doubtful whether the
disturbances which are so often associated with dentition do
exactly determine the predisposition to disease of the cord. It
is quite as reasonable to suppose that, the predisposition being
already present, dentition merely serves as the exciting cause,
and thus calls forth the disease. At all events, it seems that if
dentition really stood in a causal relation to the spinal paralysis
of children, the disease would necessarily be far more frequent
than it is.
Another fact, which is now sufficiently established, viz., that
of the occurrence of the disease at later periods of life, also goes
to disprove the intimate connection of dentition therewith. In
fact, the disease has been observed at all ages up to the sixties,
although with much less frequency than during childhood.
Sex seems to exert no influence on the liability to the disease ;
it is about equally divided between the two sexes.
On the other hand, according to Wharton Sinkler, there seems
to be no denying the influence of seasons of the year. Among
fifty-seven cases collected by this observer not less than forty-
seven occurred between May and September. Sinkler attributes
this increased tendency to the disease during the summer months
to the warm weather. :
In the majority of instances there is no evidence whatever of
any hereditary influence or neuropathic tendency. Duchenne
even states that he never saw two cases in the same family.
But Hammond reports its occurrence in two brothers, and Mor.
POLIOMYELITIS ANTERIOR ACUTA. 669
Meyer saw it arise simultaneously in twin brothers after measles.
Duchenne, jiZs, reports a case in a child whose father afterwards
died of tabes, but considers this as a mere coincidence. I have
seen a similar case.
Neither do the dyscrasias often present in childhood (rachi-
tis, scrofula, syphilis) appear to have any demonstrable influ-
ence in the production of this malady. Heine expresses himself
very positively on this subject. On the contrary, it is just the
most blooming, robust, and strong children that are most fre-
quently attacked by the disease.
Our knowledge with regard to the exciting causes of acute
spinal paralysis is just as scanty as that concerning the predis-
posing causes. Ina large number of instances not the slightest
cause can be assigned. Children are often attacked with the dis-
ease in the midst of the most blooming health, and physician and
parents strive in vain to discover any cause therefor.
In a minority of instances the fact of taking cold has evi-
dently been shown to be the cause. This has been repeatedly
and undoubtedly demonstrated in children as well as adults. In
Miles’s case the disease appeared immediately after a cold bath,
which the patient had taken while sweating, and after lively sex-
ual excitement.
In other cases—and they are tolerably frequent—no other
cause can be assigned than normal or difficult dentition. ‘‘The
irritation of teething’’ has, from all time, been a favorite method
of explanation for every conceivable trouble of infancy, espe-
cially those of a nervous character. At the same time, it is sup-
posable that the circulatory and nervous disturbances which are
undoubtedly often associated with dentition might develop this
disease in a spinal cord predisposed thereto.
Traumatic influences of various kinds have repeatedly been
regarded as causes, with what degree of justice it is hard posi-
tively to determine.
It is undoubtedly true, however, that the outbreak of the
affection is not rarely connected with some acute disease. The
entire symptomatic picture of acute spinal paralysis has repeat-
edly been seen to arise in children during the progress or soon
after the subsidence of measles, starlatina, varioloid, typhus,
670 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
intermittent fever, etc. And the same thing has repeatedly been
seen to occur in adults after the same diseases, or after severe
puerperal disease. Authorities may conflict as to whether these
attacks are to be ranked with those forms of poliomyelitis ante-
rior acuta which arise spontaneously ; but there appears unques-
tionably to be the same localization of the disease, and in all
probability a very similar anatomical process, in these well-de-
fined ‘‘paralyses after acute diseases.’”? We must trust to the
future to settle this question.
Pathological Anatomy.
In spite of the numerous investigations of the past few years,
the pathological anatomy of acute spinal paralysis can only be
incompletely given. We are, no doubt, justifiable in laying
down as a strict requirement that only those cases shall be con-
sidered as affording conclusive anatomical results which have
been accurately observed during life, and which have presented
the well-marked clinical characteristics of the disease. Many of
the cases thus far described do not sufficiently fulfil this require-
ment. Many have been satisfied with the proof that there was’
paralysis during childhood without inquiring into the precise’
history of the beginning of the malady. Changes in muscles,
bones, and nerves, which may notoriously be the results of very”
varied processes in the nervous system, have been accepted’
merely as the sequels of the ‘‘spinal paralysis of childhood.”
In this way probably very varied anatomical processes, not hav-
_ ing the same significance, have been cited as belonging to this
disease. When we see what diagnostic daring is developed in
some authors by the desire to publish new observations on any
rare form of disease, we shall be the more disposed to adhere to
the postulate above uttered. sly
Secondly, we have a right to demand that only the most re-
cent cases obtainable should be examined, with a view to deter-
mining the true essence of the pathological process present.”
Cases which are examined from twenty to sixty years after the’
fresh attack certainly cannot give safe and positive data for a
judgment with regard to this disease. The literature of the sub-’
So s
POLIOMYELITIS ANTERIOR ACUTA. ; 71
ject shows that this requirement, too, has hitherto been but little
complied with. The earliest anatomical examination which has
thus far been reported (Roger and Damaschino) was made two
months after the beginning of the disease.
I am convinced that it is only by the rigid observance of the
two requirements above indicated, and by the careful criticism of
observations, that we shall gradually succeed in learning the
essential anatomical changes in this disease, and be enabled to
separate them from those that are non-essential and accidental.
It can hardly be otherwise than that a disease with so sharp and
well-characterized a clinical picture should have some uniform
anatomical lesion as its basis.
From the anatomical observations at present before us, it
would at least appear most probable that this essential anatomi-
cal change consists in a more or less diffuse acute myelitis of the
anterior gray substance, which reaches its greatest intensity in
the lumbar and cervical enlargements of the cord and, as a rule,
leaves no permanent and irremediable alterations excepting at
these two points. In many instances, a moderate extension of the
process, both in the gray substance and to the neighboring white
(antero-lateral) columns, can be demonstrated, but probably this
is only secondary and not essential.
The conditions which have been discovered, and upon which
these views are based, must be divided into two groups, viz.:
those which have been observed soon after the beginning of the
illness (2 to 20 months), and those which have been observed
very long after (17 to 61 years). Unfortunately, we are as yet
entirely without any observations on the earliest stages of the
disease (the first few days and weeks).
Observations made at an early period of the disease (Roger
and Damaschino, Roth, Leyden’s second case, Parrot and Jof-
froy, probably also the case very briefly reported by Rinecker'
and examined by von Recklinghausen) show that sometimes
nothing abnormal about the spinal cord can be discovered by the
naked eye; sometimes the substance of the cord seemed tougher
at the height of the cervical or lumbar enlargements, and there
Jahrb. d. Kinderheilkunde. 1871" New series. V. p. 118,
672 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
was a slight dwindling of the cord, especially at the expense of
the antero-lateral columns. On making a transverse section, the
markings were somewhat indistinct, the anterior gray substance
was more or less discolored, whitish or reddish, sometimes soft
and diffluent ; sometimes a diminution can be shown in the volume
of the gray anterior horns, The anterior roots—corresponding to
the main seat of the disease—are gray, translucent, and atrophied.
The membranes of the cord usually show nothing abnormal.
Nothing short of a microscopical examination, however, re-
veals the exact seat, variety, and extent of the alterations. The
principal trouble is found in the gray substance of the anterior
horns, constituting a tolerably diffuse lesion with regions of
greater intensity at the enlargements of the cord, particularly at
the lumbar enlargement. Here we find, usually on both sides,
though sometimes only on one side, an area of softening in the an-
terior gray horn of greater or less longitudinal extent (10 to30 mm.
or more, 75 of an inch to 14 inches), which is sometimes situated
more towards the centre, sometimes more towards the front of
the horn, and is separated from the surrounding parts by a more
or less sharp line of demarcation. Similar areas are often also
found in the cervical enlargement of the cord, more rarely at
other points, in the dorsal or upper cervical portion. These areas
of softening represent inflammatory softening; their substance
is friable, soft, and disseminated with numerous granulation
cells ;' closer examination demonstrates an increase in the num-.
ber of nuclei and in the amount of connective tissue and more
than ordinary fulness of the blood-vessels. The most striking
discovery, however, is the more or less entire disappearance of
the large, multipolar ganglion-cells ; those still remaining are
found partly in all stages of degeneration and atrophy, partly,
however, quite well preserved. It has not yet been possible to
demonstrate any regular localization of these changes in definite
groups of ganglion-cells within the anterior horns. The nerve-
‘In Leyden’s case there were no granule-cells (Kérnchenzeller); in the place of
them there were numerous large, bladder-like, nucleated cells, like those of endothe-
lium, in the gray substance, in part crowded together and in part more scattered,
which, perhaps, had the same significance, in the morbid process, as the granule-
cells,
a
—
POLIOMYELITIS ANTERIOR AOUTA. 673
jibres and azis-cylinders within the area of softening are also
found to have entirely disappeared. In the immediate vicinity
of the softening there is frequently quite a striking multiplication
of nuclei, as though preparation were being made for a species
of encapsulating process. The anterior horn, as
a whole, appears diminished in size and wasted.
These areas, or foci, sometimes extend, by
means of little prolongations, backwards, or
towards the sides. The tissue surrounding them
may be more or less completely or approxi-
mately normal, with well-preserved ganglion-
cells. Generally, however, slighter and more
diffuse changes can be demonstrated through-
out a greater or less portion of the gray sub-
stance, usually throughout the entire dorsal
portion, consisting of single granule-cells scat-
tered through the tissue, the multiplication of
nuclei, dilatation of blood-vessels, the disap-
pearance of individual ganglion-cells. The ac-
companying diagram gives a clear picture of the
localization and extent of the softening in the
lumbar enlargement of the cord, according to
Roth. Fra. 15.—Localization of
Z G. 15.— zation 9
At this stage there is generally not much to the diseased area in the
anterior horns of the lum-
be seen in the antero-lateral columns ; still they >, enlargement of tho
cord in a child two years
have repeatedly been proved to be diminished in {it ,feyen, months after
size and the seat of a slight sclerosis. At other fhingintheright small
times a thickening of the trabecule has been eoitmn ; 1, 28, 90,3, and
found, atrophy of individual nerve-fibres (Jof- nation of the cord, After
froy, Damaschino), solitary granule-cells or
Leyden’s cells within the tissue ; at all events, however, no very
high degree of alteration takes place.
The anterior roots are diminished in size, atrophied, and
under the microscope show the signs of degenerative atrophy.
In observations made at a late period the picture is, of course,
radically different. We have such observations made between
seventeen and sixty-one years after the origin of the disease by
Cornil, Prévost, Vulpian, Lockhart Clarke, Charcot and Joffroy,
VOL. XIII.—43
é
674 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Petitfils and Pierret, Leyden, cases 1 and 3, Gombault, Déjerine,
F. Schultze, and others.
Now atrophy and shrivelling of certain portions of the spihad
cord are much more evident, even to the naked eye, the wasting
of the antero-lateral columns and the shrinking of the anterior
horns being especially prominent. These are irregularly reduced
Fra. 16.—Spinal cord with Poliomyelitis anterior acuta, forty-three years after the beginning of the dis-
ease, a, Section through the lumbar enlargement ;. both anterior horns and antero-lateral columns strongly
shrivelled, more on the left side than on the right. No ganglion-cells. 6. Section through the cervical en-
largement ; the left anterior horn and antero-lateral column very strongly shrivelled. No ganglion-cells.
The posterior columns and posterior horns in both sections are normal, After Charcot and Joffroy,
in their dimensions in various directions, narrowed, and shrivelled
so that the entire form of a transverse section of the cord, as
well as its markings, seems to be changed ; this is especially
prominent if the lesion is limited to one side (see Fig. 16). The
antero-lateral columns often appear somewhat gray and translu-
cent; the posterior columns, on the contrary, are Bm! normal.
x
“iat = Sa
POLIOMYELITIS ANTERIOR ACUTA, 675
The anterior roots are to a high degree atrophied, and the seat
of gray degeneration.
On making a fresh transverse section of the cord there is fre-
quently not much to be seen that is abnormal, aside from the
alterations in form; after hardening, however, the principally
degenerated areas generally appear with greater distinctness.
On microscopic examination the circumscribed foci first
strike the eye; these will be found within the anterior horns at
the lumbar and cervical enlargements, to a variable number and
extent. In addition to this, in the majority of cases, there is also
a more or less diffuse change in the gray substance, and a higher
grade of alteration in the white columns.
The anterior horns are highly atrophic and shrunken ; witha
the foci which they contain there is a more or less firm, fine-fibred
connective tissue, rich in nuclei, this wealth of nuclei being. not
rarely most striking just in the peripheral border zone; thicken-
ing and enlargement, and probably multiplication of the blood-
vessels, can be demonstrated ; granule-cells are generally absent,
but immense numbers of corpora amylacea are to be found,
as well as pigment, etc. In the foci the ganglion-cells, and
all nerve-fibres, are more or less completely destroyed. The
ganglion-cells that may remain are in all stages of degenerative
atrophy, pigmentary degeneration, and shrivelling. Well-pre-
served ganglion-cells are only to be found outside of the foci.
‘*Clarke’s columns’’ have generally been found intact; in two
cases, however, they were also involved and their cells destroyed.
In the remaining divisions of the gray anterior horns—in the
dorsal region, for instance—the ganglion-cells are less numerous
than is normal, the connective tissue increased, there is a great
wealth of nuclei, and numerous corpora amylacea. ;
. In the antero-lateral columns a greater or less degree of scle-
rosis may be discovered, thickening and multiplication of the
neuroglia, with or without pronounced atrophy of the nerve-
fibres. This sclerosis may vary greatly in extent; sometimes it
is confined to thé immediate vicinity of the anterior horns of gray
matter, sometimes it is distributed more diffusely over the entire
antero-lateral columns, especially the posterior part of the lateral
columns. It generally stands in most intimate relations. to those
676 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
parts of the anterior horns which are most prominently diseased.
The anterior bundles of roots within the antero-lateral columns,
as well as the anterior roots themselves, present an unequivocal
picture of degenerative atrophy.
When we take a comprehensive view of all these conditions,
we find, after all, that there is more unity in the picture than
appeared on the first glance. It would be highly desirable to
have our knowledge completed by some cases from the first few
days or weeks of the disease. But even without this, so much
appears certain, that we have to deal essentially with an acute
inflammatory process in the anterior horns of gray matter; we
do not know yet whether this is nothing more than an ordinary,
acute myelitis, or whether it is distinguished by certain specific
peculiarities. This process is spread, more or less diffusely,
over the greater part of the gray anterior horns, but attains its
greatest intensity in certain favorite spots—the lumbar and cer-
vical enlargements—and there causes distinct areas of softening.
In these, besides the inflammatory changes in the neuroglia, the
most striking and constant changes consist in the complete de-
struction and disappearance of the nerve-elements, especially of
the multipolar ganglion-cells.
This process soon passes over into a chronic stage; after it
has entirely receded in some places, it gradually leads, in the
principal seats of the disease, to the development of cicatricial
connective tissue, without any restitution of the nerve-elements.
In the further progress of the disease, probably only secondarily,
as a rule, the antero-Jateral columns are affected, and show a
higher or lower grade of sclerosis. If the process has been de-
veloped during the age of childhood these columns are generally
retarded in their d»velopment; they appear narrow and atro-
phied, and, together with the shrinking of the anterior horns by
cicatricial contraction of the foci, cause more or less serious
changes in form in the spinal cord. The posterior horns and pos-
terior columns almost always entirely escape the disease.
If all the anatomical conditions hitherto made public under the name of acute
spinal paralysis do not entirely agree with the representations here given, this is
doubtless in part due to the circumstance mentioned above, that quite heterogene-
ous diseases have sometimes been brought into the list, all that was necessary to
LT oer VR
POLIOMYELITIS ANTERIOR ACUTA. 677
their admission being to prove that they were developed in childhood, and left
behind them paralysis, muscular atrophy, paralytic contractures, and all sorts of
deformities. But we know that various diseases of the spinal cord (multiple scle-
rosis, hematomyelitis, simple myelitis, etc.), provided they affect certain divisions
of the gray substance, will produce exactly the same manifestations, and leave be-
hind the same results, It would certainly be wrong to count all these as cases of
acute spinal paralysis, for they are other forms of disease which happen to have a
certain resemblance to it. For the present, therefore, we should be disposed to
regard these unusual conditions as probably not belonging to this disease at all.
A question which has been raised by authors, and discussed
with great liveliness, and which, it appears to us, cannot be de-
termined with the material now on hand, is, whether the affec-
tion is originally a parenchymatous or an interstitial myelitis.
Charcot, and after him Joffroy, Petitfils, and others have asserted
that the primary step in the affection was the lesion of the large
ganglion-cells, that, therefore, the disease is parenchymatous
myelitis; while Roger and Damaschino, Roth, and others believe,
on the ground of their examinations in fresher cases, that inter-
stitial myelitis is the primary affection, and that the atrophy
and disappearance of the ganglion-cells are secondarily caused
thereby. In our opinion, no conclusive evidence has yet been
obtained in favor of either view. We therefore decline to enter
‘into any elaborate discussion of this difficult question, the more
so as it is very elaborately treated of in the works of some of the
authors above named, and as it does not yet appear to us to be
of any great practical value, however much scientific interest it
may possess. It is enough for our purpose to know that almost
all authors agree on the fact of there being acute myelitis, and
we may be content to leave it to the future to decide whether
this myelitis is parenchymatous or interstitial ; perhaps, as Du-
jardin-Beaumetz suggests, it may be decided that the connective
tissue and nerve tissue are simultaneously attacked by the irrita-
tive process.
In those sections of the cord which are especially involved in
‘the poliomyelitis, the anterior roots always appear very thin,
gray, translucent, and atrophied. The microscope shows degen-
678 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
erative atrophy of the greater part of the ‘nervé-fibrés, well+
marked proliferation and sometimes fatty infiltration of the inter-
stitial connective tissue, thickening of the blood-vessels, ete. ;
- The peripheral nerves have not yet been examined with the
care that we could wish. The results of examination by electri-
city show with tolerable certainty that degenerative atrophy
must exist at least in the motor filaments of many of these
nerves. In a somewhat old case, F. Schultze found undoubted
and considerable increase of.the interstitial connective tissue
with moderately numerous atrophic fibres. Déjerine also found
atrophy of the nerve- fibres with i increase of the connective tissue
and nuclei.
The muscles of the paralyzed limbs always show the highest
degree of alteration. Even with the naked eye the most varied
gtades and steps of such alteration can be recognized alone
of one another in one and the sanie patient.
_ In the first stages of the disease the muscles merely appear
lean, atrophied, pale, and soft ; later they become more grayish,
or of a pale reddish yellow, bathe streaked partly with white
connective tissue bands, and partly with intensely yellow bands
of fatty tissue, which keep increasing’ more and more in number
and in width. In the later stages the muscles acquire somewhat
the. appearance of decayed or withered leaves (welkes Laub), and
finally they are entirely replaced by. fatty tissue, which looks
exactly like subcutaneous fatty tissue, and by its volume often
more than restores the form and mass of the lost muscle. An-
other portion of the muscles dwindles into puré, connective: -tis-
sue fibrous strands containing no development of fatty tissue. —
_ All these alterations take place to very varied degrees of ex-
tent; they may be seen irregularly intermingled in the various
Rupees of an extremity; not infrequently one may see several
stages of change in one single muscle. The older the process is,
the more will connective tissue and fatty tissue predominate,
and in old cases some BrOnES of muscles appear merely as great
masses of fat.
The microscopic examination of these changes has unfortu-
nately not been carried out in a rigidly systematic manner. But
from what has been discovered by various observers, at the most
——— Ue
POLIOMYELITIS ANTERIOR ACUTA. 679
different stages of the disease, thus much would appear to be
certain, that the principal conditions found are those of the vari-
ous stages of degenerative atrophy of muscles, as we have more
particularly described it in another portion of this work,’ that in
addition to this, in some muscles, simple atrophic conditions and
simple lipomatous conditions are found, but that these are of
quite subordinate significance. |
In the earlier stages of the disease, in the first months and
years, we find at first a high degree of atrophy and wasting of
the muscular fibres; in many of these the nuclei are greatly in-
creased in number, the transverse striations are indistinct if not
unrecognizable. At a later period there is cloudiness of the
muscular fibres, at first caused by soluble molecules, afterwards
by fat molecules; finally, the muscular fibres disappear alto-
gether or almost so; individual fibres, however, or even whole
bundles of them, may remain for a long time well preserved in
the midst of the diseased muscle.
Eyen in the very first stages of the disease a simultaneous pro-
liferation of the interstitial tissue begins ; the width of the inter-
stices is increased, they appear to be filled, here and there, with
accumulations of nuclei, the walls of the vessels appear thick-
ened and infiltrated with cells. This proliferation of connective
tissue increases more and more ; in all the later stages the muscle
has scattered throughout it an abundance of firm-fibred connec-
tive tissue, rich in nuclei, so that some have spoken of it as a
regular sclerosis of the muscle. When all the muscular fibres
have finally disappeared from such a muscle, nothing but a firm,
fibrous strand of connective tissue remains. — |
Sooner or later, however—and in youthful subjects this seems
to occur comparatively soon—an abundant deposit of fat takes
place in this interstitial tissue ; whole rows of fat cells appear
between the atrophied muscular fibres, which are in part found
in a state of complete fatty degeneration ; these rows multiply
increasingly, overrun the entire tissue, and finally, after the de-
struction of the muscular fibres, the entire muscle is replaced by
fatty tissue. This may go so far that the original volume of the
1 This Cyclopedia.*Vol. XI.
680 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
degenerated muscle may be considerably exceeded by the volume
of the fatty tissue that has taken its place. Thus a species of
pseudo-hypertrophy of the muscle is brought about.
To my mind it does not admit of the slightest doubt that the
changes briefly described above represent the various and espe- —
cially the latest stages of degenerative atrophy, as it is known
and has been carefully studied especially in severe traumatic
paralyses.
Even the ¢endons not rarely appear as narrow bands, atro-
phied, thin, and stretched.
The bones are always retarded in growth, both as to length
and thickness, when the disease occurs during childhood; their
epiphyses are stunted, the normal protuberances and processes
less developed. Their external, hard lamella is thinned, friable,
flexible, the medullary portion comparatively increased, its fatty
contents more abundant (osteoporosis). ;
The joints are also strikingly lax, often regular dangling
joints (Schlottergelenke), their ligaments thinned, stretched, and
loose; the articular extremities are stunted, ground off, eroded ;
the articular cartilages are atrophied. The most manifold de-
formities are produced in this way, especially the severest forms
and grades of club-foot. Extraordinary degrees of curvature of
the spine are also not rarely produced in the same manner.
The external skin and the internal organs of the body, in the
majority of instances, are quite normal, or only show such
changes as are in no way connected with the disease of the
spinal cord, and only bélong to diseases accidentally acquired by
the individual. |
The brain is reported as entirely normal in almost all reports
of post-mortems, and really seems to have nothing directly to do
with this disease. Great scientific interest, however, is attached
to an observation of Sander’s, according to which the separation
of the brain from a great part of the muscular apparatus of the
body appears not to be without serious reaction upon certain
motor divisions of the brain. In one case of “spinal paralysis
of childhood ”’ (which, it is true, was associated with ‘‘idiocy’’),
in a boy fifteen years of age, Sander found the two central con-
volutions and the lobulus paracentralis (which in man is sup-
TE Be aD
POLIOMYELITIS ANTERIOR ACUTA. 681
posed to be the seat of the so-called motor centres) materially
stunted in their development. It is to be wished that there were
more careful and more frequent examinations of this relation.
Pathology of Acute Spinal Paralysis.
Symptoms.
Hitherto this disease, as it occurs in children and as it occurs
in adults, has almost always been treated of separately. This is
surely not right; it is evidently precisely the same disease in
both cases. ‘To be sure there are certain variations in its picture
of symptoms caused by the period of life, by the subsequent
growth, by the different excitability of the organism of the child
and the adult. For this reason a separate consideration of the
symptoms at least would seem to be justified.
We will first delineate in detail the more important and fre-
quent picture of the disease as it occurs in children, and add to
this a short account of the same in adults.
a. Poliomyelitis Anterior Acuta in Children.
General picture of the disease.—The onset of this disease is
marked by more or less severe fever, the significance of which
may at first be entirely unrecognized. This sometimes follows
certain premonitory manifestations (pain in the back and limbs,
psychical changes, a tendency to be frightened, etc.), or may
follow more or less difficult dentition, but most frequently it
arises without any warning and while the child is in the midst
of apparently perfect health. Very soon the heat and restless-
ness are followed by more seriows symptoms ; evidences of
congestion of the head appear, giddiness, confusion of ideas,
drowsiness, which may afterwards increase to somnolence and
coma. Children that are old enough to tell of their sensations,
complain of severe pain in the back and in the limbs. Not
seldom general convulsions, of greatér or less severity and extent,
682 ERB.—DISEASES OF THE SPINAL CORD AND -ITS ENVELOPES,
then arise, eclamptic seizures, which may occur once or repeat-
edly, but are generally of but short duration.
In many cases, however, such stormy manifestations are lack-
ing, and the beginning of the disease is introduced merely by
slight fever and a transitory ill feeling. Indeed, it is not rare
for no initial symptoms to be noticed, and the characteristic
paralysis may appear in the night, or during the day too, while
the child is apparently perfectly well.
But even the most alarming symptoms generally disappear
again. in a very short time (from half a. day or a day to three
days), the fever subsides, the child’s general health seems good,
and one is inclined to think that the trouble is all past. |
About this time the parents generally notice, with alarm, that
amore or less extensive paralysis has imperceptibly crept on.
This is made manifest when the child is taken out of bed, when
it is bathed, or when it is expected to walk. Either one limb or
all the limbs hang down, relaxed and powerless, are incapable of
motion.
It is but rarely that this is observed during the febrile and
somnolent stage, and still more rarely that it has been possible
accurately to follow the development of the paralysis. This
seems to progress pretty rapidly ; one leg may be paralyzed in
the course of half an hour, or of a few hours, the other leg fol-
lows soon, then the arms; thus the paralysis may reach its full
development during a via or in from one to two days; it rarely
requires a longer time (a week).
Sometimes during the first few days there is also ets of
the bladder, usually incontinence, more rarely retention of urine;
this is of course hard to prove, with certainty, in little children.
This may last a connie: of days, or even weeks, but then ata
disappears. |
So far as.can be he in aaiayan the sensibility of the para-
‘lyzed parts is completely retained. |
The further course of the affection is remarkably natant in
different cases. The paralysis attains the maximum of its in-
tensity and extent very soon after the. beginning of the disease.
It does not increase any more, but merely decreases. .The extent
to which it may decrease varies very much in different instances.
POLIOMYELITIS ANTERIOR ACUTA, - 683
In the rarest cases, improvement’ begins very soon; in from
one to three weeks, being at first seen in single little movements,
and then gradually extending further; the muscles at the same
time remaining relaxed and soft, but not becoming much emaci-
ated. This improvement advances further and further until
complete recovery, which may be attained in the course of a few
months. These are the cases of so-called ae spinal paral-
ysis. ads
Generally, however, the course is not so tieoniehe. It is true
that improvement usually begins early, but it only advances to
a certain point; the arms may become entirely free, or perhaps
only partly so, the movements of the shoulders and elbows may
return while the hands remain partly paralyzed, or vice versa.
In the same way partial recovery occurs in the lower extremities ;
one limb may become entirely movable while the ‘other remains
completely paralyzed, or the thighs may return to their normal
condition while the legs remain paralyzed ; indeed, single groups
of muscles or even single muscles may again acquire the power
of motion or remain completely paralyzed, in the most multiform
manner. . .
In the great majority of cases the larger part of the muscles
thus remains paralyzed for a very long time, or permanently.
And in all these muscles a high grade of rapidly progressive
atrophy is at once set up, and examination by means of electricity
gives well-marked evidences of degenerative change.
The limbs so severely paralyzed now present a very charac-
teristic condition. There is complete paralysis and entire flac-
cidity of the muscles, a high degree of atrophy of the same with
great softness to the touch, total failure of all reflex action in
‘the limbs (both of the skin and tendons) ; the sensibility of the
‘skin is everywhere normal, the patient does not take to his bed,
the skin is strikingly cool, bluish, era and not seldom
somewhat bloated.
.Children then remain for a long time in this condition, which
may extend more or less widely over the trunk and extremities,
and may be well developed within a few weeks after the begin-
ning of the illness. Their general condition is excellent, the
vegetative functions are entirely in order, the brain is perfectly
684 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
normal, their intellectual development progresses regularly, the
growth of their teeth shows nothing especially abnormal, the
growth and development of the non-paralyzed parts advances
admirably, and these children generally make the impression of
being in blooming health.
It is only in the paralyzed limbs that further changes gradu-
ally take place, changes which are peculiarly characteristic of
the affection, and even in later life betray, to the practised eye,
at the first glance, the disease which was gone through with in
childhood. These changes are as follows:
Progressive emaciation of the muscles, up to the point of the
complete disappearance of the same, and a skeleton-like condi-
tion of the limbs; not rarely, however, there is an exuberant
production of fat in the same, whereby the atrophy may, to a
great degree, be hidden. |
The development of paralytic contractions in the most various
muscles and groups of muscles.
Retardation of the growth of the bones ; shortening and stunt-
ing of the limbs ; distortion, laxness, and unusual mobility of the
joints, displacement of articular extremities of bones, etc.
As the result of all these changes the most manifold and
extreme deformities of the limbs, the joints, the spinal column,
etc., are produced. Club-foot, which is of such frequent occur-
rence, loose dangling joints, and extreme degrees of spinal curva-
ture, usually owe their origin to infantile spinal paralysis. The
shrunken, paralyzed, crippled members, hideously distorted, in-
capable of any use, constituting a burdensome appendage to the
body rather than a necessary portion thereof, appear in striking
contrast to the well-developed, well-nourished members.
In later life these patients drag their deformities and their
weaknesses around with them, without any real improvement
ever taking place. Not infrequently, however, an apparent im-
provement occurs, because the patients gradually learn most
skilfully to use the healthy muscles and limbs in supplying the
place of those that are paralyzed, and are enabled, by the help
of the former, or by the aid of artificial supports, orthopedic
apparatus, etc., to move about with tolerable rapidity and safety,
and to work.
POLIOMYELITIS ANTERIOR ACUTA,. 685
This of course varies very much, in individual instances,
according to the extent and seat of the lesion ; sometimes but
one lower extremity is paralyzed and shortened, sometimes both ;
or the arms alone may be affected, sometimes only one arm, or
sometimes even parts of one extremity alone. The most wonder-
ful curvatures and deformities thus occur (they are very graphi-
cally depicted in the plates of Heine’s book); the most striking
cripples on the public streets, the chronic inmates of orthopedic
hospitals, the most grateful objects for the ingenuity and art of
those interested in‘mechanical surgical appliances, are, in great
part, the victims of the spinal paralysis of childhood.
The duration of life does not seem to be in any way influenced
by the disease ; its victims, aside from their deformity and paral-
ysis, remain well and fresh, and may reach old age. They fulfil
their calling, so far as they are capable of having a calling, get
married, have children, and comport themselves like healthy
men and women, with the exception of the defects left behind by
the disease of their childhood.
There does not even seem to be any increased disposition
remaining to further disease of the spinal cord. I have thus far
met with but two cases in which adults, who showed signs of the
acute poliomyelitis anterior of which they had suffered in child-
hood, were attacked with spinal disease (in one case with tabes,
in the other with sclerosis lateralis amyotrophica), Raymond
saw progressive muscular atrophy developed at a later period in
such an individual. In one case I afterwards observed the de-
velopment of epilepsy.
Value of the Individual Symptoms.
The initial fever has been but very little examined and in-
vestigated as yet. It may be very insignificant or very severe. In
some, although rare instances, it appears to be entirely lacking ;
according to Duchenne, Jr., this is claimed to have been true in
seven cases out of seventy ; the correctness of this statement does
not, however, seem to have been tested by the thermometer. It
is certainly present in the majority of instances, although of very
varying intensity and duration. It ugually lasts but one or two
686 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
days, sometimes only half a day or a few hours; rarely for from
six to eight days, or even fourteen. It is not yet determined
whether the fever stands in any definite relation to the intensity
and extent of the disease in the initial stage; but it certainly
appears as though the intensity of the fever bore no definite re-
lation to. the extent of the disturbances that are left behind.
Probably no one would dissent from the view that the initial
fever is simply of an inflammatory nature, and is dependent on
the acute process localized in a large part of the spinal.cord.
In most instances the initial brain symptoms are very promi-
nent. They also appear in extremely varied degrees of intensity ;
sometimes the outbreak of the severer manifestations of disease
are preceded for a few days by light nervous symptoms; greater
psychical irritability, unusual liability to fright, uneasy sleep,
gritting the teeth during sleep, frequent. rolling of the eyes, par-
oxysms of terror, and the like, are noticed in children. With
the beginning of fever, confusion of ideas with slight somnoleney
is generally soon observed; all sorts of delirium, sometimes
light and sometimes active, appear; occasionally there is pro-
found unconsciousness. .
But the most striking and alarming manifestations are the
convulsions which occur in many cases, and which may be of a
light or a severe form. If light they may be confined: to convul-
sive twitchings of the face and extremities, to grinding the teeth
and rolling up the eyes; if severe they consist in an outbreak of
general convulsions, which remind one of eclampsia, but which
are generally repeated but a few times, and not rarely. terminate
with the first attack. This symptom also is liable to great varia-
tion ; sometimes the attacks only last one or two hours, at others
they occur frequently during one or two days; the individual
attacks are sometimes lighter, sometimes more severe ; they may
be accompanied with vomiting... But although they és look
very threatening, they do not appear to cause any immediate
danger to life. It remains to be proved, however, whiether the
convulsions, which carry off some little children within a few
days, may not sometimes belong to the initial ‘stage of acute spi-
nal paralysis. | : .
' Finally, however, there are also numerous instances in which —
POLIOMYELITIS ANTERIOR ACUTA. | 687
severe initial brain-symptoms can be demonstrated, in which, at
all events, all convulsive manifestations are entirely lacking.
The pathogenetic explanation of these initial brain-symptoms
has not yet been found. It may appear doubtful whether they
are to be regarded as mere manifestations of fever; it is not
proved whether the sudden irritation of a large part of the spinal
cord makes an impression on the brain of a child sufficiently.
powerful to induce such severe disturbances. Neither has there
as yet been furnished any demonstration of a simultaneous lesion
of the brain, during the initial stage ; this would have to be of a
very transitory nature ; and it certainly is not plausible to sup-
pose, like Frey, that this lesion consists in a cerebral hyperemia
which is induced by paralysis of the spinal vaso-motor tracts
for the cerebral vessels, and which disappears again with the
speedy abatement of the inflammatory swelling of the cord. Per-
haps a number of these causes work together to cause the re-
markable occurrence of severe initial brain-symptoms in this
spinal disease.
Unquestionably, however, the essential syEnitom of the dis-
ease is the paralysis with subsequent atrophy of the muscles.
This lends to the picture of the disease its main peculiarity, and
is almost exclusively responsible for the severe sequels of the
affection.
The development of the paralysis often occurs quite unno-
ticed. It is not until the febrile manifestations have subsided,
when the child wants to use its limbs, when it is to walk or
stand, when it is bathed or dressed, that one notices the paraly:
sis which has in the meantime crept on, and even then it is not
unfrequently looked upon as being nothing more than the lassi-
tude resulting from the fever. This error is naturally cleared up
by the further course of the affection. Children of a somewhat
older age often notice the paralysis earlier and call attention to
it in good time.
The paralysis is almost alvays developed with great rapidity,
and appears well-nigh simultanedusly in all the parts attacked:
It does not, however, come on with the quickness of apoplectic
paralysis, but several hours always pass, half a day or a night,
before it- reaches its maximum. In,yome few cases a slower
688 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
spread of the affection is observed, so that it may not reach its
acme for several days. Again, it has been seen to arise in sey-
eral successive onsets, so that the several extremities were at-
tacked at intervals of eight days; each single onset, however,
then goes on with a certain degree of rapidity.
Whatever the precise method of development may be, this
much is certain, and is to a high degree characteristic of this
very disease, that the paralysis reaches the maximum of its ex-
tent and intensity at the very beginning of the disease, or at
least within a short time thereafter ; that from this time on it
advances no further, but merely recedes. The paralysis, there-
fore, has distinctly no progressive character.
The paralyzed muscles now appear entirely flaccid and soft,
and show no trace of contraction; the limbs are capable of free
passive motions in all directions; they hang on the body like
limp, dead masses. The turgescence of the muscles appears at
the same time to be diminished, likewise the turgescence of the
skin. Reflex action is completely extinguished in the paralyzed
muscles; no reflex action can be aroused by the strongest irrita-
tion to the skin or tendons, although this irritation may be very
distinctly felt by the little patients.
The distribution of the paralysis is extraordinarily different
in different cases. The lower extremities are almost always at-
tacked ; sometimes, however, the upper extremities are seized at
the same time, as well as a great part of the muscles of the trunk,
especially those of the spinal column, and sometimes also of the
neck. Not rarely but one lower extremity is attacked, and
sometimes the paralysis occurs in the form of hemiplegia, the
arm and leg of the same side being affected. This form, the
existence of which was denied by Heine, has been observed by
Duchenne, is declared by Volkmann not to be at all rare, and
was found by Sinkler eight times in eighty-seven cases. Du-
chenne saw one case of crossed paralysis in the arm and leg. It
is rare for but one arm to be totally or partially paralyzed, still
more rarely does the paralysissseem to be confined to the upper
extremities without participation of the lower. It is very com-
mon, however, to meet with a quite partial paralysis of single
muscles and groups of muscles, especially on the lower extremi-
POLIOMYELITIS ANTERIOR ACUTA. 689
ties, and, at all events, in the majority of cases, even where the
paralysis is exceedingly wide-spread, there is a very non-uniform
implication of the various groups of muscles and even of single
muscles in a given nerve-domain. Hence arises such a manifold
variety in individual cases as to defy all description, and we
must therefore refer our readers for details to the reports of
cases accumulated in literature. We merely mention, by way
of example, that in the domain of the peroneal nerve the tibialis
anticus not rarely occupies an exceptional position, either being
paralyzed alone or alone free ; that in the domain of the crural
nerve the sartorius or the tensor vaginze femoris often give the
same history ; that in the domain of the radial nerve the same
is true of the supinator longus; that the deltoid is not rarely
attacked by paralysis alone, and other instances of the same
kind.
Very soon, sometimes within a few days, but generally not
until within the next few weeks, a gradual improvement of the
paralysis sets in, affecting a greater or smaller part of the mus-
cles involved, while the rest usually remain paralyzed perma-
nently or, at least, for a long time. This very symptom of the
partial restitution of muscles is also very characteristic of the
disease. Very rarely this restitution is complete, extending to
all the paralyzed muscles, so that the improvement once begun
advances to complete recovery (so-called temporary spinal paral-
ysis). |
The upper part of the body, and the upper extremities gener-
ally, improve soon, and are the parts most likely again to regain
their full activity ; a part of the muscles of the trunk also almost
always takes part in the improvement, while others, particularly
the muscles of the back, remain permanently paralyzed. In the
same way a partial restitution often takes places in the lower
extremities ; one limb may become entirely or partially capable
of performing its functions again, while the other remains para-
lyzed ; it is very common for single portions of an extremity to _
remain permanently paralyzed, often single muscles alone; this,
too, afterwards gives great variety to the picture of the disease.
As a general rule, the progress of this improvement only lasts
for a time ; this progress is most manffest during the first four to
VOL. XIII.—44
690 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
eight weeks, and then often inspires delusive hopes. At a later
period the progress is slower, and after six or nine months from
the beginning of the disease there is no question of any further
spontaneous improvement; if any is then observed, it is as a
rule only apparent, caused by use and practice of the restored
or unaffected muscles. Doubtless, however, during the later
stages of the disease, too, appropriate (electrical) treatment may
still effect improvement in some muscles, which is sometimes
very striking, although generally but slight.
In almost all muscles whose mobility is not very soon restored,
and which remain more or less permanently paralyzed, a well-
marked and rapidly progressive atrophy very soon appears.
This begins in the first weeks of the disease, and even those mus-
cles that are but slightly affected generally give unmistakable
evidence of a slight degree of emaciation ; this soon disappears
again, however, on the restoration of mobility. In the muscles
more severely affected the atrophy is generally very distinct in
the course of a few weeks. The muscles become more and more
flaccid and attenuated, and may so completely disappear that
the skin seems to lie immediately upon the bone, and the limbs
assume a skeleton-like appearance. During the further course of
the affection the volume of many of these muscles is again in-
creased, so that there appears to be a muscular mass present
again; this is caused, however, by the secondary deposition of
fat in the connective tissue, and it is generally easy to prove, by
the test of galvanism, that not so much as a trace of muscular
tissue remains in these pseudo-muscles. In some cases the
atrophy of the muscles is completely masked from the very
beginning through the more abundant development of fat in the
subcutaneous connective tissue, or by early deposits of fat in the
muscles themselves; this is especially true in well-nourished,
well-developed children. In such cases, however, advanced atro-
phy is always to be recognized by the extreme softness and flac-
cidity of the muscle as compared with one that is healthy, even
if the tape-measure indicates no material difference in compari-
son with the healthy side.
Another sign which may be mentioned as being often ob-
served in adults, although more rarely established in children, is
POLIOMYELITIS ANTERIOR ACUTA. 691
that during this rapidly advancing process of atrophy the mus-
cles are quite sensitive on pressure.
The alterations in the electrical irritability of the motor
nerves and of the muscles, which are always to be found in the
spinal paralysis of childhood, stand in most intimate relations
to atrophy of the muscles. The earlier authors, it is true, only
tested the relations of faradic irritability, and Duchenne, in par-
ticular, is entitled to the credit of having carefully investigated
this in every direction, and of having established important diag-
nostic and prognostic rules. Duchenne found that in muscles —
which are severely affected, faradic irritability begins to sink
very quickly ; that it is materially diminished at the end of three
to five days, and entirely extinguished by the seventh day or
during the course of the second week. All the paralyzed mus-
cles, however, in which this does not occur during the course of
the second week, in which faradic irritability is only more or
less diminished, but not completely lost, do not remain perma-
nently paralyzed, but regain their mobility, and do so the more
promptly the less their faradic irritability has been diminished.
These statements have been confirmed by all subsequent ob-
servers.
But our knowledge on this subject did not widen nor gain in
precision until the paralyzed nerves and muscles were also tested
by the galvanic current. Then it became at once manifest that
the loss of faradic irritability found by Duchenne was nothing
else than a part of the phenomena of degeneration. Indeed, as
might have been expected, a priori, in view of the degenerative
changes in the nerves and muscles, the alteration in electrical
irritability which seems to be always capable of demonstration,
in its various stages in the spinal paralysis of children, consti-
tutes the reaction of degeneration. So far as 1 know, Salomon
was the first to establish the characteristic alterations of galvanic
irritability in the muscles in the spinal paralysis of children, and
since that this alteration has often enough been observed again,
though it has also often enough been overlooked. The course of
the alteration is about the same as that in severe traumatic paraly-
sis. There is rapid loss of faradic irritability in nerves and mus-
cles, either permanently or, at least, for a long time, that is, until
692 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
mobility returns; and then the familiar fact is often observed
that faradic irritability returns much later than voluntary motion.
There is equally rapid loss of galvanic irritability in the nerves ;
in the muscles, however, during the first weeks and months of
the paralysis, there is an increase of galvanic (and mechanical)
irritability with the characteristic qualitative changes (AnSZ =
or > KaSZ; contraction slow, tonic, prolonged).
In the course of two or three months the galvanic irritability
sinks again, often far below the normal standard, but retains the
characteristic qualitative alterations, and these constitute the
main point in the examination. In the course of one or two
years and more after the beginning of the disease there is gener-
ally nothing but a trace of galvanic irritability in the muscles ;
but not unfrequently the characteristic sluggish jerking can still
be shown here too, and, indeed, it is often possible to prove, by
means of the galvanic current, that muscular substance is still
present where this was thought to have entirely disappeared. In
still older cases there is generally nothing definite to be estab-
lished. In those muscles that do not atrophy, a greater or less
simple diminution in the faradic and galvanic irritability is gener-
ally found ; the same thing is true in all those muscles and nerves
which have regained their mobility up to a certain point; in
these the reaction of degeneration can, of course, no longer be
demonstrated.
It is desirable that these relations should be more systematically tested than has
yet been done. To be sure the material is not easily obtained, and is only to be had
by a fortunate chance, and the examination of the unruly and screaming little
patients is attended with great difficulties. It is also often out of the question
exactly to localize the current in single muscles, for the abundant layer of fat, in
children, the well-preserved sensibility, the resistance of the patient, etc., make it
much more difficult to determine the contractions. The cases which occur in adults
are too rare to furnish sufficient material for observation, which can best be obtained
in large children’s hospitals. I regard the reaction of degeneration as quite a constant
manifestation in the spinal paralysis of children, one which can generally be dis-
tinctly shown only in the first years of the disease, often not being recognizable
with certainty ata later period. I have, at least, never yet, amongst a large num-
ber of cases, failed to find the reaction of degeneration on careful search. The
above statement is based upon the examination of cases after the lapse of four,
eight, and fourteen weeks, after six, twelve, twenty-two, and twenty-four months,
i ea —
POLIOMYELITIS ANTERIOR ACUTA. 693
and from that up to several, or even many years. Furthermore, it also entirely
corresponds with the known results of electrical examination in the same affection
in adults.
The changes in the bones and joints which arise in the course
of the disease are almost equally important with the changes just
described in the muscles. The bones of the paralyzed limbs are
materially retarded in their longitudinal growth, so that, in the
legs for instance, differences of from 3 to 20 cm. (1.1 to 7.8 inches)
may occur, as compared with the healthy side. The same thing
is true in the upper extremities. The long bones, furthermore,
remain much thinner than normal; they not rarely become po-
rous and inclined to bend, yielding, and friable. Their epiphy-
ses and processes grow smaller and less distinct; the shoul-
der-blade and the patella often remain far below their natural
size, the paralyzed hand or foot is shorter, narrower, and thinner
than the sound one; even the pelvis may remain considerably
behind-hand in its development, being below the normal measure-
ments of circumference and height.
It is a remarkable fact that the interference with the growth
of the bones is by no means always in direct proportion to the
atrophy of the muscles of the same extremity ; sometimes the
one and sometimes the other is in the ascendancy, and the inter-
ference with the growth of bone may persist in spite of the dis-
appearance of the paralysis (Volkmann). I have myself had
occasion to observe this fact.
Volkmann also, not without reason, counts a case of ‘‘ unilateral paralysis of the
face,” observed by him, as belonging to the spinal paralysis of childhood. Other
cases should be tested with reference to similar connection.
The joints become deformed, abnormally movable, partly
through disappearance of the articular extremities of bone and
of cartilages, partly through relaxation and stretching of their
ligamentous apparatus. The movableness of the limbs is thus
often rendered very great, so that patients can frequently execute
all kinds of unusual movements and wonderful dislocations of
the limbs.
The changes in the skin must ‘Also be noticed. The skin
694 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
becomes flaccid, withered, doughy, sometimes dry, scaly, brittle.
The most striking characteristic, however, is the coldness and
cyanosis which is uniformly observed in the paralyzed limbs.
Heine carefully measured the lowering of temperature in many
cases, and was able to prove very marked differences as com-
pared with the healthy extremity. There can hardly be a doubt
that this lowering of temperature and cyanosis are due less to
diminished nutrition in the paralyzed limbs than to vaso-motor
paralysis, and it would be interesting to note whether, in the first
stages of the disease, there is not a temporary elevation of tem-
perature. I demonstrated this to be the case in one adult pa-
tient.
By means of the conditions above described—the paralysis
and atrophy of muscles, the interference with the growth of
bones, the changes in joints—all severer cases lead to paralytic
contractures and secondary deformities, which may cause the
most revolting distortions of the limbs, of the spinal column,
etc., and are most graphically set forth by Heine in numerous
illustrations. The atrophy and secondary contraction of the
muscles, the laxness and malformation of the joints, the curva-
tures of the spine, all combine to produce the most deplorable
and extraordinary cripples, such as, in countless numbers, excite
the sympathy of the passers-by upon the highways and in the
market-places.
What are called paralytic contractures are especially effect-
ive in the development of these deformities. According to
Heine, these do not begin to develop until the children com-
mence to use their limbs and drag themselves about with them,
whether well or ill. This statement, however, may not be so
rigidly correct.
The most varied forms of club-foot occur (talipes varus, val-
gus, equinus, and calcaneus), and various combinations of the
same (most frequently of the equinus and varus). Retrocurva-
ture of the knee, inversion and eversion of the same, are also met
with, as well as contractures in the knee- and hip-joints, ky pho-
sis, lordosis, and extreme instances of scoliosis. In the upper
extremities the deformities are liable to be much less serious;
the hands and fingers are generally found flexed, the shoulder-
|
4
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/
1
POLIOMYELITIS ANTERIOR AOCUTA. 695
joint gradually becomes immovable, the pectoralis and the latis-
simus dorsi are more or less contracted.
The occurrence of contractures is chiefly the result of a high
degree of paralysis and degenerative atrophy of the muscles.
Considered in detail, the more precise method of development
may be threefold.
1. By far the most frequent cause of paralytic contracture, in
these cases, is the continued approximation of the points of at-
tachment of the muscles, induced partly by the weight of the
parts, partly by external pressure in walking, standing, sliding,
etc. This point has been thoroughly discussed by Volkmann, on
the basis of Hueter’s investigations, and the former seeks to ex-
plain almost all paralytic contractures on mechanical grounds.
According to him the deformities are developed partly by reason
of the weight of the limbs concerned and the position which they
assume when at rest, partly through the fact that limbs, articu-
lar extremities, and articular surfaces are subjected to an abnor-
mal burden, when called into use, and are thus gradually pressed
into abnormal positions. In both instances the points of attach-
ment of certain muscles would be more or less permanently ap-
proximated to each other, and thus a gradually increasing nutri-
tive shortening of the same occurs, a permanent contracture and
deformity.
This must certainly be the explanation of all those contrac-
tures and deformities which arise when all the muscles surround-
ing a joint are completely paralyzed, or when the deformity and
contracture take place in the line of traction of those very mus-
cles which are especially paralyzed. ‘Talipes equino-varus is the
form most easily explained; the foot, being left to its own
weight, assumes this position, which becomes more and more
fixed the longer the patient remains in bed, or the longer step-
ping upon the foot, which would counteract this deformity, is
avoided, or the patient merely steps upon his toes.
Paralytic talipes valgus occurs when the patient begins to
walk again very soon after his attack, and steps on the foot
while there is more or less complete paralysis of the mus-
cles of the leg; he then steps on his entire sole, and the foot,
which is loose in its joints, gives Way, toward the outer side
696 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
(knickt soweit nach aussen um), until prevented, by physioclogi-
cal restraints, from bending any further. Even talipes cal-
caneus is said to be due principally to mechanical causes,
inasmuch as when the muscles of the calf are entirely para-
lyzed, the individual steps upon the os calcis, and this is then
gradually and mechanically pushed forward; by this means
the distance between the points of attachment of the muscles of
the sole is also diminished, and for this reason the plantar curva-
ture of the sole reaches a peculiarly high degree of development
in this variety of club-foot. It appears to us, however, that here
the co-operation of the antagonistic muscles of the front of the
leg, which are less paralyzed, is of material significance. Retro-
curvature of the knee is brought about by the fact that the joint,
deprived of its power of fixation by the muscles, is extended
backwards as far as its physiological restraints will admit, in
order to transform the leg into a firm support for the body. In
the upper extremities, too, the majority of contractures and de-
formities are developed in the same simply mechanical manner.
2. But contractures may also furthermore be brought about
by the fact that the antagonists of the paralyzed muscles remain
effective. In every voluntary action of the same their points of
attachment are approximated to each other, and there is no mus-
cular power present to draw them apart again; in many cases,
indeed, this is accomplished through the weight of the parts or
other mechanical means; but where this is not the case these
muscles fall into permanent nutritive shortening, and thus in-
crease the deformity. A certain degree of participation in the
production of paralytic contractures and deformities, even though
it be but subordinate, must certainly be attributed to this active
mobility of antagonistic muscles; thus in talipes calcaneus, thus
in contractile bending of the knee-joint with complete paralysis
of the quadriceps extensor muscle.
3. Finally, a certain part in the production and fixation of
paralytic contractures may be attributed to the proliferation of
inter stitial connective tissue and its subsequent retraction, which
takes place with the degenerative atrophy of the muscles. This,
however, would seem to be of subordinate significance.
Mechanical causes certainly play the principal réle, in this
POLIOMYELITIS ANTERIOR ACUTA. 697
matter, and the manifold and adventurous methods of locomo-
tion to which many of these patients accustom themselves, as well
as the extremely varied localization and extent of the paralysis,
account for the fact that the most wonderful and striking mal-
formations and crippled conditions occur in these very patients.
So far as concerns the pathogenetic explanation of the prin-
cipal symptoms of the disease, as described thus far, these may
doubtless all be explained in one way. The acute, inflammatory,
and destructive lesion of the gray anterior horns is undoubtedly
to be held accountable for all these disturbances. And indeed
the lesion of the large ganglion-cells—and, we may add, the de-
struction of all nervous channels of communication—seems to be
of very special importance in this respect. It is difficult to make
any more definite statement on this subject ; still the application
of what we now know about it seems pretty easily made; inasmuch
as the spinal paralysis of children is one of the very conditions,
among others, which has contributed to clear up our knowledge
of the physiological functions of the gray anterior horns.
According to all we know, the gray anterior horns are points
of passage for direct motor conduction from the lateral columns
to the anterior roots. Whether this conduction, in all cases,
passes through large ganglion-cells, and whether these, there-
fore, constitute a species of-ganglionic centres (Knotenpunkte),
is not yet certainly determined, but seems very probable. It
seems, furthermore, tolerably certain that the large ganglion-cells
exercise distinct trophic functions with reference to the nerves
and muscles (and probably also to the bones, joints, etc.). It is
still undecided whether all these ganglion-cells have at the same
time motor and trophic functions, or whether, as Duchenne and
Joffroy conjecture, and as Hammond also believes, there are two
kinds, purely motor and purely trophic; nor is this point capa-
ble of easy demonstration. At the same time the latter suppo-
sition is not exactly improbable, and is certainly more convenient
as applied to the theory of this and kindred diseases.
The more or less complete destruction of the anterior gray
horns, arising acutely, explains all the manifestations encoun-
tered in quite a plausible manner: the paralysis by the destruc-
tion of motor tracts, the atrophy of Ymuscles and the hindrance
698 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
of the growth of bones, with their results, by the destruction of
the trophic apparatus. The fact of the disease occurring in cer-
tain circumscribed areas, and the immunity of certain groups of
ganglia, explains the localization and extent of the paralysis, and
the immunity of certain single muscles and groups of muscles.
The acute inflammatory nature of the process accounts for the
sudden appearance of the paralysis; the wide extension of the
process over the spinal cord accounts for the initial fever and the
wide extent of the paralysis at the beginning. The possibility
of the partial resolution of the acute inflammation explains the
rapid disappearance of the first stormy manifestations, and the
later partial restitution of the muscles.
Upon the supposition, therefore, that our views concerning
the functions of the anterior gray horns are correct, the clinical
manifestations of the spinal paralysis of childhood are in suffi-
ciently satisfactory correspondence with the anatomical lesion.
The remaining functions of the spinal cord, with few excep-
tions, suffer no disturbances whatever, or but very slight ones.
The sensibility of the skin is almost always intact. At the
beginning of the affection there may be complaints of pain, par-
zesthesia, and the like, here or there, but they are quite transi-
tory manifestations which may easily be explained by the inflam-
matory swelling and hyperemia in the initial stage. Ata later
period sensibility is generally intact everywhere. Only occasion-
ally is there a slight, generally very insignificant dulness of sen-
sibility complained of, especially a slight diminution of sensibil-
ity to pain and lessened intensity of the sensation of tickling.
This may be explained partly by an unusual extension of the
diseased process to the central and posterior gray substance,
partly, however, also by the great coldness and poor nutrition
of the extremities.
Reflex activity, on the other hand, always suffers very severe
disturbances. It is a matter of course—on account of the degen-
erative atrophy of the muscles and nerves, if for no other rea-
son—that in all muscles which are severely attacked reflex action
is completely extinguished ; in these muscles no sign of reflex
twitching can be aroused, either through the skin or through
the tendons. But even in those muscles which are but slightly
_—_-
astindl wes a
POLIOMYELITIS ANTERIOR ACUTA. 699
attacked, reflex activity is liable to be, at least temporarily, very
much lowered or entirely extinguished. As the reflex circuits
are generally considered as being located in the anterior gray
substance, and reflex activity is thought to be connected with
the large ganglion-cells, this condition of things is readily to be
understood.
Disturbances of the function of the bladder are not exactly
rare during the first days; there may be complete paralysis of
the bladder, with retention of urine, but more frequently there
are involuntary evacuations through incontinence of the bladder
(and the same thing also holds true with regard to evacuation of
the bowels). But these manifestations always disappear com-
pletely again within three to eight days. Not seldom, however,
especially in little children, a slight weakness of the bladder,
with occasional incontinence, remains for a time. But this dis-
turbance, too, is likely to disappear within a couple of weeks or
months, leaving no trace behind, and in the later stages of the
disease bladder disturbances certainly belong to the rarest ex-
ceptions.
The occurrence of bladder troubles is sufficiently accounted
for by the occasional somewhat greater extension of the anatom-
ical lesion within the gray substance.
The sexual functions probably never suffer any disturbance,
or at least only quite exceptionally and rather indirectly (through
muscular paralysis, deformities, etc.). They generally remain
quite intact, both in men and women.
The same thing is true with regard to the functions of the
special senses, the psychical and other cerebral functions.
The vegetative functions are also usually carried on quite
undisturbed. The appetite and digestion are good, bowels some-
times rather sluggish. The general nutrition of the body is usu-
ally admirable, if some other circumstance does not incidentally
disturb it.
b. Poliomyelitis Anterior Acuta in the Adutt.
When this malady attacks adults, we have essentially the
Same picture of disease presented to us as in children. It is
700 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
merely modified, in a non-essential manner, by the fact that the
brain of the adult offers somewhat more resistance to the initial
disturbances, that the general organism is not so highly disposed
to fever, and that the growth of the bones is already completed,
and the firmness of the joints is greater.
Here, too, the disease begins with a general ill-feeling, with
Fever which is generally introduced with lively pain in the back
and the extremities, and not rarely with paresthesia (formica-
tion, a feeling of numbness, etc.). Severe cerebral symptoms are
generally wanting ; general convulsions have never yet been ob-
served, but severe headache, dulness, somnolency, and even slight
delirium occur. Well-marked gastric symptoms, vomiting, ete.,
have been repeatedly met with. In some cases the fever reaches
great intensity.
Then the paralysis is developed, more or less rapidly, gene-
rally in the course of a few hours, perhaps over night, more
rarely not until after a few days. Just as in the case of children,
it is more or less widely spread, complete, and with entire flac-
cidity of the paralyzed muscles.
Now and then temporary weakness of the bladder is also de-
veloped. Reflex action in the paralyzed muscles is either low-
ered or extinguished ; though in some cases (thus with Frey) it
may be retained, at least in those muscles which are not perma-
nently and not completely paralyzed. These statements, how-
ever, need further confirmation, through accurate examinations.
An improvement of the general condition very soon sets in—
after one or two days, rarely not till the eighth or tenth day—
and then an improvement in the paralytic symptoms soon fol-
lows. This, then, either gradually advances—usually not until
after many weeks and months—to complete restitution of the
paralyzed parts (temporary paralysis, case of Frey), or there is
merely a partial restitution of the muscles, and the rest of them
remain for a long time or permanently paralyzed. In these, as
in the case of children, rapidly progressive atrophy then follows,
with evidences of the reaction of degeneration, etc. The skin
becomes lax and withered, the extremities cool and cyanotic.
But there exists no trace of disturbances of sensation ; the
patient never takes to his bed; the bladder troubles that may
POLIOMYELITIS ANTERIOR ACUTA. 701
have existed soon subside; the sexual function remains entirely
normal; the general nutrition becomes quite good again.
In the further course of the disease the evil consequences of
the paralysis and atrophy of muscles inevitably show themselves
in the shape of paralytic and myopathic contractures and the
deformities resulting therefrom. These, however, never reach
the same degree as in children, partly because in adults there is
no interference with the growth of bones, and therefore no short-
ening of limbs, because the greater firmness of the joints and
their ligaments in adults prevents more serious deformities of the
same, and because adults notice the deformities at their very be-
ginning, and seek, by means of early treatment or careful man-
agement, to remove them, or to hinder their further development,
which is, of course, not nearly as much the case with children.
The differences between acute spinal paralysis in children and
that in adults actually reduce themselves down to this more
slight development of the secondary and consecutive alterations
in the latter. In all other respects, in the extension of the paral-
ysis and atrophy to single or to many muscles, to one or to all
extremities, or to the trunk, in the further course of the disease,
in the insignificant influence of the same on the general well-
being, etc., there is the most complete correspondence between
the two, and it is therefore.not necessary to add anything fur-
ther with regard to the affection in adults.
Course—Duration— Terminations.
There is not much to be added to what has already been said
on this subject. The typical and ordinary course of the disease
—with its extremely acute beginning and very quick transition
to a chronic stage, and with its gradual development of second- |
ary changes—is, in the majority of cases, pretty much the same,
and has been described with sufficient minuteness in the preced-
ing pages.
With reference to the course of the affection, we will only add
a few words on the subject of so-called Zemporary spinal paral-
ysis. The term ‘‘temporary paralysis’’ seems to have been first
used by Kennedy ; at least he is every where cited as authority
702 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
for the occurrence of temporary paralysis in children, and I
think unjustly so, for scarcely any of his cases belong under this
general head, and those which do belong under it were not
‘‘temporary.’’ At the same time, such temporary forms of
acute spinal paralysis do seem to occur, as has been claimed by
Duchenne, Volkmann, and others, and established by Frey with
several undoubted cases. Neither can we see any reason why the
restoration of motility, which in ordinary cases is regularly ob-
served in a part of the muscles, should not in the lighter cases
extend to ald the paralyzed muscles. These temporary forms are
distinguished from the permanent ones only in this, that in the
course of some weeks, or a few months, complete restoration of
all movements takes place, although, at the beginning, these
cases were by no means to be distinguished from the severer
forms; they may even have been characterized by atrophy with
loss of faradic irritability. These temporary forms occur in
adults as well as in children.
Nothing further need be added with regard to the duration
of the disease. |
The termination of the disease seems always to be favorable,
so far as its relation to life is concerned. There is no evidence
that this disease, of itself, has ever directly induced death. In
persons who have been affected with spinal paralysis death re-
sults from accidental occurrences, the weakness of age, or any
disease imaginable.
Cases of this affection divide themselves, quite simply, into
two classes: those in which complete recovery takes place—the
temporary paralyses just mentioned, and those in which the
recovery remains incomplete, that is, there is recovery with some
remaining defect. This defect is due to permanently paralyzed
and atrophied muscles, to the shortening and bending of limbs,
etc. Daily experience teaches that this defect, even when it is
very great, need not materially interfere with the general well-
being, nor the following of an occupation, nor the enjoyment of
life. To be sure, there are also miserable cripples enough who
have been placed in the saddest predicament for their entire lives
by means of acute spinal paralysis, even though they may still
enjoy a good appetite and a clear head.
ei
POLIOMYELITIS ANTERIOR ACUTA. 703
We would here again briefly call attention to one point. It
would be well worthy of further attention to investigate whether
persons who have once gone through with an attack of acute
spinal paralysis do not show a greater disposition to diseases of
the spinal cord, so that in later life they are attacked with other
spinal affections. I have stated above that this has occurred but
seldom in my own experience and that of others—so seldom, in
comparison with the absolute frequency of the spinal paralysis
of children in general, that I am rather inclined not to believe in
any such causal relation. Still, this experience may prove to be
deceptive, and, on closer investigation, the facts may turn out
differently.
Diagnosis.
With the degree of knowledge at our disposal to-day, and in
view of the great uniformity of the picture of the disease and its
course, it is certainly quite easy to recognize acute poliomyelitis
anterior. There will be no difficulty in making the diagnosis
where the characteristic grouping of symptoms is present;
where a sudden febrile affection, not unfrequently accompanied
by severe cerebral manifestations, is quickly followed by a wide-
spread paralysis of a high grade, with complete relaxation of the
limbs; where early improvement of the general condition, and
not long after partial recovery from the paralysis follows, while
the more severely paralyzed muscles lose their faradic irritabili-
ty and fall victims to rapid atrophy ; where reflex action is com-
pletely extinguished, but cutaneous sensibility and the functions
of the bladder and rectum are entirely preserved. Under these
circumstances it will not be necessary to wait for secondary con-
tractures and deformities, for the arrest of the growth of limbs,
etc., to confirm the diagnosis.
But, even in the lightest, and what might be called fragmen-
tary cases, it will, as a rule, be possible to make a diagnosis with
greater or less certainty by means of a thorough examination of
the nerves and muscles, careful regard to the development of the
disease, and all other circumstancey, relating thereto. During
its latest stages, likewise, the disease may still be recognized by
704 ERB —DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
its sequels, and, unless all points in the history of the case going
to show the method of its development are wanting, may be pro-
nounced upon with certainty. Here, however, it is easier to
imagine the possibility of confounding it with the sequels of
other kindred forms of disease.
We must, however, as a matter of course, be careful not to
place in this category every instance of spinal paralysis arising
in childhood, even if accompanied with atrophy. This is, alas,
still too often done. But such a stretching of the idea of what
is included under ‘‘ spinal paralysis of childhood ”’ is not justifi-
able at the present day, and it must be positively required that
in the diagnosis the characteristic signs of the disease be ad-
hered to.
Acute poliomyelitis anterior must be distinguished from the
following forms of disease : |
From acute, central, or transverse myelitis. Here the dis-
tinction will not generally be difficult, on account of the disturb-
ances of sensibility and of the bladder and rectum which are
almost invariably present in these diseases; on account of the
— occurrence of bed-sores; on account of the fact that there is
usually increased reflex action and usually no atrophy. The
principal marks of distinction are the disturbances of sensibility
and of the bladder, also the course of the affection.
Hematomyelia, or hemorrhage into the gray substance, may
present great similarity to acute spinal paralysis, on account of
the rapid development of the paralysis, the subsequent atrophy
and reaction of degeneration, the absence of reflex action, ete.
But the non-febrile beginning of the former, the entirely sudden,
apoplectiform appearance of the paralysis, the almost invariable
disturbances of sensibility, the paralysis of the sphincters, the
bed-sores, etc., insure the diagnosis of hemorrhage.
Myelitis from compression—such, for instance, as not rarely
leads to rapidly developed paraplegia in Pott’s disease—can only
be confounded with poliomyelitis anterior by reason of great
inattention, or in quite exceptional cases. The disturbances of
sensibility, the heightening of reflex excitability, the paralysis
of the bladder, the spasmodic manifestations in the lower ex-
tremities, the absence of atrophy and the reaction of degenera-
=
POLIOMYELITIS ANTERIOR ACUTA. 705
tion, the presence of affections of the vertebral column, of lively
pain, of disturbances of the general health, etc., are enough to
determine the presence of this form of disease.
The cerebral hemiplegia, which is not rare in children and
quite frequent in adults (especially what is called ‘‘ hemiplegia
spastica infantilis’’), is to be distinguished from our disease by
the more or less complete demonstration of the following symp-
toms: headache, dizziness, affection of the cerebral and spinal
nerves, strabismus, a stupid expression of countenance, paralysis
with tension of the muscles and spasmodic contractures, increased
reflex excitability of the tendons, no atrophy or but a very
slight degree of the same, the preservation of electrical irrita-
bility, involuntary additional movements on voluntary motion of
the sound side of the body, stiffness and extension of the joints,
the bones not at all or but little shortened, more or less consid-
erable disturbances of sensibility, no scoliosis, etc. These signs
are also sufficient for a differential diagnosis, even when such a
cerebral affection is bilateral.
Progressive muscular atrophy is to be distinguished from
acute spinal paralysis simply by its chronic development, the
progressive course of the disease, and the lesser prominence of
the paralysis ; furthermore, by the retention of electrical irrita-
bility, the hereditary relations-of the disease, ete.
Pseudo-hypertrophy of the muscles is likewise to be recognized
by the slow development of the disease, the absence of severe
paralysis, the increase in the volume of the muscles, and the
absence of any atrophy.
The spasmodic spinal paralysis of children, two cases of
which I have reported,’ is very easily to be distinguished by
the slow, insidious and unnoticed development of paresis (which
seldom goes on to complete paralysis), by the muscular tension
and contractions, the increased irritability of the tendons, and
the absence of atrophy and the reaction of degeneration.
The distinction between our disease and the paralysis of chil-
dren following delivery,’ which, at a certain stage, may have
1 Virchow’s Archiv. Bd. 70. Heft 3. 1877. ™
* See this Cyclopaxdia. Vol. XI. (Hrd, Diseases of the Peripheral Nerves), p. 561.
VOL, XIII.—45
706 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
some resemblance to the spinal paralysis of children, of limited
localization, is generally determined by the history of the case;
and when this is not true, by the characteristic localization, as
well as by the disturbances of sensibility that are present ; fur-
thermore, by the absence of a febrile initial stage, the occurrence
of the trouble at an early age, etc.
The peripheral paralyses of single groups of muscles and
nerves through pressure, faulty position, tight bandaging, etc.,
such as not rarely occur in children, will be correctly pronounced
on by demonstration of the cause, by the absence of the charac-
teristic initial stage, by the strict localization of the trouble in a
definite peripheral nerve-domain, by the presence of disturbances
of sensibility, by the rapid, favorable result, etc.
For the distinction between this and subacute and chronic
poliomyelitis, see the following section.
Prognosis.
Acute atrophic spinal paralysis does not appear ever directly
to threaten life; its prognosis is therefore absolutely favorable,
so far as life is concerned. The first onset, it is true, often looks
dangerous, and it does not appear exactly impossible that death
may occasionally follow during the initial stage. It is a ques-
tion which as yet remains undecided, whether some cases of
death from ‘‘convulsions”’ do not belong in this category. This
can only be decided by a very careful and intelligent examina-
tion of the spinal cord in such cases. I was forcibly struck by
the fact that in von Heine’s histories of his patients it repeatedly
appears that one or another child in the same family had died of
convulsions.
The prognosis with reference to complete recovery is quite
different. Here it may be pronounced as almost absolutely un-
favorable. The ‘‘temporary’’ forms of the disease are so rare
that they can hardly be taken into consideration; in fact, the
best we can do, almost always, is to make a prognosis of recov-
ery with greater or lesser remaining defects. The parts that do
not regain their mobility in the first two or three months, or
within the first six months, seldom do so at a later period.
POLIOMYELITIS ANTERIOR ACUTA. 707
There is then little to be expected in the way of direct attempts
at recovery, although slight and partial improvements, even at
later periods, are not exactly rare.
At the same time the usefulness of the extremities may still
be materially improved through appropriate orthopedic opera-
tions, gymnastics, electrical treatment, etc., and thus the magni-
tude of the defect be rendered less noticeable by the patient.
The prognosis in this respect depends upon the grade and
extent of the paralysis, upon the preservation and the functional
capacity of certain muscles and groups of muscles, upon the
extent of the atrophy and the amount of deformity already
present, upon the age of the patient and of the disease at the
beginning of treatment, upon the intelligence and perseverance
of the patient, and more of the same kind. <A rich experience will
of course sharpen one’s judgment with regard to the value of
these several conditions.
Therapeutics,
The treatment of acute spinal paralysis naturally falls into
two divisions: the treatment of the acute inflammatory attack,
and that of its seguels and results (the paralysis, atrophy, con-
tractures, and deformities).
The fulfilment of the first task is rendered difficult by the
fact that the endeavors of the physician often come too late, or
that his diagnosis remains in doubt until the paralysis is fully
developed.
In all cases, however, which come under treatment in good
time, the measures which would be applicable in acute myelitis
are to be adopted with all energy—of course, in a manner fitting
the circumstances, and especially with due reference to the tender
age of many of the patients. Local abstraction of blood, there-
fore (leeches, cups, etc.), is to be employed, first of all, at the
parts especially affected (the lumbar and cervical enlargements) ;
cathartics (calomel, infusion of senna, etc.) ; inunction of mer-
curial ointment to the back; the use of ergotine, belladonna, or
iodide of potassium in appropriate doses; derivatives (strips of
blister plaster the length of the spine} painting with tincture of
708 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
iodine, etc.) ; and, in appropriate cases, the application of ice, or
the employment of Priessnitz’s cold wraps about the trunk. In
cases of severe brain-symptoms, Kussmaul recommends a tepid
bath, with cold affusion to the head. Still, we need not be
immediately driven to more active interference by apparently
threatening manifestations, as experience teaches that there is
hardly ever any real danger during the initial stage. But if we
should succeed, by energetic treatment, in suppressing the mye-
litis at its outset and thus preserving a portion of the nervous
elements from positive destruction, it would be a great point
gained.
In the second stage of the disease it must likewise be our
main endeavor to induce a favorable change in the diseased focus
itself within the spinal cord, to favor the resolution of the inflam-
matory and degenerative changes, so that whatever of nerve-ele-
ments, fibres and cells, may still be capable of being saved, shall
be saved and again put in condition to perform their functions.
Those ganglion-cells which have once been totally destroyed can-
not be reproduced, but probably cells and fibres which are in the
act of degeneration may be preserved from further destruction,
and gradually brought back again to the performance of their
functions. It is only on this supposition that there can be any
sense in the further symptomatic treatment of peripheral nerves
and muscles. It is hard, indeed, to determine how far the power
of our curative measures reaches towards the fulfilment of this
indication ; up to the present time not much can be said in praise
thereof.
The galvanic current may undoubtedly be regarded as one of
the principal means of influencing the diseased area within the
spinal cord ; and it is the catalytic action of the current that is
to be tried. What we want, therefore, is a stabile action of the
current upon those portions of the spinal cord which are chiefly
diseased. Our best plan will be to place a large electrode, which
will cover the entire diseased area, over the corresponding por-
tion of the back (over the lumbar or cervical enlargement), and
to apply the other to the anterior surface of the trunk, and first
to let the anode, then the cathode act for from one to two min-
utes at a time, with a moderately strong current. The earlier
a ee
POLIOMYELITIS ANTERIOR ACUTA. 709
this treatment is begun, the better; during the later stages little
is to be expected from it, although, according to the well-estab-
lished experience of some, a favorable effect is by no means im-
possible. The treatment must be continued for a long time, or
must be repeated, at intervals, for several years.
It must be admitted that, as yet, this treatment has been fol-
lowed by no specially brilliant results ; this is perhaps partly due
to the fact that these cases almost always come under treatment
far too late, and that physicians have often contented themselves
with the peripheral application of the current to the paralyzed
muscles, instead of making the diseased area within the cord
itself the main object of galvanic treatment, as should always be
done. It is also quite evident that the faradic current is not the
one to be used in these cases. According to my own experience,
which relates almost exclusively to old cases and later stages, I
can report no brilliant results; still, I have often seen improve-
ment set in, which I was obliged unquestionably to ascribe to the
treatment, so that I cannot concur in the unfavorable verdict of
Volkmann on electrical treatment. This verdict has also already
been corrected by Hitzig and Juergensen. To be sure, we may
not expect much from inappropriate, inadequate, or purely per-
ipheral electrical treatment, and under all circumstances the at-
tainment of any considerable result requires unusual patience and
perseverance on the part of the physician as well as the patient.
The same end—healing and resolution of the changes within
the spinal cord—may be sought to be reached through the gen-
eral stimulation of tissue-changes and of nutrition. On this
ground something is to be expected from the use of baths (ther-
mal springs, saline springs, thermal saline springs rich in gas,
animal baths, pine-needle baths, cold-water cures, sea-baths, etec.).
No more precise indications for the selection of the kind of baths
can yet be given. For children, I should first use saline springs
and saline thermal springs, afterwards light cold-water treatment ;
and for somewhat larger children, also sea-baths (and sea-air).
For adults, I would recommend gaseous saline thermal springs,
and then the energetic cold-water cure.
On the same principle, a strong and abundant diet will be of
benefit, with prolonged sojourn in the open air—the air of moun-
710 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
tains and woods—and the use of cod-liver oil. It is a question
whether rubbing the skin with spirituous or other applications
may have a similar though feebler effect, by exciting the activity
of the skin and aiding the circulation; at all events, it may be
tried.
As a matter of course, all sorts of internal remedies have been
tried—iodide of potassium, iodide of iron, nitrate of silver, ete.—
all, at best, with doubtful results. Strychnine has been warmly
recommended by many for the second stage ; Heine and Sinkler
have found it alike inefficacious when used internally or exter-
nally. In view of the much surer and safer action of electricity,
its use may well be ignored. Hammond recommends ergot to be
given as early as possible, and in full doses.
Finally, symptomatic treatment is of the highest importance.
This is to be directed, first, against the paralysis and atrophy of
the muscles. The principal means to be used is electricity. In
addition to the direct galvanic treatment of the spinal cord itself,
_ the systematic peripheral treatment of the nerves and muscles is
also to be carried on. Naturally, the galvanic current is the one
to be used first, on account of the reaction of degeneration of most
of the muscles. Still, Duchenne has arrived at quite noteworthy
results even with the faradic current; this is especially applica-
ble to those nerves and muscles which have but slightly lost or
entirely retained their faradic irritability. But these muscles,
naturally, also offer the best chances for galvanic treatment. The
method of treatment is simple: the labile application of the ca-
thode over all the paralyzed muscles and nerves, while the anode
is best placed upon the vertebral column at the height of the
main lesion. For very much atrophied and but slightly irritable
muscles, changes in the current are to be recommended in which
both electrodes are to be applied to the muscle (one upon the
nerve-trunk belonging to it). The strength of the current should
be such as to produce distinct twitchings and lively redness of
the skin. The faradic application is to be made with moist elec-
trodes, and with a pretty strong current. Treatment must al-
ways be continued for a very long time—months and years—with
longer or shorter intervals. By this means some slight progress
is generally attained. -
_
POLIOMYELITIS ANTERIOR ACUTA, 711
In support of the electrical treatment, massage and kneading
of the muscles, together with appropriate gymnastic exercises,
may be undertaken. Zhe application of warmth (warm-water
compresses, sand-bags, etc.) has also been recommended to fur-
ther the blood-supply and nutrition; and for this purpose, too,
some have advocated friction of the limbs with irritating sub-
stances (oil of mustard, tincture of cantharides, strong liquor
ammonie, extract of nux vomica, etc.).
But the main portion of the treatment generally, and in old
cases always, falls within the domain of orthopaedic surgery.
It is not our province here to enter into details on the difficult
and manifold indications which arise in this connection; we
refer our readers, for that, to treatises on surgery and orthope-
dics. We will only allow ourselves a few brief observations on
the main principles of the orthopedic treatment.
The main point, and the most important task, which devolves
precisely upon the practitioner who has these cases under treat-
ment af the beginning, is the prevention of contractures and
deformities ; when these are once developed and have grown old,
they are a more appropriate object for the specialist in ortho-
peedics and for orthopedic institutions. The physician may
render considerable service in this respect, if he keeps in mind
the purely mechanical methods of origin of the majority of con-
tractures and deformities, and early enough counteracts these
mechanical causes. This is the main point, and in its accom-
plishment electricity, gymnastics, light frictions, and baths can
serve merely as mild adjuvants.
The essential point consists in watching the position of the
limb when at rest, and in guarding the movements and the gait
so as to avoid the undue burdening of one side of the body
and continuous false positions. In guarding against the oc-
currence of talipes equinus it is sufficient, according to Volk-:
mann, if, during the earliest stage, while the patient is lying,
down, the foot be fastened to a light foot-board by means of a
flannel bandage, and this be drawn up somewhat towards the leg
by a strip of adhesive plaster. On their attempting to walk,
children should be put into stout-laced boots, with a steel shank
on the outer or inner side of the boot-teg, or with the sole slightly
"12 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
thicker on the one side or the other; in this way the develop-
ment of talipes varus or valgus may be counteracted. The for-
mation of talipes calcaneus may be combated by supplying the
defective action of the posterior muscles of the leg by a strong
bridle of rubber (the best is a rubber ring), which passes from the
heel to a trough-like fixture that is applied to the leg just below
the knee, and that is held firmly in place by a side-bar fastened
to the shoe. Indeed, the lost muscular power, wherever it occurs,
may be replaced in various ways by means of elastic tugs and
the like. © j |
According to the seat and extent of the paralysis, according
to the kind and magnitude of the deformity, the most varied
machines and supporting apparatuses are to be applied, in the
construction of which orthopedic surgery has accomplished a
great deal, and which often secure to the patient a very consider-
able use of his limbs.
In the more severe deformities tenotomy and forcible means
of correction may come into play. According to Volkmann,
patients should, as far as possible, avoid the use of crutches and
similar supports, especially at the beginning of their ailment.
16. Subacute and Chronic Inflammation of the Gray Anterior
Horns.—Poliomyelitis anterior, subacuta et chronica.—
Chronic atrophic spinal paralysis.—Paralysie générale spi-
nale antérieure subaigué (Duchenne).
Duchenne (de Boulogne), Recherches électrophysiol., patholog. et thérap. Compt.
rend, de l’Acad. d. Sc. 1849—De l’électrisat. localisée. 1855. 3. édit. 1872. p.
459.—WNesemann, Heilung eines bis zur vollstind. Lihmung aller Extremititen
vorgeschritt. Falles von progress. Muskelatrophie u. s. w. Berl. klin. Woch.
1868. Nr. 37.—Poché, Quelques considér. sur les amyotroph. d’origine spinale.
These, Paris, 1874.—Frey, Fall von subacut. Lihmung Erwachsener. Berl.
klin. Woch. 1874. Nr. 44, 45.—Zrb, Ueb. acut. Spinallihm. bei Erwachs. und
iiber verwandte spinale Erkrankung. Arch. f. Psych. u. Nervenkrankh, Y.
Beob. 7. 1875.—Cornil et Lépine, Cas de paralys. génér. spin. antér. subaigué,
suivi d’autopsie. Gaz. méd. de Par. 1875. Nr. 11.—Lemoine, Paralys. de l’adulte.
Guérison. Lyon médic. 1875. Nr. 15.—Lincoln, Case of Spinal Paralysis in
an Adult. Bost. Med. Surg. Journ. 1875. March 25.—S. G. Webber, Contrib. to
the Study of Myelitis, Transact. Americ. Neurol. Assoc. for 1875. Vol. L. p.
POLIOMYELITIS ANTERIOR CHRONIOA. 713
55.—Golidammer, Ueb. einige Fiille von subacuter Spinalparalyse. Berl. klin.
Woch. 1876. Nr. 26.—Hammond, Diseases of the Nerv. Syst. 6. edit. 1876,—
Klose, Zur Lehre von der Paralys. spinal. anter. subacut. Diss. Breslau, 1876.
—Bernhardt, Beitr. zur Lehre von der acut. atroph. Lihmung Erwachsener.
Arch, f, Psych. u. Nervenkrankh. VII. §, 313. 1877.
History.
It was Duchenne who, first in the year 1849, and then again
in 1853, described a peculiar form of spinal disease, character-
ized by motor paralysis, progressing more rapidly or more’slowly,
accompanied with atrophy in bulk of the muscles, and loss of
their faradic excitability, without any other manifestations.
This statement attracted but little attention until Duchenne,
in the third edition of his ‘‘ Electrization localisée’’ (1872), again
and more emphatically pointed out the existence of this form of
disease, and gave a detailed description of the same. Influenced
in part by a hypothetical belief with regard to the anatomical
basis of the disease—which he believed to consist in chronic de-
generation of the gray anterior horns—he designated it ‘‘ Para-
lysie générale spinale antérieure subaigué.”’
Since that time the existence of the disease has been univer-
sally recognized as a clinical fact, and single instances of it have
been described by various authorities (Poché, Frey, Erb, Web-
ber, Cornil et Lépine, Klose, Goltdammer, Bernhardt, and
others).
The only point on which there is still any doubt is with
reference to the anatomical basis of the disease, although the
single reports of post-mortems thus far made by Cornil et Lépine
and by Webber, would seem strongly to confirm the hypothesis
first set up by Duchenne. Further observations on this subject
are desirable.
Definition.
Clinically considered, the disease presents itself as a motor
paralysis, usually developed without fever, with but slight gen-
eral disturbance and insignificant disturbances of sensibility.
714 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The paralysis more or less rapidly seizes the entire lower extrem-
ities—generally in the course of a few days, or at the most a few
weeks—and soon extends to the upper extremities also (much
more rarely showing the opposite order of development and be-
ginning in the upper extremities) ; it is associated with complete
jflaccidity of the muscles and loss of their reflex excitability,
and is followed by rapidly progressive atrophy in the bulk of
the paralyzed muscles, with the well-marked reaction of degen-
eration.
The disease has certainly, as a rule, an ascending course,
though it is by no means always progressive ; its development
generally comes to a stand-still sooner or later, this arrest intro-
ducing a gradual retrogression of the disturbances, which may
lead to more or less complete recovery.
The anatomical limits of the disease cannot, as yet, be de-
clared with absolute certainty ; but, according to all that we know,
there is every probability of its being located in the gray ante-
rior horns. The two post-mortem examinations thus far made
virtually confirm this, and thus, for the present, we may desig-
nate the disease as a subacute or chronic inflammation or degen-
eration of the gray anterior horns, with extensive disappear-
ance and atrophy of the large multipolar ganglion-cells.
Etiology.
. The causes of the disease under consideration are as yet ex-
ceedingly obscure. Nothing is known of any definite predispo-
sition thereto, and no hereditary influences have as yet been
demonstrated. All the cases observed thus’ far have been in
adults, and, indeed, between the ages of thirty and fifty, as is also
the case with the majority of other chronic spinal diseases.
Under the head of exciting causes, traumatic injuries have been
cited—a fall upon the hip or back ; furthermore, gross exposure to
taking cold, damp dwellings, and, in the case of Klose, free indul-
gence in beer and excesses in venery. All these are mentioned
as possible etiological conditions. In the majority of cases,
however, no definite cause for the disease can be demonstrated.
Ceri”
POLIOMYELITIS ANTERIOR CHRONICA. 715
We must, however, here briefly call attention to one etiologi-
cal factor which is, as yet, of hypothetical, though perhaps of
very great significance: that is, chronic lead-poisoning. In
speaking of the pathogenesis of lead paralysis,‘ which is such a
peculiarly characteristic affection, I have sought to show that
its origin is probably spinal instead of peripheral, and KE. Remak’*
has established this more accurately and in a more detailed man-
ner by the sifting and critical examination of a larger amount of
material. He comes to the conclusion that quite circumscribed
alterations in the gray anterior horns probably lie at the founda-
tion of lead paralysis. These alterations might well be of a
degenerative or chronic inflammatory nature, but are, as a rule,
capable of resolution. Bernhardt has also recently given in his
adherence to this view. In fact, the whole state of things in
lead paralysis, with reference to mobility, atrophy, electrical
relations, the absence of disturbances of sensibility, etc., is so
entirely analogous to that in poliomyelitis anterior chronica, that
we are almost forced to the theory of changes in the anterior
gray horns in lead paralysis. On the other hand, again, I recently
saw two cases of paralysis of the upper extremities, which, in all
their details, were so completely analogous to lead paralysis
that only the entire lack of any sort of evidence of lead-poison-
ing was sufficient to determine me to give up this diagnosis, and
accept that of a chronic circumscribed poliomyelitis anterior.
Thus, everything crowds us at least into regarding the localiza-
tion of lead paralysis and of chronic anterior poliomyelitis as the
same. It is left to further investigations to determine whether
the saturnine alterations in the gray anterior horns are the same
in kind as the others—whether, therefore, the lead-poisoning calls
forth an inflammatory affection. It would be well, at all events,
to keep this question in view in the future.
! Erb, Diseases of the Peripheral Nerves. This Cyclopedia. Vol. XI.
? Zur Pathogenese der Bleilihmungen. Arch. f. Psych. und Nervenkrankh, Vol.
VI. p. 1. 1875,
716 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Pathological Anatomy.
Up to the present time there are but two reports of post-mor-
tems before us, which certainly do not fulfil all the requirements
of a vigorous critique. We here communicate them in brief.
In one case, which terminated in death at the end of four
years, Cornil and Lépine found softening of the lowest division
of the spinal cord. The principal change was in the gray ante-
rior horns, consisting of chronic inflammation, thickening of the
vessels, an abundance of fatty, granular cells, the perivascular
spaces filled with blood, disappearance of a great part of the gan-
lion-cells, increase of the cells of the neuroglia. In the cervical
portion there was a sclerosis of the antero-lateral column en-
tirely surrounding the anterior gray horn, and being limited
farther down to the posterior divisions of the lateral column
(secondary degeneration ?). The anterior roots were atrophied ;
in the muscles the usual fatty atrophic changes were found.
In Webber’s case, which had lasted eleven months, he found
degenerative atrophy of the muscles, the anterior roots in a high
state of degeneration, the posterior roots but very slightly degen-
erated. In the gray substance there was here and there an exu-
dation and an increase of nuclei around the vessels ; disappear-
ance, atrophy, and degeneration of the large ganglion-cells in the
anterior horns; but slight changes in the ganglia of Clarke’s
columns and of the posterior horns; in the white columns a
part of the nerve-fibres were degenerated, the neuroglia hardly
changed. The same alterations which Webber ascribes to a pre-
eminently parenchymatous inflammation were found to extend
as far up as into the medulla oblongata.
From these two not altogether coinciding reports, this much,
at least, would appear evident: that even if the lesion is not
entirely confined to the gray anterior horns, it is at least most
pronounced in these ; and that what here especially attracts atten-
tion, in addition to the chronic inflammatory changes, is the degen-
erative atrophy of the large, multipolar ganglion-cells. In the
anterior roots and in the muscles those changes are to be found
which have already repeatedly been described as being charac-
teristic of degenerative atrophy of these structures.
—— EE
ee a ree
POLIOMYELITIS ANTERIOR CHRONICA. 717
Pathology of Poliomyelitis anterior chronica,
Symptoms.
It will suffice for all practical purposes to give a somewhat
minute general picture of this, on the whole, rare affection. A
more detailed pathogenetic discussion of its symptoms would
bring to light the same occurrences as constitute the principal
manifestations of the acute form.
The disease may be developed with very varying degrees of
rapidity ; sometimes in a more subacute manner, developing a
widespread paralysis within a few days or weeks, but generally
pursuing a more chronic, insidious course, so that its develop-
ment may extend over years.
Accordingly, light indications of fever, gastric disturbances
and dyspeptic manifestations, headache, and the like, may be
present or may be wanting at the beginning of the disease. On
the other hand, we shall rarely fail to encounter all kinds of
paresthesia and light manifestations of sensory irritation
(drawing and shooting pains in the back and limbs, backache,
etc.) among the precursors of the disease. It is also common to
find that for a long time such persons have suffered from great
weariness and diminished endurance in the limbs.
_ The actual beginning of the disease is generally marked by a
distinct motor weakness in the lower extremities, or in but one
of these, or at least more prominently in the one. This weak-
ness more or less rapidly grows distinct; it increases in the
course of days or weeks to pronounced paresis, so that the pa-
tient breaks down on going upstairs, and soon finds his walks
reduced to a minimum, or is confined to his bed. During this
entire development there is never any tremor, never any ataxy in
the limbs.
On examining such patients, their movements are found to be
sluggish, awkward, weak,and paretic; the movements of the knee
and ankle-joint are usually more severely interfered with than
those of the hip-joint. Sooner or later this paresis increases to
complete paralysis of single muscles and groups of muscles, or
"18 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
of the entire extremity. The rapidity with which this takes
place varies exceedingly in different cases; sometimes it occurs
within a few days, sometimes not till after the lapse of many
months, or even after years. Then the muscles are completely
flaccid and soft, the limbs easily movable in all directions ; at
first there is no sign of any contracture.
Very soon a progressive atrophy in bulk takes place in the
paralyzed muscles; the calves of the legs turn into lax, flabby
sacks, the muscles of the thigh and gluteal region grow thin
and flaccid, and the tape-measure shows a diminution in the vol-
ume of the muscles from week to week. This atrophy may
advance till it causes a skeleton-like emaciation of the limbs,
amounting to almost entire disappearance of the muscles. In its
earlier stages it is generally accompanied with more or less fre-
quent and active fibrillar twitchings of the muscles.
The feet are cold and easily grow cyanotic. Sensibility of the
skin is usually completely intact in all directions; it is but
rarely that this is slightly dulled and that patients complain
somewhat of insensibility and numbness.
Reflex action in the paralyzed muscles is completely extin-
guished ; neither through the skin nor through the tendons can
the slightest reflex twitching be produced.
It is usually not long before the affection also extends fo the
upper extremities ; these grow awkward, feeble, heavy, grad-
ually paretic, and at last completely paralyzed. Here, too, the
trouble extends more prominently or earlier to individual groups
of muscles; sometimes the extensor group of the forearm is
earlier and more severely paralyzed than the rest, sometimes the
flexors and the little muscles of the hand are more prominently
affected. In general the fingers and hands are more severely
paralyzed than the forearm and shoulder. The hands assume @
correspondingly characteristic position, the arms lie lax and im-
movable as they are placed, no trace of any contracture being
demonstrable.
Reflex action is completely extinguished in the paralyzed
muscles. Sensibility in the upper extremities, too, so far as ob-
jective examination can prove, seems to be entirely normal, or
diminished to an entirely insignificant degree. Subjectively, pa-
POLIOMYELITIS ANTERIOR CHRONICA. 719
tients sometimes complain of numbness in the fingers, of parzes-
thesia in the domain of the ulnar nerve, etc.
Here, too, rapidly progressive atrophy ensues, uniformly dis-
tributed over the paralyzed muscles, which may lead to the
highest degrees of emaciation, especially in the hands and fore-
arms.
In some instances the muscles of the back and abdomen also
share in the paralysis: the patients can no longer sit up ; expira-
tion, coughing, sneezing, defecation, etc., are rendered difficult.
There is generally an entire absence of any disturbances of the
bladder, the rectum, or the genital organs; the functions in
question are carried on undisturbed and in quite a normal man-
ner; the exceptions to this are rare.
The nutrition of the skin does not suffer in the least ; no bed-
sores occur.
The vegetative functions are also all of them normally per-
formed. The appetite and digestion, which may, at the worst,
have been slightly and temporarily impaired at first, are good ;
sleep is natural ; the general nutrition and well-being are usually
quite undisturbed. |
No symptoms at all on the part of the brain or the cerebral
nerves appear, at least during the earlier stages of the disease.
The initial headache ordinarily soon disappears.
Examination of the paralyzed and atrophied muscles by elec-
tricity gives quite the same results as in acute anterior poliomy-
elitis, only modified to a slight degree to correspond with the
much slower development of the malady.
Here, too, Duchenne showed a diminution of faradic excita-
bility occurring from the beginning, and advancing more or less
rapidly to complete loss of the same.
Here, too, according to my own experience and that of others
(Bernhardt), this is nothing more than one of the manifestations
of the reaction of degeneration. I have been able to prove this
electrical disturbance in all the more recent cases that have come
under my notice (five in all), and indeed in its most pronounced
form. The motor nerves were entirely unexcitable to both the
faradic and the galvanic current; the muscles did not respond
to faradization, their galvanic excitaDility being retained, and
'
720 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
during the first weeks and months of the disease being slightly
heightened (see the case reported below), afterwards more or less
diminished, but always changed in quality (AnSZ> KaS8Z; twitch-
ing sluggish, tonic); their mechanical irritability was at first
heightened.
At the stage in which we generally first see these cases, gal-
vanic excitability is generally already much lowered, but usually
still permits of the very distinct recognition of the qualitative
anomaly. With the cure of the disease the electrical excitability
returns but very slowly and gradually to its normal standard.
We have now become familiar with the occurrence of the ‘‘ reaction of degen-
eration” in various diseases of the spinal cord, and it would seem to be time that
we should enter briefly upon the relations of the same, in order to throw some
light upon its diagnostic significance and to indicate the important points in gen-
eral pathology which result from the connection of this with other already recog-
nized facts. )
We have found that the reaction of degeneration appears in its full develop-
ment in acute anterior poliomyelitis in the form of complete loss of faradic and
galvanic excitability of the motor nerves, loss of faradic excitability of the mus-
cles, but heightening and qualitative changes in the galvanic excitability of the
muscles. We have, therefore, in this form of disease, complete paralysis, a high
grade of atrophy, the motor nerves and muscles involved in degenerative atrophy.
Quite the same thing is found—only somewhat milder in degree, corresponding
to its more chronic course—in chronic anterior poliomyelitis : the complete reaction
of degeneration, the electrical excitability of the nerves entirely abolished, ete. ;
here, therefore, likewise entirely the same condition, viz., paralysis, atrophy, the
motor nerves and muscles degenerated.
Quite a different state of things exists in amyotrophic lateral sclerosis. A case
which I accurately examined of late showed, in the upper extremities, the faradic
and galvanic excitability of the motor nerves entirely preserved (at all events not
materially diminished) ; in the muscles an elevation and qualitative change of gal-
vanic excitability (reaction of degeneration) on direct irritation, while on indirect
irritation the muscles reacted normally (twitching like lightning, KaSZ>AnSZ);
the muscles also responded to the faradic current.: At the same time there
was a high degree of atrophy and complete paralysis of the muscles. Here we
therefore found paralysis, atrophy, the motor nerves not degenerated, the muscles —
degenerated.
In progressive muscular atrophy (typical form) it is somewhat different again.
? The same condition, therefore, exists which is characteristic of the so-called middle
form of facial paralysis and some other peripheral forms of paralysis. Compare this .
Cyclopedia, Vol. XI. :
POLIOMYELITIS ANTERIOR CHRONICA. 721
In a part of the muscles attacked, the excitability, through the nerve, is preserved
or appears to be simply lowered; in the muscles themselves faradic excitability is
preserved, but galvanic excitability is preserved with the characteristics of the
reaction of inflammation (though generally with already very much lowered excita-
bility). In another portion of the muscles—in those that are very highly atrophied—
faradic excitability is abolished, the nerve is entirely unexcitable, and the muscle
reacts only on a very heavy galvanic current with sluggish twitching, AnSZ>Ka8Z.
In those muscles, however, which are but slightly affected and which were attacked
at the beginning, electrical excitability appears still to be quite normal on direct
and indirect irritation. At least so I have found it, since paying attention thereto,
in all the cases carefully examined by me. If Bernhardt (I. c.) recently doubts the
occurrence of the reaction of degeneration, this is to be excused on the ground that,
in progressive muscular atrophy, at all events, the reaction of degeneration is very
hard to demonstrate, and may easily be overlooked in a not very careful search.
There are various reasons for this. One is the very slow development of the disease,
so that the characteristic increase of excitability subsides and the qualitative changes
alone remain; another is the preservation of the excitability of the nerves, so that
the normal neuro-muscular twitchings mark the qualitative alterations. A still
stronger reason, however, is the fact that the degeneration of the fibres within a
muscle takes place in a scattered manner; among the degenerated fibres there stil]
always remain a certain number of healthy and still excitable fibres, which respond
to irritation, and thus mark the existence of the reaction of degeneration. The
more slowly the process advances, the lower sinks the excitability of the degenerat-
ing fibres, and the increasing strength of the current required to produce an effect
may for a long time compensate for the numerical diminution of healthy fibres; so .
that the relation of things long remains obscure. It will, therefore, only be possible
to demonstrate the reaction of degeneration in its earlier stages in those muscles
which degenerate pretty rapidly, and in which larger numbers of degenerated fibres
are to be found; the later stages of this reaction (with great diminution of galvanic
excitability) can only be shown in those muscles which have already attained a
high grade of degeneration. This naturally varies in each individual case. Con-
sequently, the reaction of degeneration can always only be demonstrated in single
muscles, sometimes more and sometimes less distinctly. I have thus far always
found it in this way. ;
In progressive muscular atrophy, therefore, the reaction of degeneration exists
with retained excitability of the motor tracts (at least for a long time); but, in
contrast to amyotrophic lateral sclerosis, ne paralysis here exists until the muscles
are almost entirely degenerated. Here, therefore, the manifestations are grouped
as follows: no paralysis, but atrophy; the motor fibres not degenerated, the mus-
cles degenerated.
I recently found quite an analogous state of things in a well-pronounced case of
bulbar paralysis. ‘In the muscles of the chin and lips, and even of the tongue, the
excitability of the nerves was found retained agd almost normal; in the muscles
themselves, however, the well-marked reaction of degeneration on direct irritation.
VOL. XIII. —46
722 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
I had expected this condition on account of the analogy of the disease with pro-
gressive muscular atrophy.
Quite similar variations are also to be met with in other forms of paralysis.
Among these may be mentioned the occurrence of the well-marked reaction of
degeneration in severe peripheral traumatic and rheumatic paralysis ; the occurrence
of the ‘‘middle form” in slight rheumatic and traumatic paralysis (of the facial,
radial, etc.'); finally, the extraordinary fact, in a case of lead-poisoning made
known by me,’ where the reaction of degeneration was present in a muscle that was
not paralyzed, whereas ordinarily in lead-poisoning the muscles act just as in chro-
nic anterior poliomyelitis.
It is difficult to form a plausible conception of the course and connection of the
yarious trophic and motor tracts which might, even to some degree, enable us to
comprehend these various facts. Some of the conclusions to be drawn from the
facts briefly collected in what has been said above may even now be indicated.
If it had needed any confirmation, all the facts would have unanimously con-
firmed the doctrine that the occurrence of the reaction of degeneration is always
and everywhere associated with the existence of certain histological alterations in
nerves and muscles which we comprehend under the name of degenerative atrophy.*
But it would furthermore also appear that the motor tracts, within the central or-
gan, to some degree run their course separately from the trophic apparatuses and tracts,
as there are central paralyses with atrophy (poliomyelitis anterior) and without atro-
phy (spastic spinal paralysis), and likewise central atrophies which exist for a long
time without actual paralysis (bulbar paralysis, progressive muscular atrophy),
We can, furthermore, hardly escape the conclusion that the trophic influences
. for motor nerves are somehow separated in space from those for the muscles ; that,
accordingly, different trophic central apparatuses and tracts may perhaps exist for the
nerves and the muscles, This appears from the fact that the muscles may degenerate
alone, without the nerves taking part in the degeneration. (So in amyotrophic
lateral sclerosis, in bulbar paralysis, in progressive muscular atrophy, in the middle
form of paralysis of the facial and radial nerves, in the case of lead-poisoning
described by me.) At all events, therefore, these tracts cannot be completely
identical; they must present some differences in their localization, or perhaps only
in their resistance to influences that cause disease. |
We can, even though it may be with some difficulty, form a hypothetical idea
of the existence and position of the various apparatuses and tracts belonging here,
within the central organ as well as in the peripheral nerves, whereby we might
explain the above-mentioned differences in the different forms of disease. All the
facts go to show that these apparatuses lie principally in the gray substance of the
anterior horns. But our anatomy will not so soon show us how these are arranged
' Compare the appropriate sections in Vol. XI. of this Cyclopadia.
* Hrb, Hin Fall von Bleilahmung. Arch. f. Psych. u. Nervenkrankh. Bd. V. p. 445.
1875. )
* This Cyclopzdia, Vol. XI.
ee
POLIOMYELITIS ANTERIOR CHRONIOA. 723
and distributed there. We may, therefore, be permitted, with all due reservations,
to draw a hypothetical diagram of this arrangement, according to the Aiea
which virtually results from the facts above communicated.
In the accompanying Fig. 17, let a be the motor conduction from the brain,
which undoubtedly lies in the lateral column; let this continue through the gangli-
|
Fic. 17. Diagram of the arrangement and connection of motor and trophic centres and tracts in the spinal
cord and in the peripheral motor nerves.
onic point d (multipolar ganglion-cell ?), into which the reflex tract, s, coming from
the sensitive sphere, opens through the anterior roots and the peripheral nerves
(a—d—a’) to the muscle m. Let } be the trophic central apparatus for the mus-
cles; the tract b—0’ represents the trophic conduction tract emanating from this
apparatus and somewhere (probably at d) uniting with the motor tract. Let ¢ be
724 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the trophic central apparatus for the motor nerves (which possibly coincides with
d) and c—c’ the tract which conducts its trophic influences to the motor fibres.
With this diagram, the special arrangement of which within the spinal cord is of
course unknown—and indeed, for the present, a matter of entire indifference—one
can form quite a clear idea of the origin of the different forms of disease, provided,
at the same time, he has due reference to the phenomena of reflex action.
If the tract a alone is interrupted by disease, we have simple paralysis without
any degenerative atrophy, and without the reaction of degeneration—simple lateral
sclerosis.
If a and the centre 6 are simultaneously diseased, then there is paralysis with
atrophy of the muscles, and the reaction of degeneration in the muscles, but no
change of the motor nerves, whose electrical excitability is retained—amyotrophie
lateral sclerosis.
If the centre } alone is diseased, there is atrophy of the muscles, at first without
paralysis and without degenerative atrophy of the motor nerves, reflex action being
retained—bulbar paralysis and progressive muscular atrophy.
If b, c, and d are simultaneously diseased (or, if we suppose that all the tracts
pass through d, then on disease of @ alone), there is paralysis with degenerative
atrophy, and the reaction of degeneration in nerves and muscles and loss of reflex
action—acute and chronic poliomyelitis anterior.
If we imagine 6, c, and d to represent the different ganglion-cells of the gray
anterior horns, and the diagrammatic conduction tracts to represent the different
connections of the same among one another, with the lateral columns and the
anterior roots, then we shall readily see that this diagram to a great degree harmo-
nizes with the recently accepted views concerning the forms of disease which here
occupy us. Even the view adopted by Duchenne and Joffroy, by Hammond and
others, that there are separate motor and trophic cells, has found representation in
the diagram.
But this diagram also furnishes points towards the elucidation of the different
forms of peripheral paralysis. If the conduction d, a’ alone is disturbed, simple
paralysis, without degeneration and the reaction of degeneration, will exist (the
light form of rheumatic paralysis of the facial) ; if d, a’ and 6, b’ are simultaneously
disturbed, then paralysis with the reaction of degeneration in the muscles, but not
in the motor-nerves (the middle form of rheumatic paralysis of the facial); finally,
if in addition to d, a’ and B, b’, ¢, c’ is also paralyzed, then there is paralysis with
the reaction of degeneration in the nerves and muscles (severe form of facial
paralysis’).
But, aside from these more theoretical, and, as yet, entirely hypothetical sides of
the question, accurate electrical examination also has its diagnostic importance in
such forms of disease. So far as one can judge, up to the present time, with the
very scanty material thus far on hand, some not unimportant diagnostic facts would
seem to come to light.
? Compare my Essay, cited above—A Case of Lead-Poisoning. L. c. p. 455.
2S a a ae a.
Ss - eG Sy
POLIOMYELITIS ANTERIOR CHRONICA. 725
Well-marked, complete reaction of degeneration, with loss of the excitability of
the motor-nerves and with elevation, or, at least, without any great degree of
diminution of the galvanic excitability of the muscles, is evidence in favor of
poliomyelitis anterior, both of the acute and chronic form, It is always accom-
panied with paralysis, disappearance of reflex action, and a high degree of atrophy.
The middle form of the reaction of degeneration, without any material disturb-
ance of the excitability of the motor-nerves, and with well-marked elevation, or, at
least, without any material diminution of the galvanic excitability of the muscles,
speaks in favor of amyotrophic lateral sclerosis ; this is always accompanied with
paralysis and atrophy, but reflex action may be preserved.
The middle form of the reaction of degeneration, but with a greater or less
degree of diminution of galvanic excitability of the muscles, which is hard to
demonstrate and can only be shown in single muscles and groups of muscles, speaks
in favor of progressive muscular atrophy (and bulbar paralysis). There is then no
complete paralysis, non-uniform atrophy, while reflex action may be retained. It is
true that the later stages of the disease, such as are so often found in the little mus-
cles of the hand, cannot easily be distinguished by electrical examination alone
from similar changes caused by poliomyelitis anterior or amyotrophic lateral
sclerosis (nor from peripheral paralysis, lead paralysis, etc.), but then the diagnosis
can usually be made from the other manifestations, and from the development and
course of the disease. :
At all events, it seems worth the while to pay further attention to these relations,
as they are not only of diagnostic importance, but promise to throw light upon cer-
tain difficult problems in the physiology of the spinal cord which cannot easily be
approached in other ways. To be sure, these examinations demand great practice,
patience and technical knowledge, and I cannet too urgently recommend the
greatest care in conducting test examinations. I can guarantee the facts discovered
and communicated by me, but they urgently require to be extended and confirmed
in numerous new obscrvations.
The further course of chronic poliomyelitis anterior, after it
has been developed to the point above described, may shape
itself in various ways.
In the majority of instances the disease now remains station-
ary for some time. The paralysis increases no more, the weak-
ness or impossibility of movement remains about the same; but
the muscular atrophy does still advance. Now, too, moderate
paralytic contractures may be developed, chiefly caused by the
mechanical approximation of the points of attachment of the
muscles. No other new disturbances arise.
After a while—a couple of weeks, or months—very gradual
improvement sets in, generally first in the upper extremities ;
726 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
single movements first return, others again grow more distinct
and stronger, and thus the improvement gradually advances,
while the galvanic excitability of the muscles sinks more and
more, and.slowly gives place to the normal conditions of excita-
bility, the contractures disappearing again little by little.
But the improvement is slow; it is only after the lapse of
months that the patients can again eat, write, and use their hands
for all kinds of manipulations.
Then the lower extremities have thatr turn; first the move-
ments of the hip-joint become freer and more powerful, then
those of the knee, and not till quite late those of the foot and toes.
The course of things with reference to electrical excitability and
the contractures is precisely the same as in the upper extremities.
The question of how far this improvement goes varies some-
what in individual cases. Not infrequently it advances to com-
plete recovery, so that mobility is quite restored, the nutrition of
the muscles again becomes normal, and patients regain all their
former capabilities. This may, however, require many months
and even years.
Incomplete recovery, however, i is far more frequent. A part
of the muscles (especially those in the domain of the peroneal
nerve) remain paralyzed and atrophic, and patients retain the
defect thus induced for life.
In a minority of instances the malady advances further and
further upwards ; finally, disturbances of respiration set in, signs
of asphyxia, various bulbar symptoms, paralysis in the domain
of the facial nerve, of the tongue, of swallowing, etc., and these
manifestations gradually lead to death. Sometimes this like-
wise follows, without any further complications, through simple
exhaustion.
The duration of the disease is, accordingly, in most cases,
comparatively long; at best it is a question of months, generally
of years. The progressive cases terminate fatally in from one to
four years. S
In view of the small number of observations thus far at our
command, I may be permitted to communicate a brief outline of
the following case, of a rather subacute form, recently observed
by me.
i A Or yy
POLIOMYELITIS ANTERIOR CHRONIOA. 727
Mr. A. G., forty-two years of age, was always of robust constitution and health,
and has exposed himself with impunity to many injurious influences (heat, draughts,
travels, the free use of alcoholic drink). For a year past he has often complained
of unusual weariness,
His illness began at the end of July, 1876, with general weakness, headache,
slight dyspeptic symptoms, etc. The patient still went about, notwithstanding
increasing weakness of the legs, until the 22d of August, when, his legs giving way,
he fell down-stairs. From this time on he was bed-fast. The only subjective trou-
bles complained of were some shooting and piercing pains in the legs, with transitory
Sormication.
At the end of September similar weakness in the hands set in, so that the patient
could neither write, feed himself, nor do anything else with his hands. He never
had the sensation of a tight band about his body. The functions of the bladder and
rectum were entirely undisturbed. His general condition of late had been quite good.
Condition on examination, the 6th of October.—There was a high degree of pare-
sis and partial paralysis of the lower extremities. Movements of the ankle-joint and
toes were quite impossible, of the knee- and hip-joint quite difficult.
Sitting up in bed was very difficult. The upper extremities were also to a high
degree paretic, especially the hand and forearm. The grasp of his hand could
scarcely be felt; the extensors were completely paralyzed. The power of the mus-
cles of the upper arm was materially lowered, that of the muscles of the shoulder
least so.
The mobility of the muscles of the neck and face, of mastication, deglutition,
and of the eyes was completely intact.
The sensibility of the skin in the feet and legs was somewhat, although but very
slightly, dulled ; from the thigh upward, as well as in the upper extremities, it was
entirely normal, excepting a subjective sensation of numbness in the tips of the
fingers.
Reflex action—of skin and tendons—in the lower extremities was completely
abolished.
The muscles, which were very lax and flabby, were already considerably atrophied
in all four extremities. The bladder and rectum acted normally. No bed-sores.
Appetite and digestion regular. Sleep good. Head free.
Faradic excitability in the paralyzed muscles and the nerves belonging to them
was greatly lowered, in part entirely abolished.
The galvanic excitability of the nerves of the lower extremities was completely
extinguished ; in the muscles, on the contrary, it was raised and changed in quality
(twitching, sluggish, AnSZ>KaSZ); so at least in the domain of the peroneal and
tibial nerves. In the domain of the crural nerve, diminution of the galvanic excita-
bility could already be demonstrated with a continuation of the qualitative change.
In the upper extremities the well-marked reaction of degeneration existed only in
the extensors of the forearm and in the interossei muscles.
The mechanical excitability of a portion of the atrophied muscles was distinctly
heightened,
728 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The treatment consisted of the use of dry cups along the spine every couple of
days, Priessnitz’s cold-water compresses to the back, and iodide of potassium.
His condition very soon began to improve, At the beginning of November this
was distinctly perceptible in all the extremities, even though but to a very slight
degree.
At the beginning of December the patient was able to sit in a chair, and to move
his arms and legs much more freely. In the upper extremities the domain of the’
radial nerve was still completely paralyzed ; a slight contracture of the flexors of
the hand and of the fingers had set in. Movements of the elbow- and shoulder-
joint were now perfectly free and strong.
In the lower extremities there was still entire paralysis of the foot and the toes.
Extension of the knee-joint feeble; lifting of the leg possible; a slight contracture
of the flexors of the leg.
Sensibility and the state of the bladder were normal. The paralyzed muscles
still showed the reaction of degeneration.
He was now ordered galvanic treatment to the back and extremities.
His condition now steadily improved. At the beginning of February, 1877, the
mobility in the extensor region of the forearm was pretty well restored; the con-
tracture of the flexors had almost entirely disappeared; the hands had greatly
gained in strength, the patient could again feed himself.
The mobility of the muscles of the thigh was materially improved; the muscles
of the legs were still completely paralyzed. The atrophy was somewhat less.
Electrical examination still showed the full reaction of degeneration, although
now with distinctly diminished galvanic excitability.
Middle of March, 1877.—The mobility of the upper extremities was now almost
entirely normal; the first signs of movement in the joints of the feet now began to
appear; the general condition very good.
Middle of April, 1877.—Continued improvement. Movement of the feet and
toes is becoming more distinct and extensive, although but very gradually. The
patient is now able to stand somewhat, and, if well supported, to move a few steps.
The upper extremities are now almost entirely normal.
Diagnosis.
The picture of the disease in subacute and chronic poliomye-
litis anterior has so much that is characteristic about it, that in
cases which are at all well-marked it can very easily be recog-
nized. Especial significance is to be attached to the tout ensemble
of the disease and the successive development and consecution of
the symptoms. This disease can generally be easily distinguished
from all similar and kindred affections, notwithstanding the great
similarity that frequently exists between them, by the lassitude,
POLIOMYELITIS ANTERIOR CHRONICA, 729
weakness, paresis, and finally paralysis, occurring at first in the
lower and then in the upper extremities, the muscles being lax,
without tension or contracture ; by the progressive atrophy with
the reaction of degeneration ; by the failure of reflex action ; by
the absence of any disturbances of sensibility and of the bladder,
as well as of any tendency to the formation of bed-sores ; by its
slowly progressive course and its usually favorable termination.
The differential diagnosis between this and qaewfe anterior
poliomyelitis can only come in question when it refers to the
sequels of the latter affection. The existence of the latter is de-
termined, however, by the fact of its extremely acute beginning,
which at once causes the highest degree of paralysis. The
subacute form has a decidedly progressive course: it extends
more or less rapidly upward, the paralysis increases for a time,
the disease may at last terminate fatally, or it may run a similar
progressive course towards recovery. In both respects there
seems to me to be such an essential difference between the acute
and chronic forms that it appears to me doubtful whether the
two actually represent the same process of disease developed
with different degrees of actiteness.
Progressive muscular atrophy has very often been confonzia-
ed with chronic anterior poliomyelitis. Notwithstanding all the
resemblance which the two forms of disease may bear to one
another in certain stages, they may easily be distinguished by
the following characteristics: in chronic poliomyelitis there is
first paralysis and afterwards atrophy ; in progressive muscular
atrophy the paralysis becomes associated with atrophy which
has already long existed ; in the former there is atrophy in the
bulk of the muscles, in the latter only partial atrophy of the
same; in the former the well-marked reaction of degeneration
can be demonstrated as well as the failure of reflex action; in
the latter, if there is any reaction of degeneration it is only the
middle form, and reflex action is retained ; the former runs its
course comparatively fast and generally favorably, the latter
very slowly and always unfavorably.
The distinction between this disease and amyotrophic lateral
sclerosis is still more easy. The latter, it is true, resembles
chronic poliomyelitis in the paralysis and atrophy in bulk of the
730 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
upper extremities, but in the lower extremities it shows paralysis
without atrophy, with tension of the muscles and contractures,
with increase of the reflex action of tendons, etc. Perhaps ex-
amination by electricity may also contribute something towards
the determination of this question, if the fact should be further
confirmed that in amyotrophic lateral sclerosis only the middle
form of the reaction of degeneration occurs.
With regard to the distinction between this and the slower
forms of Paralysis ascendens acuta, see the following section.
Chronic anterior poliomyelitis will be capable of being easily
distinguished from all other forms of chronic spinal disease,
from transverse chronic myelitis, multiple sclerosis, tabes dor-
salis, spastic spinal paralysis, etc., if proper regard is paid to
the condition of sensibility, of the bladder, of the nutrition of the
skin, of reflex action, of electrical excitability, etc., quite irre-
spective of the other peculiarities of these various forms of
disease.
'. In the well-marked and more diffuse forms, therefore, the
disease is easy to recognize. But it is a question which can only
be determined by further successful’ investigations, whether an-
other series of more partial forms of paralysis and atrophy of
the extremities donot belong in the same category. It already
seems probable that this is, to a certain degree, the case in so-
called lead-paralysis. |
But I would also raise the question with regard to quite simi-
lar conditions of disease which have arisen spontaneously, viz.,
with regard to partial paralysis with atrophy and the reaction of
degeneration without disturbances of sensibility in the extremi-
ties ; with regard to a good many cases which are cited in papers
on progressive muscular atrophy, but which absolutely have not
been progressive ; whether all these do not owe their origin to a
quite circumscribed chronic anterior poliomyelitis. Of course
this question can only be solved by accurate clinical observa-
tions, made with this object in view, and finally settled only by
pathologico-anatomical investigation. I therefore recommend it
as worthy of further attention.
POLIOMYELITIS ANTERIOR CITRONICA, 731
Prognosis.
The prognosis of this disease is never to be treated lightly;
life may very easily be endangered, which never seems to be the
case in the acute form.
At the same time the prognosis is comparatively favorable, as
in the majority of cases recovery follows, and at all events the
improvement, as a rule, goes much farther than in the acute
form. At the same time patients must make up their minds to
a comparatively long duration of the disease, extending perhaps
over several years.
The prognosis is bad only in that form of the disease which
advances upward with comparative rapidity. Whenever diffi-
culty of breathing and of swallowing, labored action of the
tongue, etc., set in, a fatal termination is at least very probable.
The more partial forms are never dangerous to life, but may
lead to permanent disappearance of the muscles and correspond-
ing defects of motion.
Therapeutics,
In view of the small number of observations as yet made,
there is, of course, no question of any established, independent
treatment of the disease.
In general, those principles are applicable which we have laid
down elsewhere for the treatment of subacute and chronic myeli-
tis generally. Therefore, at the beginning of the disease, we may
employ abstractions of blood, derivatives of all sorts, hydro-
pathic applications to the back, iodide of potassium, ergot, etc.
Undoubtedly at a later period the most that can be expected
is from the galvanic current. It must be left to the future to
determine whether mineral baths, cold-water treatment, or other
similar means are of any special avail, and what internal reme-
dies promise the best results. “The best we can do at present is
to continue our trial of the curative measures appropriate in
chronic myelitis.
"32 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
17. Paralysis Ascendens Acuta.—Acute Ascending Paralysis.
—Landry s Paralysis.
0. Landry, Note sur la paralysie ascendante aigué. Gaz. hebdom. 1859. Nr. 30,
31.—Kussmaul, Zwei Fille von tédtl. Paraplegie ohne nachweisb. Ursache,
Erlangen, 1859.—T7. L. Walford, Softening of the Spinal Cord. Assoc. Med.
Journ. 1854. Nov. 11. (Canstatt’s Jahresb. III. §S. 33.)—Gomes de Valle, Obs.
d. paral. asc. aig. Union méd. 1861. Nr. 138.—LZeudet, Paral. asc. aig., rapid.
mortelle, surven. dans 1. conval. d. 1. fi¢vre typhoide. Gaz. des hép. 1861. Nr.
58.—Pellegrino-Levi, De 1. paral. asc. aigué. Arch. génér. 1865. I. p. 129.—
Bablou, Obs. d. paral. asc. aig. Gaz. hebdom. 1864. Nr. 49.—G@ru, Union méd.
1866. Nr. 152.—Caussin, Gaz. des hép. 1866. Nr. 23.—H. Jones, Brit. Med.
Journ. 1866. Oct. 27.—Hayem, Paralys. asc. aigué. Gaz. des hép. 1867. Nr.
102.—Harley and Lockhart Clarke, Fatal Case of Acute Progress. Paralysis.
Lancet. 1868. Oct. 3.—C. Lange, Om obstigende spinalparalyse. Hosp. Tid.
12. Aarg. Nr. 6-10. (Virchow-Hirsch, Jahresber. pro 1869. II. 8. 34.—Cheva-
let, Par. asc. aig. d’origine syphil. Bullet. d. thérap. 1869. Oct. 15.—Labadie
Lagrave, Gaz. des hép. 1869. Nr. 148.—0. Bayer, Heilung einer acut. ascend.
Paral. unter antisyphil. Beh. Arch. d. Heilk. 1869. 8. 105.—A. Hulenburg,
Lehrb. d. funct. Nervenkrankh. Berlin, 1871. 8. 603.—Reincke, Fall vy. Paral.
asc. acut. Deutsch. Klin. 1871. Nr. 23, 24.—Bernhardt, Beitr. z. Lehre. y. d.
acut. allg. Paral. Berl. klin. Woch. 1871. Nr. 47.—Chalvet, Gaz. des hop.
1871. Nr. 98.—LZeyden, Klinik d. Riickenmarkskrankh. I. 8. 94. IL. 8. 201.
—Herm. Levy, Paralysis asc. ac. Correspondenzbl. d. iirztl. Ver. d. Rheinproy,
1873. Sept. (Centralbl. 1874. Nr. 11.)—FPetitfils, Considér. sur Vatroph. aig.
des cell. motrices. Paris, 1873.—EZisenlohr, Zur Lehre vy. d. acut. spin. Paral-
yse. Arch. f. Psych. u. Nervenkrankh. V. 8. 219. 1874.—Calestri, Gazz. Lom-
bard. XXXIV. Nr. 20. 1874. (Schmidt’s Jahrb. Bd. 168. 8. 18.)—Salomon,
Schnelle Heilung einer schwer. ac. Riickenmarksaffection u. s. w. Correspon-
denzbl. d. arztl. Ver.im Rheinl. 1875. Nr. 15.—G@oltdammer, Ueber einige Fille
von subac. Spinalparalyse. Fall. 8. Berl. klin. Wochenschr. 1876. Nr. 26.—
Baumgarten, Eigenthiiml. Fall von Paral. asc. aigué mit Pilzbildung im Blut.
Arch. d. Heilk. XVII. 8. 245. 1876.—C. Westphal, Ueber einige Fille von
acut. tédtl. Spinallihmung. Arch. f. Psych. u. Nervenkrankh. VI. 8. 765. 1876.
—Déjerine et Goetz, Paral. asc. aigué. Arch. de Physiol. norm. et path. 1876.
p. 312.—R. 2. d. Velden (Leyden), Fall von acut. aufsteigend. spinaler Para-
lyse. Deutsch. Arch. f. klin. Med. XIX. 8. 333, 1877. |
History.
In the year 1859, Landry described some cases of disease,
under ‘‘ Paralysie ascendante aigué,” which had terminated in
PARALYSIS ASCENDENS ACUTA. 733
death, with the manifestations of spinal paralysis advancing
rapidly from below upward, and finally paralyzing the medulla
oblongata, and in which no appreciable anatomical lesions were
found. In the same year Kussmaul also described two cases
observed by him of similar, rapidly fatal spinal paralysis, with
entirely negative results on post-mortem examination.
No doubt cases of disease belonging to this category had pre-
viously been described in literature—thus, by Ollivier, in his
work, under the head of Hyperzemia of the Spinal Cord, by Wal-
ford, and others. It appears that the distinguished Cuvier also
died of this disease in 1832.
But it was not until after Landry’s publication that reports
of cases of this form of disease began to accumulate. Much,
however, was included under this head which evidently does not
belong here. Thus, cases of acute, central or diffuse myelitis (for
instance, the cases of Levy, Picard, and others), or of subacute
poliomyelitis anterior (cases of Behm and Taylor), or of infec-
tious myelitis (Baumgarten); perhaps it is also wrong to place
here those syphilitic affections which run their course presenting
the picture of acute ascending paralysis.
We may learn how difficult it is to keep these different forms
of disease separated when we remember that Petitfils has but
recently made an attempt, in the most detailed manner, to estab-
lish the identity of acute ascending paralysis and acute or sub-
acute anterior poliomyelitis,—to regard the former merely as a
variety of the latter, and to refer it likewise to acute alterations
in the large ganglion-cells of the gray anterior horns. In view
of a series of well-established, more recent, and most recent facts,
* this theory may be regarded as overthrown.
Even before this theory was advanced, cases had repeatedly
been observed which might be regarded as typical of acute
ascending paralysis, and in which even the most careful examina-
tion by a skilled and practised hand discovered no trace of any
change in the central nervous system (the cases of Vulpian, Pel-
legrino- Levi, Cornil and Ranvier, Hayem, Bernhardt, and others).
The most recent observations of Westphal are decisive, and to a
certain degree conclusive. Ina number of cases that were clin-
ically well marked, he could not find any trace of anatomical
734 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
alterations in the spinal cord, even on the most careful anatomi-
cal examination, carried out in every direction. Almost at the
same time, Déjerine and Goetz published a case belonging here,
with the same negative anatomical result. Westphal has also
rendered the clinical diagnosis of the disease more definite in
various directions.
It is thus settled, for the present, that the disease cannot a
considered as identical with any of the previously named forms
of spinal disease, but rather that it is a clinically well-charac-
terized—undoubtedly spinal—form of disease, the anatomical
conditions of which are entirely negative, so far as our present
means of investigation show. The disease may, and must, there-
fore, as yet be regarded as systemic; to be sure, we stand but at
the threshold of our knowledge thereof, and it will require addi-
tional clinical, pathogenetic, and also anatomical investigations
to give us any satisfactory idea of the same. The material thus
far at our command is far too inadequate for this purpose.
Definition.
The disease designated by the name of paralysis ascendens
acuta is clinically characterized by a motor paralysis (ascending
paralysis), which generally begins in the lower extremities,
spreads pretty rapidly over the trunk to the upper extremities,
and usually also involves the medulla oblongata, which some-
times runs its course without fever, sometimes with more or less
active fever, which but slightly involves the general sensibility
and the functions of the bladder and rectum, and which runs its ;
course without any notable atrophy of the muscles, and without
any diminution or change of their electrical excitability.
In the majority of instances the disease terminates fatally, by
asphyxia, paralysis of deglutition, and the like; but oo
cases may also end in recovery.
The anatomical characteristics of the disease are at present
purely negative. No pathologico-anatomical alterations are to
be found anywhere, and especially not in the spinal cord, which
might explain the picture of the disease. In particular are
——
PARALYSIS ASCENDENS ACUTA. 735
there no signs of hyperemia within the spinal cord, of myelitis,
of acute destruction of the ganglion-cells or nerve-fibres.
If the disease is therefore to be localized within the spinal
‘cord at all, it is a question of finer, so-called impalpable disturb-
ances of nutrition, not accessible to our present means of exam-
ination.
Etiology and Pathogenesis,
On this subject very little is known, and, in fact, nothing
positive.
Sometimes the disease arises Aeithout any demonstrable pre-
disposing or exciting causes. |
Men are most frequently attacked ; among the sixteen cases
collected by Pellegrino- Levi, only Sse were in women.
Most cases of the disease occur between the ages of twenty
and forty, but it may also occur at later periods of life.
Nothing is known of any hereditary or neuropathic influences.
Taking cold is mentioned first in the line of exciting causes.
It is not necessary here to mention the individual possibilities of
the same, as they proved to be effectual in an entire series of
cases. |
Not a few instances have been seen to arise during the course
of, or during the convalescence from, acute diseases (typhoid
fever, diphtheria, pleurisy, varioloid, etc.). Some few have fol-
lowed suppressed menstruation (through taking cold or emo-
tional disturbances). _
Bablow saw the disease break out after a man had indulged
in the act of coition while standing up. |
It is at least doubtful, as yet, whether syphilis is an actual
cause of genuine acute ascending paralysis. We are accustomed
always to find palpable alterations in syphilis, so that a syphili-
tic affection of the spinal cord with an impalpable lesion does
not seem to us exactly probable ; at the same time, such a thing
is possible. At all events, various authors (Kussmaul, Landry,
O. Bayer, and others) have decided on the syphilitic nature of
the disease, partly from the antecedents and partly from thera-
peutic results. |
736 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
Westphal has recently taken up the idea of an intoxication
as the cause of acute ascending paralysis. The same had already
been announced by Landry, and briefly touched on by Hayem
and Bernhardt. Baumgarten’s case, in which the bacteria of
splenic fever (Milzbrand) were found in the blood and in the
spinal cord, appears to give some support to this supposition ;
still, in this case, there was undoubted myelitis present, therefore
it probably does not belong here. Westphal considers it proba-
ble that some intoxication—thus far, to be sure, of an entirely
unknown variety—is the actual and final cause of acute ascend-
ing paralysis. This can only be decided by numerous further
observations.
It readily occurs to us to draw a parallel between this and
another affection, likewise spinal, which sometimes terminates
fatally within a few days, and sometimes runs a longer course to
recovery, likewise appearing in lighter and severer attacks, and
for which, up to the present time, there has likewise been found
no anatomical lesion. We refer to fetanus. This parallel does
not need to be carried out any further; but close observation
cannot fail to detect the manifold analogies of the two forms of
disease, although in the one (tetanus) it is a question principally
of manifestations of motor irritation, and in the other (acute
ascending paralysis) principally of manifestations of motor par-
alysis.
Pathological Anatomy.
The few convincing and sufficiently careful reports of post-
mortems now before us (Vulpian, Cornil et Ranvier, Bernhardt,
Westphal, Déjerine et Goetz) unanimously teach that there are
absolutely no anatomical changes present to which the symptoms
could, with any reason, be referred.
The examinations fulfil all the requirements that can be made
of them at the present time; they have furnished entirely nega-
tive results, as well with reference to the brain as with reference
to the spinal cord and the medulla oblongata, and likewise with
reference to the sympathetic nerve, the peripheral nerve-trunks,
and the muscles. The future alone can tell whether the changes
ae
PARALYSIS ASCENDENS ACUTA. 737
in the anterior roots found by Déjerine and Goetz, but unfortu-
nately not thoroughly enough examined, are of any significance.
It is not probable that they are so.
On the other hand, the older investigations, which claimed to
have proved the presence of hyperzemia here and there, of soft-
ening of the spinal cord, even of myelitis and the like, lose all
their significance ; at best-they belonged to other clinically some-
what similar forms of disease. This also holds true of the very
newest observation recently published by Leyden (v. d. Velden),
under the name of acute ascending paralysis. This decidedly
does not belong to the form of disease which we have here, in
harmony with the views of Westphal and others, described under
this name, as is abundantly evident from the clinical symptoms
(a high grade of fever, delirium, paralysis of the bladder, loss of
electrical excitability, stiffness of the back, tension of the mus-
cles, etc.). What is here presented seems rather to be an admi-
rable instance of acute disseminated myelitis, especially affecting
the antero-lateral columns and the anterior gray substance.
It may be a matter of some significance that in single cases
similar alterations have been found in the spleen, the liver, the
lymphatic glands, and intestinal follicles, etc., as they are also so
frequently found in diseases of infection—such changes as cloudi-
ness, swelling, enlargement, more abundant blood-contents, etc.
Pathology of Acute Ascending Paralysis.
Symptoms.
In most instances, though not always, the appearance of the:
characteristic manifestations of paralysis are preceded by vari-
ous prodroma, such as slight febrile action, general discomfort,
pulling and shooting pains in the back and the limbs, pares-
thesia of various kinds, as formication, numbness in the feet and
finger-tips, and the like, generally also a feeling of great weari-
ness and striking weakness. These may last for a longer or
shorter period, for one or for several days, even a week and
longer ; such premonitory symptoms J have been observed for as:
long as six weeks.
VOL. XIII.—47
738 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
The actual beginning of the disease is marked by a striking
weakness of the lower extremities, which increases more or less
rapidly, either gradually or with sudden greater steps, and very
soon amounts to well-marked paresis. Standing and walking
are soon rendered impossible, while when lying down the indi- -
vidual movements of the legs can still be executed, although with
a growing diminution of force. Gradually these movements also
fail, first in the joints of the feet, then in the knees, and finally in
the hips; and so in the course of a few days, seldom earlier or
later, there is complete paralysis of the limbs.
The legs then lie there, lax and immovable, show no traces of
muscular tension or contractures, exhibit no fibrillar twitchings,
nor any other spasmodic manifestations, do not present the
slightest resistance to passive movements, and are not subject to
pain, or but very slightly so, either spontaneously or on touch
or pressure.
The paralysis now gradually advances upwards, uniformly
and steadily, but seldom interrupted by a prolonged arrest of the
malady.
The muscles of the trunk are next attacked ; sitting up and
sitting straight are gradually rendered impossible by the paraly-
sis of the muscles moving the spinal column ; the acts of expira-
tion, of coughing and sneezing, of defecation, etc., become weak
- and powerless through paralysis of the abdominal muscles.
Not long after—though here, it is true, the rapidity of the
progress is very variable in different cases—the wpper extremities
are also attacked with the weakness and paralysis. First the
hands grow weaker and less steady, the strength of grip dimin-
ishes rapidly, ordinary acts, such as writing and feeding one’s
self, grow impossible. Then the movements of the arms grow
increasingly more difficult, finally the movements in the shoulder-
joint, too, become more or less feeble and paralyzed, so that at
last the arms, like the legs, are entirely relaxed and immovable.
Then, too, disturbances of inspiration also appear, owing to
paralysis of the intercostal and other respiratory muscles of the
trunk. | .
When the disease has become developed up to this point, an
objective examination shows very little that is marked, aside
an tet Pr ew er -_ A er —_——- “.
PARALYSIS ASCENDENS ACUTA. 739
from the motor disturbances. Asa rule, the very slight disturb-
ance of sensibility is especially noticeable.
Subjective disturbances of the same, it is true, are not rare ;
patients complain of a feeling of numbness and formication in the
fingers and toes, a diminution of feeling in the soles of the feet,
rarely of higher grades, of loss of feeling in the lower extremities.
There is generally no pain, or but an insignificant amount only
at the beginning. The spinal column is not painful, the spinous
processes not sensitive on pressure.
Objective tests of sensibility, in the majority of cases, give
quite normal results; occasionally it is found slightly though
distinctly lowered, especially towards the periphery of the ex-
tremities. More rarely higher grades of anesthesia are demon-
strated, and it may be a matter of doubt whether these cases
belong in this category at all. These statements hold equally
good for sensation of the skin and muscles.
In single cases a tolerably high grade of hypereesthesia of the
skin (hyperalgesia) has also been demonstrated.
At all events, however, the disturbances of sensibility play a
subordinate rdéle, in the picture of the disease, as compared to
the motor paralysis.
No ataxy can be demonstrated, as long as any movements
are capable of being carried out, although the feeble, trembling
movements of the paretic limbs sometimes remotely remind us of
this condition.
There is likewise no considerable atrophy of the paralyzed
muscles. During the progress of the disease more or less con-
siderable emaciation may appear, as in any one long confined to
a sick-bed ; but there is no question of a high grade of rapidly
progressive atrophy, as in» poliomyelitis anterior, and the few
cases in which such has been reported were probably wrongly
classified.
Another fact which stands in most intimate relation to the one
Just stated, and which appears to be of no less value in a dif-
ferential diagnosis, is that the electrical excitability of the para-
lyzed neryes and muscles remains entirely normal. In all the
more recent cases, carefully investigated by skilled hands (Pel-
legrino-Levi, Bernhardt, Westphal, efc.) no anomaly of electrical
740 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
excitability worth mentioning has been found, even after the
disease had existed for a number of weeks. By this very means
the disease seems to be distinguished, in a very significant
manner, from all progressive paralyses caused by gross anatomi-
cal lesions within the spinal cord (myelitis centralis, poliomyelitis
anterior subacuta, etc.). At all events the careful testing of
electrical excitability is worthy of special attention in all future
cases.
But little is said with regard to the existence of vaso-motor
disturbances. In Eisenlohr’s case there was transitory edema
of the skin, with redness of the integument over various joints.
In some cases a profuse secretion of sweat is reported.
The nutrition of the skin does not usually suffer. Bed-sores
do not occur.
The conditions of reflex action certainly deserve more careful
attention, as they are probably also of diagnostic significance.
Statements with regard to the reflex action of the skin are very
various; it also appears that this changes gradually during the
course of the disease. It is but rarely that an elevation of reflex
action is reported (Eisenlohr’s case) ; histories of cases generally
show that reflex action is preserved during the first days and
weeks of the disease, that it then diminishes more or less rapidly,
and is finally entirely extinguished. If, as a general rule, reflex
action thus entirely fails in well-marked and complete paralysis,
still this does not seem to occur as rapidly and completely as it
does, for instance, in poliomyelitis anterior. Special attention
might be paid to this point. The reflex excitability of tendons
has, thus far, only been examined by Westphal, who, in one case,
found it, as well as the excitability of the skin, to be lacking.
The condition of the sphincters is a matter of no less impor-
tance. The bladder and rectum are generally quite undisturbed
in their functions ; there are no involuntary evacuations, there is
no retention of urine—this is the rule. In individual instances,
however, slight disturbances of the bladder occur; generally,
however, even if they become more severe, they are merely transi-
tory. Usually there is no trace of the severe paralysis of the
bladder and rectum which occurs as a rule, for example, in
central myelitis, and it is only exceptionally that the use of the
PARALYSIS ASCENDENS ACUTA. 741
catheter is required (cases of Déjerine and Goetz). In one case
Pellegrino-Levi found the urine alkaline. There is usually con-
Stipation, which may, under some circumstances, become very
obstinate.
Statements vary considerably with regard to the general con-
dition of the patients; it may be more or less disturbed, although,
in some instances, it is remarkably good. In the majority of in-
stances there is said to have been no fever; at all events, it does
not belong to the essential manifestations of the disease. In some
cases active fever has been found, in others only a moderate de-
gree of the same. At other times, again, single severe attacks of
fever, with a chill, have been encountered ; or there might merely
be slight, transitory, febrile movement, extending over several
days. This question, too, requires further more careful investi-
gation.
In most striking contrast to the severe manifestations of spi-
nal paralysis (for we can hardly regard it as being anything else)
is the complete integrity of the functions of the brain, at first
and during the earlier period of the disease.. Intelligence and
memory, consciousness and the functions of the special senses
remain entirely normal; there never is any dizziness, delirium,
and the like, and even complaints of headache belong to the rari-
ties in this disease. Even the cerebral motor nerves either take
no part at all in the general paralysis, or are not involved until
very late. Actual paralysis of the muscles of the eye has not
been observed ; transitory amblyopia has been reported in two
cases. Only those motor nerves which are directly dependent on
the medulla oblongata are, as a rule, sooner or later involved in
the paralysis.
After the disease has once reached the stage heretofore de-
scribed, its further course may vary somewhat.
In most instances the disease advances still further upwards.
The movements of the head and neck now begin to be disturbed ;
the muscles of the neck grow paralyzed ; patients complain. of
weakness or of a feeling of stiffness in the neck ; sometimes dis-
tinct weakness in the domain of the facial nerve sets in. Respi-
ration grows increasingly difficult; & high degree of dyspnea
742 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
occurs, with very frequent and anxious respiration ; the activity
of the diaphragm has been impaired, and the danger of asphyxia
draws threateningly nearer. Simultaneously herewith, or it may
be earlier or somewhat later, disturbances of articulation of the
voice, of speech set in, caused by paralysis of the muscular ap-
paratus pertaining to these functions. To these are added weak-
ness and paralysis of the muscles of mastication, paresis of the
soft palate (nasal speech, the regurgitation of fluids through the
nose), difficulty of swallowing, and finally complete paralysis of
deglutition ; in a word, the complete picture of severe bulbar par-
alysis. Ifwe add that not infrequently differences in the two
pupils may be observed, and that the frequency of the pulse
often rises to a very alarming height, we shall therewith have
completed the clinical picture which indicates an advance of the
process to the uppermost divisions of the cervical spinal cord.
All these manifestations continue to increase, while evidences
of hypereemia and hypostatic congestion of the lungs appear,
and the danger of asphyxia is augmented, until the fatal termé-
nation is more or less rapidly ushered in.
The period of time which elapses before this termination is
reached may vary considerably. Sometimes it is but a few
days; the disease has been seen to run its course and end in
death within two or three days, although it may last for two,
three, and four weeks; it seems to be rare for the disease to
extend over as long a time as six weeks. The average duration
of fatal cases seems to be eight to twelve days.
But another termination is possible, having occurred in a
series of cases which may probably be counted as belonging in
this category, viz., a termination in improvement and recovery.
Landry even speaks of eight recoveries in ten cases, and Pelle-
grino-Levi found at least five cured out of fourteen diseased.
The disease may come to a stand-still at any stage of its de-
velopment ; then, some day, the paralysis extends no further.
This generally appears to be the case before the paralysis has
reached the nerves of the bulb, though instances have also been
known in which recovery took place in spite of the existence of
disturbances of respiration, deglutition, and mastication.
The favorable turn usually takes place after the disease has
a -
PARALYSIS ASCENDENS ACUTA. 743
lasted but a comparatively short time; some single movements
appear to be a little better and stronger, others return once
more ; those parts last attacked by the paralysis are the first to
show improvement. This gradually increases; the strength and
power of function of the muscles grow from day to day; first
the patients can use their hands again, gradually they learn to
sit up, finally again to stand and walk. This may occupy a con-
siderable time; it is always to be counted by weeks, and whether
it be many weeks or few, varies very much in individual cases,
and depends on circumstances entirely unknown to us. . Usually
the patients feel very weak and poorly for quite a while ; fluctu-
ations and relapses in this favorable course also seem to be pos-
sible.
Exceptionally the disease may be seen to progress downwards within the cord,
instead of pursuing the more frequent ascending course. The paralysis then begins
in the nerves of the bulb, and successively seizes first the upper and then the lower
extremities. So in the case of the distinguished Cuvier, as reported by Pellegrino-
Levi.
It may seem doubtful whether Westphal’s Case 4 belongs under this head. This
was likewise an instance of acute, fatal paralysis, with a perfectly negative result of
post-mortem examination, but confined to the nerves of the bulb; there was paral-
ysis of the tongue and lips, of deglutition, mastication, and respiration. This case
would have to be considered as one of a more rudimentary character, more limited
in its localization, and rendered rapidly fatal by this very localization. But it is
probably better for the present to regard it as doubtful, and to leave it unclassi-
fied.
Diagnosis.
The picture delineated in the preceding pages is probably
sufficiently characteristic to admit of a diagnosis of the disease
being made ina fair proportion of the cases.
The paralysis, chiefly of a motor character, progressing rap-
idly from. below upwards, the small amount of fever, the insig-
nificant disturbances of sensibility, the absence of paralysis of
the bladder, the slow extinction of reflex excitability, the ab-
sence of muscular tension and muscular atrophy, the non-occur-
rence of bed-sores, and the final involvement of the functions of
744 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
the bulb would seem to be sufficiently indicative of this disease
to point suspicion that way.
At the same time a positive decision will often not be pos-
sible, especially during the first few days, and the diagnosis may
for a time be unsettled. The affections with which acute ascend-
ing paralysis may be confounded are particularly the different
forms of acute and subacute myelitis, but on careful considera-
tion of all the symptoms one will generally be able—especially
in the course of several days—to arrive at a tolerably certain
decision.
This affection is hardly liable to be confounded with acwufe
poliomyelitis anterior (section 15) because the latter has no
progressive character, never attacks the medulla oblongata, and
never directly induces death; because it generally sets in with
fever, with very rapid loss of faradic excitability and rapid mus-
cular atrophy, etc. It is only in the light and temporary forms
of acute poliomyelitis anterior—which, however, are very rare—
that a doubt might perhaps arise. But these may perhaps be
distinguished from the light forms of acute ascending paralysis
by the entire failure of reflex excitability (?), and certainly may
be distinguished by the lowering of faradic excitability—even
though it be but slight,—and by the non-progressive character of
the paralysis.
It is an easier matter to confound this malady with those
cases of subacute anterior poliomyelitis, which pursue a com-
paratively rapid course in an upward direction. Indeed this
disease has, by a number of writers, been regarded as identical
with Landry’s paralysis. This is certainly incorrect, as will
appear on a careful comparison of the symptoms of the two forms
of disease. The first argument in favor of the existence of acute
ascending paralysis is to be found in the absence of atrophy and
in the fact that the electrical excitability remains intact; then
the longer preservation of reflex action, the possible presence of
slight disturbances of sensibility and of the bladder, the more
rapid and generally fatal termination, and the early appearance
of severe symptoms of bulbar trouble, also point in the same
direction. Generally, however, we shall be able to conclude
with certainty that a given case of paralysis is due to anatomical
PARALYSIS ASCENDENS ACUTA, 745
changes in the spinal cord, only on the development of atrophy
and of the reaction of degeneration.
As a rule, Landry’s paralysis can easily be distinguished from
acute central myelitis (see above, p. 416). In the latter there is
always a high degree of disturbance of sensibility, the early fail-
ure of all reflex actions, great paralysis of the sphincters, fever,
acute bed-sores, a lowering of faradic excitability, and a rapidly
fatal termination. Hence the distinction is not difficult.
The spinal forms of syphilis, which run their course under
the form of acute ascending paralysis, may be distinguished from
the latter, if, indeed, they are not identical with it, only by the
evidence of former or still existing syphilis in the patient, and
by the results of anti-syphilitic treatment.
Infectious myelitis, of which Baumgarten has certainly not
given us a very complete clinical picture, ought to be distin-
guished from Landry’s paralysis by the same signs which char-
acterize any other diffuse or central myelitis.
The rare cases of acute multiple newritis, one of which Eich-
horst* has recently described, could only be mistaken for acute
ascending paralysis by a very careless observer. The severe
pains, limited to single nerve-roots, the anesthesia and paralysis,
similarly limited, and especially the rapid lowering of electrical
excitability, should be enough to guard against this error.
Prognosis.
Acute ascending paralysis is always a disease of very doubt-
ful prognosis. If it is far enough developed to be diagnosticated
with certainty, then the prognosis is generally very serious. It
becomes worse the more rapid has been the ascending course of
the disease, the earlier respiration has been attacked, and the
more pronounced the evidences of bulbar paralysis.
But we have seen that there are also exceptions to this rule,
that no small number of cases even terminate favorably. It is
difficult, however, to recognize these favorable cases early ; as a
rule, this is impossible until improvement has begun. Perhaps
>
1 Neuritis acuta progressiva. Virchow’s Arch. Vol. 69, 1877.
EN
746 ERB.—DISEASES OF THE SPINAL CORD. AND ITS ENVELOPES.
further experience will give us some fixed points for such a dis-
tinction.
Therapeutics.
It is difficult, in view of our entire ignorance with regard to
the true essence of the disease, to decide on any definite thera-
peutic course.
One will be inclined, in general, to employ the treatment ai
plicable to the acute ascending forms of myelitis. But it is
question whether the good results of this treatment have a
been observed in those very cases which have been falsely diag-
nosed as acute ascending paralysis.
The main object of treatment certainly is to bring about a
change in the nutrition of the nerve-elements of the spinal cord.
This is an indication more easily set up than fulfilled.
It is more than doubtful whether the energetic application of
derivatives to the spinal column is justified by this indication.
The favorable results attained by Levy and Salomon with the
actual cautery occurred in cases which most probably did not
belong under this head. At the same time, in so serious a dis-
ease, one would not shrink from the frequent application of dry
or wet cups, from repeated blistering, and, in case life was
threatened, even from the use of the actual cautery.
Careful stimulation of the activity of the skin is more likely
to prove of benefit. This may be accomplished by frictions of
the skin with cold water, the repeated application of Priessnitz’s
‘‘nacks’’ to the trunk or to the entire body, lukewarm baths,
cold affusions, etc.
Of internal remedies, iodide of potassium is generally used as
the nearest refuge in this therapeutic extremity, or nux vomica.
Their effects are doubtful.
An agent which promises much, and is certainly worthy of
being more carefully tested, is the galvanic current. While its
value has been established beyond a doubt for the later stage of
the cases that terminate favorably, the question still remains to
be decided, when its application is to be commenced. A priori,
we would seem to be justified in beginning it very early, as there
INTRAMEDULLARY TUMORS. 747
is no fever, no inflammation, but merely an impalpable disturb-
ance of nutrition in the spinal cord. And it is against just such
a condition that the galvanic current, perhaps, shows itself espe-
cially efficacious. ‘The application of a constant, moderately
strong current the length of the spinal column might be tried
first.
As a matter of course, these patients require the most careful
nursing; their nourishment must be tonic and abundant; and
on the appearance of symptoms of paralysis which threaten life,
the free and energetic use of all the various stimulants (alcohol,
coffee, musk, camphor, ammonia, nux vomica, etc.) must not be
omitted.
In those cases which terminate favorably, subsequent treat-
ment with electricity, baths, cold water, mountain air, etc., is
indicated. :
18. Tumors of the Spinal Cord.—Intramedullary Tumors.
Lebert, Traité d’anatom. patholog. Tom. II.— Ollivier, 1. c. 3. éd. Tom. II. p. 503.
1837.—Foerster, Handb. der pathol. Anat. II. 2. Aufl. 8. 628. 1863.— Virchow,
Die krankhaften Geschwiilste. Bd. 1 u. 2.—Zeyden, Klinik der Riickenmarks-
krankh. I. 8. 468. 1874.—M. Rosenthal, Klinik der Nervenkrankh. 2. Aufl. §S.
349. 1875.—Hasse, 1. c. 2. Aufl. 8. 729-735. 1869.
' Eager, Arch. génér. 1834. Tom. 4. p. 605.—Brown-Séquard, Course of Lectures,
etc. Phila. 1860. p. 60, p. 101, etc. Paralysis of the Lower Extremities. Lon-
don, 1861. p. 92-99.—Gendrin, Tubercule comprimant, etc. cité par Brown-
Séquard. Journ. d. 1. Physiol. T. VI. p. 233.—W. Guill, Cases of Paraplegia.
Guy’s Hosp. Rep. VIII. 8. 113. 1858.—Schueppel, Gliom u. Gliomyxom des
R.-M. Arch. d. Heilk. VIII. 8S. 113. 1867.— W. Scholz, Paraplegie u. s. w.,
Bindegewebsneubildung im R.-M. Allg. militiridrztl. Zeitung, 1868. Nr. 28—
John Grimm, Ein Fall von progress. Muskelatrophie. Virch. Arch. Bd. 48. S.
445. 1869.—Z. K. Hoffmann, Gliomyxom im oberen Theil des Lendenriicken-
marks, Zeitschr. f. rat. Medic. III. Reihe. Bd. XXXIV. 8. 188. 1869.—/J. San-
der, Fall von Paralysis atrophica. Arch. f. Psych. u. Nervenkrankh. II. 8. 780.
1870.—Habershon, Clinical Cases, etc. Tubercle in the Spinal Cord. Guy’s
Hosp. Rep. XVIL. p. 428. 1872.—G@. Hayem, Tubercule d. 1. moelle ép. Arch.
d. Physiol. V. p. 431. 1873.—Charcot, Lecons sur les maladies du syst. ner-
veux. II. Sér. 2. Fasc. 1873.—Chvostek, Zwei Fille von Tuberkulose des R.-M.
Wien. med. Presse, 1873. Nr. 35. 37-39.— Westphal, Fall von Hdhlen- und
Geschwulstbildung im R.-M. Arch. f. Psych. Q. Nervenkrankh. V. 8. 90. 18'74.
—Th. Simon, Ueber Syringomyelie u. Geschwulstbildung im R.-M. Ibid. ¥.
|
.
748 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
S, 120. 1874.—Liowville, Nouv. exempl. de 1és. tubercul. dans la m. ép. Arch.
génér. 1875. Janv. p. 92.—Kiebs, Beitr. z. Geschwulstlehre. Leipzig, 1877. 8.
89. Prag. Vierteljahrschr. Bd. 126 u. 133.
In this section we shall consider those pathological neoplasms
which are developed within the substance of the spinal cord
itself, in so far as they occur in the form of tumors, and are more
or less sharply distinguished from the substance of the cord.
Tumors of the substance of the spinal cord are very rare
affections ; they are also, clinically, very difficult or impossible
to recognize with certainty, and therefore seem to be of but little
practical importance ; consequently, we shall treat the subject
briefly.
Pathological Anatomy.
There are but few forms of neoplasm that have thus far been
observed in the spinal cord itself, and but single ones of these
have acquired some degree of practical importance through the
comparative frequency of their occurrence. Such are gliomata
and tubercle of the cord. 3
The majority of medullary neoplasms appear to be developed
in the midst of the substance of the spinal cord ; only in rarer
instances do they grow from the spinal meninges into the cord.
It cannot as yet be determined whether the white or gray matter
of the cord affords the principal soil for the development of the
various neoplasms. Some writers assert one thing, some another.
Perhaps the relations vary according to the various forms of
neoplasm. According to the observations of Th. Simon, it would
almost appear as though the anterior portions of the white pos-
terior columns were the favorite seat of some neoplasms. This
much, however, is certain, that intramedullary neoplasms may
be developed from the most varied points in the gray and white
substance of the cord.
The size of the tumors can never be very considerable, on
account of the narrow space within the spinal canal. They are
generally round or longish growths, from the size of a hemp-seed
to that of a hazel-nut, or even of a thumb. In single cases,
however, extraordinarily elongated tumors have been found,
INTRAMEDULLARY TUMORS. 749
which have stretched, in various degrees of thickness, through-
out the entire cord, from the conus medullaris to the medulla
oblongata.
The substance of the spinal cord is at first only crowded apart
by the tumors, more or less compressed, and finally caused to
disappear entirely ; more rarely the substance of the cord passes
directly into the mass of the tumor. An inflammatory softening
is always developed in the neighborhood of the neoplasm, a
transverse myelitis, whence in many instances the first severe
clinical symptoms proceed. Aside from this, the secondary
ascending and descending degenerations so often spoken of are
generally developed.
In the tumors themselves processes of softening are not rare;
the same is true of the secondary development of cavities (syrin-
gomyelia), extravasations of blood, etc., as we shall see when
studying the individual forms of the affection.
Among the tumors thus far observed in the cord, glioma is
probably the most frequent variety (cases of Sander, Simon, Case
VIL. ; Schueppel, Case I.; Klebs and others). It usually appears
as a soft, grayish-red or grayish-white mass, of a roundish or more
elongated shape, often very long drawn out and irregular in form.
In many places it is merged impercebtibly in the surrounding tis-
sue. It is very vascular, disseminated with numerous larger and
smaller blood-vessels, and not rarely shows more or less extensive
hemorrhages into its substance and in its neighborhood. The
secondary development of cavities is very frequent in gliomata,
especially of the softer form, and part of the cases of disease
described under the name of syringomyelia evidently belong
here (Westphal, Th. Simon). The very vascular forms have
probably also been described as teleangiectatic gliomata. This
variety, in particular, shows especially extensive hemorrhages.
According to Virchow, gliomata proceed from the neuroglia,
and represent nothing else than a hyperplasia of the neuroglia.
They consist of cells which are imbedded in a granular or fibril-
lated, or sometimes also in a more mucous basement membrane.
Their wealth of cells varies more or less; their wealth of vessels
is generally very considerable. The mnerve-elements (fibres and
cells) have generally entirely disappeared within the tumor,
50 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
according to the reports of the majority of authors (Virchow,
Charcot, and others).
On the other hand, Klebs has recently undertaken to show that all these tumors
principally proceed from the nerve-elements, partly from true ganglion-cells, partly
from medullated nerve-fibres, and that associated herewith there is a mighty devel-
opment of blood-vessels and lymph-vessels. He therefore calls these tumors newro-
gliomata. It is claimed that the interruption of nervous conduction occurs much
later in these hyperplastic tumors than in those forms of tumor which act upon
the nerve-tracts through mechanical pressure. This might be of value from a clin-
ical point of view. Further investigations may reconcile these differences,
Gliomata of the spinal cord are said to occur principally in
the cervical portion of the same, and, according to Schueppel, to
arise chiefly from the gray substance.
Myzxoglioma (Simon, Case VIII. ; Schueppel, Case II. ; Hoff.
mann) is to be regarded as a variety of glioma. It is a bright
red, translucent, viscid tumor, in which the cell-elements are im-
bedded in a basement substance containing mucine, and which
otherwise acts just like the simple glioma, with which the myxo-
glioma is sometimes combined. The same is true of habeas
of which Westphal has described one case.
Pure sarcoma (Foerster, Tuengel in his clinical communica-
tions, Hamburg, 1864, p. 27) is certainly a very rare form of tumor
within the spinal cord. Virchow has never seen an instance of it.
Myxosarcoma has been observed here and there as a long-drawn
tumor with the development of a number of central cavities.
The cases of Hutin and Scholz, and the case of Sonnenkalb, re-
ported in Ollivier, 1. c., IL., p. 402, perhaps belong in the cate-
gory of fibrosarcomata.
On the other hand, twbercie is one of the most frequent tumors,
perhaps the most frequent, of the spinal cord (Charcot). It has
been observed in numerous cases (Gull, Eisenschitz, Virchow,
Hayem, Liouville, Habershon, Chvostek, and others).
Tubercle of the spinal cord occurs at all periods of life, most
frequently between the ages of fifteen and forty, and compara-
tively oftener during youth.
These growths may be developed in all portions of the cord,
but are especially fond of the two enlargements of the same, and
according to Hayem are especially liable to occur in the lumbar
INTRAMEDULLARY TUMORS. 751
enlargement. Sometimes they occupy principally the white, and
sometimes principally the gray substance. Their size varies from
that of a hemp-seed to that of a hazel-nut, or larger; they gener-
ally occur singly, rarely several are found at once, or a whole
group of them. Tubercle of the spinal cord is seldom the only
localization of tuberculosis within the body; there is almost
always simultaneous tubercle of the brain, or tuberculosis of the
lungs and other organs of the body can be demonstrated. Very
generally gray miliary tubercles are at the same time to be found
in the meninges of the cord.
Tubercles of the spinal cord have quite the appearance of the
well-known, far more frequent tubercles of the brain; they are
roundish, hard tumors, of a dry quality, of yellowish-white,
cheesy color, of a lamellar arrangement on their cut surface; the
peripheral layers are often more gray and hard, and contain
young tubercle granulations. Sometimes a central cavity is met
with, containing softened matter of a cheesy or pasty consist-
ence (Chvostek, Habershon).
In the vicinity of the neoplasm there is always more or less
extensive softening of the spinal cord, of an inflammatory nature;
a secondary myelitis which is especially pronounced in the gray
substance, and extends to a variable degree upward and down-
ward within this substance. Sometimes, too, a species of encap-
sulation through sclerotic tissue is met with in the vicinity.
According to circumstances—according to the position of the
tumor—there will be secondary ascending or descending de-
generation.
Syphilomata, gummata, are, on the whole, but rarely found
within the spinal cord (cases of E. Wagner, Moxon, Charcot and
Gombault, and others). They are then generally multiple, and
occur simultaneously also in the brain. They have the same
peculiarities as other gummata of the central nervous system.
Carcinoma seems never to occur primarily in the spinal cord,
if we ignore the earlier, very doubtful reports with regard to
**cancerous’’ new growths in the cord. Even the case of tumor
of the cord, reported by John Grimm as medullary carcinoma, is
probably somewhat questionable. Very frequently, however,
carcinomatous growths, taking their origin from the vertebra,
a
7
*
752 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
grow into the spinal cord, but then they run their course quite in
accord with the clinical picture of meningeal tumors.
Probably those alterations within the cord which have been
described under the names of hydromyelus and syringomyelia
may also be in part counted among tumors of the cord. Although
they are not exactly rare, they are of very little practical impor-
tance on account of frequently running their course entirely unac-
companied by any symptoms. Their method of development
seems to be various; sometimes there is an actual malformation,
sometimes a secondary widening of the central canal, sometimes
a secondary development of cavities, such as occur from processes
of softening in myelitis,or more frequently (Th. Simon) in actual
neoplasms (gliomata, myxogliomata, myxosarcomata, etc.).
Etiology.
The causes of intramedullary tumors are as yet quite obscure.
Naturally enough, here too, as in meningeal tumors, the blame
has been attached to all sorts of conditions, but it is generally’
very hard to tell with what degree of justice.
Traumatic lesions, a blow, a jar, a fall upon the spinal col-
umn, are among the causes, the efficacy of which we should be —
most inclined to recognize.
The influence of pregnancy and the puerperal state are quite
uncertain. These might more readily be believed to give occasion
for the appearance of the first symptoms where the neoplasm
already existed but was as yet latent.
It cannot be regarded as settled whether severe fright, pro-
longed trouble, and the like, are capable of causing the develop-
ment of a tumor of the spinal cord.
It is certain, however, that some general diseases and dyscra-
sias are capable of occasionally becoming localized in the spinal
cord. This is true of scrofula and tuberculosis, as shown by
tubercle of the cord ; of syphilis, as shown by spinal gummata. »
We know of nothing further to say with reference to the etiol-
ogy of intramedullary tumors.
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INTRAMEDULLARY TUMORS.
Symptomatology.
The picture of disease by which tumors of the spinal cord
betray themselves is exceedingly variable in different cases ; it is
manifold, and generally at the same time so uncertain that there
can ordinarily be no such thing as a positive recognition of the
same. This lies in the very nature of the case.
Either a more or less complete paraplegia appears, with all
the usual signs observed in every myelitis from compression
(paralysis of motion, sensation, and of the bladder, increased re-
flex action ; finally, atrophy, bed-sores, etc.). The development
of this paraplegia sometimes, though by no means always, occurs
with lively excentric pain, shooting pains in the limbs, constrict-
ing pains like a girdle, etc., similar to the symptoms in meningeal
tumors, with paresthesia, local atrophy, and the like ; sometimes
it comes on with vague and uncertain symptoms (paresthesia,
_weariness, stiffness, slight atrophy, etc.) lasting for a long time,
until the paraplegia then suddenly and somewhat rapidly de-
velops itself, evidently caused by a rapidly spreading transverse
myelitis, or it may be by hemorrhage into the tumor itself and
its surroundings. °
Or a quite partial paralysis is at first developed, which may
remain for a long time confined to one upper extremity, for in-
stance, and then, in an irregular manner, seize the other extrem-
ities until the paraplegia has become complete. In such cases,
too, the symptoms of a unilateral lesion have been observed for
quite a long while (cases of Scholz, Gendrin), which have then, in
. the further progress of the affair, developed into complete para-
plegia. Or various other groups of symptoms are called forth
(progressive muscular atrophy, symptoms of tabes, signs of
spasmodic spinal paralysis, etc.) according to the position, seat,
and principal direction of development of the tumor.
In not a few cases the manifestations during life are exceed-
ingly insignificant, and one is astonished, on making a post-mor-
tem examination, to find such extensive changes in the spinal
cord. This seems to be especially the*case when a tumor quite
centrally developed crowds the substance of the cord apart, and
VOL. XII.—48
54 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
does not entirely destroy it. Th. Simon has even reported sey-
. eral exceedingly remarkable cases which ran their course entirely
without any symptoms.
But when it is not a question of just such quite exceptional
instances, then the picture of the disease is usually that of a
transverse myelitis, being more or less rapidly developed and
extending over a transverse section of the cord. Sometimes the
disease runs a more acute, sometimes a more chronic form, and it
is but seldom that in this picture the presence of a tumor can ~
recognized as the cause of the transverse myelitis.
In some single instances the disease also appears under the
picture of a slowly ascending, chronic, spinal affection, which
runs its course under the most complicated manifestations, and
does not present the picture of the previously described chronic
diseases of the general system ; therefore, represents more the
picture of a diffuse ascending myelitis. In still rarer instances
one may also recognize a descending extension of the neoplasm,
or of the myelitis caused thereby, within the gray substance, by
the subsequent disappearance of reflex excitability, the occur-
rence of extensive muscular atrophy, etc.
The attempt has thus far been made in vain to secure, from
amongst the individual symptoms, at least a few fixed points
on which to base the diagnosis of intramedullary tumors.
The following have been claimed as such. A somewhat long
antecedent history of active local manifestations of irritation,
belt-like pains, excentric pains, definite paresthesias, local paral-
yses, as in meningeal tumors; early and well-marked atrophy,
which points to a larger involvement of the gray substance;
striking fluctuations in the course of the disease, spontaneous
improvement, and equally spontaneous growing worse again
(Schueppel) ; and finally, Schueppel has also tried to connect
the occurrence of scoliosis (curvature of the spinal column to the
side on which the tumor is situated) with the presence of a
tumor. In this he is doubtless wrong, as this manifestation
merely depends on unilateral paralysis of the muscles of the
back, which may depend on all sorts of causes. Whoever is at
all familiar with the story of chronic spinal diseases will readily
see that all these symptoms are of but very subordinate signifi-
|
|
;
3
E
:
; ,
dl
INTRAMEDULLARY TUMORS. 755
cance, and will never justify a positive conclusion as to the pres-
ence of a tumor. .
The termination of tumors of the spinal cord is doubtless in
the majority of instances fatal, with the single exception of
syphilomata, in which energetic specific treatment may bring
about a cure.
The fatal termination may be brought about in various ways.
After the disease has perhaps remained latent for a considerable
time, or has only betrayed itself by slight and insignificant mani-
festations, an acute aggravation thereof suddenly occurs, and the
disease then runs its course to death under the picture of an
acute or subacute transverse myelitis.
Or the affection progresses slowly, more and more compli-
cated and severe symptoms showing themselves gradually ; the
evidences of paralysis take an ascending course, disturbances of
respiration, paralysis of deglutition, etc., are added thereto, and
bring about the end.
Or death is induced by intercurrent diseases developed dur-
ing the progress of the spinal difficulty (typhus, variola, and the
like), to which the patient is perhaps able to offer less than the
usual amount of resistance.
The duration of the disease is not easily determined, as we
can generally arrive at no certainty with regard to the beginning
of the development of the tumor, unless very positive causes for
the same can be demonstrated. As a rule, however, but a few
years elapse from the beginning of the symptoms to the fatal
termination—sometimes but a few months.
Diagnosis.
It is evident, from what has been said above, that the diagno-
sis of an intramedullary tumor is but very rarely possible. As
a rule, one will have to be content with making out a distinctly
localized, more or less extended, chronic spinal affection, under
which one may only in exceptional cases, with a certain degree
of probability, conjecture the presence of a tumor. This prob-
ability may rest upon the etiological @onditions which may hap-
pen to be present; upon the demonstration of some previous
756 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
traumatic cause, or existing scrofula, or tuberculosis, or syphi-
lis. Among the symptoms those which perhaps deserve special
consideration are the fluctuations in the intensity of the paraly-
tic manifestations, the not complete interruption of spinal con-
duction; furthermore, it may awaken suspicion of a tumor if
the evidences of central myelitis or of hamatomyelia supervene
upon those of a long-continued, insidious spinal affection. |
If once the general presence of a tumor within the spinal
canal has become probable, it will still be difficult to distinguish
an intramedullary from a meningeal tumor. An argument in
favor of the former will be found in the slighter intensity of the
initial signs of irritation and in the frequently occurring gradual
upward advance of the disease. <A positive conclusion, however,
will but rarely be possible.
Prognosis.
The prognosis of spinal tumors—with the exception of the
syphilomata—is, of course, absolutely unfavorable. In the ma-
jority of cases, however—in view of the defective diagnosis—this
is first clearly brought to our view by the fatal termination of the
case.
Therapeutics,
Consistently with the above statements we have to admit that
our therapeutics are generally quite hopeless. It is only when
syphilis exists that we shall attain any results by energetic med-
ication directed against this disease. We know at present of no
remedy for the other neoplasms. And yet we would not for that
reason oppose any attempt that may be made with iodide of
potassium, arsenic, iodide of iron, cod-liver oil, etc.
As a rule, we shall have to confine ourselves to the treatment
directed against subacute and chronic myelitis, which has been
explicitly set forth in previous sections, until we have convinced
ourselves and the patient of the hopelessness of all further at-
tempts at a cure.
3 bg? b
SECONDARY DEGENERATIONS. TD7
19. Secondary Degenerations of the Spinal Cord.
L,. Tuerck, Ueber ein bisher unbekanntes Verhalten des R.-M. bei Hemiplegien
Zeitschr. d. Ges. d. Aerzte in Wien 1850. Heft. 1.—Z. Tuerck, Ueber secun-
diire Erkrankung einzelner Riickenmarksstriinge und ihrer Fortsetzungen zum
Gehirn. Sitzungsber, d. kais. Akadem. d. Wiss. Mathem.-naturw. Classe. Bd.
VI. S. 288-312. 1851 und Ibid. Bd. XI. 8S. 93. 1853.—Leyden, Ueber graue
Degener. des R.-M. III. Deutsch. Klin, 1863, Nr. 18.—Bouchard, Des dégén-
erations secondaires d.1. moélle épin. Arch. génér. de méd. 1866. Vol. I. pp.
272, 441, 561. Vol. IL. p. 273.—Charlt. Bastian, Case of Concussion-lesion with
Extensive Secondary Degeneration of the Spinal Cord, etc. Med. Chir. Trans.
L. pp. 499. 537. 1867.—H. O. Barth, Ueber secund. Degener. des R.-M. Arch.
d. Heilk. X. 8. 433. 1869.—Vulpian, Expériences relat. a la pathogénie des
atrophies second. d. 1. m. 6p. Arch. d. Physiol. II. p. 221. p. 661. 1869. III.
p. 521. 1870.— Westphal, Ueber ein eigenth. Verhalten secundiir. Degenerat,
des R.-M. Arch. f. Psych. u. Nervenkrankh. II. §. 374. 1870.—Ueb. kiinstl,
erzeugte secund. Degener. einzelner Riickemarksstriinge. Vireh. Arch. Bd. 48,
8. 516. 1869. und Arch. f. Psych. u. Nerv. IL 8. 415. 1870.—W. Mueller,
Beitrige zur pathol. Anat. und Physiol. des R.-M. Leipzig. 1871. Beob. 1.—@.
Lange, Forelaesninger over Rygmary. Patologi. 1. Heft. Kopenhagen. 1871.
Fall von Myelit. interstit. chronica. Hosp. Tid. 14. Aarg. 1871 (s. Virchow-
Hirsch, Jahresber. pro 1871. Bd. II. 8. 77).—C. Lange, Om lednings forhol-
dene i Rygm. Bagstriinge, etc. Nord. med. Arkiv IV. Nr. 11. 1872 (s. Vir-
chow-Hirsch, Jahresber. pro 1872. Bd. II. 8. 79).—7Z2. Simon, Tumor im Sack
der Dura spin., die Cauda equina comprimirend, mit fortgeleit. Degener. d.
Hinterstriinge u. s. w. Arch. f. Psych. u. Nerv. V. 8. 144. 1874.—Leyden,
Klinik der Riickenmarkskrankh. II. 8. 301-317. 1876.—F. Schultze, Zur Lehre
von der secund. Degener. des R.-M. Centralbl. f. d. med. Wiss. 1876. Nr. 10.
—A. Pitres, Atroph. muscul, consécut. a une sclérose descend. Progrés méd.
1876. Nr. 8.—Des dégénérat. second. d. 1. m. épin. dans les cas de lésions cor-
ticales. Gaz. méd. de Par. 1877. Nr. 3.—Charcot, Lecons sur les localisat..
dans les malad. du cerveau. 1. fasc. 1876. p. 145-168.—P. Flechsig, Die Lei-
tungsbahnen im Gehirn und R.-M. des Menschen. Leipzig, 1876. S. 230 ff.—
Ueber Systemerkrankungen im R.-M. Arch. d. Heilk. XVII. 8. 101 S. 289.
1877.—P. Schiefferdecker, Ueber Regeneration, Degenerat. u. Architectur des
R.-M. Virch. Arch. Bd. 67. 8. 542-614. 1876.
A, Vulpian, Influence de l’abolition des fonct. des nerfs sur la région d. 1. m. épin.,
qui leur donne origine, Exam. d. 1. moélle dans des cas d’amputat. d’an-
cienne date. Arch. d. Physiol. I. p. 448. 1868.—Sur les modific. qui se pro-
duis. dans 1, m. épin. sous l’influence de la section des nerfs d’un membre. Ibid.
IL. p. 675. 1869.— Dickinson, On the Changes in the Nervous System which
Follow the Amputation of Limbs. Journ. of Anat. and Physiol. Nov. 1868.—
Friedreich, Ueber progress. Muskelatrophie u. s. w. Berlin, 1878. 8. 188,—Ley-
758 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
den, 1. c, Il. §. 814. 1876.—A. Genzmer, Veriinderung im R.-M. eines Ampu-
tirten. Virch. Arch. Bd. 66. 8. 265. 1876.
G. Hayem, Des altérations d. 1. moélle, consécut. 4 Varrachement du nerf sciatique
chez le lapin. Arch. d. Physiol. V. p. 504, 1873.—Compt. rend. Vol. 78. p.
291. 1871.
History. |
We are indebted to L. Tuerck (1851 and 1853) for the discov-
ery and the most thorough examination of certain secondary
processes of degeneration which frequently occur within the spi-
nal cord. He was the first to make extensive reports with regard
to these processes, and his observations, which, in spite of the
defective methods of examination then employed, still pass mus-
ter at the present day, gave us a well-nigh exhaustive explana-
tion of the state of things, to which the most recent research
has added but little.
Some few observations belonging under this head doubtless
received passing notice even before Tuerck’s time; thus, for
instance, in the ‘‘Sepulcretum’’ of Bonetus. Cruveilhier also
found secondary atrophy extending to the pons and the pyra-
mids in diseases of the brain, though he found nothing of this in
the spinal cord itself. Rokitansky had the same experience.
Tuerck, however, was the first one who thoroughly and almost ,
definitively cleared up the question of secondary degenerations .
within the spinal cord. His statements, however, chiefly refer
to the localization and extension of the process under various ;
circumstances.
The first somewhat more accurate teachings with regard to
the histological conditions in secondary degeneration are those
of Leyden, in 1863.
After various French and other observers (Charcot, Cornil,
and others) had published single cases which belonged under this
head, Bouchard (in 1866) issued a work treating of this question
in all its phases, in the most masterly manner, wherein he not
only sets forth the pathologico-anatomical relations, but also
most specifically the pathogenesis and symptomatology of sec-
ondary degenerations,
Wi eS Se ee eee et
SECONDARY DEGENERATIONS. 759
The communications which followed, consisting chiefly of
reports of cases, developed nothing new that was of any signifi-
cance. The only thing of importance was the demonstration
furnished by Westphal—previously sought in vain by Vulpian,
but afterwards confirmed by him—that secondary degeneration
could also be experimentally produced in dogs. This is a fact
of which, alas! no one has as yet availed himself for the purpose
of submitting to an experimental test various still obscure ques-
tions connected with secondary degeneration.
Quite recently again the doctrine of secondary degenerations
has been materially advanced, and in some respects cleared up,
by two important and larger works. Flechsig, in his compre-
hensive work on the paths of conduction within the human spi-
nal cord, has also examined and tested secondary degenerations
more carefully, has compared the results of this testing with the
very noteworthy results of his investigations into the history of
development, and has found them to agree in a way that is en-
.tirely satisfactory.’ Schiefferdecker too, has, at least in one
direction, most carefully worked up a large amount of experi-
mental material (in dogs whose spinal cord von Goltz and Freus-
berg had divided at a certain point, for purposes of physiological
investigation). He has fully confirmed the former doctrines
and somewhat extended them, |
In spite of all this, many a problem still remains to be solved,
and although the examination of secondary degenerations has
already been of the greatest value in advancing our knowledge
of anatomical, physiological, and pathological problems, yet just
at this very point there is still a rich field for experimental inves-
tigations, which will undoubtedly lead to numerous and impor-
tant results.
Etiology and Pathogenesis.
Since the investigations of Tuerck, it is known that certain
diseases of foci lying owtside of the spinal cord (especially within
‘In his work, in the Archiv der Heilkunde, whigh is as yet but partly made public,
Flechsig returns, in a more detailed manner and with more positive declarations, to the
‘question of secondary degenerations.
760 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
the brain), and having a definite seat, are followed by a secondary
disease of quite definite paths of conduction, which disease is
extended for great distances into the spinal cord ; and that simi-
larly, in certain diseases within the cord, secondary disease of
quite definite paths of conduction extends upward as well as
downward, far beyond the limits of the original focus of disease.
Finally, the same thing, even though to a more limited degree,
holds true of certain diseases of the peripheral nerve-tracts.
Therefore, in diseases which are either developed in its own
substance or in some portion of the nervous system lying outside
of the same, the spinal cord, in a portion of its tracts, is seconda-
rily involved in disease, and, indeed, as has appeared on more care-
ful observation, this occurs in a perfectly regular manner and
according to certain laws. Those changes in the spinal cord
which are thus caused are designated as secondary degenera-
tions. They act quite differently, according to the seat of the
lesion which causes them. We must therefore distinguish seve- —
ral groups.
a. Secondary degeneration of the spinal cord in diseases of
the brain. This is, of course, always descending in its progress,
and is as good as exclusively confined to the so-called ‘‘ pyram-
idal tracts’’ (Flechsig); that is, on the one hand, to the motor
conduction-tracts united into a large bundle in the posterior half
of the lateral columns (‘‘ Pyramidenseitenstrangbahnen”); on
the other hand, to the uncrossed pyramidal tracts lying together,
usually in a narrow bundle at the inner surface of the anterior
columns (‘‘ Pyramiden- V orderstrangband’’—Flechsig, ‘‘ Hiilsen-
Vorderstrangband ’’—7werck).
This degeneration can be followed upward through the pyra-
mids and the pons into the crura cerebri and the fibrillations of
the inner capsule ; it extends downward, always growing nar-
rower and becoming limited to a smaller number of fibres, into
the lumbar portion of the cord, to disappear gradually in the
lower half of the same.
Descending secondary degeneration of the pyramidal tracts
occurs in all destructive diseases of the brain which involve the
direct motor paths between the pyramids and the corona radiata
(perhaps more accurately the direct motor tracts of the inner
ee
ee
see"
Pd
SECONDARY DEGENERATIONS. 761
capsule—Charcot). This degeneration is called forth by effusions
of blood, foci of softening, neoplasms, scleroses, and chronic
inflammations, which to any considerable extent involve the
pons, the peduncles, the optic thalamus and corpus striatum, the
lenticular nucleus, etc. It has also been found in chronic hydro-
cephalus (F. Schultze). An indispensable prerequisite to the
occurrence of this degeneration, however, seems to be that the
direct motor tracts which run from the pyramids to the inner
capsule* must be involved in the lesion ; affections which are
rigidly confined to the gray substance of the lenticular nucleus,
the optic thalamus or the corpus striatum, call forth no secondary
degeneration (Charcot).
It is furthermore demonstrated that lesions of any consider-
able extent in the centrum ovale, in case they are not situated
too far from the foot of the corona radiata, call forth this degener-
ation. ’
Finally, it appears, from both older and more recent observa-
tions (Tuerck, Bouchard, Charcot, Pitres, Flechsig), that this
descending degeneration also takes place in diseases of the cortex
of the brain (if they are not very superficial only); but this is
only true when such lesions are situated in the so-called ‘‘ motor
sections” of the hemispheres—in the central convolutions and
their immediate neighborhood. _Here even a comparatively small
focus of disease is sufficient to cause the degeneration, while in
the non-motor portions of the brain-cortex even larger lesions
exist without secondary degeneration.
In all these brain affections, therefore,—and they constitute
no small number of brain diseases generally,—after the lesion
has existed for some time, descending degeneration of the pyram-
idal tracts takes place, and in the spinal cord this is situated
on the opposite side from the brain-lesion in the lateral columns
1 I see by the continuation of Flechsig’s work in the Archiv der Heilkunde, which
has appeared since the completion of my manuscript, that the statements of Charcot
and Fechsig materially differ with regard to the position of the pyramidal tracts with-
in the inner capsule. Charcot places them in the anterior, /lechsig in the posterior
divisions of the inner capsule, This question, which,can doubtless be definitely settled
by further investigations, is of primary interest in connection with the pathology of
the brain, )
762 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
(therefore crossed) and on the same side with the brain- lesion in
the anterior columns. Flechsig has shown that these two tracts
are doubtless physiologically of the same significance or function,
and that the pyramidal tracts are distributed variously to the
lateral and anterior columns, so that in one case all the pyram-
idal tracts run through the crossed lateral column, in another
case a great part of the same take their way through the anterior
column of the same side. In secondary degeneration, therefore,
the circumstances of this distribution may also vary.
The case made public by F. Schultze must, thus far, be considered as standing
alone. In a sarcoma of the anterior division of the corpus callosum there was de-
scending degeneration in the external posterior columns [“ Keilstrang ”—“ Funi-
culus cuneatus” of Burdach], reaching down to the dorsal portion of the cord,
while Goll’s columns and the lateral columns were free. The microscope showed
absence of the greater part of the axis-cylinders and marked atrophy of those that
remained ; the medullary sheath was chiefly preserved, the neuroglia not increased,
no proliferation of nuclei, no granule-cells, no fatty degeneration of the vessels—
therefore a picture differing from the one usually found in secondary degeneration.
The entire condition of things in this case is unique, if not inexplicable, and it
may therefore seem doubtful whether it belongs here at all.
b. Secondary degeneration of the spinal cord in diseases of
the cord itself.—In all severe diseases of the spinal cord (trans-
verse myelitis, myelitis from compression, heematomyelia, sclero-
sis, tumors, etc.), as we have already stated in various places in
this book, if these diseases involve the entire transverse section
of the cord, or also certain definite portions of the same, second-
ary degeneration of definite divisions of the cord will take place.
If the disease involves the entire transverse diameter, or at
least the greater portion thereof, ascending as well as descending
degeneration will be found as soon as the affection has lasted a
certain length of time.
Ascending degeneration extends: a, to the posterior columns,
and especially to the inner halves of the same, which, in the up-
per division of the spinal cord, are more sharply divided from
the outer halves, and are generally known under the name of
*‘tender columns,’’ or ‘‘Goll’s columns.’’ In the immediate
neighborhood of the lesion the degeneration extends to the entire
width of the posterior columns, but it very soon becomes strictly
SECONDARY DEGENERATIONS. - 763
limited to Goll’s columns, diminishes in extent as it ascends, buf
can always be followed into the restiform bodies, where it ends.
This form of ascending degeneration is very frequent, and is
generally easy to recognize by its sharp e-meayingiegs and usually
very distinct gray discoloration.
8. Ascending degeneration, again, may occupy @ narrow zone
at the outer periphery of the posterior lateral column, which
begins with its greatest width at the point of the gray posterior
horn, and extends forward over the greater part of the periphery
of the lateral column, as a border which is all the while growing
narrower. This degenerated zone can be followed upward to the
cerebellum. It was known, although but imperfectly, to Tuerck,
was afterwards often overlooked, and has recently again been
restored to its legitimate place, and more carefully studied by
Flechsig and Schiefferdecker. The tract thus degenerated, which
closely and intimately touches the descending degenerated pyram-
idal tract of the lateral column, is designated by Flechsig as
the ‘‘direct cerebellar tract of the lateral column” (‘‘ directer
Kleinhirn-Seitenstrangband ’’).
Descending degeneration in affections of the spinal cord also
extends almost exclusively to the ‘‘pyramidal tracts,’ just in
the same manner as in diseases of the brain, that is, with variable
distribution to the tracts in the posterior lateral columns and the
tracts in the internal anterior columns, only with the non-essen-
tial difference that here the gray degenerated spot in the lateral
column usually has a somewhat larger extent. Naturally in
spinal affections the descending as well as the ascending degener-
ation is generally bilateral.
Aside from this, Schiefferdecker states that transverse section
of the anterior and lateral columns shows scattered fibres of de-
scending degeneration, but they are only to be found in the
neighborhood of the point of lesion.
In lesions which only affect a portion of the transverse section
of the cord, we shall also find only correspondingly partial second-
ary degenerations.
Thus, for example, in trawmatic unilateral lesions, the ascend-
ing as well as the descending degeneration is confined to the side
of the injury.
764 -ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
In affections that are confined to the fundamental bundles of
the posterior columns (‘‘ Keilstrange’’—‘‘ bandelettes externes ”’)
we meet only. with ascending degeneration of Goll’s columns
(perhaps also of the cerebellar tracts of the lateral columns), a
condition which probably exists with tolerable regularity in tabes
dorsalis.
In case of partial lesion of the lateral columns (a cireum-
scribed sclerosis, effusion of blood, wound, tumor, etc.), we shall
find only descending degeneration of the lateral column of ——
side.
It has not yet been determined whether certain lesions of the
gray substance can also call forth secondary degenerations, and
so far as we know the question has not yet been very closely -
investigated. ‘It would doubtless be worth the while more care-
fully to test the anatomical conditions, with reference to this
point, in amyotrophic lateral sclerosis, in the spinal paralysis of
children, in progressive muscular atrophy, etc.
c. Secondary degeneration of the spinal cord in disease of
the peripheral nerves. Such a condition is, thus far, known with
certainty to exist only in lesions of the spinal nerve-roots, and,
indeed, it would appear, only of the posterior roots. A certain
number of observations exists (Cornil, Th. Simon, C. Lange,
Leyden) in which tumors on the cauda equina compressed the
nerve-roots lying within the same without directly injuring the
spinal cord itself, and in which an exquisite ascending degenera-
tion of the posterior columns was found, extending to the entire
transverse diameter of the same in the lumbar region, and being
limited, higher up, to Goll’s columns.
Lesion of the motor roots, or lesion (section, crushing, ete.) of
the peripheral nerve-trunks is not followed by any secondary de-
generation in the cord.
After having thus enumerated the causes of secondary degen-
erations in the spinal cord, we have to add that the pathogenesis
of the same is by no means, as yet, satisfactorily cleared up.
Closer observation teaches that descending degeneration oc-
curs in.undoubtedly motor pyramidal tracts, that is, in those
leading in a centrifugal direction, only when conduction in these
tracts is interrupted at some point of their course.
SECONDARY DEGENERATIONS. 765
Furthermore, that ascending degeneration occurs when the
posterior roots—therefore, tracts leading in an undoubtedly cen-
tripetal direction—are interrupted in their conduction ; likewise,
if the posterior columns, which are probably to be regarded as in
great part leading in a centripetal direction, are injured ; and
finally, if the same thing happens to certain tracts of the lateral
columns (the direct cerebellar tracts of the lateral columns).
Whether the latter lead ina centrifugal or centripetal direction
is not yet determined ; at all events, this is not indicated with
entire certainty by the direction in which these tracts degenerate
on the interruption of conduction.
Some authors, then, explain secondary degenerations simply
as follows: that the degeneration follows in the direction in
which the conduction of physiological excitation occurs, and that
the interruption of these processes of conduction—the functional
inactivity of the nerve-tracts—is the actual cause of the degener-
ation. Therefore the motor tracts have always been found de-
generated in a centrifugal, the sensitive always in a centripetal
direction.
If this were true, then, when a peripheral nerve was cut
through, the sensitive fibres ought to degenerate only in a cen-
tripetal direction, that is, in the central piece, the motor fibres
only in a centrifugal direction, that is, in the peripheral piece.
But this is notoriously not the case, both kinds of fibres degen-
erating in a centrifugal direction and only in the peripheral
division of the nerve.
If this were true, then in every descending secondary degen-
eration of the pyramidal tracts, in consequence of lesion of the
brain or cord, the anterior roots and the motor peripheral nerves
would have to degenerate, for these, too, are entirely disturbed
in their function. The contrary, however, is true; the anterior
roots and the peripheral motor tracts remain intact in the vast
majority of cases (if no special complications exist).
The view, therefore, that the degeneration is due to the funce-
tional inactivity cannot be looked upon as sufficiently well found-
ed, as has, indeed, been satisfactorily proven by Bouchard.
In my opinion, the only conclusion which can thus far be
drawn is, that secondary degeneration occurs as soon as certain
"66 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
definite conduction tracts are separated from their trophic cen-
tres, their centres of nutrition (Bouchard, C. Lange, and others)
Where these centres (centres of development? Flechsig) lie,
and how they are related to the different tracts, is, to be sure, as
yet tolerably unknown. There are only some points in regard
to which we can thus far draw conclusions with more or less prob-
ability of being right ; thus, for instance, that the trophic centres
for the sensitive tracts ascending with the posterior roots (there-
fore, probably, also for the greater part of the tracts subject to
ascending degeneration) are probably situated in the spinal
ganglia; that the trophic centres for the anterior roots and the
motor nerves are certainly to be sought in the gray anterior horns,
But it is as yet entirely unknown where the trophic centres for
the pyramidal tracts lie; they may, perhaps, be situated in the
gray cortex of the brain, in which, according to recent investiga-
tions, large, multipolar ganglion-cells have also been found, such
as exist in the gray anterior horns of the cord. The trophic cen-
tres for the direct cerebellar tracts of the lateral columns are ala@
as yet entirely unknown.
Consequently quite an array of important problems sfill re-
mains to be solved. And however great the advantages which
have already accrued to our knowledge of the anatomical struc-
ture and physiological functions of the spinal cord, through the
study of secondary degenerations, it is equally to be desired that
still further and particularly experimental investigations on this
highly important question should be undertaken. |
Those changes in the spinal cord which have been seen to arise after amputations
and the resection of nerves only stand in a very distant relation to actual secondary
degenerations. After amputation, a non-symmetrical condition of the spinal cord
has been found, with narrowing of the entire half of the cord on the side of the
amputation, sometimes mostly affecting the anterior, and sometimes the posterior
column, and generally also involving the gray substance. Some observers report
slight histological changes, diminution in size of the ganglion-cells and nerve-fibres,
very slight increase of connective tissue, possibly some diminution in the number of
the ganglion-cells; but in the majority of instances the histological condition of the
spinal cord was quite normal. The asymmetry was generally more marked in pro-
portion to the youth of the individual at the time of the operation, and the length
of time that had elapsed since the operation. No doubt here it is a question in part
of an arrest of development through the early disuse of the part; probably partly,
eS SS ee meee rh rl —
SECONDARY DEGENERATIONS. 767
also, of simple atrophy from the same cause; and, least of all, also, of the results of
a chronic irritative process travelling along the nerves from the point of amputation
upward into the spinal cord. All this requires still further investigation. Thus
much, however, appears to be certain already, that these changes in the cord arising
after amputations, etc., have nothing to do with the secondary degenerations we are
here considering; also that they are of very little practical significance.
-An entirely different matter is the condition of things which Hayem found in
the spinal cord of squirrels after tearing out the sciatic nerve. Here it is a question
of a direct wounding of the spinal cord, and of a traumatic myelitis arising thence,
the more careful study of which promises to be of great importance to the doctrine
of acute central myelitis. Exceptionally such a central, ascending myelitis (which
leads to progressive atrophy of the muscles) also arises after simple resection of the
trunk of the sciatic nerve in the squirrel.
Pathological Anatomy.
The macroscopic appearance of secondarily degenerated por-
tions is, in general, that of gray degeneration, more or less dis-
tinct and pronounced ; gray or grayish-yellow discoloration some-
times disseminated with fine, whitish lines (vessels with an abun-
dance of granule-cells). In more recent cases, a brilliant, pure,
milk-white color is also to be recognized (C. Lange), Not seldom,
however, in the fresh preparation, nothing at all, or nothing very
definite, can be seen with the naked eye; and thus, in a fresh
specimen of the cord, no correct idea can be obtained of the
existence and extent of the secondary degeneration. This is
generally brought out with great distinctness by the familiar
coloration of the specimen with chromic acid (a bright yellow
appearance), and can then be very well recognized ; but a truly
accurate conclusion, especially with reference to the extent of the
degeneration, can, after all, only be reached by microscopic
examination.
After the affection has lasted a considerable time, there is
generally no trouble in recognizing distinct atrophy and. shrivel-
ling of the degenerated columns; the form of a transverse section
of the cord may appear somewhat altered thereby, the gray horns
being somewhat displaced in one direction or another. In one-
sided degeneration, particularly, the asymmetry of the two halves
of the spinal cord, on transverse section, thus stands out dis-
tinctly.
768 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
The microscopic conditions have not yet been developed
with the completeness which we might wish, in all the different
stages of the degenerative process, so that a complete account
of the histological processes in the same cannot, as yet, be
given with certainty. The statements and views of different
investigators, with regard to the method and the essential
character of the process, also differ as yet in a manner that is
not pleasing.
In considering them, we must separate the earlier stages
(which are far from being satisfactorily investigated as yet) from
the later stages (which come under observation by far the most
frequently).
In the earlier stages of the process we meet principally and
almost exclusively with alterations in the nerve-fibres. Their
medullary sheaths are found strikingly altered in their reaction
with carmine and osmic acid; they break down and become
fissured, suffer fatty degeneration, and finally disappear alto-
gether. For some time the axis-cylinders alone remain (or per-
haps also the horny sheaths recently discovered by Kuehne and
Ewald). Along with these processes of degeneration an exceed-
ingly abundant development of granule-cells also sets in, which
gives a characteristic appearance to the-microscopic picture, and
which formerly served exclusively for the recognition of second-
ary degeneration. During all this the connective tisswe is not
materially increased ; this does not occur until much later. On
the walls of the vessels an abundant deposition of fat-granules
and fatty degeneration may be recognized. Aside from this,
there is always a not inconsiderable number of well-preserved
and apparently normal nerve-fibres to be observed.
In the later stages the degenerated tissue appears shrunken,
as a whole; most of the nerve-fibres have entirely disappeared,
or their remnants alone can still be demonstrated as narrow,
rigid fibres (axis-cylinders? horny sheaths?). The ¢issue of |
the neuroglia is materially increased, and is changed into a
dense, finely fibrillar tissue, which contains numerous nuclei and
spider-like cells. The granule-cells have become more scanty,
or have entirely disappeared; not rarely numerous corpora amy-
lacea can be seen. In this entirely degenerated tissue, likewise,
il
SECONDARY. DEGENERATIONS. 769
single, more or less numerous, well-preserved nerve-fibres are
still to be seen.
It is evident, then, that these later stages of the process are
in no way to be distinguished from ordinary gray degeneration
(in tabes, multiple sclerosis, chronic myelitis) ; the histological °
picture is almost exactly the same. Whether this is also the
case in the earlier and earliest stages, we must leave undeci-
ded, as no investigations especially directed to this point exist ;
indeed, the two processes (Secondary degeneration and primary
sclerosis) have certainly often been confounded with one another.
We should think that quite considerable differences would cer-
tainly appear, and we consider it as one of the most important
tasks devolving upon the students. of the pathological anatomy
of the spinal cord, finally to clear up these fundamental ques-
tions.
Not until this is done shall we be able to give a decided
opinion as to the method and the essence of this degenerative
process, with regard to which the views of different authors at
present materially differ. By some the entire process is regarded
as an irritative or inflammatory one, which propagates itself
directly from the point of lesion by definite tracts, or which is
developed in these very tracts by the breaking down of the
nerve-fibres. Almost all the facts in the case argue against the
theory of an inflammatory process propagated directly from the
point of lesion; and if the more recent statements of careful
observers are correct, that the first changes are to be recognized
exclusively in the nerve-fibres, and that alterations in the con-
nective tissue do not occur until many weeks later, then it will
be impossible to sustain this view. After comparing all the
statements now before us, it appears to us most probable that we
have here to deal with a process entirely analogous to those
changes which arise in peripheral nerves after they have been
divided ; that secondary degeneration, therefore, is nothing else
than the degenerative (neurotic) atrophy of certain definite tracts
of the spinal cord separated from their nutritive centres. We
shall have to leave it undecided for the present, whether the pro-
liferation of connective tissue which arises later is called forth
by the irritation caused by the products of degeneration of the
VOL. X1II.—49 ”
770 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
nerve-fibres, or whether it constitutes an essential part of that
degenerative atrophy.
Statements differ materially with regard to the period with
which secondary degeneration is developed after the occurrence
of a lesion which causes it. Tuerck’s opinion, that about half a
year is required for this purpose, is evidently incorrect ; all more
recent observations have approximated the end of the period
much nearer to the occurrence of the causative lesion, and in
cases falling under this head we may be sure of finding the
degeneration distinctly developed and easily recognizable after
four, six, or eight weeks. Schiefferdecker, in his experiments
on dogs, found the beginning of the degeneration at the end of
fourteen days. At the end of four to five weeks the well-marked
picture of the same was completed, and it was not until the
eighth week that he saw changes arise in the connective tissue. —
The peculiar form of degeneration in ring-shaped figures, which Westphal
described, and which was caused by a massive, peculiarly localized accumulation
of granule-cells, has not been seen by others, and its significance is as yet entirely
unknown. C. Lange thinks it was not a case of secondary degeneration, but a
peculiar form of myelitic alteration; perhaps it belongs under the head of what
Schiefferdecker calls ‘‘ traumatic degeneration.”
The distribution, as to space, of secondary degeneration in —
the spinal cord is, in almost all cases, strictly according to rule,
and extremely characteristic.
Descending degeneration spreads first, in all cases, to the pos- ~
terior half of the lateral columns—not entirely, but in greater
part filling out the space between the periphery, the posterior
gray horn, and the region near the point of attachment of the
ligamentum denticulatum. On making various transverse sec-
tions, the transverse picture of the degeneration produced is
somewhat varied (see Fig. 18).
In the secondary degeneration which follows diseases of the
brain, the degenerated portion, at least in the upper half of the
spinal cord, does not reach the periphery of the lateral column,
but remains separated from the pia mater by a narrow margin of
sound tissue, and is generally also somewhat separated in the
same way from the limits of the posterior gray horn. Further
downward, on the other hand, this healthy peripheral margin
a
SECONDARY DEGENERATIONS,
disappears, and the degeneration, although, as
a whole, it has grown smaller, reaches entirely
to the pia mater in the lower dorsal and lum-
bar portions of the cord.
The secondary degeneration in such cases
can generally be first demonstrated in the me-
dullary substance of the crus cerebri; then in
the pyramid of the same side, to be followed
through the crossing of the pyramids into the
lateral column of the opposite side ; the greater
part of the degenerated fibres takes this course,
while a smaller part often remains on the side
of the lesion, to.continue its course downward
in the pyramidal tract of the anterior column
of the same side.
The degeneration of the lateral column is
most extensive in the cervical portion, and here
has more of a triangular form, with the apex
directed inward (Fig. 18, 1 to 3); in the dorsal
portion it becomes gradually narrow and as-
sumes more of a roundish form (Fig. 18, 4 and
5); in the lumbar portion it moves more to-
wards the periphery, again assumes more of a
triangular form, grows narrower and narrower,
finally to disappear entirely at the height of
the origin of the third or fourth sacral nerve
(Fig. 18, 6 to 8).
Aside from this, in descending degeneration,
the inner surface of the anterior column (pyram-
idal tract of the anterior column) on the same
side with the cerebral lesion is usually found
degenerated to a greater or less extent. It
constitutes a narrow zone, which generally
does not extend as far down the cord as the
degeneration of the lateral column, but disap-
pears entirely (Fig. 18, 1to6). The occurrence
of this degeneration depends on the distribu-
tion of the pyramidal tracts in the transverse
x
SSSeeVse
Fic. 18.--Secondary de-
scending degeneration of the
pyramidal tracts in primary
lesion of the lefé half of the
cerebrum. The pyramidal
tracts of the lateral columns
of the right side of the cord
are degenerated down to the
lowest portion of the lumbar
division (1 to 8); the pyram-
idal tracts of the anterior
columns of the deft side are
degenerated as far down as
the beginning of the lumbar
enlargement (1 to 6).
772 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
GY
Fic. 19.—Myelitis trans-
versa dorsalis, with second-
ary ascending and descend-
ing degenerations (half sche-
matic). Seat of the lesion
at the height of section 5.
Above this (1 to 4), second-
ary ascending degeneration
in Goll’s columns and the di-
rect cerebellar tracts of the
lateral columns. Below the
lesion (6 to 8), secondary de-
scending degeneration in the
pyramidal tracts of the late-
ral and anterior columns,
diameter of the spinal cord, as has been more
carefully investigated by Flechsig; only the
pyramidal tracts degenerate. Accordingly, in
one-third of all the cases the lateral column
alone is found degenerated ; in the remaining
two-thirds the degeneration also involves the
anterior column of the opposite side. Thus
far no instance has been found of degeneration
of the pyramidal tract of the anterior column
alone.
In diseases of the spinal cord the relations
of descending degeneration are precisely the
same. Only the transition into the original
focus of disease is usually very gradual, so
that the secondary degeneration is only sepa-
rable, little by little, from the more diffuse le-
sion of the spinal cord. Here the degeneration
everywhere reaches the surface of the cord
and can generally be recognized glimmering
through the pia mater (Charcot, C. Lange).
The distribution to the lateral and anterior
columns is the same as in diseases of the brain
(Fig. 19, 6 to 8). Naturally, in affections of
the spinal cord the degeneration is generally
bilateral ; still it may also be the same in bilat-
eral brain affections.
Ascending degeneration of the posterior
columns involves that portion of the posterior
columns lying next to the posterior fissure,
usually having a very sharp outline (Fig. 19,
1 to 4). In the upper portions of the cord it is
strictly confined to the columns of Goll, its
apex usually not quite reaching the posterior
commissure. In the neighborhood of the orig-
inal focus of disease the degeneration spreads
over the entire transverse diameter of the pos-
terior columns, thus gradually to pass over
into the diffuse lesion,
4
SECONDARY DEGENERATIONS. — 773
yo
Above, the ascending degeneration extends into the medulla
oblongata and ends here with the ‘*‘ Funiculi graciles”’ (of Bur-
dach—‘‘ zarten Striinge’’ of Erb), in the region of the nuclei of
the same.
In tumors of the cauda equina with secondary degeneration,
the posterior columns are degenerated to their entire width, in
the lower division of the spinal cord ; the degenerated zone grows
gradually narrower and is finally strictly limited to the columns
of Goll (Th. Simon, C. Lange). This diminution, according to
Schiefferdecker, does not occur progressively and uniformly, but
by steps.
Ascending degeneration in the lateral columns is liable to
occupy but a very insignificant amount of space. It appears in
the form of a narrow peripheral zone, not sharply defined towards
the inside, which begins at the hindmost end of the lateral col-
umn and extends around the periphery of the same to a greater
or less distance forward—often to the neighborhood of the ante-
rior columns (Fig. 19, 1 to 4). Below, this degenerated zone
arises gradually from the more diffuse lesion of the spinal cord ;
farther up it can always be traced on the outermost periphery of
the cord in the restiform bodies and until the entrance of the
same into the cerebellum. Schiefferdecker states that this sec-
ondary degeneration also diminishes by steps.
Secondary degenerations, in the vast majority of cases—in
fact we may say regularly—confine themselves to the white col-
umns of the cord. The gray matter generally remains entirely
intact (Tuerck, Bouchard), and but very exceptionally takes part
in the process. Nevertheless, in descending degeneration of the
lateral columns a spread of the (irritative ?) process to the gray
anterior horns has repeatedly been observed (Charcot, Pierres,
Pitres), resulting in degeneration of the large ganglion-cells and
muscular atrophy. ‘This has thus far been observed principally
in the cervical enlargement, but belongs, as above stated, to the
rare exceptions. 3
"74 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
.
Symptomatology.
Ascending secondary degeneration (in the posterior columns
and in the cerebellar tracts of the lateral columns), so far as we
are at present informed, appears to occasion no sort of clinical
manifestations; that is, it adds no new disturbances to those
caused by the fundamental malady. At the same time the ques-
tion might be raised, whether the manifestations of sensory irri-
tation in the paralyzed side of the body (paresthesia, formica-
tion, pain, a sensation of burning, of heat and cold, etc.), which
arise so often in the myelitis of compression and similar condi-
tions, may not be connected with ascending degeneration of the
posterior columns, and originate and be maintained thereby.
This does not appear to us so entirely improbable, although it
might, indeed, be hard to prove.
However positively, therefore, we may expect the occurrence
of secondary ascending degeneration in certain affections of the
spinal cord when their diagnosis is once fairly established, and
however regularly we also find evidence thereof on the dead
body, yet this certainty is by no means founded upon any defi-
nite clinical symptoms; it rests, the rather, upon constant patho-
logico-anatomical experience.
It is somewhat different with the descending degeneration of
the pyramidal tracts. Of course this can produce no change in
the phenomena of paralysis caused by the original malady. But
since the work of Bouchard it has become toa high degree proba-
ble that the slowly developed contracture of hemiplegic subjects
(the “contracture tardive’’ of the French), which becomes asso-
ciated with the paralysis at a later period, stands in connection
with the secondary degeneration of the pyramidal tracts, and is
the result of the same. Bouchard is of the opinion that it is not
so much the degeneration of the tracts directly affected by the
paralysis which causes the contracture, as the irritation of other
nerve-fibres, of different origin, running in the same region of the
cord, which irritation is caused by a sclerosis arising in conse-
quence of the degeneration. This will, at all events, be a hard
matter to prove; and, indeed, it is not easy, as yet, to form
-
SECONDARY DEGENERATIONS. 775
any satisfactory idea of the mechanism of the origin of contrac-
tures.
An argument in favor of this view is, nevertheless, found in
the fact that the secondary contractures in hemiplegia are liable
to occur about the same time at which one may expect the occur-
rence of secondary degeneration—that is, one or two months
after the first appearance of paralysis. Furthermore, that in
the spinal affections, likewise, which lead to secondary degen-
eration of the pyramidal tracts, muscular tension and contrac-
tures in the lower extremities are developed after a short time
—about simultaneously with the appearance of these degen-
erations. Furthermore, that in amyotrophic lateral sclerosis
contractures are regularly to be found along with the sclerosis of
the pyramidal tracts, just as muscular tension and contractures
belong to the most constant symptoms of supposed primary
lateral sclerosis.
It cannot be denied that these proofs are by no means conclu-
sive, and that, thus far, there is merely a probability—to be sure,
a pretty great one—in favor of the dependence of secondary con-
tractures upon secondary degeneration of the pyramidal tracts.
It will require further and varied material for observation in
order to raise this probability to a certainty.
Matters are still more uncertain with regard to another symp-
tom which is likewise almost- constant in all cases in which
secondary degeneration of the pyramidal tracts exists, viz., in-
crease of the reflex excitability of the tendons. There can
scarcely be a doubt that this stands in connection with disease
of the spinal lateral columns, but it is not certain whether it is
the result of interruption in the conduction of certain tracts in
the lateral columns (limiting reflex action ?), or of the subse-
quently developed secondary degeneration of the same ; in other
words, whether it is a symptom co-ordinate with the paralysis
or with the secondary contractures. This question could only
be determined by careful clinical observations on the point of
whether the elevation of reflex excitability of the muscles oc-
curred simultaneously with the paralysis, or simultaneously with
the contracture, or earlier or later than either ; whether it always
occurs in connection with secondary ‘contractures, or may also
176 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
arise without them, etc. On account of the short time that has
elapsed since the discovery of the reflex excitability of tendons,
such observations do not exist in sufficient numbers. I only find
some statements in Westphal,’ that after apoplexies and the like
the elevation of reflex excitability of the tendons is present in
from seven to twenty-one days after the attack, and in some
cases was not present during the first four days. But we can-
not form much of a conclusion from this, as the statements with
regard to the time of occurrence of secondary degeneration are
as yet very uncertain. It appears to me, for the present, the
more probable that the elevation in reflex excitability of the
tendons is the result of interrupted conduction in tracts control-
ling reflex action, and is not the result of secondary degeneration
of the pyramidal tracts. At all events, this question demands
further investigation.
It is at least not likely that the epileptic and epileptiform
attacks, which are so frequent in hemiplegic patients, have any
relation whatever with secondary degeneration of the pyramidal
tracts (especially in the medulla oblongata), as was supposed by
Bouchard.
Diagnosis.
From all that has hitherto been said, it is evident upon how
unsafe a footing the clinical diagnosis of secondary degenerations
as yet stands.
Secondary ascending degeneration is simply not to be recog-
nized by any clinical manifestations; but, in case of the well-
established diagnosis of a definitely localized affection of the
spinal cord (myelitis from compression, trauma, etc.), it is merely
to be expected, with some certainty, as a necessary result of the
same.
In secondary descending degeneration the only sign which
points towards it with some probability is the occurrence of late
contractures (and of increased reflex excitability of tendons).
When, therefore, in the course of a hemiplegia or paraplegia,
’ Arch, f. Psych. u. Nervenkrankh, V. p. 810.
~
SECONDARY DEGENERATIONS. 177
muscular tensions and contractures set in after some weeks, we
may infer, with great probability, the existence of descending
degeneration of the pyramidal tracts.
If this should be confirmed in the future, then the demonstra-
tion of the presence or absence of this secondary degeneration
will perhaps admit of our arriving at a conclusion with regard to
the localization of the fundamental cerebral affection. For, as
we have before remarked, this degeneration does not by any
means occur in all, but only in very definitely localized affections
of the motor portions of the brain (Charcot). This is a question
that will have to be decided by cerebral pathology.
Prognosis.
The more exact history of the course of secondary degenera-
tions, under various possible circumstances, is a matter yet to be
investigated.
In general, the prognosis is the same as that of the funda-
mental affection, and we have every reason to believe that, with
the cure of the fundamental affection, the secondary degenera-
tions may also tend towards resolution and recovery. But this is
not so very certain under all circumstances, and although a com-
plete regeneration of the degenerated nerve-tracts appears possi-
ble in the earlier stages of the process (similar to what occurs in
the degenerative atrophy of peripheral nerves), yet this is, to say
the least, improbable in the later stages of the affection, and the
prognosis of secondary degenerations, after they have existed for
a long time, is, therefore, to be regarded as decidedly unfavor-
able.
Naturally, under some circumstances, the prognosis of the
fundamental malady is seriously vitiated by this means, and
Charcot unhesitatingly regards descending degeneration of the
pyramidal tracts as one of the main causes of the persistence of
motor paresis in hemiplegia, even when the fundamental affec-
tion runs a favorable course. There is furthermore no doubt
that secondary contractures often cause much greater interfe-
rence with the use of the extremities than would result from the
degree of paresis or paralysis actually present. And if these
778 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
contractures should be the results of the secondary degenera-
tions, then Bouchard’s statement might here be of interest, that
he had never seen hemiplegia end in recovery when the develop-
ment of secondary contractures had taken place.
All this will therefore have to be taken into consideration in
forming the prognosis of the’ cerebral or spinal fundamental
affection.
Therapeutics.
There has thus far not been much talk of any special thera-
peutics of secondary degenerations ; indeed, this could not well
be the case, in view of the difficulties which stood in the way of
the diagnosis of these alterations.
The essential point, of course, is the treatment of the funda-
mental affection, with regard to which we need not here expati-
ate.
But after what has been said above, the question may well be
raised whether a further and not inconsiderable improvement
might not be attained through direct treatment of the secondary
degenerations at a certain stage of the fundamental malady ;
whether, after the causative cerebral malady had, to a great
degree, undergone resolution, and after cerebral conduction had
again been restored by direct or by vicarious tracts, the paresis
and contractures which still remained might not be removed by
the removal of the secondary degeneration.
This question may doubtless be answered, with probability,
in the affirmative; and it therefore appears to be indicated,
when the fundamental disease has improved and is in the act
of retrograde development, to institute direct treatment of the
secondary degenerations.
The ways and means to this end are, it is true, yet to be
found. A priori, one will feel inclined to resort to the employ-
ment of the therapeutic measures commonly used in chronic mye-
litis and in sclerosis in general (baths, cold-water cures, galvanism,
etc.). The galvanic current is doubtless entitled to the most
confidence, and admits of the most practical and safest method
of application. It is not necessary to say anything further here
DEFORMITIES AND MALFORMATIONS. 779
with regard to the methods of its application in these degenera-
tions of the cord. I will merely add that in some old cases
of hemiplegia with contractures I believe I have seen decidedly
favorable effects on paresis and contractures follow direct gal-
vanic treatment to the spinal cord, instituted in addition to the
other galvanic treatment. In such cases, however, it is naturally
very difficult to be sure about our therapeutic experiences.
20. Deformities and Malformations of the Spinal Cord.
Ollivier, 1. c. 3. 6d. I. p. 159-240. 1837.—Cruveilhier, Anatom. patholog. Livrais.
XVI. —Virchow, Die krankhaften Geschwiilste. I. S. 169. 1863.— Foerster,
Handb. d. path. Anat. 2. Aufl. IL §. 621. 1863.—P. Schiefferdecker, Asymme-
trie d. grauen Subst. des R.-M. Arch. f. mikrosk, Anat. XII. 8. 87. 1876.
Bardeleben, Lehrb. d. Chirurg. u. Operationslehre. Bd. IV.—JLorinser, Spina bifida
in Pitha-Billroth, Chirurgie. Bd. III. 2. 8. 5.—Smith, An Unusual Form of
Spina Bifida. Transact. of the Pathol. Soc. XXI. p. 1. 1871.—J. Roose, A Case
of Spina Bifida. Philad. Med. Surg. Report. 1872. March 30.—A. Petit, Ana-
lyse d’un liquide de spina bifida. Bull. génér. de thérap. 1873. p. 256.—Th.
Simon, Ueber Syringomyelie und Geschwulstbildung im R.-M. Arch. f. Psych.
u. Nervenkrankh. V. 8. 121. 1874.—Zeyden, Klin. d. Riickenmarkskrankh. L
§. 195. 1874; Hydromyelus u. Syringomyelie. Virch. Arch. Bd. 68. S. 1. 1876.
We have but little to say in this section that is of interest to
the practical physician and really necessary for him to know.
First in order comes quite a series of things which are of in-
terest only in a pathologico-anatomical point of view and in con-
nection with the history of development; and which, to the
practical physician who is primarily concerned with living human-
ity, will prove all the less interesting because they occur only in
the still-born foetus, or at least in one incapable of sustaining life.
On the other hand, there are certain anomalies in the configu-
ration and position of individual divisions of the spinal cord
which one must know in order to avoid the possibility of con-
founding them with pathological changes. This also is a matter
which more particularly interests the pathological anatomist or
the special investigator of the pathology of the spinal cord. The
practical physician will but seldom obtain a sight of these things,
which do not betray themselves by anysymptoms during life.
780 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
Finally, we have to deal with conditions which are congenital,
are carried into later life, and are perhaps still further developed
at a later period—conditions of extension and widening of the
cavities lying within the spinal column itself or surrounding the
same, with more or less considerable accumulations of fluid ,
within the same and corresponding degrees of secondary changes
— displacements, adhesions, the development of clefts of the
cord itself, or of the parts surrounding it (hydromyelus, hydror-
rhachis, and spina bifida). These things, being, in part at least,
forms of disease susceptible of clinical diagnosis and therapeutic
interference, must be taken up and discussed. But, in view of
the pre-eminently surgical interest which attaches to the most
important of these anomalies—spina bifida—we may be tolerably
brief in its discussion.
Among the first group of anomalies, as mentioned above, are
the following :
1. Amyelia, or absence of the spinal cord. This is a com-
paratively rare malformation. Ollivier counts up a series of
older observations of the same. If the spinal cord is missing,
then the brain is always missing too (amyelencephalia). Entire
absence of the spinal cord, when the brain is present, does not
seem to occur. The peripheral nerves may be entirely preserved,
the nerve-roots partly so; remnants of the spinal membranes
may also sometimes be found in connection with rudimentary
development of vertebree. It is not necessary here to enter upon
any more minute description.
It is also stated that during the latter months of pregnancy
the greater part of the spinal cord may be destroyed by hydro-
myelus—the brain, as wellas the peripheral nervous system, being
maintained intact. This, too, is of no practical significance. All
such products of generation are incapable of life.
2. Atelomyelia, or imperfect development of' the spinal cord.
The upper end of the spinal cord is lacking, or is imperfectly
developed, in all cases in which the brain is lacking (anence-
phalia), or in which the greater part of the head is defective
(acephalia). The medulla oblongata is then lacking, or exists
only ina rudimentary form, sometimes still in conection with a
part of the nerves usually given off from it. Farther down, the
“ye
DEFORMITIES AND MALFORMATIONS, 781
development of the spinal cord may then be quite regular.
Sometimes, however—in acephalia—a larger piece of the upper
division of the cord is entirely wanting ; in that case there is also
usually spina bifida of the cervical vertebral column.
In rare instances the lower part of the spinal cord is also
found stunted, ending in a club-shaped extremity ; this is gener-
ally accompanied by still further anomalies of the organs of the
trunk,
The interference with development may also show itself in the
fact that the two lateral halves in which the spinal cord is de-
veloped do not unite, but either remain entirely separated, or
unite only throughout a portion of their extent; so that the
spinal cord, either for its entire length or merely at its upper or
lower end, appears separated into two lateral halves—diastemato-
myelia. This malformation generally occurs with anencephalia,
and is, of course, of no practical significance.
3. Diplomyelia, or duplication of the spinal cord.
Double monstrosities of various kinds and of various grades
also show these malformations of the spinal cord, corresponding
to the rest of their bodily development ; so that either the upper
part of the spinal cord is single and is divided into two cords
below, the vertebral column and the entire lower half of the body
also being double, or the lower part of the cord is single and
terminates in a double cord above.
We are not yet in possession of more accurate information
with regard to the method of duplication or the connection of
the parts at the point of bifurcation, which would certainly
afford very interesting pictures on transverse section.
In such cases the form of the spinal cord probably has but
little influence on the entire development and life-history of these
monsters.
Turning to our second group, we may first mention those
slight anomalies in the length and thickness of the cord which
are now and then met with. In some.men the spinal cord is
found strikingly thick and voluminous, in others strikingly thin
782 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
and insignificant, without either the one class or the other hay-
ing presented any spinal symptoms during life. If, at the same
time, microscopic examination demonstrates no alteration in the
structure of the spinal cord, then we are evidently dealing with
irrelevant, individual anomalies.
This is regularly the case with abnormal length (the cord has
been seen to descend to the third lumbar vertebra) or abnormal
shortness of the cord (sometimes it ends at the eleventh or twelfth
dorsal vertebra), if there are no other special malformations or
diseases present.
Abnormal smaliness of the entire spinal cord and medulla
oblongata, with corresponding smallness of the nerve-cells and
fineness of the nerve-fibres and axis-cylinders, has lately been
demonstrated by F. Schultze,’ in one of Friedreich’s cases of
‘“‘hereditary ataxy,’’ and he propounds the interesting query,
whether this faulty development of the entire organ is not the
predisposing cause of the sclerosis of the spinal cord developed
at the time of puberty. This question would be well worth test-
ing in future cases. : ae
Those alterations which sometimes show themselves in the
configuration of the spinal cord, and which must not be con-
founded with pathological changes, with actual diseases, are
more noticeable.
This is especially true of asymmetry of the gray substance ;
unequal width, depth and form of the symmetrical gray horns,
on a transverse section. Starting with the supposition that the
symmetry of these parts was very complete, some observers have
often declared deviations from the same to be pathological ; but
this is not permissible, unless accurate histological examination
demonstrates actual pathological changes which account for such
asymmetry (atrophy, sclerosis, the loss of ganglion-cells, etc.).
Schiefferdecker has demonstrated that such asymmetry is not
rare, occurring even to a very considerable degree, and may be
confined to single divisions of the spinal cord; the same thing
was stated long ago by other observers, and every one who occu-
' Friedreich, Ueber Ataxie mit besonderer Beriicksichtigung, u. s. w. Nachtrag.
Virchow’s Archiv. Vol. 70. p. 140. 1877.
OL
ON Se eee
DEFORMITIES AND MALFORMATIONS, 783
pies himself with the histology of the spinal cord will often meet
with this fact.
_ The non-uniform distribution of the pyramidal tracts upon
the two sides of the spinal cord, as demonstrated by Flechsig,’
whereby each pyramid may send its mass of fibres into the spinal
cord either entirely crossed or only partly crossed, sometimes
leads to very pronounced asymmetry, which here affects the
white substance exclusively, and, indeed, the antero-lateral col-
umns. |
In cases of congenital absence or intra-uterine stunting of cer-
tain extremities, we not rarely see secondary atrophy of definite
portions of the spinal cord, and thereby the production of asym-
metry which is limited to the cervical or lumbar enlargement,
according to the extremity that is affected. Thus Troisier,’ for
example, found a unilateral diminution in size of the spinal cord
especially affecting the gray matter, running through the entire
extent of the cervical enlargement, in a case of congenital stunt-
ing of the corresponding upper extremity (hemimyelia). In this
case, without any further demonstrable changes, the only thing
that could be shown was a diminution in the number of the
ganglion-cells.
- Unusual outgrowths of the gray matter, or the absence of
portions of the same, which are generally present (for instance,
the tractus intermedio-lateralis of Clark’s columns), are condi-
tions occasionally met with; likewise, in some cases, duplications
of the one or the other gray horn, for a longer or shorter distance.
These are matters the true value of which we can generally arrive
at, without much difficulty, on careful investigation.
In the third group we turn our attention first to congenital
enlargement of the central canal in the spinal cord, what is
generally called hydrorrhachis interna, also hydromyelus (or
better, hydromyelus congenitus).
' Die Leitungsbahnen im Gehirn und Riickenmark des Menschen. Leipzig, 1876.—
Ueber Systemerkrankungen im Riickenmark. Archiv der Heilkunde. XVIII. 1877.
* Arch, de Physiologie. IV. p. 72. 1871-72.
ee es
"84 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
This anomaly is not so very rare; but by no means all those
cases in which this condition has been thought to exist have
been actual congenital malformations; they have oftener repre-
sented changes acquired at a later period, as the result of disease; _
and more frequently yet these have not been cases of dilatation
of the central canal itself at all, but of newly-formed pathologi-
cal cavities—cavities which have only been confounded with true
hydromyelus on account of their central position in the spinal
cord, and which would be better designated ‘‘syringomyelia.”’
This subject will be touched on again at greater length, in the
following section (No. 21).
The malformation which concerns us here depends on an
accumulation of fluid in the fetal central canal. This may
reach very varied grades.
In the lighter grades we recognize the formation of a central
cavity in the spinal cord, more or less extensive in length, and
varying in width from that of a knitting-needle to that of a crow’s
quill. This may extend throughout a greater or less portion of the
cord, sometimes running through the entire length of the same,
at other times restricted to certain portions thereof (the cervical
or lumbar portion) ; sometimes the dilatation assumes the form
of a string of beads (moniliform), dilated portions ‘alternating
with those of normal width ; sometimes, too, the canal is obliter-
ated in the centre, its anterior and posterior walls having grown
together, leaving both sides open, so as to produce the appearance
of a double canal, etc.
In such cases, as a rule, the dilated central canal can be rec-
ognized as such, with certainty, by the position of the cavity
relative to the other portions of a transverse section of the cord
(relative to the anterior and posterior commissure, to the central
veins, the gray matter, etc.), by the lack of any trace of another
structure which might be the central canal, by the fact of its
being lined with cylindrical epithelium, etc. The spinal cord
itself is otherwise well developed, and appears to be without
any other pathological changes, aside from the displacement
which its other portions may have been subjected to through the
great dilatation of the canal.
This is also a positive test for the Separation of congenital
-
DEFORMITIES AND MALFORMATIONS. 785
dilatations of the central canal from those caused by pathologi-
cal processes. The latter are not rare, for instance, in periepen-
dymal myelitis, in transverse myelitis, in neoplasms of the spinal
cord, and we shall recur to them again later.
Simple congenital hydromyelus appears to produce no symp-
toms whatever ; much of the observations under this head have
been made accidentally, in persons who had complained of no
spinal symptoms during life; and where such symptoms have
existed and ‘‘hydromyelus’’ has been found on post-mortem ex-
amination, these pathological processes have undoubtedly, as a
rule, co-operated in the production of the same.
In the higher grades of hydromyelus entire disappearance of
the spinal cord takes place, or it appears split in two halves, for
a greater or less length ; the cavity of the central canal is in free
communication with the cavity of the dura mater and the hydror-
rhachis interna is merged into hydrorrhachis externa, as not
rarely occurs in spina bifida. This condition of things, too, may
be developed in very different grades and to a variable extent.
An abnormal accumulation of fluid within the cavity of the
dura mater—that is, in the subarachnoidal spaces, in connection
with a greater or less degree of alteration and deformity of the
vertebral column, constitutes what is called
Spina bifida (partial ny EER CIN hydromeningocele, and |
hydromyelocele).
We shall have to spend a little more time on this, as being,
practically, the most important malformation, although, for all
more minute details, we refer our readers to the text-books on
Surgery and Pathological Anatomy.
Spina bifida presents itself as a sac-like dilatation and pouch-
ing of a more or less circumscribed portion of the cavity of the
dura mater, which is generally coincident with the cleaving (or:
absence) of one or more vertebral arches, and protrudes like a,
hernia through the cleft thus formed, raising the skin in the form,
of a more or less considerable tumor. This pouching but seldom,
occurs between two vertebral arches without cleaving of the same,.
and if it does, is always a comparatively small tumor. (If the:
vertebral column remains quite normal, and there is only an in-.
creased accumulation of water in thesvertebral canal, then we
VOL. XIII.—50
7 _
786 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
have simple hydrorrhachis externa—a common manifestation in
hydrocephalus. )
Opinions still differ as to the exact method of origin of spina
bifida, and it is at least probable that this condition may be
brought about in various ways. It is either a question of a pri-
mary dropsy of the central canal, with disappearance of the cord
and secondary widening and distention of the spinal membranes,
or merely of a dropsy of the sub-arachnoideal spaces, which dis-
tends the membranes and pushes them forward like a hernia. If
these changes take place before the vertebral arches are closed,
their closure is prevented, and thus the cleft of the vertebral
column takes place. But it is also possible that this is the pri-
mary step, and that the hydrorrhachis is not developed until
afterwards.
Spina bifida is not exactly a rare malformation. Chaussier
found it present in about one case in every thousand births.
The more special relations of spina bifida are about as fol-
lows:
Its general seat is in the sacral and lumbar region, much more
rarely in the dorsal or cervical portion of the spinal column;
generally there is but one tumor present, more rarely, several ;
these are almost always situated in the median line, seldom
deviating to one side or the other.
They differ very much in size, varying from that of a nut to
that of a head. In form they are usually round or elliptical,
or also pear-shaped ; but they may also be extended in length,
stretching over a more or less considerable portion of the entire
spinal column. The tumor is either flat or pedunculated, some-
times lobulated or divided into two.
The skin over the tumor is either quite normal or highly
stretched, thinned, reddened, involved in ulceration; not rarely
an umbilicated depression may be seen at some point on the
height of the tumor, caused by the insertion of the end of the
spinal cord in the interior of the sac.
Passing beneath the skin, one usually comes upon the dura
mater, which may be thickened or normal, or also very much
thinned ; sometimes it has entirely disappeared or has split, and
the soft membranes alone protrude. Next comes the arachnoid,
a
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DEFORMITIES AND MALFORMATIONS. 787
which, in most instances, actually encloses the fluid. If hydro-
myelus exists, the pia mater also takes part in the formation of
the sac.
The neck of the sac is more or less narrow and leads into the
spinal canal. Not unfrequently it is closed by adhesion, and
thus the cystic tumor lying under the skin is isolated from the
cavity of the dura mater within the vertebral canal.
The condition of the spinal cord varies in individual cases.
In the majority of instances the spinal cord is certainly essen-
tially normal, and takes no part, or but a very subordinate part,
in the existing alterations. It happens still more frequently that
its lower extremity is adherent to the sac at some point, and
causes an umbilicated depression of the same, visible from with-
out. The spinal cord is often materially lengthened by this
means, its extremity being drawn clear out of the vertebral canal,
and not seldom thinned and flattened. The nerve-roots then run
their course from this portion back along the walls of the sac
(or floating free within the same), partly into the vertebral canal
and to their intervertebral foramina, partly directly through the
walls of the sac to their appropriate plexus. More rarely there
exists simultaneously a hydrorrhachis interna, with its evil conse-
quences so far as regards the form of the cord; then the lower
extremity of the cord is more or less destroyed, atrophied, and
the cavity of the sac communicates directly with the dilated and
open central canal.
The jlwid contained in the spina bifida is generally quite
light, colorless, and clear, and perfectly identical with the usual
cerebro-spinal fluid, consequently very rich in water and poor in
solid ingredients ; it is but rarely turbid or bloody ; its quantity
may amount to from 500 to 1,000 grammes (8 oz. to 2 lbs.) or
more.
Symptoms of Spina Bifida.
Children affected with this deformity are generally born with-
out hindrance, are capable of sustaining life, and show nothing
abnormal except a more or less extensive tumor in the sacral or
lumbar region, rarely at a higher point of the spinal column.
788 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
If the tumor is very large and the skin over it thinned, the
sac may burst during birth and its contents escape; the child
is then ordinarily born highly asphyxiated, and perishes within a
couple of hours, or, at the outside, in a couple of days.
If this is not the case, however, the tumor either remains un-
changed, or, more frequently, gradually increases in size, the
skin over the same becoming more and more thinned, ete.
It is but rarely that such a tumor is first developed some time
after birth. See Genga’s case in Ollivier.
The tumor itself, varying very much in size, is roundish, pear-
shaped, or divided into two parts and lobulated, tense, elastic,
and distinctly fluctuating. In smaller tumors the skin over the
same is unaltered, in larger ones it is more or less stretched and
thinned, bluish or reddish; at the same time the entire tumor
not rarely looks translucent, like a hydrocele. In worse cases,
the skin is superficially ulcerated and secretes a watery, purulent
fluid ; it may in part be entirely destroyed or absent, so that the
distended spinal membranes alone constitute the wall of the
sac.
A characteristic found in many cases is that the fluid con-
tained in the sac can be pressed away. In other words, it can,
by pressure, be partly emptied into the spinal canal, so that the
tumor grows smaller; but this does not occur without sometimes
causing disturbances of cerebral innervation—drowsiness, sleep,
twitchings, etc. If there is coincident hydrocephalus, swell-
ing and increasing protrusion of the fontanelles can be demon-
strated during such pressure; on the other hand, pressure on
the hydrocephalic skull increases the tension and size of the
spina bifida. The swelling likewise somewhat increases on as-
suming the erect attitude, on screaming, on pressure, etc. ; an
increase of swelling has also been observed associated with move-
ments of the pulse and of respiration. Not infrequently the
tumor is sensitive on pressure. In those cases, however, in which
communication with the spinal canal has been cut off by closure
of the sac, all these manifestations are, of course, no longer to
be found.
In the majority of cases the manifestations above described
are the only ones in spina bifida. The children thus affected are
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DEFORMITIES AND MALFORMATIONS. 789
otherwise normal, show no sort of manifestations of paralysis,
develop well, learn to walk,and may arrive at a considerable age
without being troubled by their deformity otherwise than, at
most, in a simply mechanical manner.
This, however, is the exception; as a rule, the tumor ad-
vances in growth, and not long after birth all sorts of severe dis-
turbances begin to show themselves, caused by compression of
the lower division of the spinal cord and the cauda equina.
Increasing paralysis and paraplegia set in, incontinence of urine
and of feces, bed-sores, etc., and the patients thus gradually
perish.
Much more rarely these severe manifestations exist at the
very beginning, and this is regularly the case whenever there is
coexistent hydrorrhachis interna. Paraplegia and paralysis of
the sphincters are then present from the very start, and the days
of the little patient are numbered.
But these children by no means always perish as the direct
result of the spinal paralysis thus caused; much greater and
more urgent dangers threaten them from the numerous acts of
violence and accidental wounds to which the tumors are exposed.
Knocks, pressure, dragging, direct wounds, prolonged lying upon
the back, and the like, are all of them capable of bringing about
arupture of the sac. This results in purulent inflammation of
the same, which—if the communication with the spinal canal is
still open—extends into the latter, and induces a purulent spinal
meningitis which ordinarily puts an end to the life of the little
one within a few days. It has happened, although but very
rarely, that such an occurrence has passed over favorably and
has even led to the cure of the malady; this is only to be ex-
pected when the perforation is very minute and the fluid flows
out quite slowly. If the opening is large and the fluid is, by
any accident, rapidly evacuated, death may follow very quickly,
within a few hours, under general convulsions and increasing
debility.
The terminations of the disease have been sufficiently indi-
cated in what has just been said. Life is but rarely maintained
for any considerable length of time ; still, isolated cases have been
known to live to the age of 20, 30, 35, and even 50 years. Prob-
790 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
ably in all these the communication with the cavity of the dura
mater was closed early, or was very narrow.
In most cases death occurs much earlier, and, indeed, the
more certainly and quickly the larger the tumor. The immediate
cause of death is most frequently rupture of the sac; this
comes about either through the fact of the tumor gradually grow-
ing in size, and finally bursting of itself or through some acci-
dental wound ; or through the fact of some traumatic injury,
wound, blow, or the like, causing a sudden rupture ; or through
the fact of the sac being purposely opened and emptied for thera-
peutic purposes. If, in such cases, the emptying takes place
quickly and in a stormy manner, death may occur within a few
hours, under general convulsions and increasing weakness ; or—
and this is more frequently the case, especially after operations
—an acute purulent meningitis is developed, which leads to the
death of the child in a few days.
In a minority of instances death follows without bursting of
the sac, through general prostration in consequence of the severe
spinal disturbances.
The rarest result of all is that such an accidental perforation
is survived, and becomes the starting-point of a positive cure.
More frequently, though by no means frequently enough, this
favorable result follows in consequence of a carefully undertaken
Operative evacuation of the sac.
Diagnosis.
The recognition of spina bifida is generally not difficult ; only
in the smallest forms of the same, when the orifice of communi-
cation is very small or entirely closed, can this present any con-
siderable difficulties.
The following may be mentioned as distinguishing marks: a
tumor on the vertebral column, of the form and size described
above ; tense, fluctuating, translucent ; its size capable of being
reduced by pressure, whereupon the fluid is emptied into the
spinal canal, causing the appearance of severe nervous disturb-
ances (finally also protrusion of the fontanelles) ; the edges of
the cleft vertebrae, the ends of the vertebral arches being some-
— I i » , eines A the
1 ai: eee ee -
DEFORMITIES AND MALFORMATIONS. 791
times distinguishable to the touch as light prominences. By
these means spina bifida will, as a rule, be easily diagnosticated.
It isof special importance—in a prognostic point of view, as
well—to demonstrate the presence or the absence of communica-
tion with the spinal canal ; this is not easily done in all cases.
The distinction between this and the displacement of abdomi-
nal and pelvic viscera (bladder, rectum, ete.) resulting in a sacral
tumor, to which Lorinser calls attention, will generally be easy.
There will likewise be no difficulty in recognizing the other
malformations and defects which not rarely coexist with spina
bifida ; viz., hydrocephalus, deformities of the lower extremities,
anomalies of the genital apparatus, inversion of the bladder with
congenital fissure of the abdominal walls, and the like.
Prognosis.
The prognosis of spina bifida is by no means very favorable.
Very many cases perish by the spontaneous accidental opening
of the sac or through the progressive growth of the tumor; not
a few, likewise, die in consequence of operations undertaken to
effect a cure.
The prognosis becomes more unfavorable the larger the tumor
is, as a whole; the higher it is situated on the vertebral column
(the cases where it is on the sacrum and coccyx are by far the
most favorable) ; the larger the orifice of communication with the
spinal canal; the more it isa case of true myelocele, and not
mere meningocele—therefore, the more there is of hydromyelus ;
the more distinct the signs of hydrocephalus; and, finally, the
feebler the constitution of the child thus affected. Keeping these
points in view, one will generally be able to form a conception of
what is to be expected during the further course of the malady.
Therapeutics.
Nothing at all is to be expected from the treatment of spina
bifida with internal remedies, with inunctions, baths, etc. The
attempts to cause the disappearance of this condition by deriva.
792 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
tion to the skin, by blisters, the actual cautery, etc., may be
designated as downright objectionable.
But it is just as little permissible in most cases to leave the
thing to itself and expect time to effect a cure. Experience
teaches that this trouble is almost always of a progressive char- ©
acter, and sooner or later leads to death.
Nothing remains, therefore, but surgical treatment, which
must, however, be undertaken with the greatest caution and
care, if the results are not to be altogether too unsatisfactory.
Very. different operative measures have been undertaken,
naturally with very various results. Lorinser is opposed to all
operative interference as long as a communication with the spinal
canal can be demonstrated. This is probably, after all, somewhat
excessive caution, although it is evident, in and of itself, that
those cases which have but a very narrow communication, or
none at all, with the cavity of the dura mater, promise far better
results than those with a very wide communicating orifice, as the
main danger of the operation is always to be found in the exten-
- sion of an inflammatory process to the membranes of the spine.
Among the operative procedures hitherto proposed, there are
a number that are to be positively rejected, because almost
always accompanied by fatal results. First among these is the
passing of a hair cord through the tumor ; this is inevitably
followed by inflammation and suppuration, and could only be
considered reasonable if one were quite sure that the external
tumor was entirely shut off from the spinal cavity. The incision
or amputation of the twmor is likewise commonly followed by
fatal meningitis, and is therefore to be avoided.
Ligature of the sac, which implies that it is pedunculated,
seems to be almost equally dangerous; the sac sloughs off, the
orifice of communication cicatrizes, and a cure may thus be
effected ; but here, too, purulent meningitis, with a fatal result,
very often follows. At the same time a number of favorable
results, following this method, have been reported. Thus, by
Rizzoli and Oldoini,' by Parona,? who availed himself of a pair
’ Lo Sperimentale. XXXVIII. (Centralblatt f. d. med. Wiss. 1876. No. 50.)
* Annal, universal. Vol 235, Aprile, 1876.
—
el et i rate
DEFORMITIES AND MALFORMATIONS. 793
of compressing forceps for carrying out the operation ; by von
Brunn,' who undertook the compression of the pedicle by means
of an ovarian clamp; by Colognese,* who used an elastic liga-
ture, a rubber tube, for this purpose.
In view of the better results attending them, the following
methods of operation are probably the only ones worthy of con-
sideration at the present day: methodical compression of the
tumor ; simple, repeated puncture of the sac, repeated according
to the necessities of the case ; and puncture, with the subsequent
injection of iodine.
Methodical compression, by means of adhesive plaster, ban-
dages, appropriate compresses, and the like, certainly in some
cases effects nothing but an apparent improvement, inasmuch as
it mechanically presses the fluid back into the cavity of the
Spine ; as soon as the compression ceases the tumor again returns
to its former volume. At the same time, Heister claims to have
attained a favorable result thereby. The carrying out of com-
pression by means of painting with collodion is highly recom-
mended by Behrend, and has been repeatedly employed with a
good result. He first paints the tumor with a mixture of collo-
dion with castor oil, afterwards with pure collodion, and finally
applies a compressory bandage. |
Experience teaches that simple puncture must generally be
often repeated before accomplishing its end. Still, even this
method is not without danger, even when carried out with the
greatest caution, to say nothing of the fact that it is often with-
out any result. The best way is to evacuate the fluid through a
very fine puncture (for instance, to draw it out with a hypoder-
mic syringe), not to empty the sac altogether, and afterwards
to apply a light compressory bandage.
A surer result, although, perhaps, attended with somewhat
greater risk, is to be attained by puncture with the subsequent
injection of iodine. This method was first introduced by the
French, is probably more employed at the present day than any
other, and has been especially lauded in England (Morton,*
? Berliner klin. Wochensch. 1871. No. 17.
* Annal. univers. Vol. 239. p. 143. 1877. '
* Brit. Med. Journ, April 6th and June 15th, 1872:: Lancet, Dec. 2d, 1876.
2 Ae ne eh mae
794 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
Watt,' Ellis’). Morton, in particular, seems to have practised
this method with great results; he recently reports fourteen cases,
of which eleven were cured. Recovery followed in a// the cases
seated in the lumbar region—which constitute, as is well known,
the great majority of such cases. He first makes a test puncture ;
this is repeated in five days, and then only half the fluid present
is withdrawn, whereupon an injection is at once thrown in, con-
sisting of about four grammes of a solution of iodine in glyce-
rine (pure iodine, 0.60 grammes [ten grains], iodide of potassium,
2 crammes [thirty grains], pure glycerine, 30 grammes [ 3 vijss. ]).
Others have used other solutions (tincture of iodine and distilled
water, equal parts; alcoholic solution of iodine and iodide of
potassium ; and some merely alcohol), and have also modified
the method of the injection in various ways, allowing the injected
fluid to flow out again, etc. In all such cases it will be well to
prevent, so far as possible, the penetration of the injected fluid
into the spinal canal by compression of the pedicle during the
injection. The subsequent treatment will be governed by the
signs of irritation that may arise. |
The main point in any of these operations will always be the
careful and accurate carrying out of the same, and the attentive
after-treatment.
In cases that are not suited to operative treatment—very large
tumors, very wide clefts of the spine and orifices of communica-
tion, very feeble subjects—we must endeavor to protect the tu-
mor, so far as possible, by means of appropriate bandages, com-
presses properly hollowed out, and the like.
21. Rara et curiosa.—Rare and Doubtful Diseases of the
Spinal Cord.
In the foregoing chapters I believe I have presented every-
thing that can now be regarded as to any degree established in
the pathology of the spinal cord, and that may be of importance
to the practical physician. That this does not, by any means,
1 Brit. Med. Jour., April 26th, 1873.
* Philadelphia Med. Times, No. 114. 1874.
(el i vee
—_—s—
————
SYRINGOMYELIA. 795
exhaust the entire pathology of the spinal cord, I am myself
very well aware.
’ There is another class of cases, in which even very serious
alterations may be found in the spinal cord, but which are rare
in themselves, and, furthermore, by no means admit of a positive
diagnosis ; cases which are to be regarded more as curiosities, or,
at best, as valuable material towards the construction of a future
and broader pathology of the spinal cord. There are likewise
cases enough which must, in all probability, be localized in the
spinal cord, without our being able, at present, to adduce any
positive proof to that effect. Finally, there are those in which
Severe spinal symptoms are merely a part of the manifestations
of general processes of disease (severe intoxications, infections,
and the like), and are, therefore, more or less disregarded in the
general picture of the disease, and usually also receive no thera-
peutic attention.
Such and such-like matters will be briefly discussed in this
section, while, at the same time, I wish to give special emphasis
to the fact that, owing to the essentially practical tendency of
this Cyclopedia, we are not justified in entering more minutely
upon many questions of the highest scientific interest, which are,
nevertheless, still awaiting their solution. I must therefore con-
fine myself to more or less aphoristic notices, and would fain, by
this means, give the practitioner some stimulus more accurately
to observe, and to publish any cases he may encounter of such
and similar rare forms of disease.
a, The Pathological Formation of Cavities in the Spinal Cord.—Syringo-
myelia.—Hydromyelus acquisitus,
G. Namias, Di una specie d’atrofia della midolla spinale. Gaz. med. ital. Lomb.
1851, Nr. 35. (Syringomyelia.)—- W. Gull, Case of Progress. Atrophy, etc. Hy-
dromelus, Guy’s Hosp. Rep. VIII. 1861.—oehler, Monograph. d. Meningit.
spinal. Leipzig, 1861. Beob. 17.—Zancereaux, Cas d'hypertrophie de l’épen-
dyme spinale, etc. Gaz. méd, d. Par. 1862. Nr. 31.—0. Schueppel, Ueber Hy-
dromyelus. Arch. d. Heilk. VI. 8. 289. 1865.—Ein Fall von allgem. Anisthes.
Ibid. XV. 8. 44. 1874.—John Grimm, Ein Fall von progress. Muskelatrophie.
Virch. Arch. Bd. 48. 8. 445. 1869.— Leyden, Klinik der Riickenmarkskrankh.
I, 8. 199. 1874.—Hydromyelus und Syringomyelie. Virch. Arch. Bd. 68. 8. 1.
796 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
1876.— Westphal. Hohlen- und Geschwulstbildung im R.-M. Arch. f. Psych. u.
Nervenkrankh. V. S. 90. 1874.—Simon, Ueber Syringomyelie und Geschwulst-
bildung im R.-M, Ibid. V. 8. 121. 1874.
Whereas formerly all central cavities developed in the spinal
cord were regarded at once as dilatations of the central canal,
and, in part, as congenital faults of development, the conviction
has recently been reached, through the careful examination of a
large number of cases, that there are not only pathological dila-
tations of the central canal itself which have been developed
secondarily, as the result of various diseased processes estab-
lished in the centre of the spinal cord, the dilatations themselves
not being developed till later in life, but that newly formed cen-
tral cavities also occur within the spinal cord, which have noth-
ing at all to do with the central canal, but lie within the patho-
logically altered tissue, and have been developed out of the same
by various processes of metamorphosis.
All these cases may be grouped together under the name,
already used by Ollivier, of ‘‘ syringomyelia.”’
After Hallopeau had shown, to a demonstration, that certain
chronic inflammatory processes within the spinal cord, which he
designated as periependymal myelitis, might lead to secondary
dilatation of the central canal, Th. Simon, in particular, in a
large and exhaustive work, established a correct understanding
with regard to a great part of the conditions that had previously
been thrown together under the name of hydromyelus. On the
other hand, Leyden has again recently introduced some new fea-
tures into the doctrine of syringomyelia which, it would appear,
necessitate a modification of Simon’s views.
Pathogenesis and Pathological Anatomy of Syringomyelia.
Simon sums up the results of his studies on syringomyelia as
follows: that an extensive dilatation of the central canal is tole-
rably frequent in foetal life, and is rare during later extrauterine
existence ; that, on the other hand, most of the cases designated
as hydromyelus are either of very doubtful authenticity, or cer-
SYRINGOMYELIA. 797
tainly represent no dilatation of the central canal itself, but are,
rather, newly-formed cavities, which are most fond of developing
themselves in the foremost portion of the posterior columns,
therefore, behind the central canal. It is a question here of pio-
cesses of softening with complete absorption of the softened (and
usually also newly formed) tissue. But undoubtedly genuine
dilatations of the central canal also take place, arising secon-
darily through shrinking of the newly-formed tissue which sur-
rounds the central canal. Generally, however, it is a question
of newly-developed cavities, which are especially easily formed
through the breaking down of tumors that are rich in blood
(gliomata, gliomyxomata, etc.), and which may sometimes even
be lined with a coating of cylindrical epithelium. Such cavities
may be looked upon as the true central canal only when their
topographical position with reference to the other portions of a
transverse section of the cord justifies this view.
In addition to the above we may add that such newly-
Jormed cavities may be developed in very different ways, and as
the result of the most varied pathological processes, among which
are the following:
Through breaking down and softening in the centre of neo-
plasms (gliomata, gliomyxomata, gliosarcomata, etc., cases of
Westphal, Grimm, Simon, and others). Not infrequently there
is such a complete breaking down that only remnants of the
tumor remain, or even only the connective tissue outline of the
same. The same tissue as that of which the tumor was formed
can then often still be demonstrated above or below the cavity.
These centres of softening arise in part through hemorrhage into
the interior of neoplasms (so particularly in the teleangiectatic
forms), in part through simple softening and cyst-formation
within the same. Sometimes there is a development of multiple
cavities ; once Simon even found a cavity with an epithelial lin-
ing (a shut-off portion of the foetal central canal 2).
Through the dreaking down and softening of apoplectic foci,
by the same process, therefore, that leads to apoplectic cysts
within the brain.
Through more or less extensive central softening in areas of
gray degeneration and chronic myelitis. To this category be-
798 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
long the formation of canals which Friedreich’* found in a case
of tabes of the cord ; the formation of cavities which Charcot and
Joffroy * found in a case of progressive muscular atrophy ; the
formation of a cleft which Langhans °* describes in a case of lepra
anzesthetica, and more of the same sort.
Finally, through complete interruption of the continuity of
the spinal cord at some point, as occurred in the experiments of
Naunyn and Eichhorst.‘ These observers found, in dogs in whom
they had cut or crushed the spinal cord at some point, during
their earliest youth, some weeks later, numerous most noticeable
cavities, extending a considerable distance upward from the cica-
trix. These cavities had, at first, nothing to do with the central
canal, and were considered by these observers to be due to an ob-
struction of the lymph-passages. Westphal, in his case, found
something similar in man, and advocates the possibility of a
tumor occasionally also inducing such obstruction.
In addition to the foregoing we then still have the true dila-
tations of the central canal, which may arise secondarily as the
result of various processes, probably oftenest through the so-
called periependymal myelitis of Hallopeau, which has also been
fully recognized and confirmed by Simon. Here it is a question
of a proliferation of the connective tissue surrounding the central
canal and of subsequent shrinking of the same, whereby the
canal is passively dilated.
Adhesions of the pia mater to the dura mater, chronic menin-
geal processes at certain definite points, appear, according to
Simon, also to have a definite relation to acquired hydromyelus
—perhaps by a simple extension of the inflammation from the
pia mater to the periependymal tissue, perhaps, also, by means
of the fact that shrinking meningitic layers of adventitious tis-
sue, by their pulling, mechanically cause the widening of the
canal.
Finally, obliteration of the central canal at some point
1 Ueber degenerative Atrophie der spinalen Hinterstriinge. Virchow’s Arch. Vol.
XXVI. Case IV. 1863.
? Deux cas d@’atroph. muse. etc. Arch. a. Physiol. II. 1869. Second case.
8 Virchow's Arch. Vol. LXIV. p. 175. 1875.
* Arch. f. experim. Pathol. u. Pharm. II. p. 225. 1874.
SYRINGOMYELIA. 799
(through inflammation, external pressure, and the like) may
lead to dilatation of the neighboring portions.
Leyden has again recently sought to re-establish a more inti-
mate relation between syringomyelia and congenital hydromye-
lus. He considers the two as essentially identical, basing his
opinion on the observation of two two-year-old children who
were affected with hydrencephalocele, and furthermore showed
the development of cavities in the spinal cord. Inasmuch as he
does not recognize the significance of the tumor-like masses in
the neighborhood of such cavities as being that of true tumors,
but regards them as mere hypertrophy of the ependyma and of
the neuroglia, he comes to the conclusion that congenital hydro-
myelus is the usual starting-point of the syringomyelia arising
later in life, and that even the abnormal cavities situated in the
posterior columns are merely remnants, that is to say, extensions
of the central canal, hampered in its development. He considers
this view as being supported by the history of the development
of the central canal, and thinks such cavities should be regarded
as portions of this canal which were early cut off. This view
may be the correct one for a certain series of cases, but can
hardly claim to hold good for all cases of syringomyelia.
The pathologico-anatomical condition varies very much in
different cases. Cavities of very variable length are met with;
often only of a few millimetres-or centimetres in length, but not
rarely of a length extending throughout the entire spinal cord.
These cavities are almost always more or less centrally located,
and it is only on more careful examination that we can determine
their precise situation and their relations to the central canal.
The width of these cavities varies much—from one to ten mil-
limetres, from the size of a needle to that of one’s little finger.
Their form, on transverse section, is roundish, oval, angular, sinu-
ate, etc. Sometimes several cavities are found alongside of one
another. Their contents consist of a fluid which is light and
clear, or turbid yellowish, brownish, etc.; in many cases no ac-
curate statement is made on this point.
The walls of the cavities may be smooth and firm, often pro-
vided with a layer of cylindrical epithelium, or sometimes rough,
ragged, uneven, etc.. In their vicinitywwe may, according to cir-
re a
‘ t
800 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
cumstances, find a hard, cirrhotic tissue or gray degeneration, or
the various new formations spoken of above.
The spinal cord, as a whole, is often materially altered there-
by, thickened, misshapen ; but frequently, also, nothing unnatu-
ral can be noticed about it externally. On transverse section the
substance of the spinal cord either appears simply crowded and
pushed out of place by the syringomyelia, or more or less exten-
sively destroyed, partly through simple degeneration and atro-
phy, partly through gray degeneration, neoplasms, extravasa-
tions, and the like.
Symptoms of Syringomyelia.
All experience thus far teaches that the development of cavi-
ties, as such, produces no sort of symptoms by which it could be
recognized during life. In many instances the syringomyelia is
only accidentally discovered in the bodies of persons who pre-
sented no sort of spinal symptoms during life, and who died of
some other disease. :
In other cases the most manifold spinal symptoms exist:
paresis and paralysis, atrophy of muscles, disturbances of sensi-
bility of various kinds, ataxy, paralysis of the sphincters, etc.,
in the most varied combinations. These are doubtless exclu-
sively the results of the primary alterations (the neoplasms,
chronic myelitis, apoplexy, etc.) with which the formation of
cavities has been associated later and as an accidental complica-
tion. No special symptom, no peculiarity in the course of the
disease betrays this complication.
Hence it appears that we are at present possessed of no means
to establish the diagnosis of syringomyelia during life. As a
rule we shall not be able to entertain anything more than vague
conjectures on the subject.
Consequently there is also no question about prognosis or |
therapeutics. The only indications for the same are to be found
in fundamental disease when it is demonstrated.
A —
— om =
SALTATORY SPASM. - 801
b. Saltatory Spasm.
Bamberger, Saltatorischer Reflexkrampf, eine merkwiirdige Form von Spinalirrita-
tion. Wien. med. Woch. 1859. Nr. 4 u. 5.—P. Guttmann, Ein merkwiirdiger
Fall von sog. saltator. Kriimpfen. Berl. klin. Woch, 1867. Nr. 13.—A. Frey,
Ueber den saltator. Reflexkrampf. Arch. f. Psych. u. Nerv. VI. §S. 249. 1875.
—P. Guttmann, Fall von saltator. Reflexkr. Ibid. VI. S. 578. 1876.—A.
Eulenburg, Lehrb. d. function. Nervenkrankh. S. 699. 1871.
Under the name of saltatory spasm [‘‘ saltatorischer Krampf”’ |
Bamberger, in 1859, first described two remarkable cases in
which, as soon as the patients placed their feet upon the floor, such
a lively clonic twitching of the lower extremities set in that the
patients were thrown into the air over and over again, innumer-
able times—in other words, they fell into a rapid and vehe-
ment, involuntary act of hopping and jumping. Afterwards P.
Guttmann reported two similiar cases from Griesinger’s policlinie,
and recently A. Frey, in communicating a valuable case from
Kussmaul’s clinic, has worked up the question in detail and
presented us with a number of suggestive points.
The form of disease under consideration is, on the whole, ex-
ceedingly rare. Inasmuch as, according to the unanimous view
of all authors, which I also share, it evidently represents a
functional disturbance of the spine, I consider it justifiable briefly
to discuss it at this time.
For the information of the reader the five cases thus far ob-
served will be narrated in outline.
1. Observation of Bamberger (Case 1). A man nineteen years of age had been
taken sick with acute pneumonia; during convalescence from the same, severe
spasms, of a remarkable character, occurred. At the moment when the patient's feet
touched the floor a tetanic rigidity of his legs took place, accompanied by the most severe
concussions, so that the patient was thrown into the air ; this was repeated with great
rapidity as long as the patient was maintained in an upright position. At the same
time his face wasvery red, his heart’s action much accelerated ; he had no pain.
In a lying or sitting posture there was not the slightest anomaly to be recog-
nized in the patient. The sensibility and motility of the legs then appeared entirely
normal, But when his feet were pressed against the foot of the bed similar
convulsions took place; the spasm could also be originated by tickling the soles of
VOL. XIII.—51
802 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
his feet, and then it sometimes extended to the arm. No atrophy; no pain —
the vertebree.
In the further course of the case, while the reflex excitability of the lower ex-
tremities still increased, twitchings of the face also set in, as well as increased 1
heart’s action, dyspneea, oscillating movements of the iris, etc. “
The administration of morphine seemed to have a decidedly favorable effect on
the spasm, and in the course of a few weeks recovery took place.
2. Observation of Bamberger (Case 2). A hysterical woman, thirty years of age,
suffering from chlorosis and cardialgia, and complaining of a great general sense |
of weariness. One day when she got up, the same spasms were noticed in her as in ~
the first case. As soon as her feet touched the floor she was at once tossed into the air
and this was repeated as long as she maintained the upright posture. Her face was at
the same time distorted into an anxious expression and the heart’s action was yery
tumultuous. The spasm also extended as far up as her head; after the atte
certain rigidity remained, accompanied by slight twitchings, for a quarter of a
hour after the patient was put to bed.
Motility and sensibility seemed normal. Tickling the soles of the feet calle
forth no reflex action. On pressing the feet against the foot of the bed twitching
occurred only in the upper half of the body. Nothing else particularly abnor
was recognized. r
Subsequently excitability was still further increased, to sink again soon’ _
then to remain stationary. At a later period all sorts of hysterical forms of el sm
were developed. The saltatory spasm did not disappear until after quite a whik
3. Observation of Guttmann. A man forty-six years of age. Sixteen yee
before, he had fever with congestion of the head and hallucinations. Afterwards hi
had had frequent repetitions of this congestion, with shooting pains in his limbs
Three years ago he had the same pains again, followed by trembling in the limt bs
first in the left foot on walking, then also in the right; at that time, already, he hs
saltatory spasm, which was sometimes stronger, sometimes weaker, but on the wh
gradually grew worse. Now there is very well-marked bounding as soon as the 7
touches the floor unless he has a strong support for his arms. He is flung into ta
with great force and rapidity ; his head and trunk are, at the same time, bent bacl
ward, thereby putting him in danger of falling upon his back. He also -
severe pain at such times, with a sense of oppression. The spasms are especial
severe in the morning, towards evening they often disappear altogether. Psychi
disturbances especially favor their occurrence. The attacks are generally prec .
by a sort of aura in the form of a painful drawing sensation in the legs and k
as far up as the back of the head. He complains of pain along the spine, a
somctimes of parzesthesia. a <
Objectively, sensibility seems to be normal. The spinous processes of seve
tebre are tender on pressure, and severe pressure on these is sometimes —
originating a rudimentary attack. Cutaneous irritation of the soles of the feet ‘
without effect. The spasms only occur at certain times; during the interval h c
patient can walk about, stamp on the floor, etc., without inducing an attack.
bs
Se
°_ iS een ie
a do SPR Tt
MN DLEM A tg ce!
SALTATORY SPASM. 803
All therapeutic interference proved unavailing. The patient kept his trouble
unchanged (with the aura, and influenced by psychical excitement) until his death,
which followed five years later from typhoid fever.
4, Observation of Frey. A man seventy years of age, who had been very much
reduced by previous diseases, suffered for two months from rheumatic pains in both
legs and in the left arm, which have grown stiff and weak. At a later period trem-
bling set in when motions were executed, first in the right leg, then in the left arm.
The trembling assumed a more and more convulsive character, and after fourteen
days fully developed spasms were present. On passive and active muscular move-
ment, severe clonic spasms, starting from the left arm, which is in a state of moder-
ately flexed contracture, show themselves in that arm, throwing the entire extremity
upward with great violence about three hundred times in a minute; then they pass
over to the right arm and enact just the same scene there. If the left arm is held
up still longer, the spasms now pass to the right leg, and finally to the left leg.
After a few minutes the intensity of the spasms abates, and they disappear again
gradually in the reverse order from that in which they arose. All attempts to pro-
duce the spasms by purely cutaneous irritation were unavailing.
Quite the same state of things existed in the right leg. This showed distinct
muscular tension; on the attempt to make active or passive movements, severe
clonic twitchings (about 300 times in a minute) set up in this leg, which at once
passed to the left leg, then to the left arm, and finally to the right arm, gradually
disappearing again in the reverse order. Here, too, the spasm could not be called
forth by irritation of the skin alone, nor by pressure upon the sole, as long as the
foot was not moved.
If the patient attempts to stand on the floor, as soon as the soles of his feet touch
it he is thrown into the air with great force by clonic spasm of the muscles of the calf,
which at first occurs in both calves at once and afterwards becomes alternating, so
that a very curious tripping step, of extreme rapidity, results. At the same time there
is intense pain in the legs. As soon as the patient sits down, the spasms cease.
No disturbances of sensibility. Electrical excitability normal. Moderate atrophy
of the muscles, |
A singular fact was observed, viz.: that the most violent spasms could be
quickly quieted by pressure upon the bellies of the muscles of the left arm and
forearm in the neighborhood of the elbow (control of reflex action). The same
thing was true of the right leg through pressure on the quadriceps femoris a little
above the knee.
The malady underwent no improvement under the use of various remedies.
5. Observation of Guttmann: A soldier, nineteen years old, was taken sick with
dizziness, headache, great sensitiveness of the spinal column and cramps in his fect.
The manifestations quickly increased. At the end of five weeks, as soon as the pa-
tient is set up alone on the floor he is at once thrown into the air, and this is repeated
with increasing frequency and violence of the movements until, after a few minutes, the
patient threatens to sink to the ground exhausted. Xt the same time he has pain in
the lower extremities, palpitation of the heart, dyspneea and a red face. The clonic
804 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
spasms are confined to the muscles of the leg and thigh; all the remaining muscles
of the body are free. In the sitting posture, when the soles of the feet touch the
ground, spasms also set in, but more feebly, in the form of a convulsive tremor of
the feet. If the sole of one foot is tapped with the finger, as in percussion, the clontg
twitchings are at once set up; on strong percussion, they are developed even in
both legs. The same thing occurs on pressing the feet against the foot of the bed.
The twitchings cannot be aroused through any other portion of the body.
No disturbances of sensibility and none of mobility in the lower extremities. The
spinal column was painful on pressure in three places.
In the course of a year, gradual improvement set in.
These are the only cases thus far known in literature, in
which the symptom of ‘‘saltatory spasm”’ has so far stood in
the foreground as to be deemed worthy of special notice. Simi-
lar conditions of enormously increased reflex excitability are
alluded to, here and there, in the pathology of the spinal cord,
and yet only in cases that presented much more severe and com-
plicated diseases of the spinal cord. From more recent litera-
ture I mention, for instance, the case of Mosengeil,’ in which,
after a traumatic injury of the spinal column, a very high degree
of increase of reflex excitability was developed, together with
simultaneous paralysis. A recently published case of Chouppe’s*
no doubt also belongs in this category, even though it is not
entirely identical with ‘‘saltatory spasm.’’ The case is that of
a man forty years of age who has been diseased for ten years
without change. When he begins to walk nothing abnormal can
be noticed, but when he has walked thirty to forty yards the
extensors of his legs and thighs contract powerfully and sud-
denly so that the patient makes a leap that raises him some eight
or ten inches from the ground. Then the muscles remain con-
tracted, the limbs are cold, hard, and painful. This condition
lasts about a minute. If the patient goes on walking this attack
either recurs again soon or he may walk great distances without
noticing anything more. 3
’ Berl, klin. Wochenschrift. 1875. No. 43. p. 588.
* Contracture des membres inférieures provoguée par la marche. Gaz. méd. de
Paris. 1877. No. 11. p. 138. Soc. d. Biolog,
j
a
a
ay
~
A
> |
SALTATORY SPASM. 805
The foregoing five cases have this characteristic in common,
that in all there was a very extraordinary increase of reflex ex-
citability, but only in certain nerve-tracts ; that, as a result of
the same, on standing up, or on touching the sole of the foot to
the floor, a singular spasm occurs, which has been very appro-
priately designated as ‘‘ saltatory ;”’ and finally, that this in-
creased reflex excitability appeared as an isolated fact, without
any other or with but insignificant spinal symptoms; that, in
particular, there was no serious paralysis.
An elevation of reflex excitability, even to a very astonishing
degree, is by no means a rare manifestation in the pathology of
the spinal cord; this can be demonstrated in every instance of
myelitis from compression, in every high grade of spastic spinal
paralysis, and several other forms of spinal disease. Here, how-
ever, if is generally associated with paralysis and other severe
spinal symptoms. On the other hand, the almost isolated and
quite preponderating occurrence of increased reflex excitability
is certainly very rare, and proves that the reflex apparatus as
well as the tracts that control reflex action are certainly but
rarely diseased alone. But it likewise appears, from the above
cases of saltatory spasm, that such isolated or well-nigh isolated
disease may yet occur.
The method of action of saltatory spasm has something very
peculiar about it; this being thrown upwards as soon as one’s
feet touch the floor, this severe spasm of hopping, which puts the
whole body in motion with great rapidity, is extremely charac,
teristic ; it constitutes the most prominent symptom and belongs
to all cases of the disease, although in some instances various
other spasmodic manifestations are also reported.
With regard to the true essence and the starting-point of this
peculiar cramp we are not yet altogether in the clear, in spite of
the careful observation of cases, and in spite of the peculiarly
accurate examinations of Frey. It is a pity that, at that time,
the reflex excitability of tendons was unknown. Although Gutt-
mann believes that no relation can be established between this
and saltatory spasm, yet I cannot rid myself of the idea that the
tendons are the very parts that mustalecidedly have something
to do with these spasms. At least in Frey’s case it was positively
806 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
demonstrated that the reflex action did not originate in the skin.
Frey regards it as due to the tension and stretching of the mus-
cles, but it is a question whether the tendons were not at the
same time also stretched and irritated. The fact that in several
cases pressing the feet against the foot of the bed, and that in
Guttmann’s case tapping on the sole of the foot (sic/) aroused.
the reflex spasm, speaks strongly in favor of my opinion. The
well-known dorsal clonic spasm of the feet in its higher grades,
in which both legs fall into a lively convulsive trembling (trepi-
dation épileptoide) must, in my opinion, bear a very great re-
semblance to saltatory spasm, and I can readily imagine that the
patients who show this phenomenon would also develop salta-
tory spasm if it were possible to set them on their feet and keep
them standing; but they are generally the victims of severe
paraplegia. These considerations at all events inspire the wish
in future cases more accurately to test the question of whether
saltatory spasm does not bear a certain relation to the reflex
excitability of tendons—whether it does not represent an increase
—certainly to a very high degree—of dorsal clonic spasm of the
feet. At the same time, Bamberger’s first case seems to show
that the reflex action may also originate in the skin ; this, how-
ever, is in part also true of dorsal clonic spasm, and may be
explained in other ways.
There cannot be the slightest doubt that the phenomenon is
really nothing else than a reflex spasm ; this appears, to a dem-
onstration, from all observations, and quite particularly from the
case of Frey, in which the subsidence of the reflex manifestations
followed in quite a typical manner. The fact, too, of the check-
ing of the reflex action by strong mechanical irritation of the
structures lying beneath the skin may also be understood in the q
same sense. .
We have, therefore, in all cases to deal with a peculiar form —
of spasm caused by extraordinarily increased reflex excitability —
of the spinal cord, and principally localized in certain nerve- —
tracts. | |
But does this constitute a distinctive, well-characterized form
of spasm, perhaps somewhat similar to tetanus, or is it only one
—ertainly very striking and remarkable, but yet single—symp-
SALTATORY SPASM. 807
tom of disease which may occur in various affections of the
spinal cord ?
For the present I should be more disposed to accept the latter
alternative. Just as is the case with ataxy, with muscular ten-
sion, with partial paralyses of sensation, and many other things,
so saltatory spasm might also only be a peculiar symptom be-
longing to the localization of diseased processes in quite definite
portions of the cord. Whether this symptom can be the main
and essential one in a certain definite form of disease ; whether
it will, therefore, be possible, in the future, to gather together
cases of this increased reflex excitability under the name of “sal-
tatory spasm,”’ taking only the purest cases and those most free
from other manifestations ; can only be determined by future in-
vestigations. And in these it would be desirable to give special
prominence to the more accurate study of reflex action itself and
its starting-points, and to settling the question, so far as possible,
of all other concomitant manifestations.
The cases at present before us, although they are bound
together by the common symptom of ‘‘saltatory spasm,”’ can
hardly be considered as the same in kind and belonging to a
definite form of disease. One case (Bamberger’s 2d) is decidedly
of hysterical origin; in another (that of Frey) the paresis, the
. contractures, and the atrophy that were present, speak in favor
of the existence of chronic myelitis; in the other three cases
(Bamberger’s 1st, Guttmann’s 1st and 2d) no other spinal func-
tions seemed, to any considerable degree, affected ; sensibility
and motility were quite normal. In these cases it would at least
seem natural to regard them as peculiar forms of disease, whose
main symptom was the saltatory spasm. They would constitute
the germ of a subsequent more accurate array of cases of this
form of disease.
The main causes of this disease would seem to. be previous
illnesses, debilitating influences, neuropathic disturbances.
The distribution of the spasms differs very much in individual
cases ; sometimes they are confined to the legs ; sometimes they
also extend to the back, the neck, and face, even to the organs
of circulation and respiration, and to the pupils. In all cases
the arms remained free during the actual saltatory spasm, and
808 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
could be used by the patient for his support. The spasm was
almost always accompanied by lively pain in the legs. In one
instance the spasm occurred only on standing ; in others it could
also be called forth by appropriate irritation when lying down.
Psychical influences could be shown in a number of instances
either to favor or to control the spasm.
After giving the above reports of all the known cases, it is
not necessary further to delineate the picture of the disease.
The diagnosis of saltatory spasm will, as a rule, be easy, on
account of the extremely characteristic occurrence of the hop-
ping movements as soon as the feet touch the floor.
As regards the therapeutics of this manifestation, no great
results can yet be shown. In most instances all possible thera-
peutic measures (warm baths, cold sponging, ice to the back, gal-
vanism, arsenic, iodide and bromide of potassium, etc.) proved
entirely ineffective ; the trouble remained stationary, or ran its
course to a favorable termination, apparently uninfluenced by
therapeutic measures. Only in the first case of Bamberger did
the administration of morphine seem to exert a decidedly bene-
ficial influence on the spasm.
The treatment of this peculiar condition is therefore still to
be discovered. It might be desirable, first of all, to keep our eye
on trials of bromide of potassium, calabar bean, ergotine, and
atropia (see this Vol., p. 189).
¢. Tonic Snasms [Cramps] in Muscles Capable of Voluntary Movement.
Charles Bell, Affections of the Voluntary Nerves. Physiological and Pathological
Investigations of the Nervous System. German by Romberg, 1832. p. 367.—
M. Benedict, Ueber spontane u. reflector. Muskelspann. u. Muskelstarre.
Deutsche Klin. 1864. Nr. 80-34.—Elektrotherapie. S. 184 ff. 1868.— Leyden,
Klinik u. s. w. I §. 128. 1874.—J. Thomsen, Tonische Krimpfe in willkiirlich
beweglichen Muskeln in Folge yon ererbter psychischer Disposition. Arch. f.
Psych. u. Nerv. VI. 8. 702. 1876.—A. Seeligmueller, Ton. Kriimpfe in wilk.
bewegl. Muskeln (Muskelhypertrophie?). Deutsch. med. Woch. 1876. Nr. 33
u. 34,
After attention had been directed for a long time to certain
conditions of muscular rigidity which occur in some diseases of
eh ie
TONIC SPASMS, 809
the spinal cord, and also in other nervous affections, cases were
more recently described by J. Thomsen and Seeligmueller in
which such muscular tension and regular tonic spasms, on volun-
tary motion, formed almost the only demonstrable manifestations
of disease. These were cases that probably depended on a con-
genital anomaly of the nervous system that occurred repeatedly
in one and the same family, and were hereditary through several
generations—cases which caused the individuals thus attacked
great annoyance, and often led to their being falsely judged and
unjustly treated.
As these cases are of decided practical importance, and may
acquire the most serious significance to the individual—in case
of his being subject to military duty, for instance—and as they
are, furthermore, probably of spinal origin, they will here be
briefly noticed.
We will first, as a sample of this peculiar disturbance, com-
municate the case very fully investigated and described by
Seeligmueller.
Richard Kroitzsch, a recruit, twenty-two years of age, had well-nigh driven his
drill-sergeant to despair, because he could not learn to handle his musket with
anything like the requisite rapidity and precision, and, furthermore, repeatedly let
his piece fall, in the midst of the drill, or even fell to the ground himself, without
losing consciousness. The recruit stated that a certain stiffness and tension in his
arms and legs, especially after long rest of the extremities, prevented the rapid and
precise carrying out of the movements. An older sister suffers from the same
affection.
The patient has been affected with this trouble from his earliest childhood. He
never could execute rapid movements; was prevented for this reason from becom-
ing a waiter, and was obliged to adopt a sedentary occupation. The stiffness is
very great after sitting still for a considerable time, and also on getting up in the
morning. It is claimed that his extremities always grow more supple, and are under
better control after prolonged movement ; this also proved to be the case after drilling
for a long time. His speech is also somewhat hesitating. His legs and forearms
often have the subjective sensation of being asleep and of formication. No pain
and never any cramps in the calves of the legs.
Objective examination showed a man of medium stature, with but a slight layer of
fat, but with well developed, and in part even athletic, muscles. The domain of the
facial nerve and the tongue were normal. Speech good. There was no tenderness
on pressure over the spinal column, the nerves or muscles of the extremities. Reflex
movement on tickling the soles of the feet increased, _
810 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
There was an enormous development of single symmetrical groups of muscles, thus
of the calves of the legs, the quadriceps and trapezius muscles, the glutei, the biceps
muscles, etc. The measurements given showed an unusual size of the individual
parts. This massive development is comparatively uniform for the upper and lower
extremities. There is considerable lordosis of the lumbar portion of the spinal
column. Skin and panniculus normal. Almost all the muscles show an wneven,
knobby surface, which becomes more distinct on motion. The muscles feel as hard
as boards, especially when they are set in action, when they swell up into knotty
ridges. This is also the case when they are irritated, mechanically or electrically,
On tapping over them, the parts affected at once contract into firm masses, standing
out in relief. The same thing takes place on irritation with the faradic current,
and it appears, furthermore, that the tetanus thus called forth continues dispropor-
tionately long (five seconds and more) after the action of the faradic irritation has
ceased. The same manifestations were also called forth through a strong galvanic
current.
In the muscles of the upper arm and shoulder there were distinct jibrillar con-
tractions. The active movability of the extremities did not appear to be materially
disturbed, during the examination—only the rotation of the shoulder-joint was a
little slow and hesitating. Consideruble obstacles were opposed to passive motion in
most of the joints, particularly the knee-joint. There were no disturbances of co-
ordination. Climbing stairs was executed with the legs somewhat spread. No
muscular tetanus could be called forth by compression of the trunks of the nerves
or arteries. The galvanic and faradic excitability of the nerves and muscles proved
to be quite normal.
Seeligmueller was induced to report the preceding case by the
description which Dr. J. Thomsen had given of this peculiar form
of disease. Thomsen himself has suffered from the affection
since his youth, and has demonstrated its existence in his own
children, in his brothers and sisters, and in his ancestors, includ-
ing numerous cases, and running through not less than four
generations.
The description which he gives, somewhat concisely, of him-
self and of one of his sons who, by reason of the imperfect judg-
ment formed concerning his case, had to suffer much at the
hands of the military surgeons, agrees in all essential points
with Seeligmueller’s case. !
The difficulty begins in earliest youth ; Thomsen was able, in
part, to recognize it in his children even in the cradle. It con-
sists in a deficiency in the influence of the will on the muscles,
which fall into a state of rigidity and stiffness, and even into
cdl
eT; »
a
TONIC SPASMS. | 811
complete tonic spasm when they attempt to obey the will. This
appears the more prominently the more powerfully patients
exert their will to overcome the obstacle, the more they are ob-
served, or are the subjects of psychical excitement generally.
This condition may become so extreme that patients fall to the
ground and tumble around helpless until the spasm abates. On
the receipt of sudden severe psychical impressions a sudden
painful sensation shoots through all the voluntary muscles.
Low temperature, taking cold, and all conditions of disease in-
crease the evil, warmth and movement diminish it. The sphinc-
ters are not involved. When the patients once get agoing, and
the will has attained its influence over the muscles, then they are
as capable of movement as well people.
No other disturbances of any kind are to be observed. Psy-
chically these people are well, although the fear of betraying
their condition before people, and the wish to conceal it, rule
them and influence their character. There is nothing abnormal
to be found in their corporal condition; the muscular system,
particularly, may be quite admirable and well developed. In
Rostock they excised a piece of muscle from Thomsen’s son
and found it perfectly normal.
The heredity of the trouble is very remarkable, as is strik-
_ ingly manifested in Thomsen’s family. The great-grandmother
of Dr. Thomsen died of puerperal mania, and her two sisters
were afterwards psychically diseased. His grandfather was also
mentally weak. Of his four children, two had the stiffness to a
high degree, the other two (including Thomsen’s mother), to but
a slight degree. Among the children of this generation, the evil,
as well as conditions of psychical weakness, was very wide-spread ;
of thirteen children borne by the mother of Thomsen, seven suf-
fered from this rigidity. Among the thirty-six descendants of
Dr. Thomsen and his brothers and sisters, on the other hand,
but six suffer from this complaint. Four of his own five sons
have the disease. This is, therefore, a very classical example of
‘neuropathic encumbrance” [‘‘neuropathischer Belastung’’] in
a family.
I furthermore find a case in Leyden (I. c.) which plainly be-
longs here, and some details of which I wish to mention, as it
812 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
may serve in certain respects to complete the description of
Seeligmueller.
A merchant, twenty-eight years of age, whose brother suffers from a similar
muscular affection, and whose muscles are developed in quite an athletic manner,
shows a striking stiffness in all his movements, which he has had from his earliest
youth. Individual groups of muscles do not promptly obey the will, and, when a
certain movement is intended, come to a stand-still half way in a state of tetanic
rigidity. His speech is slow and awkward, as are also the movements of the tongue.
Some of the motions of the eyes, and of those muscles controlled by the facial
nerve, are also sluggish. If the patient clenches his fist powerfully it is impos-
sible for him to extend his fingers again immediately; this is accomplished but
slowly, as if he had to overcome a serious obstacle. After these attempts have been
repeated a number of times the movements are accomplished more easily. The
same manifestations occur in the lower extremities, etc. Aside from this the patient
is perfectly well. The malady remained uninfluenced by any treatment. :
In Benedict, too, there are some observations in which this
appearance of muscular stiffness stood out in a very prominent
manner. This is particularly true of observation No. 88, in his
‘* Klectrotherapy,’’ while observation No. 86 doubtless represents
a somewhat more complicated, but, in certain respects, a similar
case. :
Charles Bell, too, has undoubtedly seen the affection here dis-
cussed, and has described it—even though in quite hasty lines—in
that portion of his celebrated work cited above. |
I myself very recently observed a case which, at least, gave
indications of quite similar manifestations. The patient, twenty-
one years of age, came to me on account of symptoms indicating
multiple sclerosis in process of development, and stated that from
his youth up he had been the butt of his comrades on account
of his being so stiff and unhandy. He had always felt a cramp-
like stiffness in his limbs whenever he endeavored to use them
rapidly, especially if he was being observed by others. This was
noticeable in rising from a chair, in going up stairs, etc.; if he
took a firm hold of any slender object with his hands, he was
unable to let go of it again immediately, etc. This condition was —
worse in the cold. When once started in walking his movements
followed much more easily.
Signs of these conditions are often enough met with in per-
TONIC SPASMS. 818
sons with disease of the spinal cord, but then they are always
complicated with other and more severe spinal symptoms. This
peculiar stiffness and awkwardness of motion, and the fact that
many patients walk and move worse when they are being ob-
served, are known to every experienced physician.
On the other hand, the almost isolated occurrence of these
disturbances, as it appears in the cases given above, is certainly
a rarity, though it might be worthy of the special attention of
military surgeons.
Briefly stated, the picture of the disease, as based upon the
scanty material at hand, is about as follows:
From their earliest youth—doubtless, as a rule, under the
influence of hereditary conveyance—these patients suffer under a
peculiar disturbance of movement, which is but rarely developed
for the first time in adults. This disturbance of movement con-
sists in a peculiar stiffness and rigidity of the muscles which are
intended to be set in action by the will; a stiffness which may
increase to a regular tonic cramp, so that movements are entirely
hindered, the patients fall to the ground, etc. Just as the vol-
untary contraction of the muscles is opposed by a strong internal
obstacle, so the termination of a contraction that has once set in
also follows but slowly, as if overcoming an obstacle ; the con-
tractions which were accomplished with difficulty persist long—
patients cannot at once let go of articles which they have seized
firmly. It is only when, after repeated powerful efforts of the
will, the tracts for motor excitation seem, as it were, to have
become free again, that movements follow with increasing free-
dom and ease, and are but little to be distinguished from healthy
movements. Psychical influences, sudden mental impressions,
the effort of paying attention, the presence of strangers, cold,
etc., act unfavorably on the condition ; warmth, moderate move-
ment, a good state of mind, a high degree of self-confidence,
relieve it. Aside from this these patients are well; their bodily
and mental functions are accomplished normally ; their muscular
system may be admirably developed and even capable of accom-
plishing a large amount of labor. Sometimes (always ?) tension
of muscles takes place on making passive movement, and on
mechanical and electrical irritation of the muscles strikingly
814 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
powerful tonic contractions of the same set in. With all this,
such patients are unfit for many of the duties of daily life and
for the exercise of various callings, and above all are unqualified
for military duty.
We will not here enter into far-reaching speculations with
regard to the essence of this remarkable form of disease. Thom-
sen thinks that it depends on a disturbance falling principally
within the domain of psychical influences. Seeligmueller does
not share this opinion. Whereas he originally thought it to be
a peculiar form of muscular hypertrophy, the doctrine of a con-
genital or inherited affection of the lateral columns of the cord
afterwards appeared to him most probable. I must confess that
I have thus far been unable to form any definite idea of the seat
and the variety of affection lying at the foundation of this diffi-
culty, although, owing to the occurrence of analogous symptoms
in so many diseases of the spinal cord, I should first of all think
of a spinal affection. The question can only be decided by fur-
ther observation.
There is also wide play left here for therapeutic endeavors,
which, in the cases thus far reported, seem to have been entirely
without results.
d, Intermittent Spinal Paralysis.
Macario, Gaz. méd. de Paris. 1857. Nr. 6.—Romberg, Lehrbuch d. Nervenkrankh.
I. p. 752.—Hartwig, Ueber einen Fall von intermittirender Paralysis spinalis,
Diss. Halle. 1874.
The occurrence of purely intermittent attacks of paraplegia
and paralysis, which, according to all appearance, are of spinal
origin, and which make a most striking impression as contrasted
with the usual stability of spinal paralysis of similar severity, is
undoubtedly one of the rarest and most remarkable forms of
manifestation of malarial infection.
Literature contains but very few instances of this form of
spinal paralysis.
I find one case of Macario’s cited in Hertz,’ in which a
1 This Cyclopedia, Vol. IL, p. 601, foot-note.
ee eee ee
eae
INTERMITTENT SPINAL PARALYSIS. 815
woman, two days after her confinement, was attacked with for-
mication in her feet without any known cause, which extended
over the trunk to the upper extremities. The extremities be-
came paralyzed and anesthetic, and the tongue, too, was para-
lyzed. These manifestations were repeated in a quotidian type
three times, and were cured by quinine.
Romberg describes quite a similar case.
A woman, sixty-four years of age, after being quite well the day before, was
suddenly attacked with paralysis of the lower extremities and the sphincters. Sensi-
bility was unchanged, consciousness clear, the temperature cool, pulse 80, small and
empty, no pain in the spinal cord. The next day there was an astonishing change
in the condition. The patient can walk again, and void urine voluntarily, and
only complains of weakness in the legs. The next morning there was paraplegia
again, which had set in at the same hour as two days before. A third paroxysm
was awaited, which also set in at the appointed time, although without paralysis of
the sphincters. Quinine effected a rapid cure.
In a recent dissertation at Halle, Hartwig has reported in
detail an observation belonging under this head.
This observation is in relation to a vigorous laborer, twenty-three years of age,
who had suffered from tertian intermittent for a few weeks five years before, but since
that time had remained perfectly well and strong. In November of 1873, he first
noticed weariness in the legs, which gradually increased, and the- arms, too, were
attacked. On the third day he was obliged to take to his bed, and the night follow-
ing he was completely paralyzed—his legs, trunk, arms, and even the movements of
his head were paralyzed, but not the muscles of the face ; speaking, breathing, and
swallowing were somewhat hindered ; there was no paralysis of the sphincters, sen-
sibility was intact, the head entirely free, no pain. The secretion of sweat was
excessive. After this condition had lasted for twenty-four hours it let up, and in
half an hour, generally with an increased secretion of sweat, all the muscles again
became movable.
During the succeeding twenty-four hours the patient remained free from any sign
of paralysis, merely complaining of weariness and heaviness of the limbs. Then
the attack of paralysis recurred again, in the same way as at first, and then there
followed regular successive free intervals and attacks, both of about twenty-four
hours’ duration. Gradually the time occupied by the attack extended to forty
hours, the interval being much shorter. Under the use of arsenic the intervals also
extended over a period of about forty hours. On first using quinine the attacks
remained altogether absent for four days. After hypodermic injections of strych-
nia the tertian type of the attacks was re-established. Between two days, on
which the patient is completely paralyzed on both sides, he has a day of tolerably
816 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
free mobility of all his members. The sphincter ani was likewise affected a few
times; the general condition of the patient had not materially suffered.
At the end of March, 1874, the following condition was found to exist during
an attack: The patient lay there completely paraplegic; only the muscles of hig
face acted normally; the flexors of the hands and feet show a minimum amount of
motion. The pupils reacted well; the special senses were normal. The head
could not be moved; on inspiration, it was principally the diaphragm that was
active; expiratory efforts were reduced to a minimum. Speech and swallowing
were somewhat difficult. Respiration 20, pulse 72, temperature 99.5°; sensibility
of the skin and muscles normal. Reflex action is entirely wanting; the electrical
excitability of the muscles is almost entirely extinguished (during the intervals it is
only diminished). No pain, only formication and a feeling of numbness in the
parts affected. Evacuations voluntary.
In the course of the succeeding months greater and lesser irregularities occurred
in the course of the disease. The use of quinine sometimes prevented the attacks for
a number of days, but then they returned again in spite of itscontinued use. On the
whole, however, the disease retained its intermittent or strongly remittent type, and
gradually a certain degree of cachexia began to show itself, with marked emacia-
tion of the muscles, etc. After the trouble had lasted for seven and a half months
no radical improvement could, as yet, be demonstrated, and nothing is stated with
regard to the final termination of the case.
These three very remarkable cases have the following features
in common: that they all present a rapidly developed paraple-
gia, advancing to complete motor paralysis, with or without
anesthesia and paralysis of the sphincters; that this paraplegia
disappears again in the course of a few hours, sometimes with
the appearance of a critical sweat, to give place to a complete or
well-nigh complete intermission; that this process is then re-
peated, ina more or less regular manner, in the quotidian, ter-
tian, or quartan type; and that the entire affection is either
promptly cured by quinine, or at least favorably influenced
thereby.
It is in the highest degree probable that we here have to deal
with a malarial infection; the intermittency of the paroxysms, |
their termination in a Sweat, and the efficacy of quinine, all argue
strongly in favor of this intermittent paraplegia being nothing
else than a masked intermittent. To be sure, this cannot, as
yet, be considered as rigidly proven.
It may probably be even more positively asserted that the
seat and starting-point of this disturbance is to be found in the
of) on
|
|
|
——
TOXIC SPINAL PARALYSIS. 817
spinal cord. The entire character and grouping of the symp-
toms, the limitation of the paralysis to purely spinal nerves, the
entire immunity of the brain, the great resemblance to other
general paralyses of notoriously spinal origin, speak with such
positiveness in favor of this belief that no reasonable doubt on
the subject can be raised.
But it is, unquestionably, a matter of the greatest difficulty
to determine what actually takes place within the spinal cord in
this malarial paraplegia,—whether any, and, if so, what anatomi-
cal changes take place therein during the attack. Hartwig as-
sumes that it is a question of transitory hyperemias and serous
transudations in the substance of the spinal cord ; a supposition
which appears to me untenable, from the mere fact that the dis-
turbance is always confined to the motor portions of the cord,
leaving the sensitive portions entirely free. It is probably safer
to say that the essential conditions of malarial spinal paraplegia
are at present unknown to us, and that we can only hope for
light on this subject from the future.
The diagnosis of ‘‘intermittent spinal paralysis’’ is very
easily arrived at from the picture of the disease. And when the
diagnosis is clear the treatment is plain. The treatment ap-
plicable to intermittent fever in all its forms—quinine, arsenic,
removal from a malarial region, etc.—must be undertaken with
energy. If this remains without results, then the therapeutic
measures laid down in various portions of this work for acute
and chronic spinal paralysis will claim consideration.
e. Toxic Spinal Paralysis,
Raoul Leroy d’ Etiolles, Des paralysies des membres inférieures. II. p. 1-75. Paris,
1857.—Jaccoud, Les paraplégies et l’ataxie du mouv. pp. 821-334. Paris, 1864.
Leyden, Klinik. Il. 1. Abth. pp. 280-297. 1875.
In connection with the foregoing cases of infectious spinal
paralysis, it may, perhaps, be appropriate to give some particu-
lars with regard to similar instances of paralysis called forth by
known and actual poisons.
It is claimed that such paralysis (in various forms, as paraple-
gia, as paralysis of single groups of muscles or extremities, as
VOL. XIIl.—52
818 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES,
general paralysis, etc.) has resulted from intoxication with ar-
senic, phosphorus, lead, quicksilver; furthermore, as the result
of poisoning with carbonic oxide, sulphide of carbon, tobacco,
camphor, ergot, lathyrus sativus, alcohol, absinthe, mushrooms,
balsam of copaiba, etc., entirely apart from the severe acute
paralysis of the nervous system, such as is called forth by
opium, belladonna, strychnine, etc.
All these poisons are distinguished for their powerful though
varied influence on the nervous system; they cause lasting
paralysis, as a rule, only when their action is slow and repeated,
more rarely when it is quite acute. They cause the most varied
forms of paralysis and paraplegia, from simple weakness and
paresis to complete paralysis, sometimes acute, sometimes more
chronic, with or without muscular atrophy, with or without dis-
turbances of sensibility. In many cases, however, the causal
connection between these and the antecedent intoxication is by
no means placed beyond all doubt.
Furthermore, we know almost nothing with regard to the
changes that may exist in the nervous system (especially in the
spinal cord) in such paralyses. We have virtually no anatomi-
cal reports on this subject that carry any weight with them; the
localization in the spinal cord cannot even be asserted, with any
degree of positiveness, on the ground of the clinical symptoms.
Great uncertainty still reigns even with regard to the most fre-
quent and best known of these forms of paralysis, viz., lead-
palsy. What is to be said and conjectured on this subject has
already been given in other portions of this work.
The pathology of the spinal cord has, therefore, not as yet
experienced any advancement through the study of toxic paraly-
sis, and there is all the less reason why we should here enter
upon these matters in detail, because this would carry us into
the domain of toxicology, this being the field where, for the pres-
ent, the scientific working up of these questions will have to take
place. The reader who is more particularly interested in this
direction will find that, aside from the hand-books on Toxicology,
the works above cited contain more detailed accounts of these
matters, even though the results may still be unsatisfactory.
PARAPLEGIA DEPENDENT ON IDEA. 819
f, Paraplegia dependent on Idea,
J. Russell Reynolds, Remarks on Paralysis and other Disorders of Motion and Sen-
sation dependent on Idea, British Med. Journ. 1869. Nov. 6.
In a very readable essay, and one of importance to the prac-
titioner, Russell Reynolds some time ago pointed out the fact
that severe disturbances of the nervous system (paralysis, cramp,
pain) may depend upon diseased action of the mind, and upon
imagination ; that such disturbances, under the garb of affec-
tions of the brain or spinal cord, may long bid defiance to all
treatment, and only disappear after the removal of the erroneous
ideas. Such conditions may occur quite independently of psy-
choses, of hysteria, hypochondriasis or simulation; they are
often associated with general debility, and even with actual, well-
defined diseases of the nervous system, and, if a correct diagnosis
is made, may easily be removed by appropriate treatment.
Everybody knows the powerful influence which imagination
and lively mental operations have upon pathological manifesta-
tions in the nervous system, and we are not surprised if these
influences make themselves felt in the domain of sensation and -
feeling ; we are less accustomed to the idea of such psychical
impressions manifesting themselves in the form of severe motor
disturbances also, although there is no reason, a priori, why this
should be impossible.
Taught by our own experience that such conditions actually
do occur, and perhaps occur more frequently than one would
think, we consider that it would not be amiss to give a brief rep-
resentation of Russell Reynolds’ views, so far as they refer to
disturbances in the sphere of the spinal functions. The reader
will agree with us that the easiest way to familiarize him with
the subject is by the brief narration of the most significant one
of Russell Reynolds’ cases.
A young lady who had seen better days was admitted into the hospital as para-
plegic. She had become so gradually, and was much emaciated. She had been
unable to stand for two or three months, and was now bed-fast. Her expression of
countenance was anxious, mixed with a glimmer of hope; she expected to be cured
8290 ERE.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
as the result of entering the hospital,—a step upon which she had resolved with
difficulty.
Her paralysis was almost complete; she could move the toes somewhat, and
raise the heel a little from the bed. But the sphincters were normal, and there was
no local atrophy. Sensibility was intact; electro-muscular sensibility and contrac-
tility normal; reflex action hard to accomplish ; no conditions of cramp ; no pain,
even on movement of the legs or on pressure over the spinal column. No hysteria;
no traumatic injury; no cachexia demonstrable.
Her previous history is as follows: Her father, who is her only relative, was
brought from affluence to poverty, a year and a half ago, through commercial dis-
asters. He bore it bravely, as did also his daughter ; he set to work again, and she
assumed duties and responsibilities which she had never known before. At first all
went well, but suddenly the father became paralytic, and his daughter nursed him
with tender self-sacrifice. But they soon found themselves in actual want. The
daughter worked as daily governess, was obliged, as a matter of economy, to walk
a great deal, and walked fast, so as to gain time for her father. Thus she worked
for many a weary week, the thought of paralysis always before her, her brain over-
burdened with thought and anxiety, her limbs weary with walking, her spirits
hardly equal to the constant effort to appear cheerful. Her legs often hurt her, and
she thought, with shuddering, what if she should grow lame like her father! This
thought acquired an increasing power over her; she was gradually obliged to give
up walking, then to stay at home, then in her room, and finally in bed. Her legs
grew more inactive from day to day until complete paralysis was present.
She was told, and all those about her were told, in confidence, that she would
soon he able to walk perfectly well. A light tonic was administered ; her legs
were faradized, though more for the sake of the psychical impression ; her legs and
back were rubbed and she was obliged to walk up and down the hall for five min-
utes every four hours supported by two nurses. The day after the beginning of
this treatment she could walk with but little support. After four or five days she
could walk quite well, and at the end of two weeks she was as strong and capable
as ever before in her life.
Not less interesting are the other examples which Russell
Reynolds gives. I have likewise met with quite similar things
in my own practice, even if not so well marked in degree, and
have repeatedly seen improvement set in through appropriate
psychical impressions made upon the patient.
It is, of course, by no means always easy to recognize such
conditions aright and to separate them from real diseases with
an anatomical basis. Such conditions are by no means always
associated with hypochondriasis or hysteria, or mental disturb-
ances, although this may occur:-still less are we to suppose that
——
a
Py ae eee wr eer ie ees bet lee bk,
PARAPLEGIA DEPENDENT ON IDEA. 821
such patients are indulging in malicious simulation; they are
themselves firmly convinced of the reality of their symptoms. A
certain general debility not rarely accompanies such conditions,
and all possible debilitating influences---diseases, cares, anxieties,
overexertion, etc.—may be followed by the same. But it gener-
ally requires, in addition, that the attention be habitually di-
rected to certain portions of the body or to certain forms of dis-
ease in order to call forth such ‘‘imaginary”’ disease. On this
ground Russell Reynolds believes that a part of the neuroses
caused by railroad accidents may be classed under this head,
wherein the attention of the victim is influenced in the most un-
fortunate manner by the stories of friends, by the inquiries of
| his physician, the talk of his attorney, and the sober face of the
; company’s physician.
The diagnosis of such forms of disease is based on the follow-
| ing circumstances: on the method of development of the symp-
toms, and especially on the demonstration of some ruling idea of
| the mind; on a judgment with regard to the symptoms present,
| and especially on the demonstration of such symptoms as cannot
| be reconciled with the theory of an organic lesion. In this re-
spect Russell Reynolds calls attention to the following points:
i that the patient cannot lift his heel from the bed nor draw it up,
while he can raise himself up or lie down without any help, or
turn from one side to the other; that in apparently complete
motor paralysis there are no signs of paralysis of sensation, no
trophic disturbances and no diminution in the electrical excita-
bility ; that sometimes there is complete inability to stand on
one’s legs, whereas the legs can be moved in every possible direc-
tion. Finally, the diagnosis is also said to be aided by the fail-
ure of ordinary treatment and the success of treatment directed
to the removal of the false idea. That it will not always be pos-
sible to make a positive diagnosis on the ground of these signs,
{ is a fact which will be admitted by every one familiar with the
pathology of the spinal cord.
In the way of treatment Russell Reynolds gives the follow-
ing recommendations: Let the case be taken hold of earnestly ;
excite the hope of recovery, if a definite plan of treatment is fol-
lowed out, and let this be done not only by the physician but by
|
|
|
|
|
EL ESL eS
SE
892 ERB.—DISEASES OF THE SPINAL CORD AND ITS ENVELOPES.
those around the patient—hence the importance of hospital
treatment ; compel the patient to walk at certain definite times,
supported on both sides; use faradization to the muscles, fric-
tion and passive movements of the limbs; apply dietetic and
medicinal treatment such as the general condition of the patient
requires.
So far as we know, these matters, which are certainly not
without practical importance, have thus far not received the at-
tention which they unquestionably deserve. It would be inter-
esting to receive communications from others regarding similar
manifestations ; perhaps it would be possible after a while to gain
somewhat more insight into the pathogenesis of these processes,
which thus far almost elude all scientific explanation.
DISEASES
MEDULLA OBLONGATA.
ERB.
EEE
I, Anatomical Introduction.
The chief works to be consulted are: B. Stilling, Untersuch, tib. d. Textur u. Func-
tionen der Medulla oblong. Erlangen. 1843.—Untersuch. tiber den Bau des
Hirnknotens oder der Varol’schen Briicke. Jena. 1846.—Schroeder v. d. Kolk,
Bau u. Function der Medulla spin. u. oblongata. Braunschweig. 1859.—
Deiters, Unters. tib. Gehirn u. Riickenmark des Menschen u. der Siiugethiere.
1865.—Stieda, Ueber den Ursprung der spinalartigen Hirnnerven. Dorpat. med.
Zeitschr. II. 1873.—Meynert, Stricker’s Handbook. Vol. 2.—Skizze des
menschlichen Grosshirnstammes, etc. Arch. f. Psych. und Nerv. IV. 387-431.
1874.—Henle, Handbuch der Nervenlehre. 1871.—Huguenin, All. Pathologie
der Krankheiten des Nervensystems. I. Anatom. Einleitung. 1873.—Flechsig,
Die Leitungsbahnen im Gehirn u. Riickenmark des Menschen. Leipzig. 1876.
—Ueber Systemerkrankung im Riickenmark. Arch. d. Heilk. XVIII. 1877.—
Farabeuf, in Diction. encyclo. des sciences médic. 2 Sér. tome VIII. p. 299.
1874.— W. Krause, Handbuch d. menschl. Anatomie. I. 1876.—Duret, Sur la
distribution des artéres nourriciéres du bulbe rhachidien., Arch. de Phy. norm.
et pathol. 1873. p. 97.
Many points, and these perhaps the most important, in the
anatomy of the medulla oblongata, are still unsettled. Indeed,
the relations here are, more than elsewhere, difficult to disen-
tangle. The connections between the different structures of the
medulla oblongata and those, first, of the spinal cord below, and
second, of the central nervous system above, are so extremely
complicated, numerous, and entangled, that even the most care-
ful and thorough anatomical investigation can scarcely make
them understood. This is quite sufficient explanation for the
fact that the views of the best observers on the finer structure of
the medulla oblongata are still at great variance with one another
on several points.
The space in this handbook does not allow of an accurate
826 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
and exhaustive description of the outward form and internal
structure of the medulla oblongata. Yet we can scarcely avoid
giving a short sketch of the principal points, in order to refresh
the practitioner’s memory: on anatomical relations, to put him
au courant with the latest investigations, and acquaint him
somewhat with the present nomenclature, and thus, we hope,
facilitate his comprehension of the morbid anatomical details in
the following pages.
The best way of attaining this object will be to begin with the
structures of the spinal cord, with which we are already
acquainted, and follow these into and through the medulla
oblongata, and after this to give a short description of the other
parts which are peculiar to the medulla. To suit the practi-
tioner’s interests, we shall endeavor, first of all, to give a clear
and correct idea of the topography of the parts, leaving aside
the details of the course of the fibres and their manifold connec-
tions, partly because these are wholly uncertain, and in many
instances in great part unknown.
Even the external boundaries of the medulla are still a matter
of dispute among anatomists, though every one agrees to bound
it inferiorly with the roots of the first cervical pair of nerves.
The superior border, however, is undecided, some considering
it as formed by the inferior border of the pons (which would
correspond on the posterior surface to the upper strize acustice) ;
but most writers include the whole floor of the fourth ventricle,
z. €., the whole rhomboid sinus ; these latter boundaries, too, are
better suited for clinical purposes. We should then take for the
upper boundary the processus cerebelli ad corpora quadr. (which
form the lateral walls of the fourth ventricle) and the entrance
of the Sylvian aqueduct; thus, we may regard the pons as a
cerebral structure, which bounds the medulla oblongata on one
side, and then we need concern ourselves no more with its struc-
ture or pathology in this article.
From a superficial examination of the exterior, one would be
led to think that the columns of the spinal cord run without
ee ae FP Em, —_=
eg Cae ee
ANATOMICAL INTRODUCTION. 827
interruption into: the structures of the medulla oblongata ; but
closer observation proves the error of this view, and shows that
the most manifold transpositions take place, which contribute to
bring new and important structures to the surface, and produce
the characteristic appearance of the medulla.
If we follow up the anterior spinal columns, they appear to
ascend directly and run into the pons. But, on drawing apart
N =n MCA.
SV... Meotpe
MT lene ME
: -- Mazp
Fra. 20.—View of the anterior surface of the medulla and pons. Enlarged, On the right side of the
Medulla the roots of the nerves are removed. a, Anterior column; 8, lateral column; c, decussation of the
pyramids; d, pyramids; e, groove between anterior column and pyramid; J, olivary body ; g, corpus resti-
forme; #, pons; i, fibre arciformes; V-XVZ/, roots of the fifth to twelfth cerebral nerves; Ncla, anterior
roots of the first cervical nerves ; Nclp, posterior roots.
the lips of the anterior median fissure, we perceive that, at the
level of the first cervical nerves, it is obstructed for a distance of
from six to seven mm. by coarse bundles of fibres, which pass
from one side to the other, decussating in fact, and then con-
tinuing their course on the opposite side, along the anterior
fissure. Here we see a crossing of fasciculi, which come to the
surface from the interior, and then usurp the position of the
828 - ERB.—DISEASES OF THE MEDULLA OBLONGATA.
anterior columns in their course upwards. This is the so-called
decussation of the pyramids (Fig. 20, c), and the columns which
go from this to the pons, and take the place of the anterior
columns, are called the pyramids (Fig. 20, d). They issue from
between the anterior columns (Fig. 20, @), which latter retreat
and disappear into the interior of the medulla. This arrange-
ment is often rendered evident by a distinct groove (Fig. 20, é)
running obliquely upwards, and forming the boundary between
the pyramids and the anterior columns proper.
The lateral columns of the spinal cord proceed directly
upwards through the medulla, and are now surrounded by the
(motor) roots of the hypoglossus (Fig. 20, XZZ) and the (chiefly
sensory) roots of the glossopharyngeus (JX) and vagus (X),
which replace the anterior and posterior roots of spinal nerves. —
In the upper half, almost immediately behind the pons, projects
an almond-shaped structure, like a long prominence, and bor-
dered on either side by attenuated stripes of the lateral columns ;
this is the olivary body (Fig. 20, 7). Its prominence is subject
to considerable individual variation. The upper portion of the
lateral column is here often called the olivary column. A small
portion of the lateral column (Flechsig’s direct cerebello-latero-
columnar tract), belonging to the periphery of the postero-late-
ral column, passes in the medulla obliquely backwards, and
takes part in the formation of the corpus restiforme, and also of
the pedunculi cerebelli.
The posterior spinal columns at first continue their parallel
course upwards; a little above the superior termination of the
decussation, however, they part at rather a sharp angle, and
pass into the cerebellum under the form of round columns, much
increased in size. These columns are the pedunculi cerebelli
(Fig. 21, g) or funiculi restiformes. The increase in size would _
alone indicate that these are not the mere prolongation of the
posterior spinal columns; in fact, new bundles contribute to the
formation of the cerebellar peduncles. The components of the
posterior columns proper appear to run directly into the pedun-
culi; the funiculi graciles (Goll’s cuneiform columns) (Fig. 21,
6), forming the internal portion of the pedunculi, at the point of F
the angle swell to nodules, the clava (Fig. 21, d), and are
ANATOMICAL INTRODUCTION. 829
usually connected with the cuneiform column of the other side
by a slender band of white substance, the obex (Fig. 21, @).
The sulcus intermedius posterior (c), which divides the graci-
lis from the cwneiform column proper, continues its course up
to the strize acustice. The cuneiform column runs upwards
alongside the sulcus, increasing considerably in size, as it is rein-
°
4,
Zz
:
9% yj <
F1G. 21.—View of the posterior surface of the medulla, the roof of the fourth ventricle being removed,
to show the rhomboid sinus clearly. The two halves are drawn somewhat apart. Enlarged. a, funiculi
cuneati, et b, graciles; a+b = posterior spinal column ; ¢, sulcus intermedius posterior; @, clava; e, obex ;
J, corpus restiforme ; g, pedunculus cerebelli (= @+06-+-/); h, crus cerebelli ad pontem; i, crus cerebelli
ad corpora quadr.; #, corpora quadr.: 7, striae medullares s. acusticee; m, fibre arciformes; 2, eminentia
teres (genu neryi facialis); 0, fovea anterior; py, locus coeruleus; g, funiculus teres: 7, nucleus of the hypo-
glossal: s+ ¢, ala cinerea; 8, nucleus of vagus; ¢, nucleus of accessorius; uw, nucleus of acusticus; Neip,
posterior root of the first cervical nerve.
forced by other fasciculi, which form the lateral half of the
pedunculus cerebelli. These fasciculi receive the name, corpus
restiforme (f'),and are frequently marked off from the cuneiform
column by a distinct groove (dotted line in Fig. 21), so that they
have been divided by some (Henle) into median and lateral cune-
iform columns; this latter distinction can be more easily de-
830 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
tected ina transverse section (Huguenin). The corpus restiforme
is partly made up of superficially situated bundles, which have
been described under the name of fibre arciformes (Fig. 20, 7;
Fig. 21, m). These arise partly from the bottom of the anterior
median fissure, between the pyramids, and partly from the late-
ral fissure, between the pyramids and olivary bodies. They
appear to be derived from the anterior columns, and form an
arch round the anterior and lateral surfaces of the medulla,
sometimes of large, sometimes of small dimensions ; finally, they
disappear almost completely into the cuneiform columns. They
are generally best developed at the posterior angles of the
olivary bodies, sometimes even covering these. But the corpora
restiformia receive numerous other bundles of considerable size
from the neighborhood of the olivary bodies, and probably, too,
from the bodies themselves.
The separation of the pedunculi cerebelli exposes the deep-
seated gray substance to a considerable extent, thus producing a
slight depression, which is bounded inferiorly and laterally by
the diverging pedunculi cerebelli, superiorly and laterally by the
converging crura corporum quadr.—this lozenge-shaped depres-
sion is called the rhomboid sinus, or floor of the fourth ventricle
(Fig. 21). Its superior angle is formed by the union of the crura
cerebelli ad corp. quadr. at the entrance to the Aqueductus
Sylvii, and its inferior angle lies between the pedunculi cerebelli,
behind the obex at the point of separation of the funiculi graci-
les. Just here too the central spinal canal opens into the poste-
rior longitudinal fissure, and thus communicates with the fourth
ventricle. The obtuse angles on either side are formed by the
junction of one crus with the peduncle of the corresponding side.
The floor of the fourth ventricle is divided symmetrically by
a longitudinal shallow groove. <A superficial inspection shows
us here a number of grooves, depressions, projections, and gray
patches, etc., which are all connected with important structures
in the interior, and thus of practical importance to us.
Of these certainly the most striking are the strie medullares
(Fig. 21,7). In numbers varying from one to twelve, these bun-
dles run horizontally at right angles to the median fissure, from
which they emerge, and cross the pedunculi, and, passing round
> -_—. =
ANATOMICAL INTRODUCTION, 831
them, join the nervus acusticus. They divide the sinus into a
superior large, and an inferior smaller space. Above the striz,
and in the right angle formed by them with the median fissure,
lies a small, rounded, white prominence, corresponding to the
genu nervi facialis and the neighboring nucleus of the abducens
(Fig. 21, 2). Laterally and anteriorly to this we find the so-
called fovea anterior (Fig. 21, 0), a depression which is generally
colored with a dark pigment, and presents the appearance of
a contracted scar. At some depth below this lies the newcleus
proper of the facial nerve.
Going from this towards the superior angle of the fourth ven-
tricle and slightly outward, we strike another gray depression,
called the locus ceruleus (p), which borders on the motor nu-
cleus of the trigeminus.
The gently elevated cords which traverse the inferior triangle
of the rhomboid sinus, parallel to the median fissure, receive the
name of funiculi terctes (Fig 21, 7). Beneath them lies on either
side a nucleus of the hypoglossal (Fig. 21, 7), extending longi-
tudinally for some distance. Passing outwards, we are met by
a light-gray triangle, with its apex pointed to the strie, and its
base resting on the clave. Thisis called the ala cinerea (sand Z).
Its anterior portion (s) is coextensive with the nucleus of the
vagus, while the posterior (¢) contains the upper end of the nw-
cleus accessoriz, which extends far down into the spinal cord,
In the interior of the medulla, somewhat anterior to the ala cine-
rea, the nucleus of the glossopharyngeus comes in contact with
that of the vagus. The posterior median nucleus of the acoustie
forms the anterior and lateral boundary of the vagus nucleus.
It comes nearer the surface than the glossopharyngeus, and oc-
cupies nearly the whole space between the ala cinerea and pedun-
culus, up to the upper border of the striee. Henle has described
it under the name of nucleus acusticus swperior.
The internal structure of the medulla oblongata is so ex-
tremely complicated that no one has yet been able to throw the
slightest light on the general course of the fibres and the connec-
tion between its paths of conduction. Though some structures
have been recognized as undoubtedly analogous to certain com-
ponents of the spinal cord (gray nuclei—gray columns, commis-
832 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
sures, etc.), still we meet with so many new and problematical
forms, the different parts combine in so various and complicated
manners, and the fibrils run in such entangled, tortuous and
interwoven courses, that we must almost despair of ever follow-
ing them up accurately. In fact, up to the present the most
careful and exact investigations have thrown but a very feeble
light upon the subject.
Very little is known with certainty and accepted by all, and
the few facts of this nature may be well described as landmarks
in an unknown region. With the rest we need not further oc-
cupy ourselves, since there is no practical value to be derived
from studying all the conflicting views of the hour. Our task in
this direction only extends to the indication of those regions
about the structure of which next to nothing is known.
The value and significance of successive sections, which are
here too the chief method of investigation, can be studied in
anatomical text-books. From the nature of the subject we can
imagine how imperfect must be the results.
The first material change in the spinal cord—that, indeed,
which leads to the distinction between it and the medulla oblon-
gata—takes place on a level with the first cervical pair of nerves,
consisting chiefly in the decussation of the pyramids.
Large bundles of fibrils collect from the posterior division of
the lateral columns, and pass obliquely forward and upward,
and simultaneously forward and inward towards the anterior
longitudinal fissure. They appear here more or Icss as continu-
ous bands, though frequently interrupted by vertical fibrils.
They cross the fissure, and then run up the other side in the ©
place of the anterior columns, which they have now displaced.
There is likewise a considerably enlarged anterior commissure,
here called the decussation. The bundles of the pyramids too
divide the anterior gray columns from the central gray sub-
stance, and displace them outward (Fig. 22).
These decussating fasciculi are to be regarded as chiefly mo-
tor. They form the coarse-bundled decussation which we see in
the anterior fissure, and are called the inferior or motor decussa-
tion of the pyramids.
Higher up too we may perceive bundles of quite considerable
ANATOMICAL INTRODUCTION. 833
dimensions, arising from the posterior columns, bending forward,
passing the central canal, crossing the middle line, and finally
running up in the pyramid of the opposite side, where they
generally occupy the exterior portion. This is the anterior or
sensory decussation. Huguenin describes a bundle from the
posterior cornua as taking part in this, but Flechsig’s latest
investigations have, to say the least, thrown great doubt upon
the significance of these fibres and the exactitude of their course.
Flechsig positively denies any connection whatsoever between
this anterior decussation and the pyramids proper. Still, these
fibrils most undoubtedly alter the configuration of the gray sub-
stance in the spinal cord, dividing the head and neck of the
Fia, 22.—Transverse section through the infer‘or portion of the medulla oblon. at the level of the decus-
sation of the pyramids. a, Anterior gray columns; 8, head of the posterior column and ascending rcot of the
trigeminus; c, anterior columns (pyramids); funiculi, d, cuneati, et e, graciles; Jf, decussation of the pyra-
mids; g, formatio reticularis; 4, roots of the accessorius ; 4, nucleus of the gracilis; *, nucleus of the cunei-
form.
posterior gray cornua from the central gray substance (Fig. 22).
At the same time, these parts are displaced somewhat outwardly
towards the periphery, since the lateral columns diminish in size.
The increase of volume in the posterior gray columns enables us
to follow them on transverse sections through the greater part of
the medulla and in their gradual outward course (ef. Fig. 22, 3,
Figs. 24-26, c). In the peripheral portion of these sections we
observe large bundles of fibrils ascending vertically ; these are
the large ascending roots of the trigeminus (Fig. 22, 6), which
may be followed down to the second and third cervical nerves
and upward as far as the exit of the sensory trigeminal roots.
VOL. XIII.—53
834 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
The motor decussation has lately been submitted to thorough
investigations, and appears to be derived mainly from the pos-
tero-lateral columns. The diagram (Fig. 23) enables us to see
this, and observe how the fibrils, before crossing the middle line,
bend gradually forward, and how they displace the anterior col-
umns after their passage across. The figure demonstrates too
the bundles from the anterior columns which join the pyramids
Fig. 23,—D‘agram of the motor decussation. Transparent longitudinal view of the medulla, with only
the anterior and the decuszation of the postero-lateral columns left, a, a, Anterior columns; 6, 6, pyramido-
postero-lateral columns: the pyramidal columns of the right side (c), arising from the left lateral column. and
reinforced by a slender bundle from the right anterior column, are left unshaded, those of the left side are
dotted. The part of the anterior columns which disappears behind the pyramids is shaded with vertical lines.
on either side and pass up along with these wundecussated
(Flechsig). Thus we see that the pyramids contain not solely
the decussated fibrils of the postero-lateral columns, but also
some additional undecussated elements, varying in number, from
the anterior columns. Flechsig positively denies the association
with the pyramids, at an anterior point, of bundles from the pos-
terior columns and cornua, though it has been asserted that this
takes place, and that these run with the pyramids into the pons.
e—— Ul
ANATOMICAL INTRODUCTION, 835
The deflection of so many bundles from the lateral and poste-
rior columns produces a number of fibrils, which lie horizontally
on a transverse section, completely interwoven, and embracing in
their meshes the vertical fibrils, after these latter have split up
in every direction. Thus from the reticular processes of the
spinal cord we get the formatio reticularis (Fig. 22, 9). This
latter structure occupies more and more space in the transverse
section as we follow it upwards, and connects all the fibrils and
structures of the medulla. But its complicated mesh-work is
scarcely to be unravelled. Thus the transverse section even of
the inferior portions of the medulla assumes the altered ap-
pearance we see in Figure 22. The four cornua are separated
from the central gray substance, and the posterior are further
very much dislocated. The centre of the section is occupied by
the remaining gray substance and an enormous formatio reticu-
laris. In addition, we see the development of new gray substance
around the different bundles and columns. On particularly good
sections one may often recognize the horizontal fibrils of the
roots of the accessorius, arising from the neighborhood of the
lateral cornua, 7. e., from the tractus intermedio-lateralis (Fig.
22, h).
Higher up, while the formatio reticularis is visibly increasing
in size, we are met by new structures, the significance of which
is only in part known.
Of these structures the most striking are the olivary bodies
(Figs. 24, 25, 26, 6). They arise in the territory of the lateral
columns, close upon the pyramids, and attain the length of 14
mm. ‘They resemble an extremely irregular disc, and contain a
number of small ganglion-cells. On the whole, they look like a
bean or an almond, with the hilus directed inwards. A number
of nerve-bundles, coming from all points, enter at this hilus,
some terminating in the gelatinous substance of the olivary
bodies, while others pass through in the form of fine bundles.
This appears to bring about an extremely wide connection with
all the different parts of the medulla oblongata.
Further on we perceive here a number of gray nuclei, most
of which are connected with some cer@bral nerve, and must be
regarded as medullary roots. The first of these is the hypoglos-
836 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
sal nucleus (Figs. 24, 25, 26, g), situated beside the middle line,
and falling back with the central canal. At the entrance of this
canal, just below the floor of the fourth ventricle, we find it lying
on the edge of the median fissure. |
This nucleus attains the length of about 18 mm.; it is cylin-
drical, attenuated, and contains a number of large ganglia, re-
sembling in every respect the multipolar cells of the anterior
cornua. It corresponds exactly to the anterior cornu, though it
retreats along with the central canal, which opens posteriorly,
while an increasing number of fibrils pass over into the anterior
Fia. 24.—Transverse section of the medulla through the inferior portion of the olivary body and the
superior termination of the nucleus of the accessorius, a, Pyramids; 0, olivary body; c, gelatinous substance,
and ascending root of the trigeminus; d, corpus restiforme; e, funiculi cuneati, f. graciles; /, nucleus
accessorii; g, nucleus hypoglossi; fasciculus rotundus (respiratory fascicle of Krause); i, nucleus funiculo-
rum gracilium et cuneatorum; XJ and XJ/, radices accessorii et hypoglossi; internal parolivary bodies
(nucleus of the pyramids). 7g
portion of the medulla. Thus the anterior end of the hypoglos-
sal nucleus comes to be situated on the floor of the fourth ven-
tricle. The roots of the hypoglossus (Figs. 24 and 25, X77) run
horizontally between the pyramids and the olivary bodies to join
their nucleus, and their whole course is easily followed.
Somewhat posterior to the nucleus hypoglossi, and in the
inferior portion of the medulla, we find the nucleus of the acces-
sorius (Fig, 24, 7). It, too, is represented by a columnar, attenu-
ated, gray structure, which extends to the tractus intermedio-
lateralis of the spinal cord (cf. Part L, p. 16), and with this it
gradually alters its position in relation to the other parts of the
ANATOMICAL INTRODUCTION. 837
section. From it the superior roots of the accessorius run later-
ally and somewhat posteriorly.
The nucleus accessorii is immediately bounded by a gray
mass, which is situated in this region, beside the nucleus hypo-
glossi. This is the nucleus of the vagus. It contains a number
of small and middle-sized ganglia, and lies in the fourth ventri-
cle, along with the hypoglossal nucleus, in the so-called ala
cinerea, immediately beneath the surface.
Immediately adjacent to the internal portion of this nucleus
comes a clearly defined, round fascicle of coarse fibrils (Figs. 24
and 25, 2). We can trace this along the whole course of the
Fra. 25.—Transverse section through the centre of the olivary body, and of the vagus-root. a, Pyra-
midal fasciculi; 6, olivary body; c, gelatinous substance and trigeminus-root; d, corpus restiforme; e, fu-
niculi graciles et cuneati: jf, nucleus vagi: g, nucleus hypoglossi; h, fasciculus rotundus (respiratory fasci-
cle); i, parolivary body (external); &, fibre arciformes; /, nucleus of the same; m, motor nucleus of the
vagus (Meynert); X, XJJ, fasciculi of the vagus and hypoglossal roots,
nucleus vagi, and find it composed of fascicles from the vagus,
glossopharyngeus, and accessorius. It runs down into the cer-
vical portion of the cord, and is said to come into connection
with the phrenic (Krause’s respiratory fascicle). According to
Stieda, the roots of the three above-mentioned nerves are derived
from this lateral ascending longitudinal fascicle, and not from
the gray structures, which are generally designated as their
nuclei.
The nucleus of the vagus is bounded, too, by another gray
structure, which comes into immediate contact with it, and is not
separated by any distinct boundary ; it lies, however, somewhat
838 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
less superficially, and is designated as the nucleus of the glosso-
pharyngeus (Fig. 26, h). The roots of the glossopharyngeus run
almost horizontally from it, outwards and forwards, making their
exit from the medulla above the roots of the vagus.
Meynert and Huguenin describe further a motor nucleus of the vagus and glos-
sopharyngeus, which is situated more in the interior, between the olivary body and
ascending root of the trigeminus. We have indicated its position in Fig. 25 by m.
Stieda looks upon it as the nucleus proper of the vagus.
The posterior median nucleus of the acusticus (Fig. 26) (nu-
cleus acust. sup. of Henle; median nucleus of the posterior root
of the acusticus of Krause) comes likewise into contact with the
K
Fic. 26.—Transverse section of the medulla through the superior end of the olivary body, where the pos-
terior median acoustic nucleus occurs. a@, Pyramids; }, olivary body; c, gelatinous substance and ascending.
trigeminus-root; d, corpus restiforme; e, funiculi cuneati et graciles; /, posterior median acoustic root; g,
anterior termination of the hypoglossus nucleus; 2, glossopharyngeus nucleus; 7, posterior lateral aco
nucleus; X%, fibre: arciformes; VZJ//, posterior acoustic roots.
vagus; but it is more superficially situated, and somewhat to
the outer side of the glossopharyngeal. It occupies the whole
space included between the ala cinerea and pedunculus cerebelli,
up to the anterior border of the striz medullares. The posterior
root of the acoustic takes its chief origin from this nucleus, and
passes out partly in superficial fasciculi (strie acustice), and
partly through the body of the medulla. Between these two
fasciculi we find the posterior lateral acoustic nucleus (Fig. 26, 7)
(nucleus acust. inferior of Henle) lying beside the peduncle, in
the form of a small gray nodule. Besides these, the acoustic
possesses two other nuclei, belonging to its anterior roots, and
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ANATOMICAL INTRODUCTION. 839
situated in that portion of the medulla which lies anterior to the
strie. The first is the anterior median acoustic nucleus (Fig.
29, VZZZ) (median nucleus of the anterior acoustic roots of .
Krause), and occupies the external angle of the fourth ventricle,
about the middle of the pedunculus cerebelli. The second ap-
pears like a prolongation of the postero-lateral acoustic nucleus
beside the peduncle, and is wedged in between the peduncle, the
crus cerebelli ad pont. and the flocculus. It receives the name
of anterior lateral acoustic nucleus (nucl. acust. lateralis of
Henle), and gives origin to the portio intermedia Wrisbergii.
We have now described in the medulla oblongata, below the
level of the pons, all the structures that are at all well known.
There are, however, a few other gray nuclear bodies, whose sig-
nification and connections are but little known. These are the
following:
The nucleus of the pyramids (internal parolivary body, Fig.
24, 7:), a structure which is bent at a sharp angle, and runs verti-
cally, consisting of gray substance of the same structure as the
olivary bodies. They lie opposite the pyramids in front, and to
the inside of the olivary bodies, corresponding nearly with the
position of the former anterior cornua.
Then we have the parolivary bodies (external, Fig. 25, 2),
similar, slightly concave bands, which occupy a position exactly
bounding the internal half of the posterior border of the olivary
bodies.
Further, we find the nucleus of the cuneiform column arising
from what was the anterior cornu, a longish, gray body on the
inner border of the cuneiform column, and enlarging as it ascends
(Fig. 22, k, Fig. 24, 7).
Fourthly comes the nucleus of the funiculus gracilis, in the
shape of a longitudinal pillar of gray substance. It arises from
the centre of the funiculus gracilis, and produces the enlarge-
ment in this, known as the clava (Fig. 22, ¢7, Fig. 24, 7). It
ascends with the nucleus of the cuneiform column, and both
* extend to the posterior end of the postero-lateral acoustic nu-
cleus.
The last on this list is the nucleus of the lateral column, a
small, cylindrical, attenuated column of cells in the posterior
840 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
portion of the lateral column between the olivary body and ses
caput cornu posterioris.
The remainder of the transverse section is occupied by the
formatio reticularis, which attains its maximum dimensions and
symmetry parallel with the olivary bodies. This structure is con-
stituted of a number of fascicles, which run horizontally in an
arched course, though sometimes radially, and embrace in their
meshes a number of vertical bundles. All through its substance
we see numerous ganglia, so that we find the most intimate inter-
mixture and intertwining of white and gray substance. The
place of the anterior commissure below the decussation of the
Fig. 27.—Transverse section of the medulla throngh the inferior border of the pons, on a level with the
facial and abducens roots. Somewhat diagrammatic. The right half represents a section made a little below
the left section. a, pyramids; b, transverse fasciculi of the pons; ¢, gelatinous substance and ascending tri-
geminus root; d, pedunculus cerebelli ; é, nucleus of the abducens (nucleus common to the facialis and abdu-
cens); J, genu nervi facialis; g, descending limb of the facialis root; % nucleus of facialis; 4, anterior
olivary body; V7, root-fascicle of abducens; VII, do. of facialis,
pyramids is filled above this point by the raphe. This structure
enlarges in its antero-posterior axis as it ascends, and consists
both of longitudinal and transverse fibres. We have further to
mention the fibre arciformes, which surround almost the whole
outer surface of the medulla in the form of a layer (varying in
dimensions) of fibres that take a horizontal or an oblique course.
They increase in size as they ascend, and generally run into the
raphe (Figs. 25 and 26, x).
Almost parallel with the most anterior stria we are met on
ANATOMICAL INTRODUCTION, 841
the anterior surface of the medulla by an enormous body of
transverse fasciculi, 7. e., the pons Varolii (Fig. 27, 6, Fig. 28). It
is this structure which produces the characteristic appearance of
the anterior portion of the medulla. The pons consists of numer-
ous and well-developed transverse bundles, between which we
can trace scarcely anything but the main longitudinal fibres,
namely, the pyramids.
The most important and best-studied parts of this anterior
portion of the medulla are the nuclei of the fifth, sixth, and
seventh cerebral nerves.
The best and longest known of these is the nucleus of the
abducens (mixed nucleus of the facialis and abducens, Fig. 27, é).
It lies in the continuation of the hypoglossus, only divided from
this by a very short interval, and occupies a position just above
the striz on the side of the median fissure, which extends about
six or seven millimetres in the form of an attenuated gray col-
umn. The roots of the abducens run almost horizontally from
the pyramidal region towards the pons, at the inferior border of
which they diverge slightly.
This nucleus appears, too, to be connected with the facialis,
for the facialis root takes its course from the lateral region of the
pons towards the median fissure of the rhomboid sinus, close
to the abducens-nucleus. From the descriptions of Henle and
Huguenin, there can be no doubt that the facialis root gives off a
number of fibres which pass into this abducens-nucleus; hence it
has been designated as ‘‘ posterior facial nucleus.’”’ After this,
the facial root takes a sudden backward turn, and runs for a
short distance parallel to the median fissure. Turning again
sharply (genu nervi facialis, Fig. 27, 7) it presses forward and
into the interior of the medulla, where it meets a longish fascicle
of gray substance, the nucleus proper of the facialis (Fig. 27, h).
Thus we see the root of the facialis only passes round the abdu-
cens nucleus in a horseshoe course, and is certainly in but very
small part derived from this nucleus. The latest observers return
to the old view, and deny even the remotest connection between
the facialis and the nucleus of the abducens.
The question about the facial nucléus does not appear to have
received its final answer. Amongst others, Lockhart Clarke de-
842 ERB:—DISEASES OF THE MEDULLA OBLONGATA.
scribes a so-called ‘‘inferior’’ facial nucleus in the inferior por-
tion of the medulla on a level with the hypoglossal and acces-
sorial nuclei, and indeed pathological facts (bulbar paralysis)
seem to confirm its existence.
In connection with the trigeminus, the complication is still
greater. We have already described one of its roots, the ascend-
ing, which belongs to the caput cornu posterioris, and may be
traced down through the whole length of the medulla into the
cervical region of the spinal cord. So we are justified in regard-
ing the caput cornu post. as inferior sensory trigeminal nucleus
(Fig. 23, 6, Figs. 24-28, c). The motor trigeminal nucleus is
ing with the exit of trgeminne’ Bemt-dingrammation « pyramide; & golaiinent schetates saan
motor undlens and soct of trigeminus’’% middle eehsoey trigemitial necleas: ¥, root sasaae Gea
situated on the floor of the fourth ventricle, close to the upper
border. Its anterior termination coincides with the entrance of
the Sylvian aqueduct, and from this it extends in form of a fine,
gray column to the border of the facialis roots. This nucleus
gives origin to the portio minor of the trigeminus. At the point
where the roots of the portio trigemini major separate, and run
some forward, and the rest backward, we find a small gray
mass lodged between the two, representing the middle sensory
nucleus of the trigeminus (Fig. 28,7). The smaller portion of
root-fascicles (Fig. 28, 6), which takes an anterior course, passes
to the far side of the corpora quadri., and terminates there in the
ANATOMICAL INTRODUCTION. 843
superior sensory trigeminal nucleus. Thus we can count up four
nuclei for the trigeminus, as we did for the acoustic.
In addition to these gray nuclei we meet in the superior por-
‘tion of the medulla: 1, the swperior olivary body (27, i), a long-
ish, gray column, which is situated in the pons just in front of
the facial nucleus, and 2, the pons nuclei, consisting of patches
of gray substance scattered through the whole pons.
The remainder of the transverse section through the anterior
part of the medulla is taken up by the transverse fibres of the
pons, and the formatio reticularis.
S21
Fic. 29.—Transparent view of the medulla from behind. On the right hand the nerve-nuclei are dia-
grammatically represented, and lettered with Roman numbers. V, motor trigeminal nucleus; V’, median, and
V”, inferior sensory trigeminal nuclei; V/Z, nucleus of abducens; VJ/, facial nucleus; V/ZI/, posterior median
acoustic nucleus; V///’, anterior median, V///’” posterior, and VZ//’’’, anterior lateral acoustic nuclei; LX,
glossopharyngeal nucleus; nuclei of X, vagus, X/, accessorius, and X/J7Z, hypoglossus, 1, crus cerebelli ad
pontem ; 2, crus cerebelli ad corp. quadr.; 38, crus cerebelli ad medullam; 4, eminentia teres; 5, striw
acusticz : 6, ala cinerea. The Roman numerals (V.—XII.) beside the figure represent the corresponding
nerve-roots. The Arabic numerals (22, 24-28) are attached to the transverse section of roots, which bore the
same numbers in foregoing figures.
It is evident from the complicated relations between all the structures we have
been describing that it is no easy matter to get a correct idea of the topographical
anatomy of the fresh unhardened organ, one that will take in every particular, and
enable us at a post-mortem examination to say without hesitation what nuclei or
nerve-fascicles, etc., coincide with some small patch of softening, some diminutive
apoplexy, or with some defined sclerotic centre. In order to lighten the practition-
er’s task in this direction, we insert two diagrammatic sketches, which give lateral
844 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
and front views of the approximate situation of the most important gray centra.
We here follow the example of others, such as Stilling, Krause, et al. These diagrams ~
do not of course make the very slightest pretensions to extreme accuracy, but still
we hope they will give an easily comprehensible picture of the topography, and
one that will act as a key to this anatomical labyrinth. .
Fig. 29 represents a transparent view of the medulla oblongata from behind,
on the right side of which all the above-mentioned nuclei are represented and their
names attached, while on the left side, to aid comparison, nothing is given but the
superficial structures, such as the ala cinerea, strie medullares, etc. By this means
Fig. 30.—Transparent lateral view of the medulla, showing the relative positions of the most important
nuclei; right half of the medulla, seen from the surface of section; the parts that lie closer to this surface are
deeper shaded. Diagrammatic. Py, pyramidal tract; Py Ar, decussation of pyramids; 0, olivary body ;
Os, superior olivary body; V, motor, V’, middle sensory, ¥”, inferior sensory nucleus of trigeminus ; A
nucleus of abducens; Gf, genu facialis; VJ, nucleus facialis; VZ/T, posterior median acoustic nucleus; LX, “i
glossopharyngeal nucleus; XY, nucleus of vagus; XJ, accessorius nucleus; X//, hypoglossal nucleus ; ;
nucleus of the funiculus gracilis; # V, trigeminus root; those of the R V J, abducens and R VZJ, facialis. — ‘at
one sees plainly the nuclei of the sixth and seventh, of the fifth and eighth, the
hypoglossal nucleus, and the inter-connected nuclei of the ninth, tenth, and eleventh |
pairs. Of course, neither the form nor size of the diagrammatic nuclear structures ag
is exactly true to nature, the only thing that is aimed at being a faithful representa- _
tion of their situation as relates to one another and the surface. Further, we have
sacrificed a number of details to the clearness of the sketch.
Fig. 30 gives a transparent view of the right half of the medulla, seen from the 4
surface of section (i. ¢., antero-posterior, through the middle line, and vertical), so
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ANATOMICAL INTRODUCTION. 845
that what is nearest to the observer in the diagram is nearest to the middle line.
* In this figure, too, only some of the gray nuclei are represented, in order clearly to
display their relation to the exterior and their internal relations of space. The
nuclei nearest the observer (i. ¢., nearest the middle line) are deeper shaded, while
those that are further from him, and consequently nearer the surface of the
medulla, have only a light shading. Amongst the nerve-tracts which communicate
- with the nuclei we have given only semi-diagrammatically those of the fifth, sixth,
and seventh nerves, especially the latter, in order to render the genu nervi facialis
more distinct. Only the three nuclei of the trigeminus, which lie within the medulla,
are sketched, and only the principal nucleus of the acoustic.
Connection between the histological elements, and the course
of the nerve-jibres in the medulla oblongata.
Notwithstanding all the investigations that have been made
and the incalculable trouble expended on this subject, we are
scarcely acquainted with the barest outlines. We know just as
little about the fate of most of the fasciculi, which enter the me-
dulla from below and from above, as we do of the significance of
numerous striking structures in the medulla. Their connection
with one another and with the gray nuclei, the mode of inter-
ruption and where it occurs, their transposition and their termi-
nation, all remain a mystery.
Still we know somewhat more about the course of the root-
jibres from their entrance into the medulla till they reach their
proper nuclei, where they temporarily end. The root-fascicles of
the hypoglossus, and perhaps, too, those of the abducens, are the
only ones which run directly and almost horizontally from their
point of entrance, and can be followed on a transverse section
along nearly their whole course. Most of the other root-fibres
take a more or less oblique course and are oftentortuous. Part-
ly, indeed, their course is comparatively simple ; but sometimes
they break up into separate fascicles, and sometimes press in-
wards towards the nuclei in more compact masses; such are the
root-fascicles of the accessorius, vagus, and glossopharyngeus.
But others are much more tortuous, and split up in all directions
to join nuclei that lie far apart ; to this category belong the roots
of the trigeminus and acoustic. The roots of the facial, finally,
as we described them above, form a large arch with its crown
(genu) touching the posterior surface*ef the medulla, and its pil-
lars in the facial nuclei.
846 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
There have been many investigations made, and much discus-
sion, on the possibility of a decussation of the root-fibres in the
medulla. It seems, however, to be settled beyond doubt, that
by far the greater part of the fibres of every nerve that enters
the medulla remains on the same side, and ends in the gray
nuclei of the side. The decussation of some few fibres has been
asserted, but by no means proven. Krause’s words on this sub-
ject represent truly the present extent of our knowledge ; he
says: ‘‘The roots of the abducens, of the portio trigemini minor,
the anterior acoustic and the inferior accessorial roots most cer-
tainly do not decussate ; a partial decussation (of some fibres) of
the portio trigemini major, of the posterior acoustic roots, of the
glossopharyngeus and vagus may take place ; possibly, too, of
the facial, the superior accessorial, and the hypoglossal, but the
assumption of the partial decussation of these latter may be due
to misconceptions.’’ In any case the decussation of all these
tracts (and we are compelled by a number of clinical facts to
assume their decussation) takes place after they have passed
their nuclei, further up in the medulla or in the pons. But the
exact place where it occurs is totally unknown, since even the
central continuation of all these nerves after they pass into their
nuclei is almost completely a blank to us. We can only conjec-
ture that these tracts are to be looked for in the formatio reticu-
laris, and that they then successively cross in the raphe, and
afterwards join other tracts (e. g., the pyramidal) at different
points as these come up from the spinal cord to the brain.
Our knowledge, too, is at the same low point as regards the
course of the different tracts into which we can dissect the spinal
cord, and as regards the ultimate course of the spinal columns in
the medulla oblongata.
The course of the pyramidal tracts has, however, been settled
beyond all doubt by the thorough investigations of Flechsig.
They are collected from the posterior portions of the lateral and
the internal fasciculi of the anterior columns, and after the decus-
sation of the parts alone derived from the lateral columns, they
run directly and continuously through the medulla upwards ;
they then enter the pons, and separate gradually into a number
of fibrils, but without any transposition or discontinuity, till they
— ae
ANATOMICAL INTRODUCTION. 847
arrive at the pedunculus cerebri, where they pass through the
inner capsule and further on into the brain. In the pons the
pyramids appear to be reinforced by fibres from the pons and
fibree arcuate, which probably come from, or are going to, the
cerebellum. Flechsig positively denies any addition to the
- pyramids from the so-called sensory decussation of the posterior
columns and cornua.
The direct tractus ab cerebello ad columnas laterales, which
Flechsig, too, has studied so accurately, runs completely into
the restiform body, though it is only one factor in this structure.
The two go together into the cerebellum, where their termination
has not yet been discovered. The real significance of this tract
has not been determined, but it may have some connection with
Clarke’s columns.
It is a more difficult matter when we come to the posterior
columns. The so-called funiculi graciles (Goll) probably end
in great part in the ‘‘nuclei of the columne graciles’’ at the
level of the clave. In the same way the greater part of the
funiculi cuneati terminates in the nucleus of this column; pos-
sibly, however, some of its fibres go directly as fibre arcuatze
into the formatio reticularis, olivary body, etc. But the further
course of the posterior columns is totally unknown. The old
view (which rested on external appearances) that the funiculi
graciles et cuneati continued straight into the pedunculi cerebelli,
and ran with these into the cerebellum, while the external por-
tion of the pedunculi (the corpus restiforme proper) was derived
through the fibre arcuatze ext. et int. from the antero-lateral
column—this view was most decidedly a false one. But the
modern view, which has been worked out chiefly by Meynert,
has not passed without opposition. Meynert considers that the
greater part of the posterior columns (or their continuation) runs
into the olivary and parolivary bodies of the same side, and that
then their continuations pass across the raphe, finally forming
the restiform body of the opposite side. Accordingly we should
have the virtual continuation of the spinal posterior columns in
the restiform bodies of the opposite side, and the olivary and
parolivary bodies thrown into their couwse. What are defined as
funiculi graciles et cuneati in the pedunculi cerebelli, and which
848 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
lie in the middle line, these Meynert describes as structures of new
origin and springing from the formatio reticularis, which higher
up join the spinal columns of the same name, and take their
place, without being continuations of these, in the same manner
as the pyramids take the place of the anterior columns.
Space does not allow us to give in detail Flechsig’s objections ~
to this view of Meynert’s. We shall only mention that Flechsig
describes a great number of fibres which come from the nuclei of
the funiculi graciles (anterior decussation) and accompany the
pyramids for some distance. They soon, however, leave the
pyramids, and rejoin the formatio reticularis in the neighborhood
of the olivary and internal parolivary bodies. Flechsig, too,
asserts the existence of an extensive connection between the oli-
vary body and the cuneiform column of the same side. Accord-
ing to the same author at least a portion, the outer portion, of
the restiform body is composed of fibres, which spring from the
formatio reticularis and the region of the olivary decussation.
The remainder of the anterior, after deduction of the pyra-:
mido-anterior columns (Flechsig’s fundamental anterior column)
_ Tuns directly upwards into the so-called posterior longitudinal
fascicle of the medulla, which is situated posteriorly between
the roots of the hypoglossus and the raphe. This fascicle is
then continued through the posterior portion of the pons into
the cerebrum. |
What remains of the lateral columns, when we put aside the
pyramido-lateral tract, is lost in the formatio reticularis, and is —
here possibly in direct connection with the corpora quadrigemina
and the thalamus opticus. From the latter two structures, as we
must not forget, a very considerable number of fibres descend to
the medulla, and take part in the construction of the formatio
reticularis. In that portion of the formatio reticularis which
lies between the olivary bodies, Flechsig describes the fibres that
are connected with the corpora quadrigemina, and in a region of
the format. retic. posterior to this he places the fibres which come
from the optic thalamus.
After we have exhausted all that we know perfectly and in
part in the medulla, there remains a vast field of which we know
nothing whatsoever. The exact connections and significance of
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ANATOMICAL INTRODUCTION. 849
the olivary and parolivary bodies, the pyramidal nuclei, etc.,
are all totally unknown; further, we know nothing of whence
the innumerable fibres of the substantia reticularis come, and
whither they go. Weare equally ignorant of the central tracts
of all the different bulbar nerves, and of the ending and signifi-
cance of the fibres of the pons. Nor are we acquainted with
the origin and function of the majority of the peduncular tracts.
Further, none of the centra, the existence of which has been
assumed to explain physiological facts, the centra for the respir-
atory and cardiac movements, and for deglutition, the vaso-
motor centra and the centrum for convulsions—in fact, all the
great reflex tracts of the medulla—none of these has been recog-
nized by the anatomists. Doubtless the formatio reticularis does
display the most suitable anatomical structure for the accom-
plishment of every possible reflex action, and so it is perhaps
allowable to conjecture that this formation chiefly serves for re-
flex processes; but there is an extremely wide gulf between a
conjecture like this and a certainty which clears up every detail.
We consider it advantageous to give a diagram of the course of the fibres (after
Flechsig, Arch. der Heilk. XVIII. Taf. VI.) to enable the reader to get a general
conception of the subject, and at the same time show him how complicated the
study is. Figure 31 represents the medulla, pons and the neighboring structures,
leaving out all the gray nuclei except the olivary bodies, and only giving the for-
matio reticularis as a shaded space. The sketch gives a general view of the most
important and best-known tracts, which ascend from the anterior, lateral, and pos-
terior columns of the spinal cord (V, 8, H). We can see plainly how the pyram-
idal tracts (Py) are formed from the pyramido-anterior (a) and pyramido-lateral
(d) tracts. And then we can follow the course of the cerebello-lateral columns (e-e)
which ascend to the pedunculi cerebelli. Then we observe how the internal por-
tions of these pedunculi (P.c.7) are lost in the formatio reticularis, whilst the exter-
nal (Pc.e) run into the olivary bodies, The remainder of the anterior (}) and lateral
(c) columns end in the formatio reticularis, The fibres of the funiculi graciles (/),
after piercing the nucleus of the funiculus (/’), form the anterior decussation of the
pyramids, join the pyramidal tracts, and then immediately fall back into the oli-
vary bodies and the formatio reticularis, The tracts of the cuneiform column (g)
after they reach their nuclei, spread out into the olivary bodies, and partly into
the formatio reticularis. This formation further receives fibres from the thalamus
opticus (7hal.) and corpora quadr. (C.g./). From the latter structures, too, fibres
pass into the olivary bodies (Cg. 0). .
Thus we see that the formatio reticularis receives fibres from every quarter, and
VOL. XIII. —54
850 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
that these fibres are here woven into a complete chaos of threads. If we only imagine
the addition of a number of other gray nucleolar structures (to which we have here
made allusion), and all their afferent and efferent fibres, the root-fibres, the fibre
arcuate, the fibres of the pons, etc., we shall then have a painfully acute idea of the
structure with which we have to deal, and the hopelessness of ever unravelling it;
we shall then, too, comprehend how our knowledge of the finer structure of the
medulla has remained so extremely incomplete, in despite of all the work and trou-
ble bestowed upon it,
Thal.
_
WN Wie:
-”
WN
WS
WS
(UWwov WG
\\ NYG WSEAS WN
CRY
WOK WS\ \
\\
Ol.
Fia. 31,—Diagram of the chief tracts in the medulla. The formatio reticularis is represented by shad-
ing. Ol, olivary body; V, anterior, S, lateral, and H, posterior spinal funiculi: a, pyramido-anterior
tract ; d, pyramido-lateral tract; Py, pyramidal tract ; b, remainder of anterior column; ¢, remainder of the
lateral column ; ¢-e, cerebello-lateral tract; f, funiculus gracilis, and /’, nucleus of the same; g, funiculus
cuneatus, and g’, nucleus of the same ; P.c.i, internal fasciculus of the pedune. cerebelli; P.c.e, external fasci-
culus of the same ; C.g.F, tract from corp. quadr, to format. retic. ; C.g.0, the same to the olivary body ; Thal.
tract from the thalamus opticus,
Vessels of the medulla oblongata.—Duret’s exhaustive inves-
tigations have proved that the medulla gets nearly its whole
supply of blood from the vertebral and basilar arteries, the lat-
ter supplying the pons portion. Here we have chiefly to men-
tion small, median branchlets which pierce into the raphe be-
"Ta +
ye oe
PHYSIOLOGICAL INTRODUCTION. 851
tween the pyramids, and are given off by the art. spin. ant. for
the bulbus and by the basilaris for the pons. They run up to
the floor of the fourth ventricle, and ramify here, forming a large,
narrow-meshed capillary network, especially round the gray
nuclei. Thus we see that they originate chiefly from the left
vertebral, for this artery generally gives off the art. spinal. ant.
when it is single, and when there are two anterior spinal arteries
the median bulbar branchlets are generally derived from the ant.
spin. sinistra. But besides these, small vessels pierce the me-
dulla along with the nerve-roots, and run to the corresponding
nuclei, where they take part in the formation of capillaries. The
olivary bodies and pyramids are supplied by small branches
from the vertebral and anterior spinal arteries. The restiform
bodies receive vessels from the art. cerebelli infer. post., whilst
the posterior spinal arteries send branchlets to the pedunc. cere-
belli and floor of the fourth ventricle. :
Most of these little vessels are so-called terminal arteries
(Cohnheim’s ‘‘ Hndarterien’’). Their ramification produces a
comparatively open-meshed network in the white substance,
while in the gray the meshes are very numerous and narrow. It
need hardly be said that numerous varieties and abnormalities of
origin and course occur amongst these little vessels, and these
are of some importance in the explanation of certain clinical
occurrences.
There is nothing special to be said of the veins, and the Zymph-
vessels in the medulla are quite analogous to those of the spinal
cord.
IL. Physiological Introduction.
Amongst others we would direct attention to: Longet, Anatomie et physiologie
du syst®me nerveux. T. I.—Schiff, Lehrbuch der Physiologie des Menschen.
I. 1858-59.—Schroeder v. d. Kolk, Bau u. Function der Medulla spin. und
oblong. 1859.— Wundt, Physiol. Psychologie. Leipzig. 1874.—Laborde, Dic-
tionn. encycl. des sc. méd. 2. sér. T. VIII. p. 604. 1874.—Poincaré, Le syst?me
nerveux central, etc. 2me édit. T. I 1877.
Besides these, the text-books of Z. Hermann, Wundt, Funke, Vierordt, etc., may be
consulted, and innumerable monographs in al] possible physiological periodi-
cals,
852 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
The physiology of the medulla oblongata is just as imperfect
and obscure as its anatomy, so that we have not become pos-
sessed of any undisputed information on the most elementary
and important facts. For instance, we know nothing of the con-
duction of sensory impressions, or of the exact position of the
chief centres.
We are, indeed, acquainted with a number of facts, which
teach us to recognize the medulla as one of the most important
divisions of the central nervous system, and which give it a
prominent part in several all-important physiological processes,
such as respiration, the cardiac movements, vascular innervation,
speech, and others. But we have got little beyond the confirma-
tion of these facts, and we are in especial darkness as to the
anatomical distribution of these functions and their components.
~ There are very good reasons for all this, and the chief of them
is the difficulty of experimentation. For the parts lie so deep
and are so well protected, the slightest injury to them is so dan-
gerous, the structures themselves are so extremely small, they
are so wonderfully connected in a complicated manner with all
possible adjacent structures, and the white and gray substances
are so intimately mixed—all these circumstances are so many
insurmountable difficulties in the way of physiological investiga-
tion.
Consequently we must not claim too much from physiology.
We should undoubtedly look for most important explanations
from careful clinical observation, combined with accurate post-
mortem examination, though this has yet been scarcely at-
tempted.
In this state of things we can and must give the practitioner
only a very brief account of the physiology of the medulla ob-
longata.
We shall first study the medulla as an organ of conduction.
Nobody can entertain the slightest doubt that the motor im-
pulses sent from the cerebrum to the spinal cord, and the sen-
sory irritations on their way from the periphery to the brain,
must pass through the medulla oblongata. Further, we are
justified in assuming that the parts of conduction for several
other irritations, which pass between the spinal cord, the cere-
he * AbAsae? - bee »*
if
PA wd baat Aird fA. abe
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a en
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eaghcls
PHYSIOLOGICAL INTRODUCTION. 853
brum and cerebellum, must likewise be situated in the medulla.
But the position of these has not yet been properly demon-
strated,
Motor Conduction.
The investigations in this direction have gone further than
any, and, indeed, have reached a certain degree of completeness.
It is almost beyond doubt that the chief paths of conduction for
voluntary motor impulses are to be sought in the pyramidal
tracts (Flechsig). We should thus have the chief conductors
for voluntary motions in the pyramids, in their inferior decussa-
tion, and in their continuations with the lateral and anterior
columns. But it appears from certain pathological facts (marked
atrophy of the pyramids without any motor affection during life),
that they are not the only conductors for voluntary impulses,
and are not necessary under all circumstances.
This function of chief motor conductor from the brain to the spinal cord has
been assigned to the pyramidal tracts chiefly on the ground of modern anatomical
and clinical discoveries. From the latest physiological experiments no binding
conclusions can be drawn, and the older experiments would rather lead to an
opposite view. The results, too, obtained by the most eminent physiologists are
directly contradictory; one saw no particular muscular contractions on irrita-
tion, while another observed convulsions; and again after section one saw no
paralysis, and the other saw extensive paralysis. According to Schiff the pyramids
are not motor conductors, whilst section of funiculi silique and laterales produces
motor paralysis. Section of the lateral columns (between the first and fourth cervi-
cal nerves in animals) stops the respiratory movements of the same side. The
uncertainty and contradiction we meet in the experimental results are easily ex-
plained by the difficulty in operating on the anterior surface of the medulla, and
the probable variation in the course of the voluntary impulses,
Nothing is definitely known of any motor conduction in the
gray substance, except what can be determined regarding the
nuclei of the nerves and their roots.
The inferior decussation gives a perfectly satisfactory expla-
nation of the decussation of the motor conducting tracts on a
level with the medulla, a fact which has been proved by numer-
ous experiments and still more numerous clinical facts. Cases
that have been observed in which there was no decussation are
854 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
to be explained by the non-decussation of the pyramido-anterior
tracts, and partly, too, by the striking variations the occurrence
of which Flechsig has so clearly proved. The pyramido-anterior
tracts, in fact, may not decussate before they reach the cord (in
the anterior commissure) ; it is further possible that their decus-
sation has taken place so far forward as the pons, namely in the
raphe; thirdly, there is a possibility of their undergoing no de-
cussation whatsoever ; but this remains to be proved. There are
certainly enough tracts in the raphe and the pons above the
motor pyramidal decussation. which would all allow of a decus-
sation of motor impulses.
Longitudinal section of the decussation of the pyramids does not produce a
complete paralysis of the animal’s body; this fact, too, argues against a total
decussation, but of course we cannot directly transfer the results to the human |
subject. Schiff’s experiments seem to prove that the decussation of the tracts
which supply the muscles of the trunk, the lower and upper extremities, occurs at
successively higher points. Schiff's assumption of a repeated (‘‘ return”) decussa-
tion in some tracts requires fresh confirmation.
Sensory Conduction.
The tracts which conduct sensory impulses in the medulla
are still quite undefined. Even in the spinal cord we cannot
trace the chief tracts with any great certainty, and in the me-
dulla this uncertainty is very considerably increased.
On this point, too, the physiologists are completely at vari-
ance. According to Schiff the tracts of the posterior columns,
which convey painful impressions, push more and more outwards,
and finally come to lie as if in direct continuation of the lateral
columns. The floor of the fourth ventricle, he asserts, and like-
wise the funiculi pyramidum and siliquee, do not react on irrita-
tion. Vulpian, on the contrary, declares that the corpora resti-
formia and the funiculi graciles et cuneati, and also the floor of
the fourth ventricle, are all equally sensitive when irritated. The
results of section are quite as contradictory, and can in no in-
stance be called unambiguous or convincing.
It is to be conjectured that the pedunculi cerebelli convey but
few sensory impressions, and that this function belongs rather to
PHYSIOLOGICAL INTRODUCTION. 855
the central gray substance (formatio reticularis), which conveys
them in all directions, so that partial lesions of these tracts never
produce any recognizable anzesthesia—of course the tracts which
have decussated in the spinal cord continue their further course
unaltered—. e., the tracts belonging to the right half of the
trunk are situated in the left half of the medulla, and vice versa.
But this decussation is by no means a total one, as experiments
show us, probably on account of the power the gray substance
has of conducting in every direction. If one side of the medulla
is cut through, one side of the face is deprived of sensation ; this
is sometimes the same as, and sometimes the opposite side to,
the section, a matter which seems to depend on the position and
depth of the section.
Thus our knowledge of the general situation of the sensory
paths amounts to nothing more than a series of conjectures. Of
course we know nothing whatsoever of the special tracts for
tactile, temperature, and pain impressions.
The functions of the medulla in the capacity of central organ
are a little more thoroughly investigated and better known. For,
in addition to the simple transmission of impressions, the medulla
can transfer centripetal irritations to centrifugal tracts ; it can, in
fact, bring about reflex functions, and these, too, of every kind
and with every complication. These appear always to be con-
nected with certain definite, more or less sharply bounded spots,
which are for this reason termed centres of the several functions.
Thus most of the centres are undoubtedly reflex centres, and it
is only in the case of few that we can assume, with any degree of
probability, that they can be thrown into activity without any
previous irritation of a centripetal tract, that they act, in other
words, as automatic centres.
In the first place, the medulla accomplishes simple or slightly
complicated reflex actions, such as those that pass from the
trigeminus in so many ways to the facialis (winking when the
conjunctive are irritated, wry faces consequent on strong impres-
sions of taste, secretion of saliva when the mucous membrane of
the mouth is irritated, sucking motion, when we put a finger into
the mouth of a new-born child, etc.). The arc of reflection must
be situated in the medulla, and the same may be asserted of the
ty, ' .
856 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
reflex actions between all the other nerves which have their origin
in the medulla.
But very much more extensive reflexes take place in the
medulla. The so-called general reflexes, or the transfer of the
reflex irritation to the whole muscular system, cannot be assigned
to any other part of the central nervous system. According to
Pflueger’s laws of reflex action the medulla oblongata is the chief
centre of irradiation for all the reflexes of every muscle, and
these are never brought into action till the reflex irritation has
extended to the bulbus. Ludwig and Owsjannikow have as-
signed the centre of origin of these general reflexes to the region
of the lateral columns in the formatio reticularis.
It is probably the same point from which general convulsions
arise in consequence of various direct or reflex irritations. Noth-
nagel proposes to give it the name centre of cramps, and assigns
it to the level of the pons in animals. This centre for cramps
can be irritated directly (as probably occurs in epilepsy) or re-
flexly in a great number of ways. According to Nothnagel the
reflex irritation is produced with the greatest certainty from two
definite points, one on each side of the median line on the floor of
the fourth ventricle.
In the human subject the exact situation of this centre is not
yet known, but is probably to be sought in the pons portion of
the medulla.
Besides these we find in this organ a large number of centres
for special processes, some of them, too, extremely important.
Some of them effect very complicated reflexes, which display a
combination of definite actions to accomplish a definite effect.
Actions of this character follow one another in a perfectly regular
order, which has its origin in the reflex mechanism and in the
performance of certain processes within it.
These centres are partly automatic as well, and their activity
persists after all centripetally conducting tracts have been re-
moved, the probable explanation being that they are excited by
a certain condition of the blood, and by the changes of the fluid.
The most important and best studied of these centres are
probably those which preside over the respiratory mechanism.
oe — hee ee ee ee ee a
PHYSIOLOGICAL INTRODUCTION. 857
The Respiratory Centres.
After Legallois had discovered the centre of respiration, Flou-
rens endeavored to localize it more accurately, and arrived at the
conclusion that it was situated in a point not larger than the
head of a pin, exactly in the middle line and at the posterior
angle of the calamus scriptorius. If this point be destroyed, res-
piration ceases and life with it (neeud vital). But of late even
Flourens himself admits two centres of somewhat larger dimen-
sions.
In point of fact, all more modern investigations point to the
existence of two respiratory centres, one in each half of the me-
dulla, situated in the superior external portion of each ala cinerea
and a little posterior to the exit of the vagus. It is possible that
the substance which connects the two may regulate the normal
harmony that exists between the respiratory motions of the two
sides of the body. Destruction of one centre only affects the
respiration of the same side of the body.
Gierke asserts that the “respiratory centre” is nothing but the sum of con-
ducting tracts, which convey the irritations, that set in motion the respiratory reflex
from the trigeminus and vagus to the motor-cells of the respiratory nerves. They
take the form of a round fasciculus composed of fine nerve-fibres, which runs down
on both sides parallel to the median line, and is identical with Krause’s respiratory
fasciculus mentioned above. So that, in the strict sense of the word, this is not
a centre, 7. ¢, a central apparatus composed of ganglion-cells, in which centri-
fugal and centripetal tracts enter into anatomical and functional connection.
Possibly a “respiratory centre” proper may be found in addition to this respiratory
fasciculus. Farther down, too, in the spinal cord there may exist similar central
structures for respiration (P. Rokitansky), but they certainly play nothing more than
a secondary part, and can never come into action independently. The same relation
probably exists between these centres as between the vaso-motor centres of the spinal
cord and of the medulla.
The centripetal tracts, which come from the periphery and
excite or inhibit the respiratory centre, are for the most part
situated in the vagus. The centrifugal tracts, which lead from
the respiratory centre, ran down through the lateral columns to
the motor nerves of the different muscles of respiration.
858 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
As this is not the place for an accurate account of the physi-
ology of respiration, we shall confine ourselves to mentioning
that a certain amount of oxygen must be contained in the blood
to maintain the irritability of the respiratory centres; that,
further, the oxygen and carbonic acid contained in the blood
must be present in certain fixed proportions to effect the irrita-
tion of the centres; that the irritation increases in proportion as
the quantity of carbonic acid exceeds that of oxygen; and that
the want of oxygen produces a greater irritation than the accu-
mulation of carbonic acid. But the respiratory centre can also
be excited reflexly by a number of different sensible nerves, such
as the vagus, trigeminus, and those of the cutis. We must add
that the physiologists consider themselves compelled to assume
separate centres of inspiration and expiration (making altogether
four respiratory centres), which appear in certain respects to have
an antagonistic action. But neither the anatomists nor experi-
mental physiologists have yet been able to localize these centres
accurately.
When the respiratory irritation increases, more muscles are —
affected, till finally general epileptiform convulsions are pro-
duced, being the result of an extension of the irritation within
the gray substance of the medulla, as far as the cramp-centre.
Sneezing, coughing, yawning, sobbing, and similar respira-
tory (partly in- and partly expiratory) reflex actions, are also
effected by the respiratory centres of the medulla, but they do
not originate in the same sensory tracts as the simple movements
of respiration. All these processes probably have their own spe-
cial mechanisms, but the anatomical structure of these is quite
unknown.
Laughing and weeping belong to the same category of reflex
actions, but they are distinguished by their combination with
mimic and secretory reflexes.
Centres for the Cardiac Movements.
Although highly probable, it is not certain whether the me-
dulla possesses a centre of acceleration of the action of the heart;
its position is, of course, unknown.
PN et Pn 2 PEE Ne PO I Onc
PHYSIOLOGICAL INTRODUCTION. 859
On the other hand, the excitement of the inhibitory fibres of
the vagus is generally assigned to a centre in the medulla, though
the position of this centre is equally unknown. This ‘‘inhibitory
centre for the action of the heart” seems also susceptible of auto-
matic and reflex irritation.
Centres of Speech.
The most important centre for voice, for the origination of
tones, is undoubtedly situated in the bulbar portion of the me-
dulla. For, after the pons has been divided from the bulbus,
reflex crying may still be produced. By this process the respir-
atory centres and the motor tracts of the accessorius (supplying
the larynx) are brought into action. Kussmaul (Appendix to
Vol. XIV. of this Cycl., p. 650) gives this centre the name of
basal phonic centre, and considers it indispensable for the con-
struction of-articulated sounds. It is situated probably close
to the centres of respiration.
Exactly the same may be said of the chief centre of articula-
tion, z. é., the structure which controls the complicated muscular
actions necessary to transform simple tones into articulate
vowels and consonants. The glossopharyngeus, accessorius,
hypoglossus, facialis, and trigeminus, all take part in the pro-
duction of articulate sounds, undoubtedly a matter of extremely
fine, complicated and carefully combined movements.
The anatomical fact that all these nerves and their nuclei lie
so close together gives weight to the assumption that the most
important centre, at least for the articulation of letters, is situ-
ated in the medulla. And this view is further strengthened by
numerous pathological facts, which show that diseases of the
bulbus, and especially degeneration of the nuclei. of its nerves,
are particularly destructive to the faculty of speech (progressive
bulbar paralysis). There is, however, a slight uncertainty in the
case, as these muscles of articulation are always positively para-
lyzed in bulbar paralysis, so that we are not fully entitled to
assume any actual disturbance of co-ordination. It is further
quite possible that the real centre of articulation lies higher up
in the cerebrum or cerebellum, and that its centrifugal tracts
860 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
only pass through the medulla, or only set in motion a series of
secondary medullary centres. We have, indeed, a parallel for
this in the co-ordinate movements of the extremities where this
process occurs farther down in the gray substance of the spinal
cord. Certainly the centres for the combination of letters to
syllables and syllables to words are situated anteriorly to the
medulla.
Nothing is known as to the position of this hypothetical centre of articulation
in the medulla. Schroeder van der Kolk wrongly assigned it to the olivary
bodies, but his view is now rejected by every one. Jaccoud tried to find it in the
bulbo-cerebellar commissural system, in the olivo-peduncular region, etc.; but we
cannot accept this proposition either. It is more to the point to say that this centre
has not yet been discovered.
Centre of Deglutition.
Swallowing is a reflex act that is performed entirely by mus-
cles the nervous supply of which originates in the medulla. It
is, in fact, a combined act of the hypoglossus, facialis, glosso-
pharyngeus, vagus, accessorius, and trigeminus. Consequently
the centre of deglutition has been assigned to the medulla, an
assumption which is well borne out by experimental and clinical
facts. But it has not been further localized, nor do we know
anything of its connections.
According to Schiff, too, the centre of vomiting is situated in
the medulla, but nothing further is known about it. Schiff like-
wise asserts that the contractions of the abdominal muscles in
defecation are co-ordinated and brought into action by a centre
in the medulla.
We can hardly assume a special reflex centre for the masti-
catory movements, as mastication cannot properly be regarded
as a reflex action. It is, in fact, only the co-ordination of cer-
tain motor impulses in order to accomplish a definite compli-
cated process ; the centre of co-ordination which serves this pur-
pose is by no means necessarily situated in the medulla. At the
same time, however, it is easy to comprehend that disease of the
motor tracts in the medulla which are involved (nucleus of tri-
PHYSIOLOGICAL INTRODUCTION. 861
geminus, hypoglossus. etc.) might impair the masticatory powers
to a great extent.
Vaso-motor Centre.
Ludwig and Thiry demonstrated a centre in the medulla
which can throw all the arteries of the body into contraction ;
and section of the cervical portion of the cord inferiorly to the
medulla paralyzes and dilates all the arteries. Later investiga-
tions, however (Goltz, Vulpian, Schlesinger, M. Nussbaum, and
others), prove beyond doubt that, even if this is the principal one,
it is still not the only vaso-motor centre ; and further, that other
secondary centres exist in the gray substance of the spinal cord,
as far downas the lumbar portion. The spinal centres are situated
one above the other through the whole cord, and appear depen-
dent, in the first instance, upon the principal medullary centre.
When this latter is removed, the spinal centres come into action
(but only gradually), and regain their influence over the vessels.
Owsjannikow and Dittmar have defined the position of the
vaso-motor centre in the medulla more accurately. They found
it, in the rabbit, between the corpora quadrigemina and calamus
scriptorius, somewhat removed from the middle line, in the late-
ral columnar tract of the formatio reticularis. The nerves for
vascular contraction which leave it are said to run down through
the lateral columns to the anterior nerve-roots (Dittmar).
In addition, centripetal fibres ascend to this centre, which
produce a reflex contraction of the vessels; these, too, are said
to lie in the lateral columns.
In conclusion, this centre can be excited or depressed by some
parts of the cerebrum (irritation of the pedunculi, blushing or
pallor resulting from mental impressions).
The latest investigations on the subject of vaso-motor nerves
compel us to assume the existence of nerves which directly dilate
the vessels. For these, too, a centre has been assumed in the
medulla.
862 ERB.—DISEASES OF THE MEDULLA OBLONGATA,
Nutritive Centres for Certain Nervous Regions.
It seems probable that the gray nuclei of the motor medullary
nerves have a nutritive effect upon their nerves and appertaining
muscles, very similar to that which the large multipolar cells of
the anterior cornua of the cord exercise over the nervo-muscular
regions dependent on them. As may be seen in bulbar paralysis,
degeneration and destruction of these cells produce granular
atrophy of the lingual, labial, faucial, and pharyngeal muscles.
Different clinical and experimental facts have led some to the
hypothetical assumption of certain centres in the brain for the
regulation of the temperature of the body. Should these really
exist, we should seek them also in the medulla.
Centres for Certain Secretions.
To Claude Bernard we owe the important discovery that the
secretion of urine, and certain nutritive processes, can be influ-
enced by irritation of the floor of the fourth ventricle.
If we merely pierce the floor with a needle, half-way between
the origins of vagus and acusticus, it suffices to produce a dia-
betes mellitus. If the needle pierces at another point, closer to
the acoustic, it produces a simple polyuria (diabetes insipidus).
And, besides this, we can frequently succeed in producing albu-
minuria by irritation of a point between these two.
In spite of numerous investigations, we are still in uncertainty
as to the manner in which this takes place, and as to the mech-
anism and anatomical structures which bring it about. Claude
Bernard conjectured that there was a nervous centre in the me-
dulla which controlled the formation of sugar in the liver. But
his view has met with many opponents, and most physiologists
now incline to the explanation of this artificial diabetes by vaso-
motor influences. This view is supported by the fact that irrita-
tion of surrounding parts produces only an increased secretion
of urine, unaccompanied by any secretion of sugar. But the
question has not yet been definitely settled.
Irritation of the anterior portion of the rhomboid sinus, close
PATHOLOGICAL INTRODUCTION. 863
to the nucleus of the abducens, produces an active salivation on
the same side as the lesion. The secretion is continuous and
abundant. It is, perhaps, produced reflexly by irritation of
some branches of the trigeminus. Possibly, however, it is a di-
rect irritation of the secretion, with or without the intervention
of vaso-motor processes. Gruetzner’s experiments go to prove
the existence of a centre of salivation in the medulla, which con-
trols both the fibres of the chorda tympani, going to the salivary
glands, and the fibres of the sympathetic. And this centre, when
directly or reflexly irritated, produces active salivation.
From all the details given in the preceding pages we can at
least conclude that a great number of the most important phy-
siological functions are united in the medulla. This very fact
compels us to admit the extraordinary entangled and compli-
cated course of the fibres, to which we so frequently drew atten-
tion.
Ill. Diseases of the Medulla Oblongata,
Introduction.
The pathology of the medulla oblongata is still in the first
stage of its development. The material for study is relatively
scarce, quite unsifted, and in great need of further enlargement ;
and the only way we can hope to enlarge it is by taking all the
modern points of view, and devoting ourselves to a careful clini=
cal study of the cases, and more especially to accurate anatomical
investigations.
As might be conjectured from its anatomy, the pathology of
the medulla resembles, in some points, that of the cerebrum, and
in others that of the spinal cord, so that diseases which are proper
to each occur in the medulla. This gives the medullary pathol-
ogy a very varied character. But, on the other hand, it is sim-
plified, as we can, in many cases, merely refer to the cerebral and
spinal diseases, which have in great part been very much better
investigated. Some cases—for instance, meningitis of the me-
dulla—we can pass over unmentioned on this account.
864 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
As yet we are acquainted with almost nothing but symp-
tomatic forms of disease in the medulla. Our knowledge was
most extensive on the subject of chronic progressive bulbar
paralysis, which had been made known by Duchenne’s investi-
gations. Gradually we became acquainted with the character-
istic symptoms of an acute apoplectic bulbar paralysis. And
soon all chronic diseases of the medulla that resulted in paral-
ysis were included under the first head, and all the acute forms
were regarded as apoplectic.
But further observation rendered matters more clear, and we
can already distinguish several different forms that have been
classed together under both of these heads, and we are probably
in a position now to draw anatomical and clinical distinctions
between these forms. |
In the following pages we have endeavored to draw these
clinical and pathologico-anatomical distinctions. At the same
time we are fully conscious that there are many shortcomings
and gaps, and that the material at our disposition is very much
too small, and in particular too inaccurate, to give us, as yet, a
sure footing on this ground.
The classification we have adopted must consequently only
be regarded as a temporary diagram, to contain, for the present,
the forms of disease with which we are acquainted. We shall
first discuss the quantitative changes of blood in the medulla, its
hemorrhages, and the obstruction of its vessels; secondly, the
results of acute and chronic mechanical lesions—acute wounds
and slow compression ; thirdly, acute inflammation of the bul-
bus; fourthly, chronic (inflammational) bulbar degeneration, first
described by Duchenne; then the other chronic and inflamma-
tional diseases of the medulla; and, finally, the neoplasmata
which occur in its substance.
We must urgently crave the reader’s indulgence for all the
imperfections and defects contained in the following description.
|
:
:
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re —
HYPERZMIA AND HEMORRHAGE. 865,
1. Hyperemia and Hemorrhage of the Medulla Oblongata.—
Apoplexia Medulla Oblongate.
Ollivier (d’ Angers), Traité des mal. de la moelle épinitre. 3me éd. IIL. p. 138-167.
1837.—Mesnet, Apoplexie du bulbe rhachid. dans sa partie supér. etc. Arch.
gén. 1861. Sept. Monit. des Sc. méd. 1861. No. 94.—Potain, Paralysie génér.
incompléte; polyurie; apoplex. foudroyante; ramollissement ancien, hémor-
rhagie de la protubérance. Gaz. d. hép. 1862. No. 98.—JLevier, Beitr. zur
Pathol. der Riickenmarksapoplexie. Dissertation. Bern, 1864. — Desnos, Cas
Whémorrhagie de la protub. annul. avec albuminurie, etc. Union méd. 1869.
No. 20.— Wilks, Labio-glosso-laryngeal Paralysis. Guy’s Hosp. Reports. XV. p.
2-17. 1870.—Hughlings Jackson, On a Case of Paral. of the Tongue from Hem-
orrhage in the Medulla Oblong. Lancet, 1872. Nov. 30. p. 770. — Dutrait,
Hémorrh. sous le plancher du 4 ventricle; albuminurie, glycosurie. Lyon méd.
1875. No. 45.—C. Browne, Hemorrh. into the Pons Varolii. Lancet, 1875.
Feb. 6.—Leyden, Klinik der Riickenmarkskrankheiten. I. p. 63. 1875.—M.
Rosenthal, Traité des maladies du syst. nerveux. p. 249. 1878.—Lichtheim.
Ueber apoplektiforme Bulbiarparalyse, etc. Deutsches Arch. f. klin. Med. XVIIL
1876.
Pathogenesis and Etiology.
Hyperemia strictly limited to the medulla must be an ex-
tremely rare occurrence, and there is reasonable doubt as to
whether such a case has ever been diagnosed with certainty, and
a real pathological change ascertained. We are not justified
here in adducing the capillary dilatations, which are so fre-
quently found in the medulla, and which are always followed
by hyperemia.
In the great majority of cases hyperemia of the medulla is
nothing more than part of a general hyperemia of the brain or
spinal cord, for the medulla is most intimately connected with
these in regard to its vascular supply. So that in every case of
general cerebral hyperemia, whether primary or secondary
(eclampsia, tetanus, mental and meningitic diseases), the me-
dulla will be found in the same condition.
Naturally the same etiological and pathogenetic conditions,
as those that were given at length in Volume XII., when treat-
ing of cerebral hyperemia, retain their force in the medulla.
We have partly to deal with active inflammational hyperzmia,
VOL. XIII. —55
866 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
resulting from hypertrophy and increased action of the heart,
or from vaso-motor disturbances, from collateral congestive in-
flammation, and from certain poisons, exposure to the sun, or
excessive mental activity, etc. But, on the other hand, it may
be the result of passive stagnation consequent on cardiac and
pulmonary disease—for instance, hindrance to the current in the
jugular veins, or violent expiratory exertions (coughing, strain-
ing, vomiting, etc.).
We need only say here that all these matters are to be re-
garded as paving the way for hemorrhage in the medulla, and
under certain conditions they actually produce it themselves.
All that Nothnagel has said, in his exhaustive and lucid trea-
tise on cerebral hemorrhage, is equally applicable to rupture in
the medulla. In regard to hemorrhage the medulla is more
closely related to the brain than to the spinal cord, 7. e., hemor-—
rhage is much more frequent in the medulla than in the cord ;
and further, the frequency is greater in the cerebral than in the
spinal end of the medulla, so that the great majority of apo-
plexies are found in the pons division. This fact alone renders
it difficult to draw a sharp line between hemorrhage in the pons
and in the medulla.
On the whole, rupture of a vessel is a rare occurrence in the
medulla. As regards its pathogenesis we may pass it over with a
few words, and refer the reader for details to Nothnagel’s treatise.
Undoubtedly the most important pathogenetic principle is
disease of the vessels (miliary aneurisms, such as Heschl de-
scribes in the pons, atheroma, fatty degeneration, capillary dila-
tation, resulting from processes of softening so clearly demon-
strated by Gerhardt’). We find extremely frequent cases of
atheroma and aneurisms of the basilar artery accompanied by
hemorrhage from its small branches in medulla and pons.
Increase of arterial tension plays a prominent part in con-
nection with these diseases of the vessels themselves; but even
without the latter the rise of the blood-pressure alone can often
produce hemorrhage. : The same result is seldom produced by an
increased tension in the veins from stagnation of their blood.
’ Jenaische Zeitschrift f. Med. und Naturw. I. 1864,
—————————— a ——“‘i—‘C;CS! =
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HYPERZMIA AND HEMORRHAGE. 867
Under the head of Hemorrhage from Excessive Tension may be
brought the cases caused by cardiac palpitation, by great excite-
ment, fits of passion, physical overexertion, and by excessive
indulgence in alcohol.
Some diseases of the surrounding parts, which not infre-
quently lead to hemorrhage of varying extent, seem to act in
two ways, ¢. e., by impairing the walls of the vessels and by
raising the collateral blood-pressure. To this class belong caries
of the cervical vertebree, purulent basilar meningitis, and tumors
in or around the medulla, etc.
In addition to this, hemorrhage, in greater or smaller degree, is
frequently produced traumatically through injuries to the skull
and back of the neck, though we can often recognize no direct,
palpable lesion in these parts. Westphal produced capillary
hemorrhage in the medulla of the guinea-pig by light blows of a
hammer on the head. Wecan imagine something analogous to
this occurring to the human subject.
In conclusion it may be remarked, that in extensive cerebral
hemorrhage, which breaks through into the ventricles, or in ex-
tended rupture in the meninges (e. g., the rupture of an aneu-
rism), the fourth ventricle is often filled with blood, and to this
may be attributed some of the symptoms that occur in such
cases.
Pathological Anatomy.
As hyperemia of the medulla is characterized by the same
anatomical appearances as cerebral hypereemia in general, we
need give no special description of it.
Nor can we draw the slightest distinction between the apo-
plectic clots in the medulla and those in the brain, either as
regards their appearance, the changes they go through, or the
condition of the surrounding parts. Fresh hemorrhage looks
like a dark-red coagulum, and is often half fluid towards its
centre. This very soon changes into a semi-solid, chocolate-
colored mass, which gradually assumes a lighter color, and is
partly absorbed. The last stage consists either in a rusty, con-
tracted scar, or in a small cyst, with a wall of dense cicatricial
868 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
tissue, with fine threads of connective tissue passing through it,
and filled with a cloudy, yellow fluid. In due course we observe
the development of a secondary degeneration, which can be
either unilateral or bilateral, according to the seat of hemor-
rhage; and this degeneration we can trace to some distance
down the spinal cord.
The size of these ruptures is usually very insignificant. Their
shape is roundish, or resembles an olive or bean, but frequently
it is quite irregular. Near the median line we often meet with
small triangular spots of hemorrhage, with the apex pointing
forwards, and the base towards the floor of the fourth ventricle,
thus corresponding pretty closely in extent with the territory of
a median bulbar artery (hemorrhagic infarct ?). As regards their
situation, these ruptures can occur at any point in the whole
medulla. If they occur near the floor of the fourth ventricle,
they have a tendency to pierce through it, and then we find a
coagulum of greater or less dimensions in this cavity. We sel-
dom meet with more than a single rupture, but occasionally
there are several together. Ollivier describes cases of from three
to six hemorrhagic points in the medulla.
In the medulla alone these effusions of blood seldom attain
to any great size, though they are frequently very large when
the pons is simultaneously attacked. In cases of the latter class
we often see undefined cystic masses, as large as a walnut or an
egg, running through the pons and medulla, usually piercing
into the fourth ventricle, and filling it with a large clot.
Capillary hemorrhage occurs, too, occasionally in the me-
dulla, in the same characteristic form as in the cerebrum, and
with just the same accompanying or causal circumstances.
Symptoms.
Very little is known of the symptoms of an inflammational
hyperemia in the medulla. It is perhaps allowable to refer
some of the symptoms of general cerebral hyperemia (dyspnea,
slow pulse, vomiting, general convulsions, certain defects of
speech, etc.) to congestion of the medulla, but this is only hypo- —
thetical. The same, too, maybe said of the assumption that
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HYPERZMIA AND HEMORRHAGE. 869
certain initial symptoms of acute bulbar disease (pains in the
head and back of the neck, spasms in the face and tongue,
formication, etc.) are to be attributed to hyperemia in the
medulla. This assumption is quite arbitrary, and no proofs
have been adduced for it.
In the case of hyperemia from stagnation, we possess some experimental investi-
gations made by Landois, Hermann, and Escher. These prove that retardation of
the pulse and dyspneea (irritation of the vagus and respiratory centres), likewise
contraction of the vessels (irritation of the vascular centre), and, finally, general
convulsions (irritation of the cramp centre), all result from intense venous stagna-
tion. All these symptoms, without doubt, originate in the medulla, and we are
forced to believe that something similar takes place occasionally in the human
subject.
Our knowledge of the symptoms of hemorrhage in the me-
dulla is more extensive, and rests upon a greater number of
observations.
Hemorrhage in this organ, even of inconsiderable extent, is
always to be regarded as extremely dangerous, commencing gen-
erally with the most alarming symptoms, and not infrequently
causing instant death.
It is, in fact, these tempestuous apoplexies (apoplexie fou-
droyante), from which death results ina few minutes or hours,
accompanied by signs of failure of respiration or circulation,
that belong usually to the medulla or pons. The patients fall
down with a cry or in epileptiform convulsions, and die instan-
taneously.
Further, we know that large effusions of blood into the hemi-
spheres and ganglia of the base, if they reach the fourth ventri-
cle, and irritate and compress the medulla, very quickly produce
death, accompanied by symptoms of vomiting and convulsions,
along with deep coma and complete general paralysis.
But slight hemorrhage in the medulla, too, generally pro-
duces immediately symptoms of an alarming and very threaten-
ing nature—symptoms which come more quickly and are more
grave the nearer the effusion is to the centres of respiration, or
when it affects these directly. In the latter case instant death
may ensue, and, consequently, medicakmen are seldom called in
for consultation or to treat the case.
870 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
Our principal interest is consequently attached to those cases
in which the patient lives on for at least some hours or days, or
in which a partial recovery takes place, and the sufferer enjoys
a somewhat longer existence, though one that is always very
materially impaired. |
Iu such cases the patients utter a loud cry, or are attacked
by buzzing in the ears, dizziness, sudden headache, vomiting, or
convulsive spasms of the body, and then follows, very quickly in
general, an apoplectic attack—. e., they fall down unconscious,
and sink into a more or less deep coma. Motor and sensory
paralyses characterize this, as well as all other apoplexies. But
we may localize them often in the medulla—on the one hand,
from their extent and combination, and, on the other hand, from
their almost unexceptional complication with a large number of
characteristic symptoms, the origin of which has been referred,
with a certain amount of probability, to the same organ.
The motor paralysis assumes very various dimensions, some-
times attacking only the lower extremities, sometimes only the
upper ; at other times it takes a hemiplegic character, though
this is only when the hemorrhage is extremely small, and then it
is usually a decussating paralysis of the extremities; but in
most cases all four extremities are either completely or partially
paralyzed, which is very characteristic, because it is hard to find
any point in the brain where all the motor tracts of the body can
be affected simultaneously, by an effusion of blood.
Accompanying this paralysis of the extremities, we always
find some of the bulbar nerves more or less completely par-
alyzed, usually the hypoglossus, accessorius, facialis, and tri-
geminus ; sometimes, too, the nerves of the orbit. These paraly-
ses also occur on one or both sides. If we have a hemiplegia,
(an effusion into one side of the medulla), the most characteristic —
symptom is that the paralysis of the bulbar nerves, caused by
injury to its nuclei and root-fascicles, occurs on the same side as —
the hemorrhage, while the hemiplegia of the extremities occupies —
the opposite side of the body, owing to the decussation that —
takes place at a point inferior to the lesion. We thus get all —
the characteristics of a hemipiegia alternans, with the extremities —
paralyzed on one side, and the facial muscles (in certain cases —
HYPERAMIA AND HEMORRHAGE, 871
this applies as well to the tongue, the muscles of mastication,
and to the abducens) paralyzed on the opposite side of the body.
The above-mentioned nerves are affected in greater or less num-
ber, according to the location of the hemorrhage.
The paralysis of sensation follows the same rules as that of
motion, only that it is on the whole not so well developed. In
Severe cases, when all four extremities are paralyzed, it is gener-
ally impossible to ascertain anything about the condition of sen-
sation on account of the coma in which the patients lie. If it is
a case of motor hemiplegia, we may assume that the sensation
decussates as well; but still, owing to the peculiar course of the
sensory fibres in the medulla, we can hardly expect a sharply-
defined anesthesia. This, of course, depends altogether upon the
extent of the effusion in transverse section. It would be ex-
tremely interesting to investigate accurately the condition of
sensation on both sides of the head and face in such cases of
apoplectic hemiplegia. For a@ priort we should anticipate an
alteration in the conditions dominant here, such as a simultane-
ous, a decussating, or even a bilateral anesthesia, always pro-
vided the so-called ascending root of the trigeminus contains the
sensory tract for the same side of the head and face.
Respiratory disturbances, as they are most threatening to the
life of the patient, may be regarded as the most important of
the symptoms produced by a bulbar lesion, and they are at the
same time very characteristic of such lesion. If fatal asphyxia
does not at once ensue, still the respiration is always greatly im-
paired ; it becomes irregular, stertorous, often intermittent, and
accompanied with the greatest dyspnoea ; the Cheyne-Stokes phe-
nomenon is frequently observed; the respiratory process then
grows more and more encumbered and paralytic, till at last death
results from asphyxia. It is only in comparatively mild cases
that the respiration can recover, or is not at all affected. But
even in cases which commence as hemiplegia, the hemorrhage
generally extends and causes further mischief.
Alterations in the action of the heart are generally less
prominent. But in every severe case we unfailingly meet with
an enormously rapid pulse, which is frequently irregular and
intermittent, and the paralysis of the*cardiac action runs a paral-
872 ERB.—DISEASES OF THE MEDULLA OBLONGATA.,
lel course with the increasing asphyxia. In the cases that have
hitherto been described, very little is noted of vasomotor changes,
unilateral or bilateral rise of temperature in the skin, such as we
might expect with certainty, especially in the period immediately
succeeding the hemorrhage.
Great importance attaches to the epileptiform convulsions
which accompany hemorrhage in the pons and medulla. They
are often among the earliest symptoms, but they may be repeated
in the first few days, and even later, assuming the most violent
character. <A d¢onic rigor has been often described in the ex-
tremities, of variable duration and frequent recurrence.
Disturbances of speech and deglutition, and unilateral and
bilateral paralysis of the soft palate result naturally from the
participation of the bulbar nerves in the paralysis. The same:
may be said of awral troubles, such as deafness and buzzing in the
ears, which will probably be more frequently detected now that
our attention has been directed to them. Vomiting of frequent —
recurrence, and a continuous troublesome singultus, which have
often been observed, may be explained in the same natural way
by an irritation of their centres in the medulla.
Potain, in a case recorded several years ago, describes the
occurrence of polyuria. Dutrait found both sugar and albumen
in the urine, but his case proves nothing, as both these sub-
stances were found before the hemorrhage as well as after. Both
Mader and Desnos confirmed the presence of albumen in the
urine in the case of an acute hemorrhage, where the kidneys
were found quite intact at the autopsy.
In a case where hemorrhage occurred in the pons portion of
the medulla, I observed a considerable rise in the temperature of
the body during the agony. Leyden and others record similar
instances, and further it agrees with well known experimental
facts.
In cases where life lasts long enough, we can test the electric
reaction of the paralyzed nerves and muscles. It probably re-
mains quite normal for some time in the extremities, though it is
stated that the irritability of the paralyzed nerves which come
directly from the bulbus soon disappears. Leyden has con- —
firmed the latter point, at least as regards the faradic current. _
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HYPERAMIA AND HEMORRHAGE. 873
Arguing from analogy, it seems highly probable that when the
nervous nuclei of the bulbus, or the nerve-roots that leave them,
are destroyed by hemorrhage, the peripheral nerves dependent on
them must lose their irritability, and that the muscles supplied
by these nerves must give a reaction of degeneration. ‘This will
be easily decided by future investigations.
The course of the disease is threefold. It is either at once
fatal, death being produced by paralysis of the respiratory cen-
tres with all the symptoms of apoplexie foudroyante.
Or secondly, death does not occur for some hours or days,
while the patient lies continuously in a state of more or less in-
tense unconsciousness and is paralyzed to a varying extent,
breathing stertorously, and with a quick pulse, sometimes, too,
with a high temperature.
In the third, and probably most seldom course, life is main-
tained for a more considerable time. This only occurs when the
hemorrhage is- relatively insignificant. The patient gradually
recovers his consciousness, some of the paralytic and other symp-
toms disappear, and nothing remains but hemiplegia or partial
paraplegia, and more or less difficulty in articulation and deglu-
tition. Apart from the fact that the actual intellectual region is
absolutely unaffected, and apart from any remnants of bulbar
paralyses, these cases, in their further course, their termination,
and the formation of secondary contractures, etc., exactly resem-
ble those cases in which hemiplegia and other forms of paralysis
have been produced by some hemorrhage in the brain anterior to
the medulla (in the thalamus opticus, the corpus striatum, the
nucleus lentiformis, the capsula, etc.).
Very little is known of the symptoms of small capillary
hemorrhage in the medulla; but they are probably similar to
those produced by emboli in the smallest arteries of the’ bulbus,
and can scarcely be detected accurately unless occurring on a
large scale. There is no evidence as to whether epilepsy can
result from this capillary hemorrhage, as Westphal’ observed it
in the guinea-pig after striking it on the head.
1 Berl. klin. Wochenschr. 1871. No. 38.
874 ERB.—DISEASES OF THE MEDULLA OBLONGATA
Diagnosis.
It is hardly possible that we shall ever be called upon to make
a special diagnosis of hypereemia of the medulla oblongata.
We can apply the general symptoms of cerebral hemorrhage
to the diagnosis of hemorrhage in the medulla, so that we need
only refer to the chapter on this subject in Vol. XII., and to
the description given above. In many cases it is very difficult
to distinguish between hemorrhage and embolism. We shall
treat of the important points for this differential diagnosis in the
next chapter.
In order to make a special diagnosis of a hemorrhagic lesion
in the medulla and pons, we must take account of the following:
In severe cases loss of consciousness, epileptiform convulsions,
and sudden death are sufficiently characteristic to establish the
diagnosis. In less rapid cases we may mention the following
Symptoms as indicative of a similarly situated lesion. Com-
mencement with general epileptiform convulsions, vomiting, sin-
gultus, more or less threatening respiratory disorders (intermis-
sion, dyspnoea, Cheyne-Stokes’ phenomenon), dysphagia, disorders
of speech, paralysis of the tongue and soft palate, of the inferior
branches of the facialis, and of the abducens, etc.; albumen and
sugar in the urine, and final rise of temperature; the extension
of paralysis to all four extremities, but particularly the unequal
degree of paralysis in the extremities of the one side, and the face
and tongue on the other side (paralysis alternans); we might
perhaps, too, adduce the cessation of all reflexes in the territory
of the paralyzed bulbar nerves.
There are some further isolated symptoms which might make
our diagnosis more accurate, but they need some additional con-
firmation. For instance, we might take the alternating paraly-
sis of the facialis (and perhaps, too, of the masticatory muscles
and the abducens) as indicative of hemorrhage in the pons por-
tion of the medulla. But we must take account of several other
symptoms according to the extent and exact position of the clot —
in the pons. As regards these we refer the reader for details to.
Nothnagel’s article in Volume XII. |
TE 0 EE
HYPERAMIA AND HEMORRHAGE. 875
We may conclude that the lesion is limited to the anterior
half of the floor of the fourth ventricle, when we see paralysis of
the abducens, facialis, and trigeminus, with aural disorders, and
sugar and albumen in the urine, etc.
Hemorrhage in the posterior portion of the rhomboid sinus
produces paralysis of the hypoglossus, facialis and trigeminus,
and of the accessorius and vagus, accompanied by grave respira-
tory disorders, and usually by paralyzed extremities; it is a
symptom probably of some importance when these latter alter-
nate with the paralysis of the tongue. Alternate paralysis of an
upper and lower extremity probably indicates that the lesion is
located in the centre of the decussation of the pyramids. In a
case described by Hughlings Jackson, a small hemorrhage, which
had occurred some considerable time before, immediately border-
ing upon the left olivary body, is made responsible for a sudden
complete paraplegia of the tongue. Whether this is justifiable
it would be hard to decide, since there were many other clots
found.
Prognosis.
The prognosis is generally very unfavorable; in the great
majority of cases, especially when the hemorrhage is of at all
large dimensions, it is absolutely fatal. There is only hope of
life in cases of very limited hemorrhage, or when the location is
very favorable, especially when it is far removed from the respir-
atory centres. The patient’s condition may then improve gradu-
ally, and partially recover. As regards details, the prognosis in
such cases is the same as in other cerebral hemorrhage.
Capillary hemorrhage, if we could diagnose it, would prob-
ably allow of a more favorable prognosis. Still, we should not
be sanguine, as the cause—namely, vascular disease—remains to
work more mischief.
Treatment.
The rules of treatment for both hyperemia and hemorrhage
in the medulla are exactly the same ag those for similar disorders
in other parts of the brain. To avoid repetition we shall merely
876 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
refer the reader once more to Nothnagel’s work, which we have
so often quoted. We should only wish to draw attention to
venesection combined with active stimulants as the most suitable
treatment in severe cases where respiration is threatened. As
the patients can seldom swallow, we must inject the stimulants
per rectum (clysters of musk), or subcutaneously (emulsions of
camphor, aromatic spirit of ammonia, port wine, cognac, etc.).
We shall not attempt to discuss the value derived in many
cases from artificial respiration, even if continued for a long time.
A suitable application of electricity is indicated in chronic
cases where paralysis continues, and where the speech and deg-
lutition, etc., are impaired.
2. Anemia of the Medulla Oblongata—Thrombi and EHmboli
in its Arteries—lNecrotic Softening.
Tuengel, Mittheil. aus d. allgem. Krankenhause in Hamburg. Virch. Arch. Bd.
XVI. p. 356. 1859.—Griesinger, Aneurysma der Basilararterie. Gesammelte
Abhandlungen. IL p. 485.—Hérard, Union méd. 1868. No. 35 (quoted by
Lichtheim).—G. Hayem, Sur la thrombose par artérite du tronc basilaire comme
cause de mort rapide. Arch. de Physiol. I. p. 270. 1868.— Wilks, Labio-glosso-
laryng. Paralysis. Guy’s Hosp. Rep. XV. p. 2-17. 1870.—Taylor, Embolism
of the Left Vertebral Artery; Paralysis of the Glossopharyngeal Nerves; Death
from Starvation. Brit. Med. Journal. 1871. Nov. 4.—Proust, Soc. de Biologie.
Séance du 17 Juillet, 1870; De l’aphasie. Arch. génér. 1872. Tome I. p. 681.
—Joffroy, Sur un cas de paral. glosso-labio-laryngée a forme apoplect. d’origine
bulbaire. Gaz. méd. 1872. Nos. 41-46.—Huret, Tribut 4 histoire de ’embolie
des artér. vertébrales. Thése. Paris, 1873.—Duret, Distribut. des artéres nourric.
du bulbe rhachid. Arch. de Physiol. V. p. 97-114. 1873.—T%rard, Thrombos.
of Vertebr. and Basilar Arteries. Med. Times. 1876. Dec. 2.—Ribard, De la
thrombose du tronc basilaire. Thése. Paris, 1876.—Lichtheim, Ueber apoplek-
tiforme Bulbirparalyse und ihre Beziechungen z. d. Erkrank. d. Seitenstr. des
Riickenmarks. Deutsch. Arch. f. klin. Med. XVIII. p. 593. 1876.—Markusy,
Zur Lehre vy. d. progress. Muskelatrophie u. progress. Bulbirparalyse. Dissert.
Breslau, 1874.—ZHichhorst, Erweichungsherd in der Varolsbriicke in Folge von
syphil. Entartung der Art. basilar. Charité-Annalen. I. p. 206. 1876.— Willigh,
Bulbiirparalyse in Folge von Embolie der Art. vertebr. Prager Vierteljahr-
schrift. 1875. Bd. 126. p. 89.—M. Rosenthal, loco cit. p. 249.—Hallopeau, Des
paralysies bulbaires. Paris, 1875. p. 98.—Note sur un fait de thrombose basi-
laire. Arch. de Physiol. VIII. p. 794, 1876.
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AN MIA. 877
Pathogenesis and Etiology.
What has been said of hyperemia can be repeated of ane-
mia of the medulla. It probably occurs seldom or never alone,
unless we take account of local compression, in which case anz-
mia only plays a very secondary part. It is generally a mere
component of general aneemia of the whole body, or at least of
the brain and spinal cord. We have not to concern ourselves
with further details of this, but refer the reader to the article on
‘‘Aneemia of the Brain.’? No doubt some of the symptoms
which we see in general anzemia are referable to a similar condi-
tion of the medulla.
Thrombosis and embolism of the vessels supplying the me-
dulla are not extremely rare. They are the commonest cause of
anemia of the bulbus ; certainly they produce at once the most
intense anzemic condition, so that, unless the circulation is quick-
ly compensated, the part at once undergoes necrotic softening.
The thrombus or embolus occurs almost without exception in
the verlebral and basilar arteries, and is very seldom confined
to the smaller branches of these. Latterly this subject has
received much attention; and the result has been that a number
of the cases which were classed together as ‘‘ acute, apoplectic
bulbar paralysis’’ (a term first used by Hérard) were produced
by emboli and thrombi in these arteries. Duret, in his mono-
graph on the arteries of the medulla (1873), mentioned all that
was important to know; Hallopeau went over the same ground
in his thesis (1875), while Lichtheim has given us an excellent
treatise (1876), containing everything known of the subject up to
the date. However, we are in possession of very few cases which
have been under accurate clinical observation, and afterwards
received a post-mortem examination. Lichtheim has collected a
great many observations, though without the confirmation of an
autopsy.
What has been said of thrombosis and embolism in the cere-
bral arteries in general, applies equally well to these processes
in the medulla. The sources of the emboli and the causes of
thrombosis are in every respect similar. The basilar artery is
878 ERB.—DISEASES OF THE MEDULLA OBLONGATA,
frequently atheromatous and contains aneurisms, and it is often
infected by syphilis, so that it constantly produces disorders in
the circulation of the pons and bulbus by means of thrombosis
and contractions in its lumen, though these are occasionally con-
fined at first to a few of the branches it gives off. Thrombi
form, too, very easily and often in the vertebral arteries ; and in
these likewise we often meet with emboli, more especially in the
art. vertebralis sinistra on account of its favorable position, given
off so directly as it is from the subclavian.
The emboli in these vessels are just as numerous and large as
in others, they undergo the same metamorphoses, and disinte-
grate in just the same way, and are then carried on by the blood.
The secondary thrombi and the development of the primary
thrombi, till they finally close the lumen of the vessel, are like-
wise indistinguishable from the process in any other vessels. So
we need not enter into any description of embolism and throm-
bosis, but the process must be borne in mind in order to get the
significance of, and enable us to comprehend, the different symp-
toms.
Pathological Anatomy,
We shall not enter into a description of thrombosis and em-
bolism in the basilar and vertebral arteries, as this can be found
in any text-book on pathological anatomy. And besides, in the
cases which have been published, the macroscopic anatomical
appearances are usually treated of with great accuracy, whilst
the consecutive changes in the pons and medulla have been very
imperfectly studied.
We shall confine ourselves eine to mentioning the facts that
either or both vertebral arteries may be completely obliterated ;
that further, the thrombosis may extend from them into the
basilar ; thirdly, that the lumen of the basilar may be obstructed
either from one end to the other, or for a short distance in its
anterior, median, or posterior division, according to which, of
course, the symptoms vary. Finally, we may state that the
branches given off from the main arteries, partially or wholly,
any or all, may be affected by the thrombosis.
Pe
AT ON NON se i ii ae illite
SAN eth Royal
ANEMIA. 879
The effect produced in the medulla is of course greater, the
quicker the obstruction is developed and the greater its extent.
Almost unexceptionally we meet with grave disorders in the cir-
culation, as most of the nutritive arteries in this region are ter-
minal. The immediate result is, of course, intense anemia of
the affected vascular territory. According to the conditions
which govern the further development of similar lesions in other
parts, the second stage consists either in an engorgement accom-
panied by effusion of blood (hemorrhagic infarct), which leads to
red, and afterwards to yellow and white softening, or we have
nothing but simple anemic yellow and white softening. The
final stage often consists of the formation of a cavity in the bul-
bus, varying in size, with walls of soft reticular connective tissue,
and delicate threads of the same traversing the interior.
If the obstruction takes place in one of the smaller vessels,
we find a number of small cuneiform centres of softening, and in
them capillary extravasations; or else we meet with similarly
shaped hemorrhagic infarcts, with their apices pointing forward
and their bases towards the floor of the fourth ventricle.
We are in possession of very few microscopical investigations on the subject of
these softenings in the medulla. Charcot found a number of corpuscles of Gluge
(Fettkérnchenzellen) in the early stages, and changes similar to what is observed in
anzmic parts of the brain. We owe a more accurately studied case to Willigk, who,
ten months after the commencement of the disease, found the basilar artery reduced
to a fine thrombotic cord, and thrombiin the art. cerebellares inferiores, whilst the
vertebrals were unaffected ; the pons was atrophied and sclerotic where it touched
the fourth ventricle; both pyramids and olivary bodies atrophied. The anterior
portion of the pyramids was sclerosed, and from here down Willigk could follow
the usual descending secondary degeneration into the lateral and anterior columns
of the spinal cord. He found a number of sclerotic vessels filled with detritus and
_ coarse granular substance in the degenerated parts of the pons and medulla, and
between these were other vessels which were dilated and admitted of circulation,
but were surrounded by lymph-cells, fat and pigment. Everywhere the connective
tissue had increased, and the nerves had nothing but disintegrated sheaths and
atrophied axis-cylinders. The ganglion-cells were manifestly altered, especially
those that lay near the thrombotic vessels; some had undergone granular disinte-
gration and pigmentary degeneration, others were in the last stage of sclerosis and
had lost all their processes; the number, too, of ganglion-cells in some parts was
greatly diminished, as, for instance, in the anterior portion of the rhomboid sinus,
‘ut not so much in the hypoglossal nucleus. An important fact was the marked
880 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
average atrophy of the cells in the olivary bodies, which bodies were themselves
diminished in size, while their fibres remained comparatively normal; the same
condition reigned in the nuclei of the pyramids. Some of the cerebral nerves, too,
had atrophied and degenerated, more particularly the abducens. The obstruction
of the basilar in this case does not seem to have taken place either very suddenly or
all at once; probably there were several subsequent emboli, which would account
for the absence of extensive necrosis and softening. LEichorst in his case found
fatty degeneration and dilatation of the vessels, and a number of the corpuscles of
Gluge; further, the nerve-fibres and ganglion-cells had degenerated, and the con-
nective tissue resolved into fat.
Symptoms.
We shall confine ourselves to the symptoms produced by ob-
struction in the arteries of the medulla, drawing a distinction
that seems advantageous, between those that take place in the
main arteries and those in the small branches.
If one or both vertebral arteries, or if the basilar is obstructed
‘(thrombosis or embolism), we usually observe the following gen-
eral symptoms: A more or less complete bulbar paralysis sets.
in suddenly or in a very short time (in the course of one or two
days, in a case of autochthonous thrombosis), frequently resem-
bling an apoplectic fit, but often, too, without any loss of con-
sciousness. This bulbar paralysis consists in paralysis of the soft
palate and tongue, loss of speech and the power of deglutition,
and partial paralysis of the inferior territory of the facialis.
These symptoms are sometimes accompanied by paralysis of the
orbital and masticatory muscles, disorders of hearing, and singing
in the ears; of extremely frequent occurrence are respiratory,
circulatory and vocal disorders. Almost without exception, par-
alysis is developed simultaneously in the extremities, usually in
the form of hemiplegia on the same side as the obstruction, con-
sequently, with greater frequency on the left side, as the art.
vertebr. sinistra is more subject to embolism ; but we very often
find all four extremities more or less completely paralyzed. Sen-
sation, apart from subjective disorders, is often quite unimpaired,
but it may also be more or less affected.
This acutely developed disease is not of a progressive charac-
ter ; at most we see a slight change for the worse in the first days,
;
i
|
= ee
ANEMIA. 881
if death from respiratory paralysis did not atonceensue. Onthe
contrary, the patients after some time generally recover to a cer-
tain degree. That is to say, the paralysis disappears in part, the
extremities contract, the tendon reflexes are more active, etc., as
in other cerebral disseminated paralyses, and the patients can
remain alive in this condition for a relatively long period.
Duret’s thorough investigations of the circulation in the me-
dulla have provided us with means of forming a judgment as to
the exact region which is principally affected by obstruction of
the different vessels, so that we can draw conclusions as to the
location of the thrombosis, from observation of the functions that
are disordered. The following is a condensed statement of
Duret’s results: The important gray nuclei of the bulbus are
supplied on the one hand by the arteries of the nerve-roots, which
spring from the vertebrals, the basilar and its branches; but
they derive by far the greater supply of blood from the median
bulbar arteries, which pierce through the anterior fissure into the
raphe, and thence to the nuclei. Thus the nuclei of the hypo-
glossus and accessorius are supplied by branches from the spinalis
anterior and vertebralis, and in a very minor degree, too, form the
cerebellaris inferior. The nuclei of the vagus, glossopharyngeus
and acusticus derive their blood from the branches given off by
the anterior portion of the vertebrals and from their junction ;
the blood-supply of the nuclei of the facialis, trigeminus, abdu-
cens, and the two anterior orbital nerves, comes chiefly from the
different branches of the basilar.
The pyramids and olivary bodies derive their blood in part
through small branches coming directly off from the vertebrals,
and partly from the spinalis anterior. The pedunculi cerebelli,
and also the lateral and posterior portions of the medulla, are
supplied by the inferior cerebellar and posterior spinal arteries.
The floor of the fourth ventricle receives terminal branches from
nearly all the arteries of the bulbus and pons, and in addition to
these some vessels from the inferior cerebral artery and from the
.choroid plexus.
If this vascular distribution were perfectly constant, we could
easily make a synthetical estimate of the results that would be
produced by the obstruction of any vessel or any point of the
VOL. XIIL.—56
882 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
same ; and on the other hand, we should be able to deduce an
exact diagnosis of the location of the lesion from the symptoms
presented to us. But the manifold varieties in the points at
which these vessels are given off, and in their course, as well as
the various possibilities of a collateral circulation, all tend to di-
minish the succcess of our efforts in this direction.
We must pay special attention to the unilateral or bilateral
origin of the spinalis anterior, and as to whether it unites to form
a common trunk or not; further, as to whether the cerebellaris
inferior is given off at an anterior or posterior point, etc. With
such anomalies a lesion located in exactly the same point of the
same vessel may produce in different cases very dissimilar symp-
toms.
Notwithstanding attempts have been made to localize the
thrombus from the symptoms in different cases, and the post-
mortem examination has in some of them given results which
agreed very well with what was observed during life, still, the
diagnostic rules we shall now give can lay no claim to absolute
constancy ; they are at most approximately true.
Obstruction of the basilar artery, as a rule, produces bilateral
symptoms, paralysis of all four extremities, and of both sides of
the face, etc. ; but indubitably the most important symptom is
the cessation of the functions of the vagus and glossopharyngeal
nuclei, severe respiratory disorders, dyspnoea, cyanosis, and
usually a rapid death from asphyxia. A rapid and complete
obstruction of the basilar generally produces instant death. Be-
sides, consciousness is lost in every case, the patients falling down
insensible and sinking into deep coma. If life does last for a few
hours, we may observe a complete paralysis of all four extremi-
ties, caused undoubtedly by anemia of the pyramidal tracts.
But in these cases, too, life soon terminates in asphyxia, the res-
piration becoming very rapid. ‘Tirard describes cases of 75 to
105 respirations in the minute.
If the obstruction only extends to small portions of the basi-
lar, or if the thrombosis is merely attached to the wall of the
artery and only cuts off the blood from a few branches, the
Symptoms are often less threatening, and individual bulbar
nerves are paralyzed, accompanied by weakness or paralysis* of
a
——————————
ANEMIA. 883
some or all of the extremities. In such cases we see the different
orbital muscles paralyzed, and those supplied by the facialis,
trigeminus, etc. The respiration may then remain uninterrupted,
provided circulation continues in the posterior portion of the
basilar and in the vertebral arteries.
Obstructions in both vertebrals simultaneously produce ex-
actly the same effects as thrombosis of the basilar artery, namely,
complete paralysis of the extremities and the tongue, difficulty
in swallowing, aphonia, and intense dyspnoea, quickly followed
by death from asphyxia. The life of the patient is not in such
immediate danger if the thrombosis is developed slowly enough
to allow time for the completion of a slight collateral circulation.
Joffroy attaches some importance to the lock-jaw that has been
observed in such cases. We are inclined to agree with Licht-
heim, who ascribes a case of Marusky’s, in which this symptom
was observed, to embolism rather than to extravasation.
Obliteration of one vertebral artery produces symptoms
which are to a certain degree hemiplegic. The lesion is more
frequent in the left artery, from which, too, the spinalis anterior
is generally exclusively or in greater part given off. It produces
occlusion of the spinalis anterior and cerebellaris inferior. This
is the origin of the hemiplegia, which occurs either on the same
side as the lesion or on the opposite, a matter that depends on
somewhat varying conditions, such as the location of the throm-
bus, the point of origin of the spinalis anterior, the completeness
of the pyramidal decussation, etc. We may also meet with
paralysis of the hypoglossus and accessorius, disorders of articu-
lation and deglutition, aphonia, paralysis of the inferior branches
of the facialis, partial paralysis and anesthesia of the soft palate,
etc.; but all these symptoms are frequently more prominent on
one side of the body. We have thus before us all the symptoms
of acute bulbar paralysis, and, in addition, a more or less pro-
nounced hemiplegia or weakness of all four extremities, gener-
ally unaccompanied by any loss of consciousness.
We can often recognize the successive occlusion of the differ-
ent arterial territories quite plainly by the grouping of the symp-
toms and the order in which they follow one another, which show
us how the thrombosis becomes more complete and increases in
884 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
its extent. This is well illustrated by the cases described by
Tirard, Hallopeau, and others.
The larger the vessel occluded and the thrombus occluding it,
and the firmer the consistency of the latter, the quicker ensues
death. If the circulation can be quickly restored by disinte-
gration or displacement of the thrombus or embolus, or by suffi-
cient collateral branches, we may hope for improvement and par-
tial recovery. Patients of this class may drag out their existence
for several years more, though generally retaining severe results
of the lesion, such as paralyses, contractures, and difficulties of
articulation and deglutition. lLichtheim has described a very
good instance of this form.
An occlusion of the very small branches in the bulbus can
certainly never be diagnosed with certainty from the symptoms
it produces. But as these vessels are generally terminal, their
obliteration is sure to be accompanied by necrosis of the parts
affected, and it only depends on the territory of such an artery
whether we get any symptoms of it or not. It is quite possible,
for instance, that these occlusions may produce partial paralysis
of the tongue, difficulties of articulation and swallowing, unilate-
ral paralysis of the facialis and abducens, respiratory disorders,
and perhaps even fits of asthma, etc. But we are seldom or
never able to conjecture such lesions.
To this category, however, belongs a case of Voisin’s, which Duret quotes, A
woman had all the symptoms of a suddenly developed bulbar paralysis, and the
post-mortem examination proved the presence of a triangular capillary clot as large
as a pea, situated in the middle line and pointing with its apex to the anterior sur-
face of the bulbus, while its base was directed towards the floor of the fourth ven-
tricle. Hallopeau, too, describes an interesting case in which the main lesion con-
sisted in a small point of softening in the bulbus, which coincided exactly with the
common nucleus of the facialis and abducens, and had paralyzed these two nerves.
An embolus of the vertebralis as well had given rise to hemiplegia on the opposite
side of the body, while a continuous incomplete thrombosis of the basilar produced
other paralytic symptoms, and finally caused death from asphyxia.
Diagnosis.
The diagnosis of a bulbar embolus or thrombus is very fre-
quently surrounded with many difficulties, though in most cases
= 7 nn
Se aa ae are eee ~
—
s —
ANEMIA. 885
we can scarcely fail to inform ourselves of the approximate lo-
cation of the well-marked symptoms. A bulbar paralysis, for
instance, with all its characteristic symptoms of difficulty in
swallowing and articulation, palato-labio-lingual paralysis, par-
tial paralysis of the masticatory and some of the orbital muscles,
with threatening disorders of the respiration and circulation, and
accompanied by either hemi- or paraplegia of the extremities,
occasionally too by epileptoid convulsions—all this is so charac-
teristic that we can hardly fail to comprehend it, and our atten-
tion is at once directed to the pons and medulla. But in fulmi-
nant and extremely rapid cases, when the patient sinks into deep
coma, and universal paralysis sets in with threatening asphyxia,
we can only make a guess as to where the lesion has occurred.
We can generally make a pretty positive diagnosis of an
acute, defined lesion in the bulbus, if the symptoms are suddenly
developed without any warning ; for, even in a case of autochtho-
nous thrombosis, we generally have a sudden attack, probably
the moment the vessels are completely occluded. But it is not
always easy to determine whether a hemorrhage or an embolism
has taken place. The general grounds for the one or other inter-
pretation are, as is well known, not at all absolute (compare
Nothnagel, Vol. XII.); nor can we always find any source of
an embolus; besides, in old persons thrombosis is just as fre-
quent as hemorrhage, and in young subjects the arteries may be
infected by syphilis. These reasons render a positive distinc-
tion, in most cases, impossible, unless the special symptoms lead
us to diagnose one cause or the other. This is, however, very
frequently the case.
We could hardly entertain thoughts of an extravasation, for
instance, in Hallopeau’s case, where the different symptoms came
on one after the other—the same effect as produced by an embo-
lus with continued development of a secondary thrombus.
Epileptoid convulsions and apoplectic attacks are of more fre-
quent occurrence in cases of hemorrhage than in those of embo-
lism and thrombosis; it is only when the whole basilar is com-
pletely occluded that we meet with a severe apoplectic attack.
The symptoms of embolism are, ig many cases, of a definite
character, owing to the regular distribution of the vessels, whilst
886 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
those of apoplexy are more dependent on chance; so that we
oftener meet with a repetition of exactly the same group of
symptoms in cases of embolus than we do in extravasation. As
an instance of this repetition, we refer the reader to Lichtheim’s
case of obliteration of the vertebral, with simultaneous bulbar
paralysis and paralysis of the extremities.
The course of the disease is very frequently quite decisive for
or against a diagnosis of embolism. Striking and rapid improve-
ment, with total disappearance of complete groups of paralytic
symptoms, seldom occurs in cases of hemorrhage.
When we have decided on a thrombus or embolus, though
perhaps only on grounds of probability, we must proceed to the
exact localization of the lesion. This will often be possible when
we can go upon the basis of the facts stated above ; but our diag-
nosis must always have a certain amount of uncertainty, owing -
to all the possible varieties of the vessels. Besides the localiza-_
tion of the paralyses, other symptoms may help us to form our
diagnosis. Thus, in diagnosing occlusion of the basilar, we
might take account of an unusually full pulse in the carotids,
and of Griesinger’s symptom (which he deduced a priori, though
we have never heard of its being practically tested) of violent
general convulsions resulting from energetic compression of both
carotids, just as in Kussmaul and Tenner’s experiments. The
practical application of this experiment seems, however, some-
what problematical.
Prognosis.
We need scarcely observe that the cases of embolism and
thrombosis with which we are now occupied are of the gravest
character. Whilst the prognosis of sudden and complete obstruc-
tion of the basilaris or both vertebrals is almost absolutely fatal,
we may say of a slowly developing, or at first incomplete, ocelu-
sion of one or more of the large vessels in this region, that it
almost unexceptionally ends in death within a short period. We
cannot expect life to last long, except in cases of relatively limited
obstruction, which happen to affect the least dangerous parts, or
where a possibility is offered of a somewhat considerable collat-
— a
INJURIES AND WOUNDS. 887
eral circulation. When such cases become chronic they share
the same prognosis as thrombotic or embolical softening of other
cerebral regions, and are consequently, in their later periods, to
be regarded as incurable.
Treatment.
We refer the reader, for the treatment of these cases, to Noth-
nagel’s article. Stimulants and tonics are plainly indicated
when the thrombosis is located in the bulbus; but, unfortu-
nately, the diagnosis is so uncertain in many cases that it is
difficult to follow out any definite therapeutical course. So that
we must be guided by the scanty symptomatic indications, which
can be gathered from a careful observation of the individual case.
At a later period electricity may be applied with most suc-
cess. Markusy derived the most wonderful results from its ap-
plication in a case which probably belonged to this class.
3. Injuries and Wounds of the Medulla Oblongata.—Chronic
Compression of the Same.
Ollivier, 1. c. 3me éd. I. u. IL. passim.— Waters, Remarkable Case of Lesion of the
Medulla Oblong. Medico-Chir. Transact, Vol. XLVI p. 115. 1863.—Viz, Fall
von einseit. Verletzung des verl. Marks. Correspondenzbl. d. drztl. Ver. im
Rheinland, 1874. Centralbl. 1875. No. 22.—JZeyden, Klinik I. und IL 1874-
76.—Hallopeau, Des paralysies bulbaires, Paris, 1875. p. 117.—C. Lange, Ein
paar ploétzliche Todesfille. Hosp. Tid. 1870. Virchow-Hirsch. Jahresber.
1870.—Levrat-Perroton, Cas de glycosurie déterminée par une tumeur colloide
renfermée dans le 4me ventricule. These. Paris, 1859.—Solbrig, Ueber die Ve-
rengerung des Eingangs des Wirbelcanals in den mit Epilepsie verbundenen
Seelenstérungen. Allgem. Zeitschr. fiir Psych. Bd. 24. p. 1. 1867—». Reck-
linghausen, Virch. Arch. Bd. 30. p. 864. 1864.—Ladame, Symptomatologie
und Diagnostik der Hirngeschwiilste. p. 43. 1865.— Voisin, Cas de paral.
glosso-lab.-lar., sans sclérose du bulbe. Annal. médic. psych. Janv. 1871. Vir-
chow-Hirsch. Jahresber. 13871. Vol. II. p. 59.—.Baelz, Enchondrom der Schii-
delbasis. Arch. der Heilkunde. XIIL p. 192. 1872. —Bouchard, Compress. de la
pyram. antér. gauche par l’apophysie odont. ; hémiplégie; convulsions épilept.
(quoted in Hallopeau’s work, p. 118).—Bourdon, Tubercule du cervelet occu-
pant l’éminence vermicul. et comprimant 1e bulbe; embarras de la parole.
ibid. p. 125.—G@arrod and Philpot, Papillomatous Tumor in the Fourth Ven-
888 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
tricle of the Brain. Lancet. 1873. March 1.— Hertz, Fall von Erweichungsher-
den in der Med. oblong. ete. Deutsches Arch. f. klin. Med. XIII. p. 385, 1874.
—Rotter, Arthritis deformans der Articul. epistropheo-atlant. etc. ibidem XIII
p: 408. 1874.— Verron, Etude sur les tumeurs du 4. ventricule. Thiase. Paris,
1874.—Hallopeau, Tumeur dans le cerveau moyen. Gaz. méd. 1874. No. 9.—
Hubrich, Geschwulst des Kleinhirns, Druck auf die Med. oblong. Arch. fiir
Psych. u. Nerv. V. p. 594. 1875.—Lanzoni, Caso singolare di paral. bulb. per
compress. di un tumore del cerveletto. Raccogl. med. 1876. Aprile. Jahresber.
pro. 1876. IL p. 111.—Morelli, Affectionen der Med. oblong. Centralbl. 1877.
No. 38.—Griesinger, Ancurysma d, Basilararterie. Gesammelte Abhandl, IL p.
472 (from the Arch. d. Heilkunde III.).—Zebert, Aneurysma d, Vertebrales,
Basilaris, etc. Berliner klin. Wochenschr. 1866. No. 28.
Notwithstanding its protected position, the medulla oblongata
often suffers from traumatic influences, and is thereby, directly
or indirectly, more or less injured and even destroyed. To this
category belong acute mechanical injuries to this vital organ,
which are of the most dangerous character, and consequently
have, as a rule, a very short clinical history.
But, besides these, there are other mechanical influences which
affect the medulla from without, but quite gradually and increas-
ing by slow degrees. These influences are neoplasmata, disease
of the bones, and dislocations, parasites, etc. They all produce
a slowly increasing pressure, and compress the medulla chron-
ically.
It appears to us quite suitable to discuss the two—the acute
and chronic forms of mechanical injury to the medulla—in the
same section.
Pathogenesis and Etiology.
Injuries of the medulla may be produced in many different
ways: for instance, by a cut or stab, which pierces easiest between
the atlas and occiput; or by foreign bodies, such as pistol and
rifle bullets, splinters of bone, etc. Such injuries can occur at any
point, accompanied or unaccompanied by injuries of the cervical
vertebree and skull. Further, these wounds may be produced
by a cut on the head, with or without fracture of the skull, and —
in many cases by contre-coup. A fall on the head or back of the
INJURIES AND WOUNDS. 889
neck, or a heavy body striking these parts or the face, produces
similar results.
Fractures, dislocations and displacements of the two first
cervical vertebre are very important and frequent causes of
wounds of the medulla. When the vertebre are fractured, as
happens from gunshot wounds, or from a fall or blow on the
head or neck, etc., we always find them more or less displaced ;
if this is not the case, the medulla may escape uninjured. The
most dangerous luxation is that of the first vertebra, as it is
almost always accompanied by backward displacement of the
odontoid process ; this process is then forced against the anterior
surface of the medulla, which it compresses and lacerates, espe-
cially when some pathological process has already produced en-
largement of the bone, or altered its natural direction of growth.
This event, followed by immediate death, can also be produced by
simple dislocation of the odontoid process. Dislocation can take
place when the head is sharply pulled forward, as in hanging, or
flexed, the epistropheus slipping from under the transverse liga-
ment. The same effect is produced by any great force acting on
the head and neck, inducing a luxation in the occipito-atlantoid
or atlanto-epistropheal articulations. A similar result ensues
from caries of the first cervical vertebree, which slackens and
destroys the ligaments and the vertebree themselves, so that quite
a trifling mechanical process, such as a sudden turn of the head,
etc., produces dislocation.
The causes of slow compression of the medulla are very vari-
ous. If any neoplasma or enlargement (whether it arises in the
bone, periosteum, meninges, in the vessels or the surrounding
parts of the brain) grows in the direction of the medulla, it may
_ produce slowly increasing compression, and thereby cause mate-
rial injury to the functions of this organ.
The processes of this class with which we most frequently
meet are osseous. Simple caries of the occipital bone and two
first cervical vertebree may produce the effect, with its exuda-
tions, abscesses, osseous tumefaction, dislocation of the odontoid,
etc.
The medulla is often compressed, too, by abnormalities in
the shape and size of the bones. Solbrig directs attention to one
890 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
of these, which is by no means of seldom occurrence, namely,
constriction of the entrance to the spinal canal, caused by some
misgrowth of the processus anonymi occipitis, of the processus
odontoideus, and of the posterior semicircle of the atlas. In nine
cases of epilepsy he found at the autopsies considerable constric-
tion, which had caused compression. And Ollivier describes
similar cases. An enlargement of the odontoid, too, is not rare.
Hertz describes a case in which this process was very much en-
larged, with its point directed sharply backwards towards the
medulla, perhaps the result of rachitis. These variations do not
seem to have any absolute significance, and are often found by
mere chance; but when combined with certain external injurious
influences or some casual effort (physical overexertion, carrying
a heavy load, etc.), they may give rise to grave disorders. In
Hertz’s case, for instance, the overgrowth of the odontoid had
produced a small centre of softening in the decussation of the
pyramids, corresponding exactly to the point of the process.
Arthritis deformans in the articulations between the occi-
put, atlas, and epistropheus, would seem to be a very much
rarer cause of compression. Rotter has lately described a case
in which the shape of the joints was immensely changed, the
odontoid process enlarged, and the ligaments very slack, so that
the occipital foramen was considerably constricted.
The medulla is much oftener compressed by twmors arising
Srom the bony parts and growing into the foramen magnum.
Baelz found an enchondroma from the base of the skull, Leyden
a cystosarcoma of the clivus, and Hallopeau a connective-tissue
tumor from the base, and we could enumerate many other in-
stances of this class.
The same effect is produced by different kinds of tumors
Javorably situated on other surrounding structures, such as
syphilitic gummata arising on the dura mater, excrescences on
the choroid plexus (Kussmaul), epitheliomata in the arachnoid
(Voisin), ete.
In this class we may further include aneurisms of the basilar
and vertebral arteries, which are of somewhat common occur-
rence ; they, however, in the majority of cases compress the
pons, but sometimes their influence extends to the medulla and
INJURIES AND WOUNDS. 891
its nerves. They are rendered still more dangerous by ‘the
thrombosis, which almost constantly accompanies them.
Lastly, we come to tumors of the cerebellum, which, when
they are large enough to compress the medulla and are favorably
situated, play a very prominent part. Cases of this kind are
numerous. Bourdon describes a small tubercle in the vermis
cerebelli surrounded by an exudation, which compressed the
inferior portion of the rhomboid sinus; Morelli had a case of
tubercle on the floor of the fourth ventricle; Hubrich saw a
glioma, probably originating in the flocculus, and wedged in be-
tween the medulla, cerebellum, and pons, which had compressed
the medulla considerably, and pushed its nerves to one side;
Lanzoni observed a glioma as large as a hen’s egg in the vermis
inferior, which covered the fourth ventricle; Voisin found an epi-
thelioma in the pia mater of the cerebellum growing in the direc-
tion of the medulla. But we need not multiply cases further.
The action in all these cases is increasing pressure from with-
out upon the medulla, and this pressure must naturally first act
upon the nerve-roots given off by the medulla, and then upon
the different parts and funiculi in the organ itself. This is what
produces the characteristic symptoms of gradually increasing
irritation and paralysis. But frequently a long time elapses
before we can observe any symptoms, or perhaps only very insig-
nificant ones; and then these cases exhibit suddenly the most
acute paralytic symptoms, ending quickly with death. This, of
course, leads us to assume an embolus or extravasation, but this
occurs by no means constantly ; on the contrary, it is almost cer-
tain that bulbar myelitis produced by compression, which ex-
tends rapidly over a large surface, is the origin of these acute
symptoms. In fact, we have an analogous case in the slow com-
pression of the spinal cord. It is the possibility of this myelitis
by compression that constitutes the chief danger ina great many
cases of mechanical injuries of the medulla oblongata.
Pathological Anatomy.
It is unnecessary to dwell upon the eauses which could pro-
duce an acute trauma in the medulla. <A few words, too, will
892 ERB.—DISEASES OF THE MEDULLA OBLONGATA,.
dispose of the anatomical changes which we observe in the organ
when wounded, lacerated, or crushed. Tney resemble in every
detail the acute injuries in the spinal cord, and their termina-
tion is similar. The location and extent these lesions occupy are
very various, and of course dependent on chance.
It would also take up too much space to describe the ana-
tomical appearances of the causes of slow compression, and we
shall content ourselves with having enumerated them above.
The medulla itself may undergo the most manifold changes
from compression: its shape may be altered, it may be dis-
located, turned on its axis, or pressed out flat or obliquely, ren-
dered unsymmetrical, or may receive a number of impressions of
various depth and size. Various parts are atrophied by pressure,
or there may be sharply-defined indentations, or one-half may be
severely compressed, whilst the other is relatively untouched, ete.
It is quite plain that.all this depends entirely upon the position
and shape of the compressing processes, and that these, too, are
accountable for the different symptoms that we may meet with.
Relatively little is known of the histological changes that
take place in such cases. We usually find the medulla anemic,
and generally softened. In Hubrich’s case the affected half was
soft and friable. Extravasations in the softened parts are of fre-
quent occurrence. In the small centre of softening which Hertz
describes, he found that the medullary sheath had disappeared,
and likewise part of the axis-cylinder ; he saw, too, a great deal
of finely granulated, soft, interstitial tissue, numerous corpus-
cles of Gluge, and corpora amylacea; the vessels were irregularly
dilated, hypertrophied, and covered. with granules of fat and
pigment, and it was around them he found most of the corpus-
cles of Gluge.
The nerve-roots given off from the bulbus are generally more
or less degenerated and compressed; they are flattened, gray,
attenuated, and undergo degenerative atrophy.
Secondary degenerations often arise from these lesions and
run down into the spinal column.
However, in future cases it would be very desirable to make
more accurate investigations on the results of myelitis of the
medulla from compression.
ee ae ea
= t+
INJURIES AND WOUNDS. 893
Symptoms.
If the injury to the medulla is a severe, acute one, the symp-
toms are generally very simple—the patients collapse as if struck
by lightning, and die instantaneously; sometimes they give
utterance to a loud cry before falling, or death may be accom-
panied by a few transitory convulsions. All this results from
sudden paralysis of the respiratory centre, and complete inter-
ruption of every conducting connection with the spinal cord and
the periphery. 3
This is the ordinary course when the occiput is dislocated
towards the atlas, or when the odontoid process is forced from
the epistropheus, or in fractures of the anterior cervical vertebra,
or in gunshot and knife wounds of the medulla, and also in a
number of other cases.
When the wounds are relatively less severe, or when the
medulla is only partially lacerated, life may last for some time;
but these cases, too, end suddenly.
Waters describes a case of this nature. The patient received a heavy blow in
the face, unaccompanied by fracture of the skull. At first the symptoms were
trifling, consisting of a slight feeling of weakness, and deafness on the right side.
There was no anesthesia; the tongue and uvula were slightly oblique; the patient
suffered, too, from singultus, and was unable to swallow. The temperature was
high on the right side. Sudden death in twenty-four hours. At the autopsy he
found both sides of the right pedunculus cerebelli lacerated, the wound extending
to the floor of the fourth ventricle. The paralytic symptoms may be explained by
laceration of the nuclei, and death probably resulted from paralysis of the respira-
tory centre.
Vix’s case cannot be regarded as anything more than a mere unilateral wound
of the upper cervical portion of the spinal cord, which was located in all proba-
bility below the decussation of the pyramids. No conclusions, however, can be
drawn from the case, as the patient survived, and an autopsy was never obtained.
It is certainly highly probable that patients sometimes sur-
vive very small injuries to the medulla. But still this is difficult
to prove; for, from the symptoms of paralyses of different kinds,
troubles of articulation and hearing, epilepsy, slow pulse, dia-
betes mellitus or insipidus, etc., we camonly conjecture that the
medulla has received some injury.
894 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
On the other hand, it is by no means certain that we must
always assume an actual lesion such as hemorrhage, laceration,
or comminution, to explain the symptoms which follow trau-
matic influences bearing upon the neck and skull. It would not
_ be difficult to account for all the symptoms by simple commo-
tion, similar to what has been found in the spinal cord ; it does
not alter the question whether they are accompanied or not by
chronic nutritive troubles. This remains to be decided. There
is no doubt, however, that our present material is not sufficient
to allow us definitely to assume the existence of a commotio
medulle oblongatee.
Special importance attaches to a number of initial symptoms
in slow compression of the medulla. These initial symptoms
develop very gradually, and may escape observation ; their form
is very variable, and they are the results of irritation and paraly-
sis of the nerve-roots coming from the bulbus and pons. In the
first place, we have symptoms of irritation, such as pains of
varying intensity in the territory of the trigeminus, or head- and
face-aches, which often assume a neuralgic character, and are
generally unilateral, though sometimes bilateral. To this class
further belong twitching of the muscles supplied by the facialis,
transitory cramps in the tongue and lips; sometimes, too, we
meet with clonic and permanent contractions in the extremities,
with buzzing in the ears, etc. When the bulbus itself is seriously
irritated, we may observe epileptoid convulsions, vomiting, dizzi-
ness, and singultus.
After these initial symptoms have lasted for a varying period,
the nerves above mentioned show signs of paralysis, usually
accompanied with atrophy, and thus we gradually get all the
symptoms of a “bulbar paralysis.’ Paralysis in the extremi-
ties and disorders of respiration and circulation very soon follow.
But the development of the disease does not always take this
course; sometimes it begins more acutely—so rapidly, in fact,
that we are induced to think of an embolus, thrombus, or some
similar lesion. Cases of this nature are recorded by Hallopean,
Bourdon, Bouchard, and others. In point of fact, this acute
commencement may be caused by thrombosis or hemorrhage in
the medulla; but in the majority of cases it results from a rap-
el
BAT Aah da +o
nm, mr ame a
INJURIES AND WOUNDS. 895
idly developing and spreading myelitis from compression, after
this latter has reached a certain intensity.
In both cases, if the symptoms are well developed, we have,
in the first place, paralysis of the bulbar nerves and centra,
varying in extent, symmetry, and intensity ; in the second place,
the extremities are paralyzed—either a perfect hemiplegia, or,
when paraplegia, the symptoms are more marked on one side
than on the other. Lastly, we meet with different degrees of
sensory disorders, both in the face and on the trunk and
extremities. But, at the same time, there is no sign of any
anterior parts of the brain being complicated, and consciousness
is generally quite unimpaired. The optic nerves are never
alfected, except when the tumor is very large, and so situated as
to extend its influence thus far.
It is a most striking fact that in this disease we usually meet
with a group of symptoms which are generally taken to indicate
bulbar paralysis, and almost all the cases of this nature have
been described under the heading of chronic bulbar paralysis.
To this class belong paralysis of the tongue and muscles of
articulation, partial paralysis of the inferior branches of the
facialis (especially as regards the lips) and of the soft palate,
troubles of deglutition, increased secretion of saliva, hoarseness
and aphonia, disturbances of the respiration and circulation, and
occasionally paralysis of the orbital muscles (especially the
abducens) and the masticatory muscles, anesthesia in the terri-
tory of the trigeminus, deafness, and singing in the ears; finally,
we may meet with vomiting, singultus, epileptic convulsions,
signs of vascular paralysis, Stokes’ respiration, and a number of
other symptoms which do not need mention. Of course, all these
symptoms do not occur, by any means, in every case, but only
one or more at a time, so that these cases of slow compression
assume very various forms. This variability of symptoms is the
great characteristic which distinguishes it from ‘‘ chronic progres-
sive bulbar paralysis.’ This latter disease, which we shall
describe later on, presents unusually constant and sharply de-
fined symptoms.
To illustrate the variability of symptoms in slow compression,
we shall give the following summaries of cases on record :
896 ERB.—DISEASES OF THE MEDULLA OBLONGATA,
Bouchard’s case: Compression of the left pyramid ; hemiplegia of the right side,
with contractures, followed by epileptoid convulsions confined to the left side. No
other lesion found in the brain.
Hallopeau : Compression of both pyramids ; consequent paralysis of both upper,
and later, of both lower extremities, with permanent contractions and violent
remittent spasms in the members ; no anesthesia; finally, dyspnoea and asphyxia.
Hertz: Myelitis from compression in the decussation of the pyramids; motor
paralysis of all four extremities, with spasms and contractures—observed in the
neck too; contracture of the masticatory muscles; speech, articulation, and sen-
sation unaffected ; remarkable temporary redness of the face; pain in swallowing,
and headache.
Rotter : Compression in the region of the inferior decussation of the pyramids,
caused by the odontoid process ; motor paralysis of the extremities of the right side
and of the sphincters; epileptoid convulsions; no disorder of sensation; speech
and deglutition unaffected. (Imperfect record.)
Baelz : Enehondroma of the base of the skull, compressing chiefly the nerve roots,
and hardly affecting the bulbus itself at all; headache; neuralgia in the trigemi-
nus; convulsive fits in the lips and tongue; in a later stage, typical bulbar paraly-
sis, with paralysis and atrophy of the tongue; finally, anesthesia of the face and
scalp ; extremities very little affected.
Hubrich: A glioma, as large as a walnut, wedged in on the left side, between the
medulla, cerebellum, and pons; headaches, buzzing in the ears, and vomiting ;
troubles of deglutition, and a fecling of fur on the hands; increased secretion of
saliva; paralysis of both inferior and of the right superior extremities ; no paraly-
sis of the lips or tongue, but speech somewhat affected ; sensation is unaffected ;
attacks of vertigo and weakness, and finally, loss of consciousness, with convulsions
and passing blindness. The patient himself assigned the lesion, with perfecke accu-
racy, to the point where it was found at the autopsy.
Leyden; A cystosarcoma which had forced its way on the right side, between the
medulla, cerebellum, and pons; severe headache; vertigo; left-sided hemiplegia ;
later, general weakness of all four extremitics, with violent pain, bulbar paralysis,
paralyzed bladder, and decubitus.
Bourdon: The floor of the fourth ventricle compressed by a small tubercle around
the nucleus of the hypoglossus ; speech very much impaired (anarthria); all other
bulbar functions unaffected ; sudden death.
Morelli: Tubercle on the floor of the fourth ventricle ; headache, giddiness, 4 im-
paired vision ; paralysis of right facialis and right abducens; weakness of the left
upper dxtreialee: fibrillar twitchings in the tongue and left masseter.
Lanzoni: Glioma on the floor of the fourth ventricle ; headache, inclination to
vomit, dyspnea, unsteady gait, strabismus, tongue to the left, difficulty in speak-
ing and swallowing, facialis paralyzed on the left side; no paralysis of the extrem-
ities, sensibility unaffected.
Chouppe (in Verron’s work, p. 49): Hypertrophy of choroid plerus, attaining a
thickness of one centimetre ; pain in the face, frequent vomiting, bilateral deafness ;
INJURIES AND WOUNDS. 897
decrease of intelligence, and amblyopia; partial paralysis of the facialis on the
right side; sensibility unimpaired ; later, delirium; contraction of the extremities
of the left side; neither albumen nor sugar.
Von Recklinghausen : Hypertrophy of the choroid plexus, unattached in the ventri-
cle; scalp-wound; later, loss of memory; diabetes mellitus ; phthisis.
Bourdon (in Verron’s work, p. 52): Tumor of the choroid plexus as large as a
_ hazel-nut, of firm tissue, and like a mulberry; secondary softening of the pyra-
mids; convulsive movements, and tremor in the extremities, tongue, and face,
rendering difficult, too, the movements of the eye and of speech; general muscular
weakness; normal sensibility ; frontal headache ; decrease of intelligence; no albu-
men or sugar; finally, continuous convulsive contractions, speech incomprehensi-
ble, respiration and deglutition unaffected, mania, vomiting, death.
Garrod (in Verron’s work, p. 57): Papilloma of the choroid plexus, one and one-
half inches long, occupying the whole ventricle, very vascular; wound on the
head; unsteady gait; ataxy; weak sight, and stagnation in the papilla; paral-
ysis of right abducens ; strength of muscles almost unaffected, and normal sensibili-
ty; pain in the back of neck; weakened intelligence; vomiting ; deafness; diffi-
culty in swallowing; disturbances of respiration and circulation; partial paralysis
of the right facialis; finally, coma, general paralysis, and a terminal rise of tem-
perature.
_ Solbrig’s cases: Contraction of the entrance to the spinal canal ; probably in all
the cases a very chronic, slow compression of the medulla; as yet only found in
epileptic insane, but probably causally related to epilepsy. But we need more de-
tails.
These cases will suffice to give an idea of the great number of
different possible symptoms, and at the same time show the dif-
ficulties we have to deal with and the points to which we must
hold fast in the interpretation of individual cases.
Diagnosis.
The diagnosis of a severe acute trawma of the medulla is sel-
dom made during life, and generally only after a post-mortem
examination ; and in the few cases in which life remains unextin-
guished for a few hours, we must hesitate to make a certain |
diagnosis on the very ground that death did not follow instan- |
taneously. In the latter case the probability-diagnosis can only
be confirmed by a sudden death. Even in lighter cases, where
the symptoms remain constant, the most careful estimation of
all the circumstances can hardly lead to anything more than a
probable conjecture.
VOL. XIII.—57
898 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
The symptoms of slow compression are so grouped and suc-
ceed one another in such an order, as to allow of a diagnosis in
many cases. Thus, when we observe a series of initial symptoms
of irritation in the bulbar nerves, sharply confined to certain
nervous tracts; and then in the same tracts symptoms of paral-
ysis which, perhaps at an early stage, prove on electrical exami-
nation to be peripheral; when we meet with giddiness, violent
headache, vomiting, and epileptic convulsions ; and when, later,
these are followed by the typical symptoms of bulbar paralysis,
complicated with paralysis, twitching, and contractures in the
extremities ; and if these symptoms of paralysis show a disposi-
tion to spread rapidly ; if they are rather unsymmetrical on the
two sides; and if, finally, the sensorium is unaffected—in such a
case we may assume a gradually increasing compression from
without with considerable certainty.
But it is different when the initial symptoms are absent or
very trifling, and we suddenly meet with all the symptoms of an
‘‘acute bulbar paralysis’’ (see next paragraph) simultaneously
with the development of a myelitis from compression or the oc-
currence of hemorrhage or thrombosis. Here it would be impos-
sible to make a certain diagnosis, though perhaps there might be
a possibility, by means of more accurate investigation, of finding
some previous suspicious symptoms from which we might con-
jecture that it was not an actual case of so-called primary acute
bulbar paralysis, but only a secondary one, originating from com-
pression from without.
The chronic cases are easiest and oftenest confounded with.
Duchenne s chronic bulbar paralysis. In our opinion it is not
so very difficult to distinguish between the two forms, provided
that we understand Duchenne’s disease as a well-characterized
and sharply-defined form, and not merely any chronic paralysis
of the bulbar nerves and centres whatsoever. We shall discuss
this point more in detail in Paragraph 5, under the head of
Chronic Progressive Bulbar Paralysis.
Cases of slow compression of the anterior half of the medulla
alone, where the pyramids are mainly involved, exhibit a very
striking likeness to spastic spinal paralysis, so that, when the
disease is fully developed, the resemblance is almost complete
INJURIES AND WOUNDS. 899
(compare Hallopeau’s case, 1. c., p. 121). Still, in most cases it
will be possible to draw a distinction, though, of course, it cannot
-be a reliable one until we become acquainted with the anatomi-
cal lesion which causes spastic spinal paralysis. The points of
distinction are: the sudden commencement of the paralysis, the
fact that it appears first in the upper extremities, and that it is
followed later by actual bulbar symptoms, dyspncea, paralysis
of the tongue, difficulty of swallowing, etc.
But, even when we do diagnose slow compression of the me-
dulla, there still remains the difficulty of determining its cause.
Here we must proceed on general principles. It often happens
that we find characteristic symptoms which enable us to say
whether it is a case of caries of a cervical vertebra, an aneurism
of the basilar artery, a tumor within the skull, or syphilis. Still,
too, these frequently fail us.
Prognosis.
Every severe acute injury to the medulla causes instant
death ; and smaller lesions, too, are usually extremely danger-
.ous, because the traumatic inflammation and softening conse-
quent on them often lead rapidly to a fatal termination. We
can seldom hope for any long duration of life.
The prognosis of slow compression of the medulla is, of course,
dependent upon the cause of the compression ; but in most cases
‘it may be pronounced absolutely fatal, as most of the processes
in this category follow an uninterruptedly progressive course.
The prognosis of the quickness or slowness of the disease in pro-
ducing death depends, on the one hand, upon the rate at which
the structure grows, and, on the other hand, upon the point at
which the medulla is attacked, and whether the vital centres
come at once or only slowly under the influence of compression.
We may form a prognosis not absolutely fatal in cases of
simple caries (as restitution is possible), in arthritis deformans,
and in syphilitic tumors.
It naturally needs an exceedingly cafeful estimation of every
circumstance and symptom before we can form a prognosis for
each individual case.
900 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
Treatment,
Little can be said on this head. Acute injuries to the medulla
must be treated in the same way as similar ones of the spinal
cord. |
Causal treatment is the chief and only method which prom-
ises success in slow compression. We can find elsewhere what
is to be done in cases of caries, syphilis, aneurisms, tumors, etc.
We must take a purely symptomatic course. But, when the
diagnosis is uncertain, it would be advisable to have recourse to
a number of empiric remedies.
4. Acute Inflammation of the Medulla Oblongata.—MUyelitis
Bulbi Acuta.—Acute Bulbar Paralysis.
Abercrombie, Abscess of the Medull. Oblong. Diseases of the Brain and Spinal
Cord. p. 103. Edin. 4th ed. 1846.—Zange, Om acute Bulbarparalyse. Hosp.
Tidende. 1868. Nos. 51-53. Jahresberichte pro 1868. II. p. 46.—Meynert, Ab-
scess in der Varolsbriicke, etc. Oesterr. Zeitschr. f. prakt. Heilk. 1863. No. 24.
—Rosenthal, loc. cit.—Leyden, Klin. der Riickenmarkskrankh. II. p. 157. 1875.
—Leyden, Zwei Fille acuter Bulbirparalyse. Arch. f. Psych. u. Nery. VIL. p.
44. 1876.—Lichtheim, Ueber apoplektiforme Bulbirparalyse, etc. Deutsches
Archiv f. klin. Med. XVIII. 1876.
It is only in the last few years that this disease has received
its due share of attention. Under the heads of apoplexy, embo-
lism, myelitis from compression, and traumatic myelitis of the
bulbus, we have, in the preceding paragraphs, treated of ‘‘apo-
plectiform bulbar paralysis.’ But there still remain individual
cases of great interest, and which must most probably be re-
garded as primary acute myelitis bulbi. Leyden was the first
who drew our attention to this form, and he illustrated it with
an accurate description of three cases.
The other cases, which are scattered over the literature of the subject, cannot be
well taken into consideration: Abercrombie’s case of an abscess appears to have
been a tubercle, and must consequently be excluded; Meynert describes an acute
abscess, but his case was complicated with basilar meningitis; Lange’s two cases
are doubtful, and perhaps belong to another form of disease. So there only remain
to us Leyden’s three interesting cases, and we have taken them as groundwork for
our description.
vo
ACUTE BULBAR MYELITIS. 901
We shall bring together under this head the processes in the
medulla oblongata of relatively acute and primary origin, which
may fairly be designated as inflammational. On the other hand,
we do not include forms of secondary origin, such as the bulbar
processes, which originate in acute ascending myelitis, and usu-.
ally bring about the fatal termination of acute central myelitis,
and ascending poliomyelitis anterior subacuta. Nor can we in-
clude the myelitic centres we find in the oblongata in cases of
basilar meningitis.
Etiology.
The causes of acute bulbar myelitis are still almost unknown.
If we put out of consideration the myelitides ascending from the
spinal cord, and also basilar meningitis and emboli as causes of
centres of softening, we have nothing further.
In Leyden’s first case he could adduce no cause ; in his second
he assumes an embolus as the probable origin, but no embolus
was found; it was preceded by rheumatic arthritis. His third
case was a hard drinker, who had suffered greatly from rheuma-
tism, but had no peculiar antecedents.
Pathological Anatomy.
Rather small centres of softening, without definite boundaries,
were found in the medulla in all three cases. In two cases noth-
ing abnormal could be seen on the fresh specimens with the
naked eye, either in the form, color, or consistence of the me-
dulla. But in the third case, even without the microscope, a cen-
tre of extravasation could be plainly seen, dotted with numerous
small extravasations. When the specimens were hardened, how-
ever, the position and size of the myelitic centres were easily
recognized. |
An accurate examination gave the following results:
Casz I.—Woman, thirty-six years of age. Region of the pyramids and olivary
bodies covered with numerous small extravasations; all around the softened sub-
stance was of a gray and reddish yellow tinge. These centres were found from
above the decussation of the pyramids up to the inferior position of the pons, occu-
902 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
pying especially the so-called internal fields of the medulla, and were more numer-
ous on the left side than on the right; on the left side changes had taken place
between the roots of the vagus and accessorius. Microscopically the vessels were
found to be hypertrophied, and surrounded partly with numerous cells and partly
with extravasations of blood. The nervous substance was in a state of inflamma-
tional disintegration, and full of pus-cells, corpuscles of Gluge, parenchymatous
centres of myclitis (swollen axis-cylinders, etc.)—in fact, a form of inflammational
disintegration with capillary hemorrhage. Ly
Case IL—Woman, fifty-two years of age. In the right half of medulla a small
centre of softening, situated between the restiform body, the olivary body, and the
roots of the hypoglossus, shaped like an olive, without any boundary above or be-
low. Consequently it affected chiefly the roots and nuclei of the vagus, glossopha-
ryngeus and accessorius; the substance of the restiform body, too, was very much
involved. Microscopie examination showed considerable cellular infiltration, with
softening and swelling of the nervous tissues. Cells were large and round, and
possessed several nuclei, and there were a few corpuscles of Gluge. The adventitia
of the vessels was full of cellular elements. In this case a commencing inflamma-
tional (embolic ?) softening. ,
Case III.—Man, sixty-two years of age. Centre of softening in the internal
fields of the medulla, extending from the floor of the fourth ventricle into the pyra-
mids, and from the centre of the olivary bodies to its anterior extremity, tapering
to a point anteriorly and posteriorly. Under the microscope the structure could hardly
be recognized, the tissue showing a tendency to disintegration; few corpuscles of
Gluge; reactive demarcation on the periphery, 7 ¢, parenchymatous myelitis,
swollen axis-cylinders and cellular infiltration, Acute softening of inflammational
character ?
These cases undoubtedly prove the existence of recent small -
centres of inflammation in the medulla, which in two cases oceu-
pied the internal, and in the other the lateral field. Further.
observations must of course be awaited, bringing with them
more knowledge.
Symptoms.
Taking up these three cases, we can draw up the following
description of the disease: The commencement appears to be:
always acute and rather sudden, accompanied by headache, gid-
diness ; occasionally, too, by vomiting or violent singultus, diffi-
culty in swallowing and speaking, pareesthesia, and symptoms of
weakness in the head and extremities. But there is never any.
disturbance in the sensorium, loss of consciousness, or apoplec-
tic attack.
Ae SSG ANTI IY eee Lak PW Ler eee bce ah Pate
a
—————
AOUTE BULBAR MYELITIS. 903
‘After a short time more or less developed and severe symp-
toms of bulbar paralysis make their appearance, which affect the
different functions of the bulbus in different degrees, according
to the situation of the lesion.
In one case swallowing was impossible, in the other the pa-
tient could only swallow with the greatest difficulty. Then,
again, the tongue is either paralyzed or almost unaffected, whilst
articulation is more or less disturbed. Symptoms of paralysis
in the region of the inferior facialis and in the soft palate varied
in intensity, and were sometimes bilateral, sometimes more uni-
lateral. Usually, at quite an early date, there were very marked
symptoms of disturbance of respiration (quick, irregular and
halting breathing, dyspnoea, feeling of oppression, cyanosis) and
of circulation (rapid, small and irregular pulse, with intermis-
sions, etc.).
Besides this, there were frequent vomiting, troublesome sin-
gultus, fits of coughing, violent headaches, small differences in
the pupils, etc.
The symptoms are rendered complete by more or less con-
siderable affection of the extremities, which can, however, vary
greatly according to the position and extent of the lesion; this
affection consists in partial paralysis of some or all four extrem-
ities, sometimes in hemiplegia (when the process approaches or
involves the pyramids). When the pyramids are spared we have
no symptoms at all of paralysis, or very trifling ones. In one
case signs of loss of co-ordination were observed (destruction of
the fibree arcuate 2).
Sensibility was objectively scarcely affected ; subjectively
complaints were made of pains and formications in the limbs
(funiculi restiformes involved ‘).
The bladder and rectum may become paralyzed at a later
stage. In Cases 2 and 3 there was a slight fever, 38.8° C. (97.9° F.)
Neither epileptic convulsions nor tonic or clonic contractions
of the muscles have yet been recorded. |
In its further course the disease makes rapid progress; the
disturbances of circulation and respiration increase ; the patient
becomes unconscious, and plainly collapses; death results from
paralysis of respiration and asphyxia.
904 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
The duration of the disease is short (four, six, or ten days).
It is not decided whether death is the one invariable result of
the disease. For the present we should scarcely venture to make
the diagnosis until we obtain a post-mortem examination, in
order thus to fix the symptoms and render the diagnosis pos-
sible in succeeding cases. It will not be possible, before this has
been done, to say whether other cases (as is quite possible and
even probable) take a more favorable course and result in con-
valescence. At present nothing certain is known of this.
Diagnosis.
It is certainly not very difficult to recognize an ‘acute bulbar
paralysis,’’ 7. é.,an acute pathological process in the medulla ob-
longata. But it is really difficult to say what the process is, and
to distinguish it from hemorrhage, embolism, or rapidly develop-
ing myelitis from compression.
The following points may perhaps be taken as indicative of
primary acute myelitis bulbi: no foregoing or initial symptoms,
no loss of consciousness, no convulsions, and moderate fever ;
rather gradual development of the paralysis and the complete
set of symptoms, a matter of at least hours or days; rapid
change for the worse.
Of course, nothing decisive can be said till we have collected
more cases. |
Prognosis.
The same may be said of the prognosis, for it is impossible
to draw conclusions sufficient to form a prognosis from three
cases which all terminated fatally.
Treatment.
The principles, means and methods which we have treated of
in the chapter on the therapeutics of acute spinal myelitis (supra,
section 9), may be applied to the treatment of bulbar myelitis.
We would recommend, too, comparison with what has been said —
of the treatment of paralysis ascendens acuta (supra, section 17.)
meine te “Impl S
PROGRESSIVE BULBAR PARALYSIS. 905
5. Chronic Progressive Bulbar Paralysis (Wachsmuth).—Pro-
gressive Muscular Paralysis of the Tongue, Soft Palate, and
Lips (Duchenne).—Paralysis Glosso-labio-laryngea (‘Trous-
seau).—Progressive Atrophic Bulbar Paralysis (Leyden).—
Progressive Bulbo-nuclear Paralysis (Kussmaul).— Primary
Atrophy of the Motor Nuclei (Hallopeau).
Duchenne (de Boulogne), Paralysie musculaire progressive de la langue, du voile du
palais et des lévres. Arch génér. 1860. Vol. IL pp. 283 and 431.—De I’électri-
sation localisée. 2. édit. 1861. p. 621.—3. édit. 1872. p. 564.—Duménil, Gaz.
hebdom. 1859. 24 Juin. p. 390.—TZrousseau, Paralysis glosso-laryngea. Clin.
méd.— Wachsmuth, Ueber progress. Bulbirparalyse u. Diplegia facialis. Dorpat,
1864.—B. Schulz, Beitr. z. d. Motilititsstérungen der Zunge. Wien. med.
Woch. 1864. Nos. 38 and 39.—Gerhardt, Capillarektasie im Pons Varoli. Jen.
Zeitschr. f Med. and Naturwiss. I. p. 196. 1864.—De Bonnefoy, De la paralysie
glosso-laryngée. These. Paris, 1866.—Mignard, De la paralysie dite glosso-
labio-laryn. These. Strasbourg, 1867.—Huber, Zur Geschichte der Paralys.
glosso-lab.-lar. Deutsches Arch. f. klin. Med. IIL. p. 520. 1867.—J. Stein, Dop-
pelseit. Lihmung des Nerv. fac. u. hypogloss. nebst allgem. prog. Muskelatro-
phie. Ibid. VI. p. 593. 1869.—ZLeyden, Vorl. Mitt. tiber progr. Bulbarparalyse.
Arch. f. Psych. und Nerv. II. p. 423. 1870.—Ueber progr. Bulbirparalyse. Ibid.
IL. p. 648. 1870; and IIL. p. 388. 1872.—Charcot, Note sur un cas de paralysie
glosso-lar. suivi d’autopsie. Arch. de Physiol. norm. et path. III. p. 247. 1870.
—Duchenne et Joffroy, De Vatrophie aigué et chron. des cellules nerv. de la
moelle épin. et du bulbe rhachid. & propos d’une observ. de paral. glosso-lab.-
lar. Ibid. IIL. p. 499. 1870.— Wilks, Guy’s Hosp. Rep. XV. 1870. p. 2.—Hun,
Labio-glosso-lar. Paralysis. Americ. Journ. of Insan. 1871.—Krishaber, L’anes-
thésie de la sensib, réflexe des voies aér. et digest. comme signe précurseur de
la paral, 1.-gl.-lar. Gaz. hebd. 1872. p. 772.—A. Hulenburg, Lehrb. d. funct.
Neryenkrankh. 1871. p. 549.—Cheadle, Glosso-lab.-lar. Paralysis. St. George’s
Hosp. Rep. V. p. 128. 1871.—Benedikt, Elektrotherapie. 1868. p. 217.—Nerven-
path. u. Elekt. 1876. p. 640.—Zur Casuistik d. progr. Lihmung d. Gehirn-
nerven. Deutsch. Arch. f. klin. Med. XI. p. 210. 1872.—Fall von diffus. Neuritis
centralis. Ibid. XIII. p. 94. 1874.—Lockhart Olarke, Progress. Muscul. Atrophy,
etc. Medico-chir. Trans, Vol. 56. p. 103. 1873. — Friedreich, Ueber progr.
Muskelatrophie, etc. Berlin, 1873. p. 322.—Z. Hoering, Ueber paralysis glosso-
ph.-lab. Diss. Tiibingen, 1870.—Blumenthal, Réflex. sur la mal. décrite par
M. Duchenne, etc. Gaz. des hép. 1872. No. 113.—Bourdon, Etudes sur les
mal, du bulbe rhach. Bull. de ’Acad. de Méd. 1872. No. 7.—Gaz. hebd. 1872.
No. 22. p. 354.—Déchery, Quelques formes d’atroph. et de paralysie glosso-
laryng. d’origine bulbaire. These. Paris, 1870.—Kussmaul, Ueber fortschreit.
Bulbirparalyse und ihr Verhiiltn. z. progr. M.-Atrophie. Volkmann’s Samm.
906 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
klin. Vortr. No. 54. 1873.—M. Rosenthal, loc. cit. 1876.—Leyden, Klin. d.
Riicken. II. p. 509-525. 1876.—Hammond, Diseases of the Nerv. System. 6th ed.
p. 502. 1876. Charcot, Leg. sur les mal, d. syst. nerv. Tom. Il. 1877.—Hitzig,
Fall von angeborn. Bulbirparal. Berl. klin. Woch. 1874. No. 37, p. 465.—
R. Maier, Fall von fortschreitender Bulbarparalyse. Virch. Arch. Bd. 61. p. 1.
1874. — Habershon, Glosso-laryng. Paralysis. Guy’s Hosp. Reports. XX. p.
334. 1875.— Winge, Case of Duchenne’s Disease. Norsk. Mag. for Ligevid.
R. 3. B. 4. (Virchow-Hirsch’s Jahresberichte for 1874. IL. p. 127).—Markusy,
Zur Lehre von der progr. Muskelatrophie und progr. Bulbirparal. Diss.
Breslau, 1874. Hallopeau, Des paralysies bulbaires. Thése de l’agrégat. Paris,
1875.—Dowse, Bulbar paralysis. Brit. Med. Journ. 1876. Nov. 11.—Foz, Case
of Bulbar Paralysis. Brit. Med. Jour. 1876. Nov. 11.—foz, Case of Bulbar
Paralysis. Ibid. Noy. 11.—R. Kayser, Zur Lehre von der progr. Bulbiarparal.
Deutsches Archiv f. klin. Med. XIX. p. 145. 1877.—Poincaré, Le syst®me
nerveux central. 2. éd. Vol. I. p. 291. 1877.—Grasset, Malad. du syst®me
nerveux. 1878. p. 433.
Introductory. Historical.
The form of disease which we shall discuss in this paragraph,
in spite of its relatively short existence in the records of science,
has accumulated quite a large literature, and can boast of an
equally long list of different names which it has received.
It is beyond dispute to Duchenne that we owe the first de-
scription of this disease, as an individual and defined clinical
form. It of course stands to reason that the disease was observed
by others before this ; but the men (Trousseau, Tuerck, Duménil)
who observed it did not treat it as a special form. Duchenne at
first gave an accurate clinical description founded on a number
of cases, but did not know anything of the nature of the patho-
logical lesion. Although often accompanied by progressive mus-
cular atrophy, he regarded the two as totally different. The one
disease consisted in a primary atrophy without paralysis,
whereas the glosso-labio-laryngeal paralysis was a primary
paralysis without atrophy. |
In the next few years a large number of cases were recorded,
some of them with autopsies, which did not, however, reveal the
real situation of the lesion, but only allowed the assumption of
a progressive atrophy of the nerve-roots as foundation for the
PROGRESSIVE BULBAR PARALYSIS. 907
symptoms. Butin the year 1861' Baerwinkel casually pointed
out that the seat of the disease should probably be looked for in
, the central nervous system, especially in the medulla oblongata.
Schulz (1864) referred it with the greatest distinctness to the me-
dulla, on both sides of the raphe, but restricted it to the region
of the facialis. Wachsmuth in his admirable treatise (1864)
declared most distinctly, on theoretical grounds, that at the next
autopsy the origin of the disease would most certainly be found
in the bulbus medulle ; and in place of Duchenne’s laborious title
he proposed to call it ‘‘ progressive bulbar paralysis,’’ a name
which has since then been universally adopted. Wachsmuth ex-
pected to find a lesion not alone of the gray nuclei on the floor
of the fourth ventricle, but also a notable change in the olivary
bodies. But later investigations only confirmed the former, and
this they have done completely. But it was some years before
_ the confirmation came. At an autopsy which Bonnefoy made
(1866), he found sclerosis of the medulla with increase of con-
nective tissue; but the investigation, which can only be carried
out properly with the aid of modern methods, was very imperfect.
Decisive results were first obtained in 1869, and published in
1870, by Charcot in France, and by Leyden in Germany, after
Charcot and Joffroy had pointed out (1869) in two cases of pro-
gressive muscular atrophy the signification of the disappearance
of the ganglion-cells of the bulbar nuclei in atrophic paralysis of
the tongue and lips. The results obtained by Charcot and Ley-
den agreed pretty well in all important points. The French
authors, however, laid particular stress on the atrophy and dis-
appearance of the ganglion-cells, asserting this to be an essential,
and sometimes even the primary and only change in bulbar paral-
ysis. Since this further anatomical investigations have been
made (Duchenne and Joffroy, Gombault, R. Maier, and others),
which merely confirmed the former views without as yet solving
the question of the primary or secondary nature of the process
in the ganglion-cells of the gray bulbar nuclei.
The numerous cases which have been recorded, and the com-
prehensive descriptions of the disease, have since then thrown
1 Schmidt's Jahrbiicher. Bd. 110. p. 296. 1861.
908 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
considerable clearness over the matter. Amongst the latter Kuss-
maul’s excellent treatise (translated by the Sydenham Society,
1877) deserves special mention, giving a most thorough investi-
gation of the pathological physiology of the disease. Kussmaul
proposes the name of ‘‘ progressive bulbo-nuclear paralysis,’ on
the ground of the pathological results.
It is beyond doubt that even at the present day a number of
non-related diseases are classed under this name and its syno-
nyms. So we shall follow the example of the better authors,
and include only one form with perfectly defined clinical symp-
toms, and with an equally definite anatomical lesion, under the
name of progressive bulbar (or bulbo-nuclear) paralysis.
Adopting this name, we shall describe a form of disease which
very frequently takes a chronic course, and is always character-
ized by the most striking regularity. The following are its cL1n-
ICAL SYMPTOMS: Progressive paralysis and atrophy of certain
muscles which derive their nervous supply primarily from the
bulbus, 1. ¢., the tongue, the lips, the soft palate, pharynx, and
larynx ; and in consequence of this, disturbances of articulation,
speech, mastication, deglutition, and of the voice; later on,
spreading of the paralysis to other important bulbar functions
(especially the respiratory function), and frequent combination
with progressive muscular atrophy. The ANATOMICAL BASIS
consists in degenerative atrophy of the gray nuclei in the floor
of the fourth ventricle, and often other extensive sclerotic pro-
cesses in the medulla and spinal cord, and degenerative atrophy
of the paralyzed nerves and muscles.
We shall deal in the following paragraphs exclusively with
this form. This excludes all those cases which, though they ex-
hibit certain bulbar paralytic symptoms, do not give the pure,
defined, and constant symptoms of progressive bulbar paralysis,
and are the result of a different anatomical lesion (compression
of the medulla, or neoplasmata in it, etc.).
Pathogenesis and Etiology.
There is as yet nothing known of the exact mode in which
the pathological process which we have just described takes
PROGRESSIVE BULBAR PARALYSIS. 909
place, and the special causes of it have been very meagrely inves-
tigated.
Under the head of predisposing causes, newropathic diathesis,
or general nervous disposition, deserves mention, though it cer-
tainly does not play a prominent part.
The period of life is of more importance—progressive bulbar
paralysis being a disease of maturity and old age, and seldom
occurring before the fortieth year; most frequently between this
and the seventieth year.
Out of nine undoubted cases there was only one patient under forty; this was a
girl of twenty. Hitzig’s case of a child six years old most undoubtedly belongs
to another class of disease. "The case Kayser records of a twelve year old boy is, to
say the least, doubtful, and was not confirmed by the autopsy. Even Wachsmuth’s
case—a girl seventeen years of age—admits of doubt on account of the presence
of unusual symptoms (paralysis of the superior branches of the facialis, loss of
faradic irritability of the nerves and muscles, absence of any motor disturbances in
the tongue) ; the first mentioned symptom, however, was present in my own case of
the girl of twenty. In any case, the occurrence of the disease in young people must
be regarded as a great rarity.
The male sex seems more liable than the female to the dis-
ease ; of the cases on record, by far the greater number are males.
The disease occurs in all ranks of society, from the highest to the
lowest, and in every profession.
The exciting cause most frequently adduced is catching cold;
and some of the cases undoubtedly owe their origin to this, and
I can produce three observations of my own as witnesses. (The
above-mentioned girl of twenty years of age attributed the dis-
ease to a severe cold she caught during menstruation ; a midwife
exposed herself, on the occasion of a troublesome delivery, to a
bad cold, etc.)
The same undoubted influence is exercised by violent and
continuous mental excitement, bodily and mental overexertion,
é. g., in nursing patients, excessive mental activity, or straining
of the muscles affected in the disease (continuous playing of wind-
instruments, long reading with a loud voice, etc.). To the same
category belong restricted circumstances—stinted nourishment.
It has not yet been proved whether progressive bulbar paraly-
sis ever originates in a slight shock Of the medulla from a fall,
910 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
especially on the feet or nates, or even on the head without in-
jury to the skull. And the same may be said of the influence of
syphilis, excessive smoking, and other causes that have been
asserted.
It often happens that allied pathological processes spread
from the spinal cord into the medulla, and thus combine with
progressive bulbar paralysis; this is undoubtedly the case with
amyotrophic lateral sclerosis and progressive muscular atrophy.
But in many cases no cause for the disease can be asserted.
Pathological Anatomy.
It is by no means an easy matter to detect the changes in the
bulbus with the naked eye. It frequently happens that for the
naked eye there is nothing there to be seen in the fresh state, not
the slightest alteration of form, color, or consistency.
Often we can, however, notice that the medulla is reduced i in
size, or unsymmetrical from general or partial atrophy; here and
there, too, an unusual hardness or an abnormal want of firmness.
We can generally detect a slight gray decolorization in some
parts of a section, and a cloudiness and want of definition in the
structure. But this is not brought out properly till the speci-
men has been hardened in chromic acid; though even this seldom
gives absolutely certain results.
In almost every case, however, the atrophy and gray de-
colorization of several nerve-roots given off from the medulla is
very striking ; these are often reduced to thin, gray threads, that
are hardly visible, and are, of course, extremely different from
the nerves that remain unaffected. This is usually most pro-
nounced in the hypoglossal and facial nerves ; while in the roots
of the accessorius, vagus, and glossopharyngeus it is usually less
intense, and often unnoticeable. Still less frequently does it ex-
tend to the roots, especially the motor roots of the abducens and
trigeminus; and the roots of the acoustic are never affected, or
only very exceptionally.
Gerhardt’s case, in which he found a small centre of softening in the pons, is
not above criticism, and the microscopic examination was very imperfect. If it was
ae
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PROGRESSIVE BULBAR PARALYSIS. 911
a case of progressive bulbar paralysis at all, it was one complicated by chance by a
centre in the pons; and besides, there was softening in the cerebellum, and changes
had taken place in the spinal cord.
It is only the most accurate microscopic examination which
can give at all satisfactory explanation of the process in the
medulla, And even this gives very uncertain and meagre results
with fresh specimens, chiefly corpuscles of Gluge, increased con-
nective tissue, and here and there an atrophied or pigmented
ganglion-cell, or a thickened vessel—seldom more than this.
The localization and extent of the pathological process and
its character cannot be distinctly and certainly made out until
the organ has been hardened and treated with the usual coloring
reagents; when this has been done, the diseased parts may be
recognized, from their bad coloring, by the naked eye, or with a
pocket-lens.
The microscopic examination of the different cases exhibited
various processes and of varied extent (because some of them
were complicated); but much, and probably all essential particu-
lars, were common to them all.
The chief point seems to be a degenerative atrophy of the
ganglion-cells in certain gray nuclei of the medulla. This was
observed in every case which was accurately examined.
This affection of the ganglion-cells may, as it would appear,
exist quite unaccompanied by other changes worth mention
(Charcot, Joffroy, Hallopeau, and others); but in the majority
of cases we observe simultaneously an increased growth of con-
nective tissue, atrophy of different nerve-tracts, conglomerations
of fat-granule- and other kinds of cells, slight changes in the
vessels—in a word, we may observe in the medulla, in varying
proportions, all that is described under the name of gray degen-
eration, sclerosis, or chronic myelitis (Leyden, R. Maier).
As we do not yet possess records of so very many autopsies
from which we can draw absolute conclusions, it is still an open
question whether the chronic myelitis is an essential or secondary
part of the process, whether the atrophy of the ganglion-cells is
only the secondary result of this myelitis or a primary change,
and merely accompanied afterwards (necessarily or casually) by
myelitic changes, and especially by alterations in the interstitial
912 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
tissue. But the atrophy of the ganglion-cells certainly appears
to be the deciding cause in the pathogenesis of the disease, and
to account for the form taken by the symptoms. But, before we
can speak on this subject with absolute certainty, we must await
further investigations, to be conducted with the greatest accuracy
and specially directed to the solution of these questions.
The changes which take place in the ganglion-cells consist in
progressive atrophy and contraction; they become filled with
yellow or brown pigment (yellow pigmentary atrophy), their
nuclei disappear, and finally the cells themselves, leaving behind,
at most, some unrecognizable remains, in the shape of angular,
glittering, pigmented masses. If we now examine the gray
nuclei, and compare them with normal specimens, we are at once
struck by the decrease in number and size. In this way we can
obtain a satisfactory general idea of the intensity and extent of
the process in the various nuclear structures.
In the individual cases the surrounding tissue was found to
contain corpuscles of Gluge in varying quantity ; increase of
connective tissue and of the nuclei, and a number of spider-cells
(‘‘Spinnenzellen’’); hypertrophy and fatty degeneration of the
vessels ; often numbers of corpora amylacea; and then the
nerve-fibres themselves were atrophied and diminished, while the
axis-cylinders were often strikingly massive and swollen ; finally,
the nerve-fibres lose their medullary sheath, and disappear com-
pletely with the axis-cylinders. In a relatively recent case,
Benedikt found changes of an undoubtedly inflammational char-
acter—z. e., congestion, hypertrophy of the walls of the vessels,
and numerous ‘‘inflammational nuclei,’’ etc.
As regards the topography of the changes, the results as yet
obtained seem to prove that the nuclews of the hypoglossus is
the starting or central point of the disease ; it degenerates earlier
and more completely than the others. The nuclei of the acces-
sorius and vagus are next attacked, while the disease does not
extend in all cases to the nucleus of the glosso-pharyngeus. The
nucleus of the facial is attacked at a very early stage—at least,
that part of it which is connected with the inferior (labial)
branches. The present pathologico-anatomical investigations
have not decided whether the point attacked is the nucleus
<a saa
PROGRESSIVE BULBAR PARALYSIS. 913
facialis proper of the latest writers, situated in the anterior por-
tion of the rhomboid sinus, or whether it is the ‘‘inferior’’ facial
nucleus in the inferior portion of the sinus assumed by Clarke.
The nucleus of the abducens is very seldom diseased; the
acoustic nuclei appear never to suffer, and likewise the trigemi-
nal nuclei ; still, the motor nucleus of the trigeminus has been
often found in degeneration, but only the merest traces of dis-
ease in the sensory nuclei.
The root-fibres, which go to the nuclei, appear to be more or
less strongly atrophied and degenerated.
Thus, we have to deal mainly with a circumscript centre of
disease, which has a tendency to spread gradually. It attacks
primarily the gray nuclei situated in the inferior portion of the
floor of the fourth ventricle, and extends from here very stealth-
ily in all directions.
As regards the other structures in the medulla, the olivary
bodies are seldom affected, though R. Maier found them degen-
erated, and Leyden found corpuscles of Gluge, in one case, in
their centre. The participation of the formatio reticularis is
doubtful and not easy to decide ; Benedikt found it universally
affected. Still, the nerve-fibres running through it are probably
involved in every case. The pedunculi cerebelli are never
attacked. On the other hand, the pyramidal tracts have been
often found diseased, full of corpuscles of Gluge, sclerosed, and
degenerated ; and this degeneration could be generally traced
up into the pons, and regularly down into the lateral and ante-
rior columns of the spinal cord; but it is quite possible that
these were all complicated cases.
In fact, combinations with spinal diseases occur very often.
These spinal diseases are sometimes degeneration of the ganglion-
cells of the anterior cornua, such as has been of late regularly
found as the lesion in the typical form of progressive muscular
atrophy ; sometimes simultaneous degeneration of the lateral
columns and the anterior cornua, producing the form Charcot
has described as amyotrophic lateral sclerosis.
Changes in the nerves and muscles. The nerve-roots coming
off from the bulbus are almost always very much degenerated,
and they exhibit the same degenerative atrophy as peripheral
_ VOL, XIII.—58
914 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
nerves after section, 7. e., fatty degeneration and disappearance
of the nerve-fibres, growth and sclerosis of the neurilemma, leavy-
ing nothing of the roots but tough cords of connective tissue,
filled with fat, and preserving generally only traces of their
axis-cylinders. These changes, though less in degree, may be
traced through the nerves and into their peripheral terminations
in the muscles. Still, in one case Charcot found but very slight
changes in the root-fibres of the hypoglossus.
The roots of the hypoglossi are usually the ones which suffer
most from the disease; then the faciales, and next a part of the
roots of the accessorius, vagus, and glossopharyngeus. In com-
plicated cases we find the same changes taking place in many of
the anterior spinal nerve-roots.
In the muscles, too, we find a very pronounced atrophy,
which varies greatly in extent and intensity. The muscles look
pale, reddish, or yellow, or a reddish gray ; they are very much
diminished in size, striped with fat, and partly changed to fatty
and connective tissue. Under the microscope, we see intensive
atrophy of the muscular fibrils, and notice their small number,
the increase of nuclei and connective tissue, and in some parts
masses of fat. According to the unanimous view of all modern
authors, the changes are exactly the same as those which take
place in progressive muscular atrophy, and they exhibit the
same irregularity and want of uniformity in their distribution.
The tongue usually suffers most, though cases have occurred in
which the degeneration could not be diagnosed with certainty
till brought under the microscope. Atrophy in different degrees,
too, has been observed in the lips and palate and in the pharyn-
geal and laryngeal muscles.
We generally see in addition similar atrophy of the muscles
of the back of the neck, especially the trapezii, and in compli-
cated cases there is usually progressive atrophy of the whole
muscular system. Even in uncomplicated cases we very fre-
quently find the initial traces of atrophy in the small muscles of
the hand, ball of the thumb, interossei, ete.
In the other organs of the body no changes characteristic of
this disease take place. Extreme wasting and emaciation of the
whole body may usually be observed, as in all other states of
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PROGRESSIVE BULBAR PARALYSIS. 915
inanition. Frequently centres of pneumonia from foreign bodies
are found in the lungs, or we have phthisis, or there are symp-
toms of some other fatal disease. But we need not enter upon
this.
Pathology of Progressive Bulbar Paralysis.
Symptoms.
General Symptomatology.—Progressive bulbar paralysis is
almost unexceptionally developed in a most stealthy manner.
Slight premonitory symptoms generally precede, but escape
observation for along time. These consist of a slight feeling of
oppression and pain in the back of the head and neck, an
unpleasant sensation in speaking, a little giddiness, etc. ; oc-
casionally we may succeed in detecting a loss of reflex irritabil-
ity in the pharynx and larynx at an early stage of the disease
(Krishaber). }
The commencement is occasionally accompanied by violent
symptoms, such as a sudden impediment of speech, with diffi-
culty in the movements of the tongue and lips; or we may have
impairment of the act of deglutition. These symptoms often
appear to result from a slight apoplectic attack, but it is doubt-
ful whether they are real cases of the disease we are discussing.
But usually the symptoms come very gradually and stealth-
ily, and the patient sees without suspicion his trifling difficulties
growing worse, till after a somewhat short and unrestrainable
course they bring his life to an end after fearful suffering.
At first the reigning symptom is a progressive weakness of
the lingual, labial, palatal and pharyngeal muscles. This does
not develop according to the same rule in every case, the weak-
ness beginning sooner and making more rapid strides sometimes
in this and sometimes in that direction. This produces a dis-
tinction between the different cases, but this is unessential.
The difficulty of speech is generally striking, proceeding from
weakness of the tongue. The pronunciation of certain letters
and syllables which are chiefly produced by the tongue becomes
difficult, hindering the articulation and rendering the speech in-
distinct. e
916 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
This is soon followed by difficulty and indistinctness of the
labial sounds, arising from weakness and stiffness of the lips.
The speech thus loses still more of its clearness, and at the
same time the patient is deprived, in part or whole, of his power
to whistle, blow, compress his lips, kiss, show his teeth, ete.
This is inseparably connected with a change in the expression,
the mouth becoming lengthened, and the naso-labial folds deeper,
and the whole expression peculiarly lachrymose.
Mastication is impaired at a very early stage, chiefly by rea-
son.of the difficulty in moving the tongue and cheeks; a real
paresis of the muscles of mastication is rare, and never one of
the early symptoms.
After a varying length of time we observe a difficulty in
swallowing. This is due in the first instance to paresis of the
soft palate, which renders the voice nasal, and often allows fluids
to escape through the nose during the act of deglutition; the
pronunciation of certain labial consonants (‘‘b’’ and ‘‘f’), too,
becomes more difficult.
The muscles of the pharynx and those that close the larynz
become gradually weaker. This is betrayed by the increasing dif-
ficulty in swallowing, which is sometimes greater with solids and
sometimes with fluids ; sometimes, too, the food ‘‘ goes the wrong
way,’ in other words, gets into the larynx, and causes fits of
coughing and suffocation.
Even at this stage the patients exhibit an extremely charac-
teristic appearance—their peculiar expression, the contrast be-
tween the upper movable and lower paretic portion of the face,
the faltering, incomprehensible, nasal speech, and the difficulty
in swallowing, all betray the disease at the first glance to a prac-
tised eye. The case is completed by atrophy, trembling move-
ments and fibrillar twitchings of the lips; by the grooved ap-
pearance and atrophy in the tongue, which can hardly be put
out, or lies helpless in the bottom of the mouth, in constant
vibration with fibrillar twitchings; by the excessive secretion of
a thick, mucous saliva, which the patient cannot swallow, and
which he must consequently wipe from his lips constantly with
a handkerchief.
But the organs of sense and the intelligence generally remain
9
PROGRESSIVE BULBAR PARALYSIS. 917
quite unaffected; the most that has been observed being a
slightly lachrymose and easily excitable temper, with an inclina-
tion to causeless laughter. Sensibility remains quite undis-
turbed ; even the taste on the tongue is perfectly normal. Re-
flex action is only diminished in the pharynx and larynx.
Thus the disease follows its slow and generally unremitting
onward course. There seldom comes a remission of any length,
and still more rarely any improvement. We can clearly see from
week to week, or at least from month to month, a change for
the worse. The speech becomes more and more incomprehen-
sible, swallowing more difficult, the secretion of saliva greater
and more annoying, the patient becomes weaker, while his men-
tal functions and intelligence remain unclouded, giving him a
mournfully clear idea of what threatens him, and thus adding
another pain to his disease.
As the disease proceeds, we get further symptoms, resulting
from the extension of the process in the medulla. Such are
weakness and loss of voice, caused by paresis and paralysis of
the vocal cords and the muscles of the larynx; and then irregu-
lar action of the heart, retardation or great rapidity and irregu-
larity of the pulse, a feeling of faintness and threatening death,
accompanied by great terror; further, we have respiratory dis-
turbances in the form of a feeling of oppression, weight on the
breast, dyspnoea with actual fits of suffocation, difficulty in
coughing, sneezing, and clearing the throat, etc. Finally, we may
observe paralysis of the muscles of mastication ; much more
rarely do we see any sensible disturbances in the region of the
trigeminus; still less frequently are the orbital muscles para-
lyzed, usually beginning with the abducens.
The contrast is striking between these severe paralytic symp-
toms and the clearness preserved in the higher functions of the
brain and organs of special sense, together with the freedom of
the extremities from any but trifling affections. Though the
extremities, with the exception of inanition from weakness,
rarely suffer from any motor or sensible affections, and more
especially any actual paralysis, till the very last stage of the
disease, still we may frequently observe the development of a
progressive atrophy in the smaller muscles of the hand, causing
918 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
the interossei to fall in, and diminishing the thenar and hypo-
thenar muscles, etc. But this complication often grows to a
complete and general progressive muscular atrophy.
At this stage the patients suffer frightful tortures. Speech-
less and harassed by salivation and the danger of suffocation,
with their intelligence perfectly unclouded, they see the ap-
proach of a death from starvation. Every endeavor to still their
gnawing hunger is vitally dangerous, and causes unspeakable
pain; artificial nourishment seldom gives them long respite.
Characteristic of the very last stage comes a state of intense ina-
nition, which in one way or another brings about the death of
the patient. It is real good fortune for those whose lives end
quickly from suffocation, or who are carried off after a short
attack of pneumonia caused by a foreign body, or for those who
are set free by paralysis of the heart or respiratory organs. Any
of these is better than death from starvation. Life frequently
terminates with a prolonged agony, often accompanied by a ter-
minal coma, rise of temperature, etc., but generally resulting in
a simple extinction of life.
Such is a sketch of the most usual and frequent cases, though
it is, of course, subject to many variations, and does not run in
exactly the same way with the constant quickness and constant
intensity. |
From our present experience it is doubtful whether the dis-
ease ever resulted in anything but death. |
Analysis of the Individual Symptoms.
Initial symptoms. Real premonitory symptoms are often
wanting, and are generally quite trifling and uncharacteristic.
There are occasionally complaints of pains in the head and back
of the neck, slight dizziness, and a feeling of compression in the
neck and breast, which rarely attains the character of actual
dyspnea. We shall not attempt to decide whether these symp-
toms are to be regarded as signs of initial hyperemia, constantly
occurring in slight attacks.
Krishaber found in two cases that, many months before any definite paralytic
symptoms appeared, the pharynx, larynx, trachea, and cesophagus were strikingly
a a i i a ee
PROGRESSIVE BULBAR PARALYSIS. 919
slow to answer reflex irritation, while their tactile sensibility remained unaffected.
But does this often occur?
The real symptoms of the commencement of the disease usu-
ally consist in a slight affection of the speech, the patient becom-
ing tired easily after speaking for some time, and finding diffi-
culty in the pronunciation of certain letters and words. The
speech, too, grows objectively less distinct.
This is followed by the first symptoms of a commencing weak-
ness in the lips and palate ; the expression of the face is altered,
the voice becomes nasal, and the patient tires after prolonged
chewing and swallowing.
This is the usual order of succession in which the symptoms
occur; but occasionally they commence with the lips and palate.
Even at this early stage we may often observe an increased secre-
tion of saliva.
The duration of the development of the symptoms varies con-
siderably ; sometimes it is rather short after a febrile disease or
after a febrile initial stage(?). But it is generally pretty long
and gradual, the worst being a few rapid periods. Kussmaul
records a rare case, which began with a sudden weakness in one
of the above-mentioned muscular regions. Actual apoplexy or
acute myelitic processes appear never to give rise to a genuine
progressive bulbar paralysis. —
It frequently happens that an intercurrent disease induces a
very rapid change for the worse.
Affection of Speech.
The affection of speech is usually the earliest symptom, and
the one most acutely felt. It consists always and without ex-
ception of an incapability (produced by paralysis) to pronounce
certain letters (and syllables and words which are formed with
these letters). The simple and combined motions of the tongue,
_ lips, etc., necessary to the articulation of the sounds, become difli-
cult or impossible. So it is a mere affection of the articulation.
Thus we have to deal with alalia (or anarthria). It is never a case
of stumbling over syllables (Silbenstolpern), a transmutation and
920 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
confusion of syllables and words; the words are never forgotten,
as in genuine aphasia. It is, in fact, always an affection of the
articulation, caused by paralysis and atrophy of the muscles
necessary to speech.
The course of the affection varies according to the order in
which the three important muscular provinces, the tongue, lips,
and palate, are paralyzed. According to this varies the order in
which the different letters become difficult of pronunciation.
Finally, all articulation becomes impossible, and the patients can
only produce grunts and groans, and even these very imperfectly
when the vocal cords are paralyzed.
Primary weakness of the tongue renders the vowel ‘‘i’’ first
unpronounceable, as its production requires the greatest raising
of the tongue. The tongue, too, is in part or altogether the pro-
ducer of the consonants ‘‘r,’’ and ‘‘sch”’ in particular, and of
6s s,”’ J vag yl a oh and finally of ‘6 qd? and AS had
Weakness of the lips causes the loss chiefly of ‘‘o”’ and ‘*u,”’
and also of ‘‘e,’ whilst ‘‘a’’ can be pronounced almost to the
last. When the lips become more affected, ‘‘p’’ and ‘‘f”’ cannot
any longer be pronounced, and lastly ‘‘b,’’ ‘‘m,’’ and ‘‘w”’ are
lost.
Paralysis of the palate renders the formation of certain la-
bials still more difficult, because the current of air necessary to
form explosives escapes through the nose, and consequently
loses nearly all its force. Thus, ‘‘b’’ and ‘‘p” are turned into
‘“me”’ and ‘‘ve.’ If we close the patient’s nose, these letters
are very much better pronounced (Duchenne). Besides this, the
nasal tone is due to the weakness of the palate.
When all these affections come together, the speech grows
rapidly more and more indistinct, and becomes at last an im-
possibility. The words sound quite differently from what they
should, and gradually only monosyllabic words can be recog-
nized, till at last even the power of producing these is lost, and
the unfortunate creatures can only give forth inarticulate, incom-
prehensible, grunting sounds.
All these affections may be easily explained either by the
lesion in the nerve-nuclei and nerves, or by the atrophy of the
muscles, both which causes injure the efficiency of the muscles
Se ee a ee ee ee of | O
i eee
PROGRESSIVE BULBAR PARALYSIS. 921
of speech. Thus we see that the affection of speech depends
essentially upon the lesion in the hypoglossal nucleus, and part
of the nuclei of the facialis and accessorius. It requires further
investigation to determine the extent to which the nuclei of the
vagus and glossopharyngeus are implicated.
If the affection spreads further in the accessorius nucleus, the
innervation of the larynx and the vocal cords becomes weaker,
from which result hoarseness, weakness of voice, and finally
complete aphonia. In the course of this process the patients are
often able to groan loudly, and laugh, sometimes in a peculiarly
boisterous manner; but, for ordinary speech, their voice is of no
service to them. In such cases the laryngoscope reveals paresis
and paralysis of the vocal cords.
Affections of Mastication and Deglutition.
These form the second important group of symptoms in this
disease. Here, too, we find variations, according to the succes-
sion in the paralyses of the various groups of muscles which take
part in deglutition.
Particles of food which get between the lips and teeth can-
not be caught up by the tongue, and consequently stick there.
This condition is rendered worse when the lips and buccinators
are paralyzed simultaneously, in which case the food “falls out”’
more readily. When the paralysis is more complete, food, es-
pecially semi-fluid and fluid, falls completely out of the mouth,
which can no longer be properly closed. In the same way, too,
saliva flows constantly, and has to be wiped away every moment
by the patient.
But when the disease attacks the motor nucleus of the trigem-
inus, and thus paralyzes the muscles of mastication, the final
and worst affection of deglutition is produced. This results in
exhaustion and increasing loss of power in chewing, until at last
the act becomes an impossibility. The patient is likewise un-
able to close his mouth, or effect the lateral motion of his lower
jaw. The utmost he can now do is to take fluid nourishment,
and even this he can hardly effect, as deglutition is so difficult.
The first stage of deglutition is affécted by weakness in the
922 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
tongue. There is great difficulty in forming the bolus, and press-
ing it back against the soft palate and into the pharynx. These
movements the patient often assists with his hands, shoving the
bolus back till it is caught up by the reflex movements of deglu-
tition.
Weakness of the soft palate finds its expression chiefly in the
imperfect closure of the choanz. At first fluids escape through
the nose, and, at a later stage, sometimes even solid food. The
regurgitation is favored by the action of the inferior constrictors
of the pharynx. In this way a considerable portion of nourish-
ment often escapes.
When the pharyngeal muscles become affected the difficulty
and danger connected with swallowing a bolus grow greater, for
particles of food are caught up in the sulci and burse of the
pharynx, and collect there and behind the epiglottis too. Some-
times the whole bolus gets fast, and cannot be moved forward
or backward, causing great danger of suffocation.
The greatest inconvenience and danger lies in the possibility
of fluids or solid bodies getting into the larynx. For, by irrita-
tion, they produce coughing and attacks of dyspnoea, or, if they
get into the bronchi, they give rise to pneumonia. This danger,
too, may assume different proportions, according to the muscles
which are first and most paralyzed.
If it is chiefly the body of the tongue which is paralyzed, the
root cannot be well brought over the fallen epiglottis, and hence
the larynx is not completely shut, so that particles of food and
fluids easily find their way into the trachea. A solid bolus
passes over more easily, as its weight presses down the epiglottis ;
but fluids enter very easily.
But, for the preservation of the larynx, the purely jatee
mechanism for closure seems still more important. This is
brought about by the accurate juxtaposition of the arytenoid
cartilages and the plice ary-epiglottice (v. Bruns). If the mus-
cles which perform this function are weakened or paralyzed (mm.
arytenoid. transv., thyreo-ary-epiglott., and thyreo-arytenoid.
ext.), the larynx cannot be closed effectively. But, if. this func-
tion is quite unimpaired, then food cannot easily ‘“‘go the wrong
way,’ even if the closure by the tongue and epiglottis is very ©
=F > SR i -
" —
PROGRESSIVE BULBAR PARALYSIS. 923
imperfect. In such cases the patients can swallow fluids and
semi-solids without much difficulty. But when the laryngeal
closure is affected, the danger in swallowing fluids is greater, as
they can penetrate through the smallest opening into the larynx.
The patients prefer to avoid this risk by taking more solid and
drier nourishment, though of course the difficulty of swallowing
this is greater.
When the paralysis extends to the cesophagus, deglutition is
a complete impossibility, and recourse must be had to the stom-
ach-pump.
The explanation we gave of affections of speech may be ap-
plied directly to deglutition. In this case, also, we are unac-
quainted with the details as to the participation of the nuclei of
the accessorius, vagus, and glossopharyngeus.
Affections of Expression.
In addition to the affections of the speech and deglutition, we
have in the expression a prominent and characteristic symptom,
due to paresis of the inferior branches of the facial. In fact, a
practised eye can make the diagnosis from the features alone.
The orbicularis oris suffers more than all; while the leva-
tores lab. sup., quadratus, triangularis, and levator menti, the
buccinator, efc., are less frequently affected, and never so in-
tensely. These muscles are almost always plainly atrophied, so
that the lips look lean, furrowed, thin, and sharp-edged. Some-
times, too, we see fibrillar contractions passing through them.
This paresis deprives the patient of the power to whistle, blow
out a light, show his teeth, point his mouth, etc. Besides this,
he can no longer keep his mouth closed ; but it is always open,
with a hanging underlip, and the saliva flows out in a constant
stream.
The expression of the face undergoes a peculiar change, the
mouth increasing in breadth, and slightly opened, the naso-labial
sulci grow more marked, thus producing a sad, lachrymose, and
somewhat stupid look, contrasting strongly with the vivacious
movement of the features of the upper half, and with the bright-
ness and motion of the eyes.
924 ERB.—DISEASES OF THE MEDULLA OBLONGATA,
The lower half of the countenance remains relatively motion-
less in speaking and laughing, and the laugh degenerates to a
peculiar grin.
The superior branches of the facial are usually unaffected,
though in very rare cases they have been paralyzed with varying
intensity.
The lesion lies, undoubtedly, in an affection of the nucleus
facialis. But there are many doubtful points connected with
this. In the first place, Why is this nucleus so regularly and so
early affected? A glance at Fig. 30 shows us that the nucleus
of the facial is rather far removed from the nuclei of the hypo-
glossus and accessorius, in which the pathological process seems
to commence. Lockhart Clarke’s assumption of a facial nucleus
at an inferior point, about on a level with the hypoglossal (close
and external to this nucleus), is undoubtedly more suitable
to explain this early participation. The second question—
Why is it that the lower branches, and almost always these
alone, are the ones that are attacked (—could also be easily an-
swered on the assumption that the process only extends to this
‘inferior ’’ nucleus, on a level with the hypoglossus, which ex-
clusively controls the inferior branches of the nerve, while the
superior nucleus is only rarely affected, and never till a late
period. The explanation of this peculiar difference in the be-
havior of the superior and inferior branches of the facial, which
occurs, too, in other cerebral lesions, we must leave to normal
and pathological anatomy. |
Affection of the Salivary Secretion.
In nearly every case—though there are exceptions—we are
struck, at an early period of the disease, by the constant flow of
saliva from the mouth. It is sometimes very watery, sometimes
more consistent with transparent mucus, and must be constantly
wiped away. It soaks through the pillow at night, causing the
patients great annoyance.
This is primarily and chiefly due to paralysis of the lips and
the muscles of deglutition. The saliva is secreted in normal
quantity, but can only be swallowed with difficulty, and conse-
a SEE
PROGRESSIVE BULBAR PARALYSIS. 925
quently collects in the mouth. But, the contraction of the lips
being imperfect, the saliva flows over them, and out of the
-mouth. It is easy to prove on one’s self that no extra secretion
of saliva is necessary, by avoiding deglutition and holding one’s
mouth open, and inclining one’s head slightly forward.
Though the salivation may be thus to a certain extent ex-
plained on the ground of paralysis, still it might be asked, is
there not at the same time an actual increase of the secretion ?
And the question in a great number of cases can be answered in
the affirmative.
Schulz estimated in one case a six- or eight-fold secretion.
Kayser asserts positively that the secretion is increased, but his
proofs are more theoretical than actual facts. His reasoning is
that the saliva is secreted uninterruptedly during sleep, and that
it does not always commence simultaneously with affection of
deglutition. In Kayser’s case he could increase the secretion by
reflex irritation, and stop it temporarily by means of atropine.
Kayser has discussed the question thoroughly, though he has
by no means decided it. The large quantity of the secretion ex-
cludes the supposition that it is mere ‘‘ paralytic saliva.’”? In
fact, we know so little of this ‘‘ paralytic’’ saliva, or of its man-
ner of production, that we can hardly discuss the question. We
must consequently assume an irritation of the salivary centres,
which, according to Gruetzner’s investigations,’ governs both the
fibres of the chorda tympani, and of the sympathetic which go
to the submaxillary gland. But he does not attempt to show
how this centre of salivation is irritated, when all the other bul-
bar functions are paralyzed, nor to localize the centre exactly in
the medulla.
Affections of the Respiration and Circulation.
The affections of respiration occur chiefly in the terminal
stage. They are as yet imperfectly known.
We have already mentioned the various affections of laryn-
geal innervation, paralysis of the vocal cords, aphonia, and the
~
' Beitr. zur Physiol. d. Speichelsecretion. Pflueg. Arch. VII. p. 522. 1873.
926 ERB.—DISEASES OF THE MEDULLA OBLONGATA.,.
attacks of coughing and suffocation caused by the entrance of
foreign bodies during eating and drinking.
The participation of the nuclei of the vagus and accessorius
in bulbar paralysis being beyond doubt, when we consider the
close relationship that exists between them and the respiratory
centre, we can hardly be surprised to find frequent affections of
the respiratory mechanism. However, this is not so often the
case, and when it occurs, it is at a late stage of the disease.
When we meet it in an advanced form, we may be sure that the
end is drawing near.
We often hear complaints of constriction and fulness in the
breast, accompanied by a want of breath which has no visible
foundation—affections in fact, connected with a decrease in the
functions of the respiratory centres. But real attacks of dysp-
noea, which are occasionally observed, would rather lead us to
think of irritation in the centres.
We may further note various troubles of expiration, such as
weak and powerless coughing, partly due to insufficient inspira-
tion, and partly to feebleness of expiration and paralysis of the
vocal cords. Then, too, they find difficulty in blowing their
noses, because part of the current escapes through the mouth.
They seldom sneeze, and often find it impossible, as the strength
of the expiration diminishes with weakness of the expiratory
centres. The loss of motility in the root of the tongue causes
them a similar difficulty in clearing their throats. Many patients,
too, complain that they can no longer smoke; but this depends
chiefly on paralysis of the tongue, and of the muscles which
lower the inferior maxillary, and of the orbicularis oris.
Finally comes the stage of weakness and paralysis of the
respiratory centres, due to degeneration. The want of breath
and the oppressive feeling grow worse, while the attacks of dysp-
nea accumulate and breathing grows constantly less powerful,
till asphyxia, either slow and resulting from gradual paralysis,
or acute, occurring in an attack of dyspnoea, ends the life of
the patient. But the slightest disease of the respiratory organs,
such as a bronchial catarrh, or pneumonia, often suffices to put
an earlier end to the patient’s life.
Little is known of the disturbances in the action of the heart.
osteo -
on aera
—-
LP a a ee Ea aly airs a
PROGRESSIVE BULBAR PARALYSIS. 927
There is no reliable record of retardation of the pulse (irritation
of the vagus). An abnormally rapid pulse (paralysis of the
vagus) has been oftener recorded, rising sometimes, just before
death, to 130, 150, and higher, in the minute. The fainting-fits
which so frequently occur, and to which the patients occasion-
ally succumb, may fairly be referred to the centres of cardiac
innervation.
Disorders of Nutrition.
One of the most constant attendants of progressive bulbar
paralysis is undoubtedly atrophy of the paralyzed muscles.
This is usually most marked in the case of the fongue. This
member grows smaller, flatter, shrunken, and marked with fur-
rows; it looks limp, and is kept in constant vibrating motion
due to fibrillar contractions. We can often, too, plainly detect
atrophy of the Zips, which grow thin like paper, emaciated, and
with sharp edges; the skin over them becomes withered, and
also exhibits in many cases these fibrillar contractions. Of
course, the atrophy must have advanced pretty far before it can
be noticed in the lips. Atrophy of the soft palate can probably
never be recognized with certainty.
Several authors assert that this atrophy is not constant, and
Duchenne himself brings the absence of atrophy forward as a
distinguishing characteristic of his bulbar paralysis from pro-
gressive muscular atrophy. But all modern observers bear wit-
ness to the complete falseness of this view. With reference to
this question, | have myself compared my notes of nine accu-
rately observed and genuine cases of bulbar paralysis, and found
atrophy recorded in every single one; though in one case it was
only found in the lips, and not in the tongue. Im six of these
nine cases, though the bulbar paralysis was far advanced, there
was no complication whatsoever with progressive muscular atro-
phy (an extremely important matter for the question in hand) ;
in two cases there was a commencing muscular atrophy, and in
one case it was slightly advanced.
But we must grant without hesitation that the atrophy does
not always appear at an early stage, and runs, by no means, a
928 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
parallel course with the paralysis. On the contrary, the paraly-
sis may have lasted some time before there is any atrophy, or,
at least, before it becomes evident. But we should not forget
that there may be a very considerable atrophy and degeneration
of the tongue and lips before we can detect it by mere inspection.
Charcot’s case proves quite plainly that the tongue may retain
quite a normal appearance, volume, and smoothness, and yet, on
microscopic examination, exhibit extensive degeneration of its
muscular fibres.
We are thus led to the conclusion that atrophy is one of the
most constant and regular symptoms of bulbar paralysis, ob-
serving at the same time that it does not run parallel with the
paralysis. The atrophy, in precisely the same manner as the
paralysis, may commence at various points, and progress from
these; and if the two do not begin simultaneously and progress
in the same direction, this only proves that they are not causally
dependent upon one another, but only co-ordinate.
In many cases we meet with local atrophy and fibrillar con-
tractions of the small muscles of the hand. This is the first indi-
cation of complication with progressive muscular atrophy, which
we shall discuss more fully later on.
It is extremely probable that the atrophy we have described
arises from a lesion of the motor nerve-nuclei in the floor of the
fourth ventricle, and that its origin is due in great part to degen-
eration of the large ganglion-cells in these nuclei. In fact, the
symptoms of bulbar paralysis themselves supply the best possi-
ble argument for the assumption of a nutritive function of at
least some of these cells.
One constant and necessary consequence of the disease occurs
sooner or later, in the form of general nutritive disturbances—a
state of extreme emaciation, increasing and finally extreme inani-
tion, all due to insufficient supply of food. It is self-evident that
this must be accompanied by great general weakness, even with-
out pronounced paralysis, and that the patients must keep to —
their beds, being, in fact, scarcely capable of stirring.
There is no fever during the whole course of the disease,
unless arising from a chance complication.
Among the rare symptoms of progressive bulbar paralysis,
PROGRESSIVE BULBAR PARALYSIS. 929
we may note affections of the auditory nerve, consisting of
buzzing in the ears and deafness. Whether they really belong
to the disease, or are only chance complications, and part of
another lesion, which was confounded with bulbar paralysis, we
cannot decide. In any case, they take no prominent part.
_ The same may be said of paralysis of the orbital muscles.
It is not a usual symptom of progressive bulbar paralysis ; still,
it is occasionally recorded. Nor is it at all strange that the motor
nuclei of the nerves supplying these muscles, especially the
abducens nucleus, should sometimes participate in the disease ;
but itis exceptional. I have myself seen cases in which ptosis
and paralysis of other orbital muscles were present, but am not
quite sure that they were genuine bulbar paralysis.
As has been already observed, paralysis of the muscles of
mastication is more frequent, resulting from the spread of the
disease to the motor nucleus of the trigeminus. Sensory affec-
tions of the trigeminus are, on the contrary, very rare, occurring
either very exceptionally, or perhaps never. The symptoms are
a furry feeling and anesthesia on both sides of the face, and
want of sensation in the tongue.
Sensory affections in the trunk and extremities are quite as
rare, though there are occasional records of furriness and loss of
sensation in the fingers, excentric neuralgia in the extremities,
pains in the back and loins, etc.
Paralyses in the trunk and extremities are, however, more
frequent. Here and there weakness and paralysis of the cervical
muscles, especially the trapezii, and of the shoulder muscles,
etc., have been observed. This is usually accompanied by atro-
phy, and thus forms a gradual transition to progressive muscular
atrophy. On the other hand, we meet with paralyses of the
lower extremities, with contractures, and increased tendon-reflex,
but no atrophy—a complication which we must regard as amyo-
trophic lateral sclerosis, and which we shall discuss later on.
Little is known of any vaso-motor affections. I observed
frequent congestions in the head in one case, a very red face, and
a feeling of heat in the limbs ; but it was a man who was always
subject to these symptoms.
There is no reliable case of diabetes mellitus or albuminuria
VOL, XITI.—59
930 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
occurring in bulbar paralysis, though Déchery makes a short
reference to one recorded by Voisin.
The symptoms in a pronounced case of bulbar paralysis are
so characteristic that they can be taken in at a glance; but still
an accurate objective ecamination in such cases is of service
in helping to fix definitely, and enlarge our knowledge of, the
whole appearance of the disease.
Besides the functional affections which we have described in
full, we may be able to detect the presence of paralysis in the
tongue, lips, soft palate, and sometimes in the vocal cords. The
tongue lies almost immovable on the floor of the mouth, and
can be extended over the teeth only with great difficulty. Its
point can no more reach the palate or cheeks, and its root cannot
be raised, though there is not much difficulty in drawing it back.
In fact, the paralysis is by no means always evenly distributed
over the whole tongue, generally affecting first and prominently
the internal muscles, the lingual muscles proper.
We described above the paralysis of the Zips. The soft pal-
ate loses its tense appearance, while the uvula hangs loosely,
though generally quite vertically, and is usually somewhat
swollen. During phonation we observe only very slight motion
—often less on one side than on the other. The laryngoscope
reveals to us the paresis or paralysis of the vocal cords.
The results of electrical examination of the paralyzed nerves
and muscles is especially interesting, though it is true that most
authors up to the last few years have left us very scanty records.
As arule, we find it stated that in progressive bulbar paralysis
both the faradic and galvanic irritability are subject to no note-
worthy change, or, at the most, a simple decrease, without any
qualitative alteration, may be detected in the very last stage.
Thus, Duchenne, M. Meyer, Grasset, and Hallopeau talk of
perfectly normal faradic irritability ; Rosenthal, Erdmann, and
Déchery consider it normal, or only diminished in a few cases ;
Benedikt found it retained for a long time in the tongue, while
it had diminished in the muscles of the face; Wachsmuth found
it completely extinguished ; Leyden asserts that the diminution of
the electric irritability is not noticeable till the very last stages of —
atrophy, and that the reaction of degeneration was not observed ;
egg coe. — “eee a
A PS oe
PROGRESSIVE BULBAR PARALYSIS. 931
Kussmaul alone observed in one case, where the faradic irrita-
bility of the orbicularis oris was well preserved, that its galvanic
and mechanical irritability had increased. Thus, it appears
there was a degenerative reaction in this muscle, although it
cannot be deduced with certainty from Kussmaul’s brief report,
and was certainly not recognized as such.
Encouraged by my observations in progressive muscular atro-
phy (elsewhere reported *), and led on by the conviction that the
form of degenerative atrophy with which we have to deal in
bulbar paralysis would be physiologically expressed by the
‘reaction of degeneration,’’ I expected certainly to find this
reaction in the disease, and my expectation was fully justified
by the first pronounced case which came under my observation,
and which I examined with great care. I found, in fact, the
most marked reaction of degeneration in direct irritation of the
muscles, both on the chin and in the lips, and even in the
tongue. At the same time, however, the electric irritability of
their nerves was normal, or but slightly diminished ; so that we
have exactly the same form of degenerative reaction which I
have described as characteristic of the so-called ‘‘ middle form ”’
of certain peripheral paralyses (cf. Vol. XI.), and I have no
doubt that we shall find the same thing, if we look carefully for
it, in all cases where atrophy of the muscles has reached a cer-
tain point. :
The patient in this case, which I intend to publish elsewhere in full, was a
woman, aged sixty-two, who had shown symptoms of progressive bulbar paralysis
for a year and a half, complicated in the last three months by a commencing atro-
phy of the thenar and interosseous muscles. At the time I examined her, the
symptoms of bulbar paralysis had reached their most typical appearance. The /far-
adie examination revealed no plain diminution of the irritability in the inferior
branches of the facialis and muscles of the lips and chin. The faradic irritability
of the tongue, both directly and through the nerve, was likewise normal, or per-
haps slightly diminished. Galvanic examination of the inferior branches of the
facialis showed no diminution of irritability, or only a very slight one; nor was the
quality altered (cathodal closing contraction was greater than the anodal, the con-
traction short, like a flash of lightning). Direct galvanic irritation of the muscles,
' Vide supra, Section 16. Compare, too, Hrd, Ein Fall von Bleiliihmung. Arch. f,
Psych. u. Nervenkrankh, V. p. 452. 1875. >
932 ERB. —DISEASES OF THE MEDULLA OBLONGATA,
however, revealed the plainest symptoms of the reaction of degeneration in the atrophic
. labial and mental muscles. When the muscles were irritated through the nerves,
there was only a slight, though normal, contraction at the cathodal closure with
eight cells, and no anodal closure contraction, while there were extensive though
sluggish and tonic contractions when the muscles were irritated directly with the
same number of cells. The contraction at the anodal closure, too, appeared greater
than at the cathodal. Even with six cells these contractions are quite distinct,
while through the nerve no effect is produced. Direct irritation of the tongue with
acurrent of four or six cells resulted in evident closure contractions, and most
unmistakably greater at the anodal than at the cathodal closure. The sluggish
character of the contraction was not distinctly recognized. We found exactly the
same condition in the thenar and first interosseous muscles.
Considering the great practical and theoretical interest of
these results, it would be very desirable to test them further and
in a greater number of cases.
Examination of the sensibility usually reveals no disturb-
ance whatsoever. It is quite normal in the particular cases of
the face, mouth, and nares. Frequently, however, the suverior
cervical vertebree are painful on pressure.
In many cases the behavior of the reflex actions -s striking.
They are often greatly diminished, or even totally extinguished,
so that we can touch and irritate (with our fingers or an instru-
ment) the patient’s tongue, soft palate, pharynx, and even
larynx, without exciting any considerable reflex action, such as
the motions of vomiting or coughing. At the same time the pa-
tient can feel and localize each touch quite distinctly. Krishaber
examined this point very accurately in two cases, and found
even the larynx extremely insensitive to the action of caustic.
This is, however, not always the case; on the contrary, IT have
in many of my cases found that the reflex irritability of the
palate and pharynx was retained till the later stages of the
disease. Still, in others I have seen it extinguished at an early
date.
In the case of which I have given the above sketch, I ob-
served very striking reflex contractions in the muscles of the
chin and lips. When percussed, their whole surface fell into
active, short contractions, but the muscles percussed remained .
perfectly passive. To prove more clearly their reflex nature, I
produced these contractions by similar percussion of the nose.
Pes Ss
To
————————
PROGRESSIVE BULBAR PARALYSIS. 933
When the cornea was irritated the diseased muscles contracted _
most actively.
In conclusion, we may call attention to a number of negative
symptoms, which are also rather characteristic. In the first
place we have perfectly normal intelligence, memory, and sleep ;
unaffected organs of special sense and unaffected movements of
the eyes; normal sensibility; absence of motor and sensory
affections in the extremities, at least in the firs: stages of the
disease-; normal function of the bladder and rectum; unim-
paired appetite and good digestion ; and finally, no fever.
Course, Duration, and Terminations.
The cowrse of progressive bulbar paralysis is always very
slow and chronic from beginning to end.
Any alteration of pace in the course is rare, though it may
halt for a little, and then go steadily on its way again. There is
seldom an improvement of any duration.
Recovery has never been observed, at least when the diag-
nosis was certain.
Asa rule, the course is fatal, and death generally results in
a few years (from one to five), either from progressive general
inanition and exhausticn, from fits of choking and asphyxia,
from an attack of syncope and paralysis of the heart, or, finally,
from intercurrent complications, which effect a more rapid ter-
mination than the condition of the bulbar paralysis would lead
us to expect.
Complications.
By far the most important and frequent complication of pro-
gressive bulbar paralysis is the typical form of progressive mus-
cular atrophy. This has been very frequently observed, and
may occur in two ways. Either an extensive progressive muscu-
lar atrophy attacks an already well-developed case of progres-
sive bulbar paralysis, or at least traces of it may be found on
the hands and scapular muscles, and fibrillar contractions occur
934 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
in different parts of the body. Or, on the other hand, we may
see a perfect case of progressive muscular atrophy, and after
some time atrophic paralysis of the tongue, lips and palate sets
in, so that at last the patient dies of typical progressive bulbar
paralysis.
It has often been discussed whether the two forms of disease
are related, and merely distinguished from one another by their
localization and the different directions in which they develop.
Duchenne, indeed, who observed the frequency with which they
occurred together, asserted that it was a mere combination of
two totally distinct diseases. According to him, bulbar paraly-
sis is paralysis without atrophy, and progressive muscular atro-
phy, on the contrary, atrophy without paralysis.
But the fact alone of their frequent combination speaks for
their close relationship. A still stronger argument is that the
clinical symptoms exhibited by the affected muscles are per-
Jectly similar ; in both cases we have weakness and atrophy,
with predominance sometimes of one and sometimes of the other,
attacking the different muscles and sets of muscles in irregular
order, and showing a tendency to progressive disease. Besides,
the changes in electrical irritability are identical, and the same
may be said of the pathologico-anatomical process in the nerves
and muscles, which is a typical form of degenerative atrophy.
And finally, we find post-mortem exactly the same anatomical
changes in the central nervous system—either a simple pigment-
ary atrophy of the multipolar ganglion-cells in the gray sub-
stance, or a chronic sclerotic myelitis, producing at the same
time the destruction of the ganglion-cells.
The great number and unanimity of modern investigations all
compel us to regard progressive muscular atrophy as essentially
resulting from degeneration and destruction of the large gan-
glion-cells of the anterior cornua. And in the same manner all
carefully made autopsies teach us that the essential lesion in
progressive bulbar paralysis is, in all probability, degeneration
and destruction of the large ganglion-cells in the motor nuclei
of the medulla oblongata. |
Now, it cannot be fora moment doubted that the gray motor —
nuclei of the medulla are prolongations of the anterior gray
*
_s
a ee ee Pe oe
PROGRESSIVE BULBAR PARALYSIS. 935
columns, and that the two are anatomically and physiologically
analogous.
We may accordingly assume that 7 both diseases the patho-
logical processes are either essentially identical, or at least very
closely related, and that it depends on their localization chiefly
whether the result is muscular atrophy or bulbar paralysis, and
that consequently these two diseases may combine frequently
and in every proportion.
This view has been very beautifully expounded and argued
by Kussmaul. Shortly afterwards Hallopeau, on the same
grounds as Kussmaul, asserted the relationship of the two dis-
eases, only distinguished by their localization. Perhaps a little
too early, he proposes for both diseases the name of ‘‘ atrophie
primitive chronique des noyaux moteurs,’ and distinguishes a
bulbar form (progressive bulbar paralysis), a spinal (progressive
muscular atrophy), and a bulbo-spinal form (a combination of
the two).
In the preceding paragraphs we have given the views of nearly all modern
neurologists, with which we ourselves, too, fully agree on the grounds of the facts
we have learned. Even Trousseau in his time declared for the relationship of the
two forms, though he did not think they were quite identical. Benedikt can draw
no distinction between cases with and those without atrophy. Leyden, Charcot,
Poincaré, Grasset and others all agree to the complete unity of the diseases; and
Kayser, in a lately published review of the question, takes the same side.
At the same time it should not be forgotten that high authorities do not take
this view. In the first rank comes Duchenne, who was the first to set up the dis-
tinction we have so often noticed, asserting that in bulbar paralysis there was only
paralysis. It is, indeed, hardly credible that so distinguished an observer as
Duchenne should have overlooked the atrophy, which is at least very frequent. At
a later period Duchenne modified his views considerably. He admitted that the
anatomical lesion in the two cases was identical (primary atrophy of the large
ganglion-cells), and allowed that they were often combined; but still he held fast
to his old clinical distinction of paralysis in the one case and atrophy in the other.
He tried to get himself out of the dilemma by the hypothetical assumption that
there exist two kinds of multipolar ganglia—motor and nutritive, and that in pro-
gressive bulbar paralysis exclusively or chiefly the motor ganglia were affected, and
in progressive muscular atrophy only the nutritive. Hammond quite agrees with
this view.
One could very easily agree to this, and temporarily accept this rather plausible
hypothesis, if it only could be proved that progressive bulbar paralysis really exists
936 ERB.—DISEASES OF THE MEDULLA OBLONGATA,
without atrophy. But this has never been proved, Instead of proofs, we meet with
the constant assertion that there is no atrophy, in direct contradiction to what is
constantly observed by all modern authors.
The histories of his own cases prove that Duchenne himself did not meet solely
with cases without atrophy. In observations 140 and 141 (Electris. localis, 2d éd.
pp. 622 and 629), Duchenne narrates that the tongue was wrinkled and furrowed,
‘“‘et en apparence atrophiée,” and then goes on naively to state that in both cases,
after a few faradic sittings, it again assumed “its normal volume,” ergo, it must
have been atrophied before.
It is quite plain that it is not always an easy matter to detect atrophy in an
organ like the tongue, and that further it may be concealed by a secondary growth
of connective tissue or deposition of fat. Naturally, too, disturbances of the action
of the tongue, which requires such precision, can be detected at a much earlier date
than the atrophy which creeps so slowly after. It is almost superfluous to adduce
as evidence Charcot’s observation, that the tongue may during life retain its normal
appearance and proportions, and still, when examined post-mortem, be found to
have undergone extensive degenerative atrophy. Consequently the anatomical
examination, and not the clinical, can alone decide the absence of atrophy. And
all observations restricted to a clinical examination, or which do not employ the
microscope at the autopsy, as well as all which relate to other lesions than degen-
erative atrophy of the gray nuclei, are utterly worthless for the decision of this
question.
Nothing can decide but a complete autopsy embracing all points, and there is
no such an one. In the only one (which was published by Duchenne himself, and
performed by Joffroy) it is a matter of extreme regret that the muscles (tongue,
lips, etc.) could not be examined. The decisive autopsy, consequently, has still to
be made.
Accordingly, Déchery’s thesis, written probably at least in part under Duchenne’s
guidance, and attempting the rescue of “‘ bulbar paralysis without atrophy,” can hard-
ly be regarded as a success. Déchery brings forward this form, without being able
to prove its existence, and since he cannot bring himself to accept Duchenne’s
hypothesis of separate motor and nutritive cells, strives to get out of the difficulty —
by assuming that in non-atrophic bulbar paralysis only a few cells in the gray
nuclei are affected, and all or a great many in the atrophic form. Duchenne’s
hypothesis certainly sounds more plausible than this.
But in the last few years the doctrine of close relationship between progressive
bulbar paralysis and muscular atrophy has found a stout opponent in Friedreich.
He devotes a special chapter, in his work on progressive muscular atrophy, to the
relationship between it and progressive bulbar paralysis, and comes to the follow-
ing conclusions: Progressive bulbar paralysis is essentially a pure paralysis, and it
is characterized clinically by the fact that the muscles retain their normal volume ;
yet sooner or later atrophy may be superadded. Now, if this bulbar paralysis
commences in a case of already developed muscular atrophy, the reason is that an
ascending neuritis, derived from the muscles, spreads to the cervical portion of the
oll
eee ~
pes we
PROGRESSIVE BULBAR PARALYSIS. 937
spinal cord, and is from this propagated to the medulla oblongata, where it
becomes established as bulbar paralysis. In cases where progressive muscular
atrophy appears as a complication of bulbar paralysis, we must assume that it is
primarily a case of paralysis, produced by propagation of the bulbar process into
the spinal cord, and that then a secondary atrophy commences in the paralyzed
muscles, an atrophy, consequently, which has nothing to do with genuine progressive
muscular atrophy. Finally, there exists a progressive atrophy of the muscles of the
face, palate, and tongue, which is, however, only a part (generally of late occur-
rence) of a very extensive general progressive muscular atrophy.
It is not in place to discuss these somewhat complicated views of Friedreich's ;
in fact, it would not be possible without a very thorough exposition of his myopathic
theory of progressive muscular atrophy, for which there is not space in this work.
We only repeat, that in opposition to Friedreich’s view, it must be asserted that the
existence of bulbar paralysis without degenerative atrophy of the muscles remains
to be proved. And further, our own experience does not lead us to believe that the
complication of bulbar paralysis with progressive muscular atrophy does not occur
by any means unexceptionally through the intermediation of a paralysis preceding
the atrophy.
With the facts at present before us, we are compelled to adhere to our convic-
tion that paralysis and atrophy are always combined in progressive bulbar paralysis,
though the relative proportions may vary, 7. ¢., in one case atrophy may occur earlier
and be more marked than in another, and vice versa. But it does not appear to us
allowable to draw a sharp distinction between the two forms of disease on the mere
ground of a difference in the degree of atrophy.
The existence of progressive bulbar paralysis without atrophy remains to be
proved, and when this is done we shall gladly recognize it, and likewise a primary,
isolated, progressive atrophy of the lingual, labial, and palatine muscles. For the
present we shall restrict the idea of the bulbar paralysis we have described in the
foregoing pages to a disease which commences with more or less early and well-
marked degenerative atrophy of the muscles, and which is, in this respect, and in
its anatomical foundation, closely allied to progressive muscular atrophy.
A second important complication of progressive bulbar paral-
ysis is with amyotrophic lateral sclerosis. Bulbar paralysis
often occurs in the last stage of this disease, which has been
described by Charcot, and causes the death of the patient. In
this case, also, it is characterized by the same anatomical lesion
—that is to say, degeneration and atrophy of the gray nuclei
of the medulla. The disease is further characterized by the
symptoms of progressive muscular atrophy in the superior
and spastic spinal paralysis (lateral sclerosis) in the inferior ex-
tremities. To this class belong a number of cases described as
938 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
bulbar paralysis or progressive muscular atrophy. It is clearly
a complication of a chronic degenerative process in the medulla,
with similar extensive chronic processes in both the white and
gray matter of the spinal cord.
The anatomical facts and clinical symptoms allow us to con-
jecture an immediate relationship between the three diseases—
progressive bulbar paralysis, progressive muscular atrophy, and
amyotrophic lateral sclerosis. But we need more numerous, em-
bracing, and careful observations before we can determine their
relations, and either distinguish sharply between them, or unite
them more closely.
Theory of the Disease.
Our whole description shows pretty plainly how little we know
relatively, and especially how few certain data we have, to found
a theory.
One fact is beyond doubt: that in bulbar paralysis we have a
progressive paralysis and atrophy of certain muscles and muscu-
lar groups, and that this corresponds anatomically to a degenera-
tive atrophy of the muscles and their nerves and nerve-roots, —
and finally, of their gray nuclei and large ganglion-cells. The
functional derangements may be satisfactorily explained by these
anatomical changes.
Probably the degenerative atrophy of the ganglion-cells is the
primary part of the disease; for, as this condition of the cells is
constant, it cannot be the degeneration of the root-fascicles, or
any other conducting tract of the medulla, which gives rise to
the symptoms.
We are still in darkness as to how this process in the gan-
glion-cells comes about, and what it actually is—whether it is a
primary (interstitial) myelitis with secondary atrophy of the
cells, or a primary idiopathic degeneration. This question seems
hardly ripe for discussion. Nor can anything more be said of
the manner in which the process is earried out.
Furthermore, there is no light on the exact relationship be-
tween what is plainly the primary central lesion, and the sec-
ondary changes which take place in the nerves and muscles. It
ee oe Pes w®
PROGRESSIVE BULBAR PARALYSIS. 939
seems to us very improbable that a descending neuritis is prop-
agated from the centre in the medulla along the nerves to the
muscles, creating in these latter an inflammational atrophy. The
centre in the medulla seems too small and limited to meet this
supposition, and shows too few signs of actual inflammation.
Besides, the changes in the nerves are not proportionate to those
in the muscles, and then, too, electric examination proves that
the nerves may be quite unimpaired whilst the muscles are far
advanced in degeneration. We must consequently regard this
degenerative atrophy as neurotic. But there is nothing to ex-
plain the relations of the different affected central structures to
the origin of the paralysis and the production of nutritive de-
rangements in the muscles and nerves.
We are here again met by the questions we have already
discussed and designated as a rewarding object of future in-
vestigations, 7. e., Are there separate and peculiar motor and
nutritive cells? Have the muscles and nerves separate nutritive
centres? How must the lesion be located to produce paralysis
alone, paralysis with atrophy, or atrophy without paralysis? Do
facts allow us to distinguish between a form of bulbar paralysis
commencing with paralysis, but leading, without fail, to atrophy
(analogous to spinal poliomyelitis ant. chron.), and another form,
in which the atrophy is primary, and in which the paralysis is
due merely to atrophy (analogous to the typical form of progres-
sive muscular atrophy) ?
These and other theoretical questions await an answer, which
can only be given by very deep researches. It would appear
advisable here to include not only all cases of progressive bulbar
paralysis and progressive muscular atrophy, but also those of
amyotrophic lateral sclerosis, and poliomyelitis anterior chronica.
Diagnosis.
When bulbar paralysis is fairly developed, the symptoms are
so extremely characteristic that it is hardly possible to mistake
them. It is unnecessary to repeat the individual characteristics
here.
But it is frequently a difficult matter fo recognize the very
940 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
commencement of the disease. We should here pay attention to
any slight difficulty of speech, a certain stiffness of the lips,
slight alteration in the expression of the face, to a feeling of pres-
sure and traction in the back of the neck, slight trembling in the
tongue when put out, traces of a nasal voice, etc., ete. Any traces
of atrophy in the small muscles of the hand are likewise of im-
portance.
It is hardly worth mention that at this stage there is no
trouble about distinguishing the disease from a simple angina, or
stomatitis simplex. |
When the disease is further advanced the great task is to dis-
tinguish between ‘‘ bulbar”? paralysis from other causes and
primary progressive bulbar paralysis.
When the bulbar paralytic symptoms (derangement of speech
and deglutition, paresis of the lips, paralysis of the tongue,
palate, etc.) are only some of many arising from extensive dis-
ease in the central nervous system—e. g., disseminated sclerosis,
general paralysis of the insane, amyotrophic lateral sclerosis,
poliomyelitis anterior chronica ascendens,—then the first matter
to be settled is the diagnosis of these diseases from the symptoms
that belong to them, in order thus to gain a clear idea of the po-
sition occupied by the bulbar symptoms, and of any special
process taking place in the medulla.
But it is more important, when the disease is actually local-
ized in the medulla, to make out its nature, whether it is a
primary atrophy of the gray nuclei on the floor of the fourth
ventricle, or whether it is a different pathological process. The
diagnosis must in this case depend upon the most accurate ex-
amination possible of the course and development of the disease,
and a careful investigation of all, and especially of the unusual
symptoms.
The manner in which the disease commences is the best guide
to distinguish it from embolism, thrombosis, and hemorrhage in
the medulla. These three always commence acutely and suddenly,
whereas progressive bulbar paralysis is very gradual. The paral-
ysis is frequently partial, limited to, or predominant on, one side.
An apoplectic attack, violent dizziness, or an epileptoid fit often
form the onset. Besides, these diseases have no progressive char-
eT, eee
PROGRESSIVE BULBAR PARALYSIS. 941
acter, but rather a tendency to improve. Nor is there generally
any difficulty in recognizing the later results of these processes,
such as hemiplegia with contractures, absence of atrophy, stabil-
ity of the bulbar symptoms.
The differential diagnosis of fwmors which compress the me-
dulla is of more importance, as their course is usually one of
slow development. Here we should note that at first the patient
nearly always suffers from violent headaches, dizziness, buzzing
in the ears, vomiting, etc. We should also look specially for
initial symptoms of irritation or paralysis of the bulbar nerve-
roots, especially neuralgia and aneesthesia in the trigeminus,
derangements of hearing, spasms and contractions in the face
and tongue, paralysis of the abducens and facialis, or of the
tongue, with early pronounced degenerative reaction of a com-
plete nature—all this is the more important, the more unilateral
the symptoms are. When the compressing body is situated
anteriorly, and acts on the bulbar roots of both sides, it is often
hardly possible to draw a distinction. Early paralysis of the
limbs with contractures is likewise of importance, when the
tendon-reflex is increased and there is no atrophy. Then, too,
repeated epileptic attacks should be noted, attacks of fainting
and temporary amaurosis, and finally all other symptoms which
indicate the presence of a neoplasm within the skull (ophthal-
moscopic examination, etc.).
It is easy, as a rule, to distinguish bulbar paralysis from a
diplegia facialis of peripheral origin. The diagnosis may be
founded on the complete paralysis of all branches of the facialis,
inclusive of the superior ones, as well as on the intense degenera-
tive reaction we generally find, the complete immunity of the
tongue, normal deglutition, and the eventual ageusis of the point
of the tongue. Nor is there much difficulty with a diplegia faci-
alis of cerebral origin, which may be distinguished by the simul-.
taneous paralysis of the extremities and perfectly unimpaired
electric irritability, and also by the manner in which the disease
is developed. |
We should not, however, forget, when dealing with symptoms
even of bilateral paralysis of the bulbar nerves, that all the
symptoms of labial, lingual, and pharyngeal paralysis may be
942 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
caused by lesions localized more centrally in the hemispheres,
corpus striatum, internal capsule, etc. In such cases we are ad-
vised by Joffroy to observe that the paralyses of the tongue,
palate, lips, and pharynx are never long complete. It is also
characteristic that they arise from two plainly separate unilateral
affections, and there is frequently a preponderance on the one
side or other ; there is no atrophy ; electrical irritability is quite
normal, and there is no reaction of degeneration ; reflex action re-
mains unaltered, or may be increased; the extremities are Lies
wise paralyzed, without atrophy.
We may mention, finally, that Jolly in a case of extensive
cerebral sclerosis ‘ saw the gradual development of a bulbar par-
alysis of most unmistakable nature, though without atrophy of
the tongue, and at the autopsy he found no notable pathological
change in the medulla, especially no alteration of the nuclei in
the floor of the fourth ventricle. This case teaches us that a
very similar set of symptoms may be produced by a lesion in the
anterior tracts, and that we cannot be too particular in making a
differential diagnosis to note every symptom, even those that
seem quite insignificant. :
Prognosis.
In all the well-observed and accurately recorded cases of
genuine bulbar paralysis, there is hardly an instance of recovery,
and but seldom a halt in the course, or a transitory improve-
ment. There are, indeed, a number of recorded cases in which
considerable improvement took place, and even some cures ; but
when we look closely at these records we see that they are not —
cases of bulbar paralysis at all, or else very doubtful ones. No
typical, genuine case has yet been treated with lasting success.
I have myself treated numbers of such cases without success ; in
fact, the only case which seemed successful, when reviewed more
accurately, cannot strictly be included, although it had certainly
very strong points of similarity with the typical form.
With our present knowledge we must, accordingly, term the
? Arch, f. Psych. und Nervenkrankh, III. p. 711. 1872.
TP SAT be
SO ATE a: FESO et em
—_ _————e all —_ — —_— ——— aie —
PROGRESSIVE BULBAR PARALYSIS. 943
prognosis absolutely fatal. We can in such cases prophesy the
patient’s death within a few years. Benedikt’s assertion that the
prognosis of ‘‘ progressive paralysis of the cerebral nerves”? is
more favorable than that of locomotor ataxy, progressive muscu-
lar atrophy, etc., applies very well to a series of diseases which
Benedikt classifies under this heading, but which have certainly
nothing to do with progressive bulbar paralysis.
In some cases a prognosis may be formed from the stage of
the disease and its principal symptoms. Intense dysphagia is,
of course, an unfavorable sign, and likewise advanced inanition,
dyspnoea, and fits of suffocation. In fact, the greater the respir-
atory derangements, the nearer is the end. Duchenne considered
the incapability of lateral motion of the jaw (paralysis of the
pterygoids) as a prognostically unfavorable symptom, as in that
case the disease is in the proximity of the nuclei of the vagus,
and death may soon be expected.
Treatment.
The prognosis we have just given speaks for the bad success
of every treatment.
However, it would be quite unjustifiable to renounce every
effort to cure the disease. Perhaps time will bring us suitable
agents and methods. Perhaps; too, when taken early, the disease
is more tractable; and then the transitory successes that are
occasionally attained stimulate us to further therapeutic efforts.
Certainly the experience we have gained of progressive muscular
atrophy is not exactly encouraging.
We have to deal with a chronic, slowly progressive degenera-
tion, which comes on with very slight symptoms of irritation and
without any evident inflammational process or growth of tissue,
and the proximate and ultimate causes of which are unknown to
us. Accordingly, the indication is to improve the abnormal
nourishment of the nervous system, and to rouse the regenera-
tive activity—in a word, the indication is ‘‘alterative.”’
In the earliest stages we should apply (according to the ini-
tial symptoms) gentle derivatives at regular intervals (Kuss-
maul), bloody and dry cupping, vesicantia, setons, Priessnitz
944 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
bandages, and shower-baths (a single stream of water should be
used very cautiously).
When the disease has developed we should, above all things,
endeavor to regulate the diet in such a manner as to avoid irri-
tation of the nervous system. The patients should, if possible,
give up their work, and avoid all excitement, and, at the same
time, take plenty of wholesome nourishment, limiting themselves
in alcoholic drinks, and tea and coffee. Care should be taken
that they get enough sleep, and they should have plenty of open
air, if possible at the seaside or in the mountains.
We may combine with this any course of treatment which
tends to a general stimulation of nutrition, and produces a tonic
effect upon the nervous system. In this respect I place most
reliance upon a cautious hydropathic treatment, which must,
however, be continued for a long time and with great regularity.
But with aged patients this is not very feasible. I think it ad-
visable, too, in suitable cases, to try the effect of warm saline
and chalybeate springs, though I should decidedly warn any-
body against hot springs, steam-baths, or mud-baths. A very
cautious trial of a hot spring (especially in the mountains)
might possibly prove of service to old and decrepit people.
But by far the most important indication is electricity, which
promises more than any other method tried. Unfortunately,
however, the results as yet obtained are similar to those of pro-
gressive muscular atrophy, not at all encouraging. Benedikt’s
reported cures are certainly very brilliant, but they plainly relate
to other forms of disease. The only two of his cases which really
belong to this class remained unaffected by his treatment. How-
ever, Benedikt’s publication contains many encouraging thera-
peutical remarks. I myself effected a cure with galvanism in
one case which had all the symptoms of bulbar paralysis, but
began with severe pains in the head and joints, and, besides, |
exhibited symptoms of dizziness and buzzing in the ears, so that
I was not certain of my diagnosis.
The most effective method of galvanism is as follows: one
vanize with stabile application transversely through the mastoid
processes, and longitudinally through the skull, the so-called
galvanism of the cervical sympathetic (anode on the nuchus, and
dee ee
pee he?
OE ae
ae OUP,
—
PROGRESSIVE BULBAR PARALYSIS. 945
cathode at the angle of the lower jaw); and then induce move-
ments of deglutition (twelve to twenty at each sitting); besides
this, apply, according to circumstances, direct galvanic or faradic
currents to the tongue, lips, and palate.
I seize this opportunity of correcting an error which has been allowed to run
through our literature for several years, the error of supposing that galvanic produc-
tion of the movements of deglutition is due to irritation of the hypoglossus. It is quite
incorrect, for it may be easily demonstrated that the current which suffices to pro-
duce these movements is by far too weak to irritate the hypoglossus; and that the
movements, too, cannot be induced by a single contraction of the tongue (especially
by a unilateral contraction) ; further, that it is more easily effected at other points
than the point of irritation of the hypoglossus; and that, finally, actual direct irri-
tation of the hypoglossus, though accompanied by visible contraction of the tongue,
produces zo movement of deglutition. It is evidently a case of reflex action, arising
from the sensible nerves of the pharynx and larynx; in fact, physiology teaches us
that irritation of the laryngeus superior induces reflex deglutitory movements. If
one tries the experiment on himself, there is immediately a sensation produced as if
one had a bolus or draught of water in the throat, and this is irresistibly followed
by a movement of deglutition.
The best method to produce it is to place the anode on the back of the neck,
and then run the cathode rapidly over the lateral surface of the larynx, repeating
this after short pauses. A healthy man requires only six or eight cells, but for bul-
bar paralysis the current must often be much stronger, and the reflex irritability is
easily exhausted. To meet this, we must reverse the current, instead of using catho-
dal closure. This treatment produces some improvement in deglutition at least for
a short time.
The electric treatment must be continued for a very consider-
able time, with from four to seven sittings a week. The duration
of a sitting should not exceed four or six minutes. The patients
are frequently irritable and sensitive to a galvanic current, so
that great caution must be taken in selecting the number of cells.
Medicines taken internally have never produced the very
faintest effect. Still, considering their success in other chronic
degenerations of the central nervous system, we shall always be
inclined to administer nitrate of silver, iodide of potassium,
iodide of iron, chloride of gold and sodium, ergotine, belladonna,
and preparations of iron and quinine, etc. We wish to warn
against the administration of strychnine and phosphorus.
As the derangement of deglutitign grows worse, the impor-
VOL. XIII.—60
946 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
tance of the patient's food increases. At first all food must be
finely divided, and very carefully cooked ; it must be soft, juicy,
and concentrated nutriment. At the same time we should not
forget to vary it suitably, and not cause distaste from monotony.
Minced meat, beefsteaks of the same, hashes, russoles, etc., beef-
tea, milk and eggs, cocoa, soups of revelenta arabica, and pre-
pared leguminosa, etc., form a basis to which may be added all
kinds of soft prepared meats, compotes, and vegetables. Wine
and beer should only be taken in moderation.
According as the deglutitory paralysis grows worse, special
attention must be given to the act of swallowing; help must
always be given, and none but easily swallowed victuals be
allowed. Afterwards all particles of food must be removed from
the pharynx, the root of the tongue and underneath it, and the
mouth carefully washed out. |
When deglutition becomes impossible, we must feed the pa-
tient through a flexible tube; but with many patients this is ren-
dered impossible by violent fits of vomiting and suffocation. In
this case nothing is left but the administration of nutritive ene-
mata, such as solution of pancreas, milk and eggs, bouillon,
wine, etc. But patients seldom endure this long.
When the only indication is to overcome increasing exhaus-
tion, gastrotomy and introduction of food through the wound
might be recommended as a ‘‘ dernier ressort.’? We might hope,
by this means, to prolong the patient’s life for a short time. But
if there are threatening signs of respiratory paralysis, the oper-
ation would be superfluous.
Fauvel, in one case, proposed and performed tracheotomy to
check the fits of suffocation and dyspnoea. If the patient con-
stantly wears a tube, and eventually has the larynx plugged at
every meal to meet these choking fits, and to prevent the en-
trance of food-particles into the trachea, it may do some good.
To check salivation, Kayser recommends atropine (subcutane-
ous dose, 7 to 4 gr. (0.0004—0.001); internally, 4 to 4; gr. (0.0008-
0.0012). We cannot abstain from the use of narcotics, mor-
phine, chloral, etc., when, towards the termination of his disease,
the patient is troubled by dyspnea and sleeplessness.
The usual analeptica and irritantia may be administered in
——-_— ~~
SCLEROTIC CENTRES. 947
cases of general weakness, syncope, etc. To close the tragic
course the physician might well think of euthanasia.
6. Other Chronic Diseases of the Medulla.
Samuelson, Kinigsb. med. Jahrb. I. p. 93. 1859, and Berliner klin. Woch. 1868.
No. 27.—J. Wagner, Ueber Hirngeschwiilste. Diss. Berlin, 1871.—Cornil and
Lépine, Cas de paralys. génér. spin, antér. subaigue suivi d’autopsie. Gaz, méd.
de Paris. 1875. No. 11.—Hallopeau, Des paralysies bulbaires. Paris, 1875.
The description of diseases in the foregoing paragraphs by
no means exhausts the pathology of the medulla oblongata.
There are several other forms of disease, some occurring as part
of the phenomena of more extensive diseases of the central ner-
vous system, and some which occur so seldom and have been
recorded so badly that they have no practical value, and are,
consequently, hardly worth mention. Probably the future will
throw much light upon this province, so that this chapter can
only be regarded as a temporary refuge for those diseases of the
medulla oblongata to which no place has been yet assigned in
our nosography.
The literature of this subject is still very small. We give the
following extracts :
Sclerotic centres, which are usually met with in the medulla
oblongata as one of the many symptoms of. multiple cerebro-
spinal sclerosis. These may occur typically in all shapes and
sizes ; they are oftenest found on the floor of the fourth ventricle,
pressing more or less deeply into the white substance, and affect-
ing the bulbar nuclei in varying degree; but they have also oc-
casionally been observed in the pyramids, olivary and restiform
bodies, and in the formatio reticularis. Sometimes, too, they
may be met with in the bulbar nerves.
The microscopic appearance of these centres is quite the same
as any other, so we may refer to the description on p. 481. The
destruction of the nervous substance proper (nerve-fibrils and
ganglion-cells) does not appear at all so complete or of the same
kind, as in bulbar paralysis, for instance.
The symptoms of these bulbar centres play a prominent part
in multiple sclerosis, and there seems to be a special connection
948 ERB.—DISEASES OF THE MEDULLA OBLONGATA,
between the symptoms of bulbar paralysis we so often meet in
this disease and these centres in the bulbus. But Jolly’s often-
cited case proves that this is not necessary, and that the symp-
toms may be produced by anteriorly situated lesions.
In such cases we often come across a strikingly deceptive
likeness to progressive bulbar paralysis; but the paralysis is
generally not complete—only a paresis ; atrophy of the muscles
is rare, and in general the whole development of the symptoms
is not so regular as in the typical form of chronic bulbar paraly-
sis. Besides, the diagnosis is readily confirmed by the presence
of numerous other symptoms of multiple sclerosis.
Possibly other individual symptoms in multiple sclerosis,
such as scanning speech, monotonous voice, paralysis of the fa- —
cialis, weakness and trembling of the tongue, salivation, auditory
derangements, etc., might be referred to the centres in the me-
dulla. We have already discussed the question, and must here
again leave it undecided whether this supposition is correct or
whether the symptoms are not due to centres situated in an
anterior portion of the brain.
It is somewhat more warrantable to connect the derangements
of deglutition, attacks of dyspnoea, syncope, cardiac palpita-
tions, and paralysis, etc., which occur in the last stages of mul-
tiple sclerosis, with the development of sclerotic centres in the
medulla.
Anatomical changes in the medulla occur, too, usually as a
part of dementia paralytica (chronic myelitis, myelitis with cor-
puscles of Gluge, gray degeneration); these changes, however,
constitute only a very small part of the lesion, which extends
over the whole central nervous system in this disease. It is still
questionable, and not at all probable, that the frequent and typi-
cal derangements of speech are dependent upon the participation
of the medulla. However, it is not a matter for discussion here.
When poliomyelitis anterior subacuta assumes an ascending |
and progressive character, the process in the spinal cord finally
PE PE? ~ Pans
So = «(earn oe, ee
7 _—
Ld
DIFFUSE SCLEROSIS. 949
attacks the bulbus, and seems to show a special tendency to set-
tle in the gray nuclei in the floor of the fourth ventricle. But
we have no decisive pathological facts on this point. If we may
draw conclusions from Cornil and Lépine’s interesting case, in
which unfortunately the exact microscopical examination of the
medulla is not recorded, we have a case of chronic inflamma-
tional changes with secondary destruction of the ganglion-cells.
When a progressive myelitis universalis finally spreads to
the medulla, the changes are probably the same, viz.: chronic
myelitis varying in extent, but probably not confined to the gray
substance, but embracing the white as well; still this is an unde-
cided question.
But the bulbar changes, which take place in the terminal
stages of amyotrophic lateral sclerosis (and also in the course of
progressive muscular atrophy) are, as we have already insisted,
exactly the same as in progressive bulbar paralysis.
In all these cases the infection of the bulbus is indicated by
the occurrence of bulbar paralytic symptoms, which gradually
increase till they assume the typical form of progressive bulbar
paralysis—derangement of speech and deglutition, and paresis
of the lips and palate, increase or decrease of saliva, derange-
ment of respiration, attacks of suffocation, and all the rest. The
appearance of the symptoms always betokens the last stage of
the disease ; the prognosis is generally very serious, and the dis-
ease can seldom be checked in its course.
Among the diseases that are well confined to the medulla a
diffuse sclerosis—chronic myelitis bulbi—has occasionally been
observed, sometimes with and sometimes without simultaneous
sclerosis of the brain or spinal cord. But details are wanting.
It is hard to say, from J. Wagner’s description, whether his
remarkable case (tumor-like hypertrophy and toughness of the
pons and the whole medulla, more especially on the right side)
was a real tumor or hypertrophic sclerosis. It was more prob-
ably a genuine neoplasm. .
950 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
Samuelson observed one case of circumscript bulbar sclerosis,
consisting of an indurated spot in the left half of the pyramidal
substance about the size of a bean. Microscopic examination
proved it to be sclerosis (fine fibrils of connective tissue with
numerous nuclei and separated nerve-fibrils).
In this case, after repeated sensory and motor derangements
had occurred, sometimes in the right and sometimes in the left
extremities, he observed a sudden right-sided hemiplegia with
apoplectiform symptoms, and accompanied by troubles of deglu-
tition and respiration, and slight derangement of speech. The
tongue was straight, and all the anterior cerebral nerves unaf-
fected; retention of urine; feeling of a hoop around the head
from the occiput to the forehead; sensibility normal; reflex
action increased. Variations in the course of the disease are
recorded, but no details given.
7. Tumors of the Medulla Oblongata—Neoplasmata in its Sub-
stance. ,
Abercrombie, Diseases of the Brain. 1845. p. 103.—Ollivier, loc. cit. 3. édit. II.
p- 514. 1837.—Levrat-Perroton, Cas de glycosurie déterminée par une tumcur
colloide renfermée dans le 4me. ventric, Thése. Paris, 1859. Canst. Jahresber.
1859. IV. p. 254.—2. Recklinghausen, Schiidelverletzung, Diabetes, Tumor im
4, Ventrikel. Virch. Arch. Bd. 30. p. 864. 1864.—Mosler, Virchow, Neubil-
dung im 4. Ventr. mit. Diab. insip. Virch. Arch. Bd. 438. p. 225. 1868,—Vir-
chow, Die Krankhaften Geschwiilste. I. pp. 183, 387, 424; IL pp. 112, 134,
664, ete. 1863-65.—Ladame, Symptomatol. u. Diagnostik d. Hirngeschwiilste.
p. 43. 1865.—Immermann, Berl. klin. Wochenschr. 1865. p. 177.—Joh. Hrich-
sen, Zur Casuistik der Tumoren des Verling. Marks. Petersb. med. Zeitschr.
1870. I. p. 105.—Hdwards, Tumour in the Medull. Oblong. Brit. Med. Journal.
1870. Feb. 5.—J. Wagner, Ueber Hirngeschwiilste. Diss. Berl. 1871.—Bour-—
don, Etudes sur les malad. du bulbe rhach. Gaz. hebdom. 1872. No. 22. p. 354.
—Garrod and Philpot, Papillomatous Tumour in the Fourth Ventr. of Brain.
Lancet. 1873. Mar. 1.— Verron, Etude sur les tumeurs du 4. ventr. These. Paris,
1874.—Hallopeau, Des paralysies bulbaires. Paris, 1875.—Carpani, Storia clin.
d’un caso di tumore d’un pedunculo cerebellare. Lo Speriment. Ottobre. 1876
(Virch.-Hirsch. Jahresber. for 1876. II. p. 111).
Pathological Anatomy—Cases.
Neoplasmata in the medulla oblongata are of very rare occur-
rence. Ladame only collected nine cases altogether, and most:
eid
~ Ee
—- a
TUMORS. 951
of these were not actually in the substance of the medulla, but
only in its vicinity, in the cerebellum, etc., and only secondarily
connected with the medulla,
Asa matter of fact, it is extremely hard to distinguish between
tumors in the medulla itself, and those in the surroundings,
which press upon and irritate it. Clinically it is in most cases
impossible, as experience teaches us that tumors, for instance,
which grow in the cavity of the fourth ventricle, and develop
in the direction of the floor, produce exactly the same symptoms
as those which grow in the floor itself, for instance, tumors of:
the ependyma. And as far as the symptoms are concerned, it
would seem @ priori that there can be no considerable difference
whether a neoplasm arises 72 the gray or white matter of the
medulla and destroys it from within outward, or whether a
similar one penetrates from without, dislocating and voMpreeses
it, and thus causing myelitis.
Thus, the anatomical and clinical appearances of the two are
intimately connected, and we can in great part refer to what has
been already said of chronic compression through neoplasmata.
It is utterly impossible to draw a sharp distinction, since most
of the recorded cases are imperfect, in as far as the tumor has
seldom been limited to the medulla, but has generally involved
the surrounding corpp. “ie .» pons, and cerebellum to some
extent.
So we shall merely mention what tumors occur in the medulla,
and then give a few short examples, and from these deduce the
symptoms. For the future the cases ought to be more accurately
observed and recorded.
Perhaps the most frequent form in the medulla is tubercle ;
they may be of any size up to the dimensions of a walnut, especi-
ally in the pons portion ; there is usually but one, but there may
be several small ones. The surrounding tissue is sometimes quite
intact, sometimes more or less affected (Ollivier, Erichsen, Aber-
crombie).
Gliomata and glio-sarcomata have been repeatedly found
(Virchow), either developed from the ependyma or in the centre
of the medulla; their size and position vary.
Myzxomata appear never to be seen except on the choroid
952 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
plexus of the fourth ventricle, and the same may be said of
psammomata, which often occur there also, both large and small.
Fibromata have been discovered in many cases (Liouville,
Virchow, Carpani), occurring in sizes up to a bean, and growing
either in the ependyma or in the medullary substance.
The secondary changes, which the medulla undergoes in such
cases, have not been much investigated ; in fact, we have but
very scanty records of the naked-eye appearances. But we can
predicate, almost with certainty, that softening processes often
occur, and sometimes extend far beyond the limits of the tumor
itself, and that further the lesion is often complicated by apo-
plexy and thrombosis.
But in general the tumor involves the neighboring parts of
the brain, and seldom remains confined to the medulla; thus the
pons is usually, the cerebellum frequently, and the corpora quad-
rigemina occasionally drawn into the process. This of course
has a great effect upon the symptoms.
Intense hydrocephalus must be considered one of the most
frequent secondary changes caused by tumors in the medulla,
and more particularly in the fourth ventricle. It is produced,
on the one hand, by compression of the veins, especially of the
vena magna Galeni, on the other hand, through the hinderance
to the return of the cerebro-spinal fluid into the arachnoid
space, caused by the tumor filling up the fourth ventricle and
rendering it impassable.
We give a few extracts of cases.
Ollivier, Case 146: Two tubercles in substance of medulla ; epilepsy for twelve
years ; an aura of violent singultus before every attack, and feeling of globus in the
throat.
Erichsen ; Tubercle the size of an almond, covering right half of bulbus along
whole length of fourth ventricle, and extending somewhat to the left; right corp.
restiforme quite destroyed; headache, dizziness, slight dilation of pupils, nau-
sea; vomiting and singultus, aphonia, anesthesia of the right side of the face ; paresis
of the right side of palate; tongue unaffected ; finally, paralysis of the bladder.
Edwards: Fibro-cellular tumor in the centre of the medulla; convergent stra-
bismus (paralysis of abducens) ; weakness in legs ; difficulty in swallowing ; incom-
prehensible speech ; later, vomiting ; hiccuping ; complete alalia; dysphagia ; abdo-
minal respiration; paralysis of sphincters and extremities.
Virchow (Geschwiilste. IL p. 184): Fibrous hyperplasia of the ependyma of
dha
Se lg gp Algae
eS SS aa
TUMORS. 953
fourth ventricle, three to four lines thick, resembling a tumor. Wound on head;
after nine years, mental depression, loss of memory, dizziness, headache, diplopia ;
Frequent urination (polyuria?) ; later on, constant vomiting and languor; move-
ments of the eyes (?), pupils, and tongue normal; sensibility unaffected; pulse 56;
finally, derangement of' speech, stupidity, etc.
Liouville (quoted in Verron’s work, p. 57): Small fibroma in ependyma in left
side of calamus scriptorius, one centimetre long and a half centimetre broad. The
patient, who suffered from heart and kidney disease, had glycosuria during life.
Carpani : Elliptical jibroma in the pedunculus cerebelli, near the pons, size of a
bean; violent pain on right side of head ; impairment of vision and hearing on the
right side ; vomiting ; atactic gait ; weakness of extremities on right side; right-
sided paralysis of abducens and facialis.
J. Wagner ; Tumor occupying the right half of pons and medulla, covered with
small prominences; this half hypertrophied to twice or four times normal size (very
inaccurately described). Violent headache and dizziness; paralysis of the right
facialis, abducens, and hypoglossus; nasal voice; paresis of all four extremities;
pain in back of neck; hearing impaired on right ride; finally, derangement of
speech and asphyxia.
Homolle (quoted in Verron’s work, p. 54): Glioma on the floor of fourth ventricle,
probably commencing in ependyma;. very vascular; processes extending into the
corpora quadr., optic thal., and left hemisph. of cerebell. Vomiting ; headache ;
transitory loss of consciousness; amaurosis; stagnation papilla; paresis of left faci-
alis ; attacks of vertigo ; somnolence ; sudden death.
Mosler-Virchow : Large-celled gliosarcoma of ependyma, pedunculated; five
centimetres long, occupying the whole ventricle; one to two centimetres in diam-
eter, causing the cerebellum and medulla to swell out. Vertigo ; vomiting ; racking
headache, with considerable remissions of some duration; finally, sudden death
with symptoms of suffocation. Diabetes insipidus in last few years.
Etiology.
As far as we have any knowledge of them, the causes of tu-
mors in the medulla are exactly the same as of any others in
the skull, viz.: traumatic influences, syphilis, tuberculosis, ete.
So we merely refer to Obernier’s article in Volume XII.
Symptoms.
Frequently tumors of the medulla cause no functional de-
rangement, and are only discovered post-mortem ; or they may
remain for a long time latent, and then suddenly in a few hours
or days cause sudden death with symptoms of suffocation.
954 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
But, generally speaking, the final catastrophe is preceded by
suffering of some duration. We need only give a short sketch
of the general symptoms, which display numerous points of simi-
larity to other cerebral tumors.
Among initial symptoms the most prominent are headache,
occurring generally in separate attacks, reaching in some cases a
frightful intensity, and localized in various parts of the head, but
generally in the occiput and nuchus; and secondly, attacks of
dizziness, and frequent, exhausting vomiting. Tinnitus aurium,
singultus, epileptic fits, are of rarer occurrence at an early stage.
The latter form a very important symptom ; they occur either
as typical fits or else as mere epileptic vertigo or petit mal.
While these symptoms remain, and often grow worse, a num-
ber of others make their appearance, which are calculated to turn
our attention to the bulbus as the seat of the lesion. These con-
sist of paralytic symptoms in the facialis, hypoglossus, and
abducens ; and we see derangements of speech and degtutition,
with paresis of the palate and a nasal tone of voice, frequently,
too, hoarseness and aphonia. Besides these symptoms, there
may be more or less extensive paralysis of the extremities,
either unilateral or bilateral paresis, with or without contrac-
tures. It is very characteristic when we see a hemiplegia al¢er-
nating with paralysis of the facialis, abducens, or hypoglossus.
We frequently meet with derangement of co-ordination, re-
minding us of ataxia, but usually partaking more of the char-
acter of the uncertain gait belonging to cerebellar diseases—this
is especially the case with tumors of the fourth ventricle.
Derangements of sensibility are less marked. They gener-
ally consist of pain in the nuchus, back, and extremities, par-
eesthesia in two similar regions, occasionally aneesthesia in the
trunk or extremities. On the other hand, anesthesia of one
or both sides of the face isa very important symptom. Reflex
action is often increased.
Special local importance attaches to tinnitus and deafness,
whilst amblyopia and amaurosis (founded on the stagnation —
papilla recognized with the ophthalmoscope) are almost constant
accompaniments of every kind of tumor within the cerebral
cavity.
oe —_-
———
TRAE 8 AMA Ee ae eer A Oe a ae ee
——
TUMORS. 955
Occasionally psychical derangements have been observed,
such as loss of intelligence and memory, depression, etc., but
this is rather rare.
Special importance attaches to a constant and lasting vomit-
ing, violent and lasting singultus, and frequently occurring epi-
leptoid convulsions, and attacks of transitory unconsciousness.
Glycosuria and polyuria, which have been often observed (espe-
cially in cases of tumor of the fourth ventricle), and probably
will be still oftener seen when looked for, deserve particular
notice.
_ The course of the disease is probably fatal in every case. Still
considerable variations, and remissions and cessations of growth
for long periods may occur, and thus the disease may extend
over a number of years. Usually, however, the course is an unin-
terrupted one. The headaches and paralytic symptoms grow
worse, vomiting becomes incessant, hiccuping is a source of per-
petual annoyance, the epileptic attacks occur more frequently,
consciousness grows clouded, and then come detiria, and after-
wards coma, and usually life terminates with increased respira-
tory derangement in an attack of suffocation. Death is generally
rather sudden.
Very little certainty as regards the symptoms of special local-
ization in the medulla can be derived from the few cases on
record. In general, we must-content ourselves with making a
probable diagnosis of a tumor in the medulla from the general
symptoms of a tumor in the brain, and the special symptoms of
bulbar paralysis. We can seldom estimate its size, or attempt
to localize it more accurately. Still this must always be the aim
of our diagnostic endeavors, and we possess even at present a few
** points de départ.”’
The most reliable points are, that ¢amors in the anterior por-
tion of the medulla, especially in the pyramids, produce uni- or
bilateral paralysis, with contractures and increased tendon-reflex,
sometimes also paralysis of the bladder, while sensibility remains
unimpaired ; and then, besides, we may have the different symp-
toms of bulbar paralysis.
Tumors on the floor of the fourth ventricle, on the other hand,
produce no marked paralysis, and usually no considerable de-
956 ERB.—DISEASES OF THE MEDULLA OBLONGATA.
rangement of sensibility ; but ataxia may occur, and the most -
characteristic symptoms are vomiting and singultus, with res-
piratory disorders and a slow pulse, while special importance
attaches to glycosuria and polyuria.
It is hardly possible to diagnose a tumor of the corpora resti-
Jormia. Wemust await further observation before we can found
a diagnosis on sensory derangements in the extremities, unilateral
anesthesia of the face, auditory troubles, ataxia, etc.
There are no diagnostic points whatsoever for twmors in the
olivary bodies and reticular formation, except the general symp-
toms of a cerebral tumor and the special ones of bulbar paralyses.
Diagnosis.
When the general symptoms of a tumor in the brain (violent
headache, dizziness, vomiting, stagnation papilla, loss of intelli-
gence, etc.) are accompanied by signs of local irritation and
paralysis, pointing more or less definitely to a lesion in the
medulla, and when, in addition, we have quite obstinate vomit-
ing, continuous singultus, and glycosuria or polyuria, we are
then enabled to diagnose a neoplasm growing in the medulla
with some certainty. But to insure against rashness, we should
hold in mind the great difficulty and uncertainty of all such
diagnoses.
As regards the distinction of these tumors from those situated
in other parts of the brain, we refer the reader to Obernier’s
exhaustive treatise. We shall merely call attention to the special
difficulties of distinction from cerebellar tumors, because, on the
one hand, tumors of the medulla often grow into the cerebel-
lum, and on the other hand, many cerebellar tumors produce an
irritative and compressive effect upon the medulla. In such
cases it is simply impossible to draw a distinction, or we must
acknowledge both parts as affected.
It is very easy, as a rule, to distinguish between a tumor and
other. bulbar disease, especially progressive bulbar paralysis, as
the latter exhibits more definite and typical symptoms than are
ever produced by a tumor. While the regular symptoms of a
tumor, such as violent headache, dizziness, vomiting, singultus,
aS es eee
ee altel ate aaa
TUMORS. 957
troubles of hearing, glycosuria, amblyopia, and stagnation
papilla, epileptic convulsions, etc., seldom or never occur in pro-
gressive bulbar paralysis.
It is a far more difficult task, or perhaps an impossibility, to
distinguish between tumors in the substance of the medulla and
those that compress it chronically from without. When unaided
by etiological circumstances, we must have recourse alone to
symptoms of disease in the nerve-roots (signs of irritation and
paralysis in the trigeminus, facialis, hypoglossus, vagus, etc.) in
order to form a probable diagnosis, that the tumor is compres-
sing the medulla from without, and is not growing in its sub-
stance.
Prognosis.
Like all other cerebral tumors, those of the medulla, with few
exceptions (gummata, etc.) are quite hopeless, and are, in fact,
worse than the others in so far as an extremely small-sized tumor
suffices to produce the most grave consequences in this vital
organ.
Though the growth may cease for some time, and striking
remissions are recorded, still, when once the diagnosis is certain,
we should give a very guarded prognosis. The few, though un-
doubted cases in which the fully developed symptoms of a cere-
bral tumor are recorded to have completely disappeared, cannot
be allowed much weight.
Treatment.
Treatment is in this case just as hopeless as in all other cases
of cerebral tumor, unless it be a syphilitic gumma. To avoid
repetition, we again refer the reader to Obernier’s article. The
physician must, as a rule, confine himself to a symptomatic
treatment after he has exhausted all the usual agerts supposed
to act upon neoplasmata.
END OF VOLUME XIII.
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INDEX.
ABEILLE, 284.
Abercrombie, 385, 900, 951.
Absinthe, poisoning by, in etiology of spinal paralysis,
818,
Acker, 188,
Acute Ascending Paralysis, 732.
Acute Atrophic Spinal Paralysis, 663.
Acute Bulbar Paralysis, 900.
Acute Inflammation of the Gray Anterior Columns,
663.
Acute Inflammation of the Medulla Oblongata, 900.
Acute Spinal Paralysis of Adults, 663.
Adler, 19.
Age in etiology of diseases of the spinal cord, 150; of
acute spinal meningitis, 229 ; of multiple sclerosis,
4%5 ; of myelitis, 388, 427; of myelomalacia, 469;
of paralysis ascendens acuta, 735; of poliomyeli-
tis anterior acuta, 667; of progressive bulbar pa-
ralysis, 909 ; of spasmodic spinal paralysis, 623 ; of
spinal apoplexy, 292; of spinal irritation, 360 5; of
spinal nervous weakness, 871; of tabes dorsalis,
524.
Alcoholism in etiology of chronic spinal meningitis,
253; of inflammation of the spinal dura mater,
222; of myelitis, 429; of spinal irritation, 360;
of spinal paralysis, $15,
Allbutt, Clifford, 87.
Ammonia in concussion of the spinal cord, 356; in
paralysis ascendens acuta, 747.
Amyelia, 780.
Amy], nitrite of, in anemia of the spinal cord, 290.
Anemia of the Medulla Oblongata, 876.
Anemia of the Spinal Cord, 281.
Anatomy of the Medulla Oblongata, 825.
Anatomy of the Spinal Cord, 7.
Andral, 278.
Aneurism in etiology of injuries of the medulla ob-
longata, 890,
Apoplectiform attacks in multiple sclerosis, 501.
Apoplexia Medullz Oblongate, 865.
Aretzeus, 285.
Arsenic in diseases of the spinal cord, 191; in inter-
mittent spinal paralysis, 817; in myelitis, 463; in
tabes dorsalis, 615; in tumors of the spinal mem-
branes, 276; poisoning by, in etiology of spinal
paralysis, 818.
Arteries, affections of, in etiology of anwmia of the
spinal cord, 282; of myelomalacia, 468; of spinal
apoplexy, 293.
Ataxia in diseases of the spinal cord, 83; in tabes dor-
salis, 543, 559.
Ataxie Locomotrice Progressive, 513.
Atelomyelia, 780.
Atrophic, Acute, Spinal Paralysis, 663.
Atrophic, Chronic, Spinal Paralysis, 712.
Atrophy, Primary, of the Motor Nuclei, 905.
Auerbach, 119.
Axenfeld, 87.
Basiow, 735.
Baden-Baden, baths of, in diseases of the spinal cord,
167.
Badenweiler, baths of, in diseases of the spinal cord,
167.
Badham, 665.
Baelz, 890.
Baerwinkel, 474, 512, 907.
Baierlacher, 264.
Ball, 126.
Bamberger, 101, 801, 802, 896, 897, 89S.
Barium, chloride of, in multiple sclerosis, 512; in ta-
bes dorsalis, 615.
Bartels, 266.
Barth, O., 119, 283.
Barthez, 665.
Baths in diseases of the spinal cord, 164; in acute spi-
nal meningitis, 250; in chronic spinal meningitis,
261; in concussion of spinal cord, 357; in inflam-
mation of the spinal dura mater, 225; in menin-
geal hemorrhage, 216; in multiple sclerosis, 512;
in myelitis, 422, 425, 459; in paralysis ascendens
acuta, 746; in poliomyelitis anterior acuta, 708 ;
in poliomyelitis anterior chronica, 731; in progres-
sive bulbar paralysis, 944; in slow compression of
the cord, 343; in spasmodic spinal paralysis, 645 ;
in spinal apoplexy, 305; in spinal nervous weak-
ness, 381; in tabes dorsalis, 610; in tumors of the
spinal membranes, 276.
*
960
Baumgarten, 390, 397, 733, 736, 745.
Bayer, O., 765,
Bazire, 651.
Beard, 184, 865, 369.
Bed-sores in chronic spinal meningitis, 257; in hemi-
plegia et hemiparaplegia spinalis, 653; in inflam-
mation of the spinal dura mater, 224; in multiple
sclerosis, 483, 487; in myelitis, 403, 433, 440; in
myelomalacia, 471; in slow compression of the
cord, 830; in spinal apoplexy, 299; in tabes dor-
salis, 586; in tumors of the spinal membranes,
272; in wounds of the spinal cord, 312, in etiol-
ogy of pachymeningitis spinalis externa, 217;
treatment of, in diseases of the spinal cord, 195.
Behm, 733.
Behrend, 793.
Bell, 269.
Bell, Charles, 647, 812.
Belladonna in diseases of the spinal cord, 190; in
acute spinal meningitis, 250; in hyperemia of the
spinal meninges, 268; in myelitis, 423, 463; in
poliomyelitis anterior acuta, 707; progressive
bulbar paralysis, 945; in tabes dorsalis, 615; in
wounds of the spinal cord, 318.
Benedict, 519, 567, 611, 812.
Benedikt, 94, 912, 913, 980, 9385, 943, 944.
Beneke, 175.
Benjamin, 265.
Berger, O., 50, 119, S70, 623, 625, 630, 639, 641,
Berlin, 474, 489, 512.
Bernard, Claude, 862.
Bernhardt, 650, 666, 718, 715, 719, 721, 733, 736, 739.
Bervliet, 284.
Bétous, 623, 625.
von Bezold, 42, 59,
Bierbaum, 230, 665.
Billroth, 128,
Bladder, affections of, in diseases of the spinal cord,
122, 131 ; in acute bulbar myelitis, 903; in chronic
spinal meningitis, 257; in concussion of the spi-
nal cord, 349; in inflammation of the spinal dura
mater, 224; in hemiplegia et hemiparaplegia spi-
nalis, 653; in meningeal hemorrhage, 213; in
multiple sclerosis, 483, 486, 503; in myelitis, 403,
409, 433, 489; in myelomalacia, 471; in paralysis
ascendens acuta, 740; in poliomyelitis anterior
acuta, 682, 699, 700; in slow compression of the
cord, 329, 334; in spinal apoplexy, 297; in spinal
nervous weakness, 874; in tabes dorsalis, 540,
548, 584; in tumors of the medulla oblongata,
955; in tumors of the spinal membranes, 272;
in wounds of the spinal cord, 311, 312; in etiology
of diseases of the spinal cord, 154; innervation
for evacuation of, 54.
Blisters in acute spinal meningitis, 249; in chronic
spinal meningitis, 261; in concussion of the spi-
INDEX.
nal cord, 356; in myelitis, 424, 459; in paralysis
ascendens acuta, 746; in progressive bulbar pa-
ralysis, 943; in slow compression of the spinal
cord, 343; in spinal irritation, 368.
Blood, affections of, in etiology of anzemia of the spi-
nal cord, 284.
Blood-letting in diseases of the spinal cord, 185; in
acute spinal meningitis, 249; in chronic spinal
meningitis, 260; in concussion of the spinal cord,
856 ; in hemorrhage in the medulla oblongata, 876;
in hyperemia of the spinal meninges, 207; in
meningeal hemorrhage, 216; in myelitis, 428; in
paralysis ascendens acuta, 746; in poliomyelitis
anterior acuta, 707; in poliomyelitis anterior
chronica, 731; in progressive bulbar paralysis,
943 ; in spinal apoplexy, 304; in spinal irritation,
868 ; in wounds of the spinal cord, 318.
Blood-vessels, changes in, in multiple sclerosis, 482;
in myelitis, 398, 434; in etiology of hyperemia of
the medulla oblongata, 866; of injuries of the
medulla oblongata, 890,
Blum, 588.
Boening, 519,
Boll, 19, 21, 22, 25, 26, 30.
Bones, affections of, in diseases of the spinal cord, 125;
in multiple sclerosis, 483 ; in poliomyelitis anterior
acuta, 680, 693 ; in tabes dorsalis, 558; in etiology
of injuries of the medulla oblongata, 889,
Bonetus, 517.
Bonnefoy, 907.
Bouchard, 265, 538, 589, 625, 758, 761, 765, 766, 773,
774, 776, T78, 894.
Boucherean, 222."
Bouchut, 284,
Bouillaud, 518.
Bourdon, 519, 569, 891, 894.
Bourneville, 298, 473, 477.
Brain, affections of, in diseases of the spinal cord,
144; in multiple sclerosis, 479; in myelitis, 447;
in poliomyelitis anterior acuta, 680; in etiology of
secondary degeneration of the spinal cord, 760.
Braun, 252, 261.
Breschet, 301.
Brodie, 128, 130, 314.
Brown, 358.
Brown-Séquard, 35, 36. 53, 61, 65, 69, 70, 74, 75, 82, _
86, 89, 95, 100, 101, 102, 109, 154, 189, 190, 195,
197, 204, 215, 261, 271, 283, 287, 290, 316, 823,
386, 423, 425, 459, 463, 465, 471, 494, 647, 649,
650, 651, 655, 658, 661,
Bruberger, 253.
Briickenau, baths of, in diseases of the spinal cord,
170, 171.
von Brunn, 793.
v, Bruns, 922.
;
i Buchwald, 474, 481, 504,
re Aaa
See ae
a
eR a ee wn eh Oe
INDEX. 961
Budge, 55, 58, 125,
Bulbar Paralysis, Acute, 900.
Burckhardt, 72, 104, 107, 116, 117.
Burresi, 650,
Busch, 186.
Buzzard, 126.
CALABAR bean in diseases of the spinal cord, 189,
Camphor in concussion of the spinal cord, 356; in
paralysis ascendens acuta, 747; poisoning by, in
etiology of spinal paralysis, 818.
Carbon, sulphide of, poisoning by, in etiology of spinal
paralysis, $18.
Carbonic oxide, poisoning by, in etiology of spinal pa-
ralysis, $18.
Carcinoma of the Spinal Cord, 751.
Carcinoma of the Spinal Membranes, 265.
Cardiac movements, centres for, in the medulla oblon-
gata, 858.
Caries of vertebre in etiology of meningeal hemor-
rhage, 209.
Carpani, 952.
Carré, Mar., 519, 524, 539, 567.
Caster, 615.
Cathartics in acute spinal meningitis, 249; in chronic
spinal meningitis, 260; in hyperemia of the spi-
nal meninges, 208; in myelitis, 423; in poliomy-
elitis anterior acuta, 707; in spinal apoplexy, 305.
Cautery, actual, in myelitis, 424; in slow compression
of the cord, 343,
Cayley, 265.
Chapman, 162. :
Charcot, 45, 76, 96, 99, 100, 101, 102, 109, 115, 116,
118, 119, 121, 123, 124, 126, 127, 180, 138, 141, 221,
222, 223, 225, 265, 286, 292, 296, 301, 322, 323, 327,
828, 333, 337, #41, 343, 386, 897, 405, 435, 436, 437,
441, 473, 475, 476, 482, 484, 491, 493, 494, 496, 499,
500, 501, 502, 505, 508, 512, 519, 583, 537, 538, 549,
550, 580, 585, 587, 588, 589, 601, 602, 614, 621, 622,
623, 624, 625, 687, 640, 641, 649, 653, 666, 673, 677,
750, 751, 758, '761, 772, 773, 777, 798, 879, 907, 911,
918, 914, 928, 985, 936, 937.
Chaussier, 786.
Childbed in etiology of tumors of the spinal mem-
branes, 268.
Chill in acute spinal meningitis, 235; in myelitis,
402; in spinal apoplexy, 299; in tumors of the
spinal membranes, 272.
Chloral hydrate in acute spinal meningitis, 250.
Chloroform in acute spinal meningitis, 250 ; in myeli-
tis, 465.
Cholera in etiology of multiple sclerosis, 476.
Chouppe, 804,
Chronic and Subacute Inflammation of the Gray An-
terior Columns, 712,
Chronic Atrophic Spinal Paralysis, 712.
Chronic Traumatic Lesion of the Cord, 819.
Chvostek, 474, 475, 539, 750, 751.
Circulation, disturbances of, in diseases of the spinal
cord, 140 ; in acute bulbar myelitis, 903; in acute
spinal meningitis, 236 ; in anzemia of the medulla
oblongata, 880; in hemorrhagein the medulla
oblongata, 871; in myelitis, 412, 447; in progres-
sive bulbar paralysis, 917, 925; in tabes dorsalis,
589; in etiology of diseases of the spinal cord,
152; of hypereemia and hemorrhage in the me-
dulla oblongata, 866; of myelitis, 428.
Clarke, Lockhart, 30, 116, 119, 386, 519, 535, 666, 673,
841, 913, 924.
Clemens, 194, 346, 353,
Climate in diseases of the spinal cord, 175; in myeli-
tis, 426, 464; in spinal nervous weakness, 381.
Cod-liver oil in concussion of the spinal cord, 357; in
myelitis, 425; in poliomyelitis anterior acuta, 710;
in slow compression of the cord, 342; in spinal ir-
ritation, 367; in tabes dorsalis, 616,
Coffee in paralysis ascendens acuta, 747.
Cohnheim, 119.
Cold, application ‘of, in diseases of the spinal cord,
162; in acute spinal meningitis, 249; in hypera-
mia of the spinal meninges, 208; in meningeal
hemorrhage, 216; in myelitis, 423; in paralysis
ascendens acuta, 746; in spinal apoplexy, 304; im
spinal irritation, 865; in wounds of the spinal
cord, 818; exposure to, in etiology of diseases of
the spinal cord, 151; of acute spinal meningitis,
229; of chronic spinal meningitis, 252; of hyper-
semia of the spinal meninges, 201; of inflamma-
tion of the spinal dura mater, 222; of multiple
sclerosis, 476; of myelitis, 889, 427; of paralysis
ascendens acuta, 7385; of poliomyelitis anterior
acuta, 669, 708 ; in poliomyelitis anterior chronica,
714; of progressive bulbar paralysis, 909; of spas-
modic spinal paralysis, 625; of spinal irritation,
260; of tabes dorsalis, 525; of tumors of the
spinal membranes, 268.
Colognese, 793.
Commotio Medulle Spinalis, 344.
Compression in etiology of myelitis, 389, 428; of mye-
lomalacia, 469.
Concussion of the Spinal Cord, 344.
Concussion of spinal cord in etiology of myelitis, 428,
Conium in diseases of the spinal cord, 189.
Connective tissue, changes in, in myelitis, 398, 433.
Convulsions in acute spinal meningitis, 242 ; in hemor-
rhage in the medulla oblongata, 872; in myelitis,
412; in poliomyelitis anterior acuta, 681, 686; in
tumors of the medulla oblongata, 954.
Cooper, A., 210.
Copaiba, poisoning by, in etiology of spinal paralysis,
818
Cord, Spinal, Anatomy of, 7.
962
Cornil, 665, 673, 718, 716, 733, '786, 758, 764, 949.
Cough in diseases of the spinal cord, 142; in spinal
irritation, 362.
Courjon, 333, 341,
Crussel, 196,
Cruveilhier, 70, 75, 266, 267, 268, 270, 295, 473, 517,
758,
Cudowa, waters of, in diseases of the spinal cord, 169 ;
in concussion of the spinal cord, 357.
Cumings, 286.
Cupping in myelitis, 459 ; in progressive bulbar paral-
ysis, 943; in tabes dorsalis, 609.
Curare in diseases of the spinal cord, 189.
Cuvier, 733, 743.
Cyon, 59, 85, 86, 87, 89, 524, 529, 567, 572, 580, 593,
Cysticercus cellulosz in the spinal membranes, 266.
Cystitis, treatment of, in diseases of the spinal cord,
193.
Czerwinsky, 612.
DAMASCHINO, 116, 666, 671, 673, 677.
Davaine, 266.
Déchery, 930, 936.
Defecation, disturbances of, in diseases of the spinal
cord, 138.
Deformities of the Spinal Cord, 779.
Degeneration, Gray, of the Posterior Columns, 5138.
Deglutition, centre for, in the medulla oblongata, 860 ;
disturbances of, in diseases of the spinal cord, 142;
in acute bulbar myelitis, 903; in anemia of the
medulla oblongata, 850; in hemorrhage in the
medulla oblongata, 872; in myelitis, 412; in pa-
ralysis ascendens acuta, 742; in progressive bulbar
paralysis, 921; in slow compression of the cord,
837; in tabes dorsalis, 589.
Deiters, 30.
Déjerine, 666, 674, 678, 734, 736, 737, '741.
Delamarre, 138, 550, 589.
Dentition in etiology of acute spinal meningitis, 231 ;
of poliomyelitis anterior acuta, 669.
Derivatives in diseases of the spinal cord, 185; in
acute spinal meningitis, 249; in chronic spinal
meningitis, 260; in hyperemia of the spinal
meninges, 207; in myelitis, 422, 458: in poliomye-
litis anterior acuta, 707; in poliomyelitis anterior
chronica, 731; in progressive bulbar paralysis,
943; in slow compression of the cord, 343; in
spinal irritation, 368; in tabes dorsalis, 609; in
tumors of the spinal membranes, 276; in wounds
of the spinal cord, 318,
Desnos, 872.
Diagnosis. See Different Diseases.
Diaphoretics in myelitis, 422.
Diet in diseases of the spinal cord, 192; in chronic
spinal meningitis, 262; in myelitis, 425, 457, 464;
in poliomyelitis anterior acuta, 709 ; in progres-
INDEX.
sive bulbar paralysis, 944; in slow compression of
the cord, 342; in spinal irritation, 367; in spinal
nervous weakness, 380; in tabes dorsalis, 616.
Digestion, disturbances of, in diseases of the spinal
cord, 188; in myelitis, 412; in spinal nervous
weakness, 874.
Digestive tract, innervation of, 53.
Digitalis in spinal apoplexy, 305.
Diphtheria in etiology of paralysis ascendens acuta,
735 ; of tabes dorsalis, 52S,
Diplomyelia, 781,
Dittmar, 36, 179, 861. .
Diuretics in chronic spinal meningitis, 261; in mye-
litis, 428.
Driburg, baths of, in diseases of the spinal cord, 170,
171.
Dubezanski, 128.
DuBois, 50, 109, 138,
DuCastel, 601,
Duchenne, 83, 105, 116, 386, 475, 518, 519, 570, 665,
666, 667. 668, 688, 691, 697, 702, 710, 718, 719, 724,
864, 906, 920, 930, 934, 935, 936, 943.
Duchenne, jun., 669, 695.
Dujardin-Beaumetz, 36, 389, 399, 401, 416, 519, 615,
677.
Duménil, 103, 519, 906.
Duret, $50, 877, 881, 884,
Dusourd, 284,
Dutrait, 872.
EAR symptoms in diseases of the spinal cord, 142; in
anzemia of the medulla oblongata, 880; in hemor-
rhage in the medulla oblongata, 872; in multiple
sclerosis, 500; in progressive bulbar paralysis,
929; in tabes dorsalis, 581; in tumors of the me-
dulla oblongata, 954,
Ebstein, 474, 476, 493, 494, 502, 504, 569.
Echinococcus in the Spinal Membranes, 266.
Eck, 615.
Eckhard, 56, 58, 59, 130, 137.
Ehrling, 323.
Eichhorst, 46, 65, 296, 745, 798, 880.
Hilsen, baths of, in diseases of the spinal cord, 171.
Eisenlohr, 740.
Eisenmann, 519, 570,
Eisenschitz, 750, i]
Electricity in diseases of the spinal cord, 178; in anze-
mia of the spinal cord, 290; in chronic spinal
meningitis, 261; in concussion of the spinal cord,
356; in hemorrhage in the medulla oblongata,
876; in hyperemia of the spinal meninges, 208 ;
in inflammation of the spinal dura mater, 225;
in meningeal hemorrhage, 216; in multiple scle-
rosis, 512; in myelitis, 424, 459, 462 ; in paralysis
ascendens acuta, 746; in paraplegia dependent on
idea, 822; in poliomyelitis anterior acuta, 708;
—_—-
STE SS a ae
ee
in poliomyelitis anterior chtonica, 731; in pro-
gressive bulbar paralysis, 944;.in secondary de-
generations of the spinal cord, 778; in slow com-
pression of the cord, 343; in spasmodic spinal
paralysis, 645; in spinal apoplexy, 305; in spinal
irritation, 368; in spinal nervous weakness, 381 ;
in tabes dorsalis, 613.
Ellis, 794.
Elster, baths of, in diseases of the spinal cord, 171,
Emaciation in hemiplegia et hemiparaplegia spinalis,
653.
Emboli and Thrombi in Arteries of the Medulla Ob-
longata, 876.
Embolism in etiology of myelomalacia, 468,
Ems, waters of, in myelitis, 423.
Enchondroma of the Spinal Membranes, 265.
Engelken, 36, 38, 179, 386, 410.
Engesser, 474, 489, 493, 495, 502, 503, 504, 569.
Epileptic seizures in diseases of the spinal cord, 101 ;
in slow compression of the cord, 337.
Erdmann, 551, 610, 930.
Erection of penis and ejaculation, innervation for, 56.
Ergot in diseases of the spinal cord, 189; in concus-
sion of the spinal cord, 356; in hyperzemia of the
spinal meninges, 208; in meningeal hemorrhage,
216; in myelitis, 423, 463; in poliomyelitis ante-
rior acuta, 707; in poliomyelitis anterior chronica,
731; in progressive bulbar paralysis, 945 ; in spi-
nal apoplexy, 305; in tabes dorsalis, 615; in
wounds of the spinal cord, 318; poisoning by, in
etiology of spinal paralysis, 818.
Erichsen, 348, 352, 355, 356, 357, 951.
Erlenmeyer, 619,
Escher, 869.
Esquirol, 266, 278.
Ether in concussion of the spinal cord, 356.
Etiology. See Different Diseases,
Eulenburg, 119, 614.
Ewald, 768.
Exanthemata, acute, in etiology of diseases of the spi-
nal cord, 153; of myelitis, 390; disappearance of,
in etiology of acute spinal meningitis, 231.
Exercise, physical, in myelitis, 426, 457. 464; in para-
plegia dependent.upon idea, 822; in poliomyelitis
anterior acuta, 711; in spinal irritation, 367; in
spinal nervous weakness, 380; excessive, in etiol-
ogy of diseases of the spinal cord, 152; of chronic
spinal meningitis, 253; of meningeal hemorrhage,
209; of multiple sclerosis, 476; of myelitis, 389,
427; of spinal nervous weakness, 371; of tabes
dorsalis, 525.
Expression of face, affections of, in progressive bulbar
paralysis, 923.
Eye symptoms in diseases of the spinal cord, 141, in
acute bulbar myelitis, 903; in acute spinal menin-
gitis, 242; in multiple sclerosis, 487, 498; in my-
INDEX. 963
elitis, 412; in paralysis ascendens acuta, 741; in
progressive bulbar paralysis, 929; in slow com-
pression of the cord, 337 ; in spinal irritation, 363 ;
in tabes dorsalis, 541, 563, 576; in tumors of the
medulla oblongata, 954.
Fasrictovs, 617.
Febrile diseases in etiology of hyperemia of the spi-
nal meninges, 201,
Fehst, 8.
Feinberg, 154, 155, 891, 399.
Féréol, 589,
Fever in diseases of the spinal cord, 127; in acute
spinal meningitis, 235, 242; in meningeal hemor-
rhage, 213; in myelitis, 402; in paralysis ascen-
dens acuta, 741; in poliomyelitis anterior acuta,
681, 685, 700 ; in spinal apoplexy, 297; in tumors
of the spinal membranes, 272; in wounds of the
spinal cord, 312, 314.
Fibroma of the Medulla Oblongata, 952.
Fibroma of the Spinal Membranes, 264.
Fibrosarcoma of the Spinal Cord, 750.
Fibrosarcoma of the Spinal Membranes, 264.
Fick, 36, 38, 179.
Finkelnburg, 87, 519, 543.
Fischer, 128, 129.
Fischer, H., 347,
Flechsig, 626, 637, 654, 759, 760, 761, 762, 766, 772, 783,
833, 824, 846, 847, 848, 849, 853, 854.
Flies, 183.
Flourens, 65, 857.
Fluxion, collateral, in etiology of hyperemia of the
spinal meninges, 201.
Foerster, 266, 499, 581, 750.
Fournié, 60.
Fournier, 528,
Frank, P., 385,
Franzenbad, waters of, in diseases of the spinal cord,
170; in myelitis, 461.
Frerichs, 286, 473, 475, 609, 617.
Freusberg, 47, 45, 50, 51, 52, 65, 104, 316, 759.
Frey, 101, 656, 700, 702, 713, 801, 803, 805, 806, 807.
Frictions, external, in diseases of the spinal cord, 186.
Friedreich, 86, 88, 119, 130, 147, 386, 499. 510, 517,
519, 523, 537, 539, 556, 560, 562, 563, 564, 565, 567,
569, 570, 578, 584, 589, 590, 591, 593, 614, 752, 798,
936, 937.
Frommann, 21, 30, 386, 897, 433, 519,
Fronmueller, 227, 308,
Froriep, 518.
Fuerbringer, P., 50, 194,
Functional Irritation of the Spinal Cord, 357.
Functional Nervous Weakness of the Spinal Cord, 369,
Functional reparation of lesions of the spinal cord, 64,
Functignal stimulation in etiology of hyperemia of
the spinal meninges, 200.
964
Garr in diseases of the spinal cord, 96; in tabes dor-
salis, 543,
Galen, 385, 517.
Gangrene in diseases of the spinal cord, 121.
Gastein, baths of, in diseases of the spinal cord, 167,
Gauné, 201, 231.
Gendrin, 649, 753.
Genga, 788.
Gerhardt, 866, 910.
Gerlach, 16, 20, 21, 22, 25, 26, 29, 30, 31.
Gierke, 857.
Gintrac, 647, 649.
Glioma of the Medulla Oblongata, 951.
Glioma of the Spinal Cord, 749.
Glio-sarcoma of the Medulla Oblongata, 951.
Glio-sarcoma of the Spinal Cord, 750.
Goetz, 734, 736, 737, 741.
Gold, sodio-chloride of, in diseases of the spinal cord,
191; in myelitis, 426; in progressive bulbar pa-
ralysis, 945; in tabes dorsalis, 615.
Goll, 25, 30.
Goltdammer, 292, 296, 713.
Goltz, 41, 42, 43, 47, 52, 54, 56, 58, 65, 70, 92, 112, 129,
133, 187, 313, 316, 568, 654, 759, 861.
Gombault, 116, 641, 649, 666, 674, 751, 907.
Gosselin, 194.
von Graefe, 576, 614.
Grancher, 399.
Grasset, 930, 925.
Gray Degeneration of the Posterior Columns, 513,
Gray Degeneration of the Spinal Cord, 426.
Griesinger, 294, 614,
Grimm, John, 751, 797.
Grisolle, 284,
Gruetzner, 863, 925.
Guérard, 475, 476.
Gull, W., 154, 188, 285, 286, 340, 386, 750.
Gummata of the Spinal Cord, 751.
Gurlt, 307, 318,
Guttmann, 101, 801, 802, 803, 805, S06, S07.
HaBersHon, 750, 751.
Hematomyelia, 291.
Hematomyelitis, 291.
Hematorrhachis, 208.
Heemorrhagia Medulle Spinalis, 291.
Haidenhain, G., 59.
Hair, changes in, in diseases of the spinal cord, 119.
Hall, Marshall, 105.
Hallopean, 886, 431, 436, 452, 666, 796, 798, 877, 884,
8S5, 890, 894, 899, 911, 930, 985,
Hamilton, 400, 469.
Hammond, 148, 196, 201, 203, 204, 208, 250, 288, 290,
361, 365, 366, 367, 368, 381, 470, 471, 494, 512, 585,
66S, 697, 710, 724, 935.
Hanot, 116.
INDEX.
Harless, 59, 385, 567.
Hartwig, 815, S17.
Hasse, 209.
Hawkins, 334.
Hayem, 116, 200, 210, 292, 800, 886, 390, 892, 397, 398,
899, 401, 402, 416, 733, 736, 75C.
Headache in diseases of the spinal cord, 75; in acute
spinal meningitis, 236; in multiple sclerosis, 484;
in tabes dorsalis, 543.
Heart, affections of, in myelitis, 412; in spinal irrita-
tion, 362.
Heart, innervation of, 52.
Heidenhain, R., 128.
von Heine, 386, 664, 668, 669, 688, 694, 710.
Heister, 793.
Helmholtz, 47, 181.
Hemiplegia et Hemiparaplegia Spinalis, 646,
Hemorrhage in the Medulla Oblongata, 865.
Hemorrhage in the Membranes of the Spinai Cord,
208.
Hemorrhage in the Substance of the Spinal Cord,
291.
Hemorrhage in etiology of hemiplegia et hemipara-
plegia spinalis, 649,
Hemorrhoidal bleeding, suppression of, in etiology of
acute spinal meningitis, 231; of chronic spinal
meningitis, 253; of myelitis, 390.
Hemorrhoids in etiology of tabes dorsalis, 528.
Hempel, 577.
Henle, 10, 21, 22, 30, 829, 841.
Hennig, 470.
Hérard, 877.
Heredity in etiology of concussion of the spinal cord,
860; of multiple sclerosis, 475; of myelitis, 427 ;
of tabes dorsalis, 523; of tonic spasms, S11.
Hermann, 869.
Hertz, 890, 892.
Hertzberg, 71, 553.
Heschl, 866.
Hine, 153.
Hippocrates, 385, 517.
Hirsch, 184, £65, 474.
His, 19.
History. See Different Diseases.
Hitzig, 262, 424, 709, 909.
Hoffmann, 750.
Horn, E., 518.
Horn, W., 518.
Hubrich, 891, 892.
Hueter, 695.
Huguenin, 38, 836, 833, 838, 841.
Huss, Magnus, 222, 253.
Hutin, 517, 750.
Hydrocephalus in tumors of the medulla oblongata,
952, ;
Hydromyelus, 783.
_
—S =~ —
INDEX. 965
Hydrorrhachis Interna, 783.
Hyoscyamus in myelitis, 465.
Hypereemia and Hemorrhage of the Medulla Oblon-
gata, 865.
Hyperzemia of the Spinal Cord, 280,
Hypereesthesia in diseases of the spinal cord, 73.
Hysteria in etiology of multiple sclerosis, 476.
INFLAMMATION, Acute, of the Gray Anterior Columns,
663.
Inflammation, Acute, of the Medulla Oblongata, 900.
Inflammation of the Spinal Cord, 382.
Inflammation, Subacate and Chronic, of the Gray An-
terior Horns, 712.
Inflammation in etiology of acute spinal meningitis,
230; of chronic spinal meningitis, 252 ; of menin-
geal hemorrhage, 209; of myelitis, 389, 429.
Influenza in etiology of diseases of the spinal cord,
153.
Injuries of the Medulla Oblongata, 887.
Injury in etiology of diseases of the spinal cord, 151;
of acute spinal meningitis, 230; of chronic spina:
meningitis, 252; of concussion of the spinal cord,
$45; of hemiplegia et hemiparaplegia spinalis, 648 ;
of hypersemia of the spinal meninges, 201; of me-
ningeal hemorrhage, 209; of multiple sclerosis,
476; of myelitis, 388; of poliomyelitis anterior
chronica, 714; of spasmodic spinal paralysis, 625 ;
of spinal apoplexy, 293; of spinal irritation, 360 ;
of tabes dorsalis, 529; of tumors of the spinal
cord, 752; of tumors of the spinal membranes,
268.
Insolation in etiology of acute spinal meningitis, 229.
Intermittent fever in etiology of diseases of the spinal
cord, 153. -
Intermittent Spinal Paralysis, 814.
Intestinal disorders in etiology of diseases of the spinal
cord, 154.
Intramedullary Tumors of the Spinal Cord, 747.
Iodine in inflammation of the spinal dura mater, 225;
in meningeal hemorrhage, 216; in slow compres-
sion of the cord, 342.
Tris, innervation of, 58.
Iron, preparations of, in concussion of the spinal cord,
857; in myelitis, 425; in myelomalacia, 471 ; in
poliomyelitis anterior acuta, 710; in progressive
bulbar paralysis, 945; in slow compression of the
cord, 342; in spinal irritation, 367; in spinal ner-
vous weakness, 381.
Isnard, 191,
JACcouD, 86, 154, 254, 284, 386, 519, 528, 567, 860.
Jackson, 212.
Jackson, Hughlings, 875,
Jacoby, 518.
_ Jakubowitch, 21,
Jean, 590.
Jelly, 119.
Joffroy, 50, 110, 116, 126, 222, 325, 386, 397, 299, 436,
474, 498, 588, 641, 649, 651, 653, 666, 671, 673, 677,
697, 724, T98, $33, 907, 911, 936, 942.
Johnson, Athol, 265.
Joints, affections of, in diseases of the spinal cord,
125; in hemiplegia et hemiparaplegia spinalis,
653; in myelitis, 483; in poliomyelitis anterior
acuta, 680, 693; in slow compression of the cord,
826; of tabes dorsalis, 540, 548, 587; in etiology
of diseases of the spinal cord, 154; of injuries of
the medulla oblongata, 890.
Jolly, 474, 482, 493, 495, 498, 504, 942.
Juergensen, 709.
KAvERT, 617.
Kayser, 909, 925, 935, 946.
Keen, 430.
Kellogg, 594.
Kelp, 474, 481, 495, 501, 504.
Kennedy, 665, 701.
Kidneys, affections of, in diseases of the spinal cord,
129 ; in multiple sclerosis, 483; in myelitis, 403,
446; in tabes dorsalis, 540, 589; in etiology of
diseases of the spinal cord, 154,
Kiesselbach, 500.
Killian, 505.
Kissingen, baths of, in diseases of the spinal cord,
168,
Klebs, 749, 750.
Klemm, 155, 399.
Klohss, 385.
Klose, 713, 714.
Knapp, 142, 577.
Kniebisbider, baths of, in diseases of the spinal
cord, 170,
Koebner, 648, 651.
Koehler, 230, 231, 241, 246, 253.
Koelliker, 21, 30.
Koenig, 246.
Kohts, 153, 268.
van der Kolk, Schroeder, 860.
Koster, 292.
von Krafft-Ebing, 610, 613.
Krause, 14, 844, 846.
Krishaber, 915, 918, 932.
Kuehne, 768.
Kussmaul, 283, 417, 431, 708, 733, 735, 859, 886. 890,
908, 919, 931, 935, 943.
LADAME, 950,
Laénnec, 210.
Lallemand, 517,
Lancereaux, 300.
Land@k, baths of, in diseases of the spinal cord, 167,
966
Landois, 869.
Landry, 87, 284, 285, 732, 733, 735, 736, 742.
Lange, C., 21, 22, 587, 602, 668, 764, 766, 767, 770, 772,
773, 900.
Langhans, 429, 798.
Lanzoni, 649, 650, 651, 891.
Lathyrus sativus, poisoning by, in etiology of spinal
paralysis, 818.
Laveran, 429.
Lead-poisoning, in etiology of myelitis, 429; of polio-
myelitis anterior chronica, 715; of spasmodic spi-
nal paralysis, 625; in spinal paralysis, 518,
Leber, 142, 577, 580.
Lebert, 266.
Legallois, 857,
Lente, 317.
Leo, 473.
Leonhardt, 524, 525.
Lépine, 713, 716, 949.
Lesch, 615,
Leube, 474, 493, 495, 497, 498, 501, 502, 510.
Leudet, 201, 341.
Leuk, baths of, in diseases of the spinal cord, 167.
Leukomyelitis Posterior Chronica, 513.
Levier, 293, 298,
Levy, 386, 733, 746.
Lewin, 424.
Lewisson, 52, 154, 155.
Leyden, 67, 70, 87, 88, 89, 102, 104, 147, 153. 154, 216,
218, 222, 230, 239, 241, 264, 270, 271, 283, 285, 286,
846, 856, 370, 386, 390, 400, 435, 468, 473, 519, 525,
587, 554, 555, 556, 567, 568, 569, 581, 610, 611, 615,
666, 671, 672, 674, 737, 758, 764, 796, 799, 811, 872,
890, 900, 901, 907, 911, 913, 9380, 935.
Lichtheim, 877, 883, 884, 886.
Liebwerda, baths of, in diseases of the spinal cord,
171.
Lightning stroke in etiology of concussion of the spi-
nal cord, 346.
Liouville, 227, 280, 293, 294, 296, 399, 474, 750, 952.
Lipoma of the Spinal Membranes, 265.
Lorinser, 791, 792.
Lovén, 56.
Lucae, 581.
Ludwig, 856, 861.
Lungs, affections of, in multiple sclerosis, 483; in
etiology of tabes dorsalis, 528.
Luys, 519.
Macario, 814.
Mader, 872.
Magnan, 222, 474,
Maier, R., 907, 911, 913.
Malarial infection in etiology of intermittent spinal
paralysis, 816,
Malformations of the Spinal Cord, 779.
INDEX.
Mannkopf, 217, 227, 386.
Marienbad, baths of, in diseases of the spinal cord,
170.
Markusy, 887.
Martin, 590.
Marusky. 883.
Masius, 65.
Massot, 300, }
Mastication, disturbances of, in progressive bulbar
paralysis, 916, 921.
Masturbation in etiology of spinal nervous weakness,
871; of tabes dorsalis, 525.
Matteucci, 179.
Mayer, A., 78.
McDonnel, 108, 314, 315, 316, 317.
Medulla Oblongata, Diseases of, 8%,
ANATOMICAL INTRODUCTION, 825; bibliography,
825.
PHYSIOLOGICAL INTRODUCTION, 851; bibliography,
851; motor conduction, 853 ; sensory conduction,
854; the respiratory centres, 857; centres for the
cardiac movements, 858 ; centres of speech, 859;
centre of deglutition, 860 ; vaso-motor centre, 861 ;
nutritive centres for certain nervous regions, 862;
centres for certain secretions, S62,
PATHOLOGIVAL INTRODUCTION, 863.
HYPERZMIA AND HEMORRHAGE, 865; bibliography,
865; etiology and pathogenesis, 865; pathological
anatomy, 867; symptomatology, 865; diagnosis,
874; prognosis, 875; treatment, 875.
Anz=MiA, 876; bibliography, 876; pathogenesis and
etiology, 877; pathological anatomy, 878; symp-
tomatology, 880; diagnosis, 884; prognosis, 886;
treatment, 887,
INJURIES AND Wounps, 887; bibliography, 887;
pathogenesis and etiology, 888 ; pathological anat-
omy, 891; symptomatology, 893; dixgnosis, 897;
prognosis, 899; treatment, 900.
AcuTEe BuULBAR MYELITIS, 900; bibliography, 900;
etiology, 901; pathological anatomy, 901; symp-
tomatology, 902; diagnosis, 904; prognosis, 904;
treatment, 904.
PROGRESSIVE BULBAR PARALYsI8, 905; bibliogra-
phy, 905; history, 906; pathogenesis and etiology,
908; pathological anatomy, 910; symptomatol-
ogy, 915; course, duration, termination, 933 ; com-
plications, 933; theory of the disease, 938; diag-
nosis, 929; prognosis, 942: treatment, 943.
Oruer Coronic Diseases, 947; bibliography, 947 ;
bibliography, 947; Sclerotic Centres, 947 ; Diffuse
Sclerosis, 949,
TuMoRS OF THE MEDULLA, 950; bibliography, 950 ;
pathological anatomy, 950; etiology, 953; symp-
tomatology, 953; diagnosis, 956; prognosis, 957;
treatment, 957.
Medulla Oblongata, anatomy of, $25. -
ee
————
INDEX. | 967
Medulla Oblongata, changes in, in acute bulbar paral-
ysis, 901; following injuries, 891; in hyperemia
and hemorrhage, 867; in progressive bulbar par-
alysis, 910.
Medulla Oblongata, physiology of, 851.
Meinberg, baths of, in diseases of the spinal cord, 171.
Melanoma of the Spinal Membranes, 265.
Membranes of cord, changes in, in multiple sclerosis,
483 ; in myelitis, 432; in tabes dorsalis, 531.
Mendel, 180, 613,
Meningeal Apoplexy, 208.
Meningeal Hemorrhage, 209.
Meningitis, cerebro-spinal, in etiology of diseases of
the spinal cord, 153.
Menses, suppression of, in etiology of acute spinal
meningitis, 231; of myelitis, 390; of chronic spi-
nal meningitis, 253; of paralysis ascendens acuta,
735.
‘Mental causes of concussion of the spinal cord, 346;
meningeal hemorrhage, 209; of multiple sclero-
sis, 476; of myelitis, 390, 427; of progressive bul-
bar paralysis, 909; of spinal irritation, 360; of
spinal nervous weakness, 371; of tabes dorsalis,
§25; of tumors of the spinal membranes, 268,
Mercury in diseases of the spinal cord, 190; in acute
spinal meningitis, 249; in concussion of the spi-
nal cord, 357; in meningeal hemorrhage, 216; in
myelitis, 423; in tumors of the spinal membranes,
276; in wounds of the spinal cord, 318; poisoning
by, in etiology of spinal paralysis, 818.
Mette, 617.
Meyer, A., 222.
Meyer, M., 184, 550, 614, 666, 668, 930.
Meynert, 838, 847, 848, 909.
Michaud, 219, 322, 323, 325, 326, 327, 333, 386.
Miescher, 36, 655,
Mitchell, Weir, 126.
Molliére, 476.
Monod, 301, 517, 647, 649.
Moos, 581.
Morbid processes, neighboring, propagation of, in eti-
ology of diseases of the spinal cord, 151.
Mordret, 285,
Morelli, 891.
Morton, 793.
Mosengeil, 804.
Motion, disturbances of, in diseases of the spinal cord,
79; in acute bulbar myelitis, 903; in acute spinal
meningitis, 235, 238; in anemia of the medulla
oblongata, 880; in anzmia of the spinal cord,
286; in chronic spinal meningitis, 256; in con-
cussion of the spinal cord, 349; in hemiplegia et
hemiparaplegia spinalis, 650; in hemorrhage in
the medulla oblongata, 870; in hyperzemia of the
spinal meninges, 203; in inflammation of the
' spinal dura mater, 220, 224; in injuries of the |
medulla oblongata, 894; in meningeal hemor-
rhage, 212; in multiple sclerosis, 484, 490; in
mye-itis, 402, 489+: in poliomyelitis anterior acuta,
682; in poliomyelitis anterior chronica, 717;
in saltatory spasm, 801; in slow compression of
the cord, 328, 331; in spasmodic spinal paralysis,
627; in spinal apoplexy, 297; in spinal irrita-
tion, 362; in spinal nervous weakness, 372; in
syringomyelia, 800; in tabes dorsalis, 542, 559;
in tonic spasms, 813; in tumors of the medulla
oblongata, 954; in tumors of the spinal cord,
753; in tumors of the spinal membranes, 268 ;
in wounds of the spinal cord, 311, 312.
Motor conduction of the medulla oblongata, 853; of
the spinal cord, 37.
Moutard-Martin, 284.
Movements, co-ordination of, 39.
Moxon, 474, 751.
Mueller, H., 65, 217.
Mueller, Joh., 518,
Mueller, R. H., 218.
Mueller, W., 119, 649, 653, 666,
Multiple Sclerosis of the Spinal Cord, 472.
Muscles, affections of, in diseases of the spinal cord,
114; in acute spinal meningitis, 236; in chronic
spinal meningitis, 257; in concussion of the spi-
nal cord, 352; in hemiplegia et hemiparaplegia
spinalis, 650; in inflammation of the spinal dura
mater, 220, 224; in multiple sclerosis, 483, 486,
495; in myelitis, 406, 410, 432, 440; in paralysis
ascendens acuta, 739; in poliomyelitis anterior
acuta, 678, 683, 687, 700; in poliomyelitis anterior
chronica, 718; in progressive bulbar paralysis,
916; in slow compression of the cord, 328, 335;
in spasmodic spinal paralysis, 628; in spinal apo-
plexy, 299; in syringomyelia, 80U; in tabes dor-
salis, 539, 587; in tumors of the spinal mem-
branes, 267, 270.
Muscular tonicity. theory of, 59.
Mushrooms, pcisoning by, in etiology of spinal paraly-
sis, 818,
Musk in concussion of the spinal cord, 356; in paraly-
sis ascendens acuta, 747.
Myelitis, 382.
Myelitis Bulbi Acuta, 900,
Myelitis, chronic, in etiology of hemiplegia et hemi-
paraplegia spinalis, 649.
Myelitis Chronica, 426,
Myelomalacia, 467.
Myxoglioma of the Spinal Cord, 750.
Myxoma of the Medulla Oblongata, 951.
Myxoma of the Spinal Membranes, 264,
Myxosarcoma of the Spinal Cord, 750,
NACHTWEYH, 617.
Nails#changes in, in diseases of the spinal cord, 119,
968
Nasse, 58, 148,
Nauheim, waters of, in myelitis, 461; im spinal ner-
vous weakness, 381; in tabes dorsalis, 611.
Naunyn, 46, 65, 71, 128, 129, 553, 798.
Nawrocki, 655.
Necrotic Softening of the Medulla Oblongata, 876,
Nenndorf, baths of, in diseases of the spinal cord, 171.
Nerves, affections of, in diseases of the spinal cord,
141; in multiple sclerosis, 480; in myelitis, 410,
432, 447; in poliomyelitis anterior acuta, 678; in
tabes dorsalis, 539; in etiology of secondary de-
generation of the spinal cord, 764,
Nervous symptoms in acute spinal meningitis, 236,
242; in multiple sclerosis, 487; in myelitis, 411,
447 ; in poliomyelitis anterior acuta, 686, 700 ; in
tabes dorsalis, 543, 582.
Neurasthenia Spinalis, 369.
Neuroma of the Spinal Membranes, 265.
Neuropathic disposition in etiology of diseases of the
spinal cord, 146.
Nieder, 129, 314,
Niemeyer, 86.
Nobili, 179.
Nonat, 300.
Nothnagel, 52, 60, 335, 856, 866, 874, 876, 885,
Nussbaum, M., 42, 861.
Nutrition, changes in, in diseases of the spinal cord,
127; in progressive bulbar paralysis, 927; in spi-
nal nervous weakness, 374; general disturbances
of, in etiology of diseases of the spinal cord, 151.
Nutritive centre for certain nervous regions, 862.
Nutritive stimulation in etiology of hyperzemia of the
spinal meninges, 201.
Nux vomica in diseases of the spinal cord, 188; in
anemia of the spinal cord, 290; in meningea,
hemorrhage, 216; in paralysis ascendens actual,
746; in spinal irritation, 365; in spinal nervous
weakness, 381,
OBERNIER, 953, 957.
Obré, 265.
Oeynhausen, baths of, in diseases of the spinal cord,
168.
Ogle, 322.
Oldoini, 792,
Ollivier, 200, 218, 273, 278, 314, 316, 317, 343, 365, 385,
889, 517, 783, 750, 780, 796, 868, 890, 951.
Operative measures in treatment of spina bifida, 792;
in wounds of the spinal cord, 318.
Opium in diseases of the spinal cord, 192; in acute
spinal meningitis, 250; in anemia of the spinal
cord, 290; in myelitis, 465; in spinal irritation,
368 ; poisoning by, in etiology of spinal irritation,
860.
Oppler, 103.
Oppolzer, 386, 389,
INDEX.
Ordenstein, 473, 495.
Oré, 301, 649.
Orthopeedic surgery in treatment of poliomyelitis ante-
rior acuta, 711. -
Osteoma of the spinal membranes, 265.
Osthoff, 553.
Otto, 474, 477, 512.
Oulmont, 519,
Owsjannikow, 856, 861,
PaGe, 316.
Pain in diseases of the spinal cord, 75; in acute bul-
bar myelitis, 903 ; in acute spinal meningitis, 235,
237; in chronic spinal meningitis, 256; in con-
cussion of the spinal cord, 349; in hyperemia of
the spinal meninges, 203; in inflammation of the
spinal dura mater, 219, 223; in meningeal hemor-
rhage, 211; in multiple sclerosis, 484; in myeli-
tis, 402; in poliomyelitis anterior acuta, 681, 700 ;
in saltatory spasm, 808; in slow compression of
the cord, 328, 330; in spasmodic spinal paralysis,
627 ; in spinal apoplexy, 297; in spinal irritation,
861; in spinal nervous weakness, 273 ; in tabes
dorsalis, 541, 547 ; in tumors of the medulla oblon-
gata, 954; in tumors of the spinal cord, 754; in
tumors of the spinal membranes, 268; in wounds
of the spinal cord, 311, 313.
Panum, 468.
Paoluzzi, 649, 651.
Paralysie Atrophique de l‘Enfance of Duchenne, 663.
Paralysie Générale Spinale Antérieure Subaigué of
Duchenne, 712,
Paralysis Ascendens Acuta, 732.
Paralysis, Bulbar, Acute, 900.
Paralysis, Bulbar, Progressive, 905.
Paralysis of Landry, 732,
Paralysis, Spinal, Intermittent, 814,
Paralysis, Spinal, Toxic, 817.
Paralysis Spinalis Spastica, 620.
Paralysis in diseases of the spinal cord, 79; in acute
bulbar myelitis, 903; in acute spinal meningitis,
2°6, 239; in anemia of the medulla oblongata,
880 ; in anemia of the spinal cord, 286; in chronic
spinal meningitis, 256; in concussion of the spi-
nal cord, 849; in hemiplegia et hemiparaplegia
spinalis, 650; in hemorrhage of the medulla ob-
longata, 870; in inflammation of the spinal dura
mater, 220, 224; in injuries of the medulla oblon- _
gata, 894; in meningeal hemorrhage, 212; in
multiple sclerosis, 404; in myelitis, 403, 489; in
myelomalacia, 471; in paralysis ascendens acuta,
738; in poliomyelitis anterior acuta, 682, 687, 700 ;
in poliomyelitis anterior chronica, 717; in pro-
gressive bulbar paralysis, 917, 929; in slow com-
pression of the cord, 328, 331; in spasmodic spi-
nal paralysis, 628; in spinal apoplexy, 297; in
————
ee
_3>*
OLE SO "Sa. PES LI FOG OM Mere =
INDEX. 969
syringomyelia, 800; in tabes dorsalis, 546, 583 ;
in tumors of the medulla oblongata, 954; in tu-
mors of the spinal cord, 753; in tumors of the
spinal membranes, 268; in wounds of the spinal
cord, 311, 312.
Paraplegia dependent on Idea, 819.
Parona, 792.
Parrot, 308, 666, 671,
Pathology. See Different Diseases.
Pellegrino-Levi, 733, 735, 739, 741, 742, 743.
Petit, J. L., 308.
Petitfils, 674, 677, 783.
Petri, 172.
Pfeffers, baths of, in diseases of the spinal cord, 167.
Pfeufer, 210.
Pflueger, 43, 47.
Phosphorus in diseases of the spinal cord, 191; in
myelitis, 463; in tabes dorsalis, 615; poisoning
by, in etiology of spinal paralysis, 818.
Physical causes of diseases of the spinal cord, 152.
Physiology of the Medulla Oblongata, S51.
Physiology of Spinal Cord, 33.
Picard, 733.
Pick, A., 588.
Pierres, 773,
Pierret, 13, 32, 116, 386, 533, 535, 536, 537, 572, 577,
578, 583, 601, 674.
Pitres, 761, 773.
Pleurisy in etiology of paralysis anterior acuta, 735,
Plombiéres, baths of, in diseases of the spinal cord,
167.
Pneumonia in etiology of diseases of the spinal cord,
153; of tabes dorsalis, 528,
Poché, 713.
Poincaré, 935, .
Poisoning theory of paralysis ascendens acuta, 736.
Poisons in etiology of diseases of the spinal cord, 153 ;
of hyperzmia of the spinal meninges, 201; of
myelitis, 429; of spinal irritation, 360.
Poliomyelitis Anterior Acuta of Kussmaul, 663.
Poliomyelitis Anterior Subacuta et Chronica, 712,
Position of body in anemia of the spinal cord, 290;
in concussion of the spinal cord, 356; in hyperz-
’ mia of the spinal meninges, 207; in spinal apo-
plexy, 305.
Potain, 872.
Potassium, bromide of, in diseases of the spinal cord,
191; in myelitis, 465; in spinal irritation, 369; in
tabes dorsalis, 615; iodide of, in diseases of the
spinal cord, 190; in chronic spinal meningitis,
_ 261; in concussion of the spinal cord, 856; in
myelitis, 423, 426, 463; in myelomalacia, 471; in
paralysis ascendens acuta, 746; in poliomyelitis
anterior acuta, 707; in poliomyelitis anterior
chronica, 731; in progressive bulbar paralysis,
in spinal apoplexy, 305; in tabes dorsalis, 615; in
tumors of the spinal membranes, 276,
Pregnancy in etiology of multiple sclerosis, 476,
Prévost, 665, 673,
Priapism in myelitis, 409.
Primary Lateral Sclerosis, 620.
Prognosis, See Different Diseases,
Progressive Bulbar Paralysis, 905.
Psychical symptoms in spinal irritation, 363.
Puerperal diseases in etiology of myelitis, 290.
Pulse in diseases of the spinal cord, 143; in acute
bulbar myelitis, 903; in acute spinal meningitis,
235; in concussion of the spinal cord, 849; in
hemorrhage in the medulla oblongata, 872; in
hyperemia of the spinal meninges, 205; in mye-
litis, 412; in slow compression of the cord, 337;
in tabes dorsalis, 589,
Putzeys, 43.
Pyrmont, baths of, in diseases of the spinal cord, 170,
171.
QuinckE, 10, 128, 129, 314.
Quinine in diseases of the spinal cord, 191; in acnte
spinal meningitis, 251; in concussion of the spinal
cord, 357; in intermittent spinal paralysis, 817;
in meningeal hemorrhage, 216; in myelitis, 425,
465; in myelomalacia, 471 ; in progressive bulbar
paralysis, 945; in slow compression of the cord,
842; in spinal irritation, 367; in spinal nervous
weakness, 381,
Rapow, 180, 209.
Radcliffe, 649.
Radlick, 497.
Ragatz, baths of, in diseases of the spinal cord, 167,
Ranke, 179, 184.
Ranvier, 21, 22, 733, 736.
Raymond, 685,
Raynaud, 550, 589,
von Recklinghausen, 671.
Rectum, affections of, in spinal diseases in general,
188 ; in acute bulbar myelitis, 903; in acute spinal
meningitis, 236; in concussion of the spinal cord,
3849; in hemiplegia et hemiparaplegia spinalis,
653; in meningeal hemorrhage, 213; in multiple
sclerosis, 486 ; in myelitis, 409; in myelomalacia,
471; in paralysis ascendens acuta, 740; in slow
compression of the cord, 329, 334; in spinal apo-
plexy, 298; in tumors of the spinal membranes,
271; in wounds of the spinal cord, 311, 312; in
etiology of tabes dorsalis, 528,
Rectum, innervation for evacuation of, 53,
Reflex action of the spinal cord, 46,
Rehme, waters of, in diseases of the spinal cord, 1683
in myelitis, 461 ; in spinal nervous weakness, 381 3
. 945; in slow compression of the spinal cord, 342;
ifftabes dorsalis, 611.
970
Reichert, 50.
Reinez, baths of, in diseases of the spinal cord, 171.
Remak E., 70, 71, 72, 178, 184, 519, 553, 581, 593, 595,
618, 715.
Remak, Sen., 529, 538,
Respiration, disturbances of, in diseases of the spinal
cord, 140; in acute bulbar myelitis, 903; in acute
spinal meningitis, 236, 241; in anzmia of the
medulla oblongata, 880 ; in concussion of the spinal
cord, 349; in hemorrhage in the medulla oblon-
gata, 871; in hyperemia of the spinal meninges,
204; in multiple sclerosis, 498; in myelitis, 412,
447; in paralysis ascendens acuta, 738; in pro-
gressive bulbar paralysis, 917, 925; in slow com-
pression of the cord, 337; in spinal irritation,
362; in tabes dorsalis, 589.
Respiration, artificial, in hemorrhage in the medulla
oblongata, S76.
Respiration, innervation of organs of, 53.
Respiratory centres in the medulla oblongata, 857,
Rest in concussion of the spinal cord, 356; in menin-
geal hemorrhage, 216; in myelitis, 422.
Reynolds, J. Russell, 153, 819, 820, 821.
Rheumatism in etiology of myelitis, 390 ; in etiology
of tabes dorsalis, 528.
Richter, Fr., 167, 173, 610, 612.
Riegel, 128, 162, 649, 651.
Rilliet, 665.
Rindfleisch, 473.
Rinecker, 671.
Rizzoli, 792.
Robertson, 142, 577."
Robin, 194.
Rockwell, 184, 2
Roessingh, 155.
Roger, 116, 666, 671, 677.
Rokitansky, P., 53, 518, 758, 857.
Romberg, 148, 286, 386, 518, 521, 558, 607, 618, 815.
Rémerbad, baths of, in diseases of the spinal cord,
167.
Rosenstein, 130.
Rosenthal, M., 148, 203, 266, 337, 340, 523, 548, 610,
611,. 930,
Roth, 116, 666, 671, 677.
* Rotter, 890.
Ruehle, 87, 218,
Runge, 172.
5, 269.
Sacus, C., 50.
Salivary secretion, affection of, in progressive bulbar
paralysis, 924.
Salomon, 148, 691, 746.
Saltatory Spasm, 801.
Samuelson, 950.
Sander, 265, 680, 749.
Sarcoma of the Spinal Cord, 750.
INDEX.
Sarcoma of the Spinal Membranes, 264,
Schiefferdecker, 26, 30, 759, 763, 770, 778, 782.
Schiff, 35, 86, 37, 38, 39, 41, 42, 45, 58, 61, 64, 69, 71,
72, 74, 75, T7, 816, 554, 655, 858, 854, $60,
Schiffer, 283,
Schlangenbad, baths of, in diseases of the spinal cord,
167.
Schlesinger, 42, 57, 58, 861.
Scholz, 169, 347, £53, 357, 370, 750, 753.
Schuele, 474, 481, 489, 498, 512,
Schueller, 186.
Schueppel, 45, 88, 90, 92, 95, 569, 749, 750, 754.
Schuetzenberger, 293.
Schultze, F., 50, 162, 227, 230, 233, 288, 428, 490, 496,
509, 602, 666, 674, 678, 761, 762, 782.
Schultze, M., 19, 117.
Schulz, 907.
Schulze, E.. 525, 528, 529.
Schwalbach, baths of, in diseases of the spinal cord,
170 ; in concussion of the spinal cord, 357.
Sclerosis, Diffuse, of the Medulla Oblongata, 949,
Sclerosis, Multiple, of the Spinal Cord, 472,
Sclerosis of the Lateral Columns, 620.
Sclerosis of the Posterior Columns, 513.
Sclerosis of the Spinal Cord, 426.
Sclerosis in etiology of hemiplegia et hemiparaplegia
spinalis, 649.
Sclerotic Centres of the Medulla Oblongata, 947.
Scrofula in etiology of tumors of the spinal cord, 752.
Scrofulous diathesis in etiology of tumors of the spi-
nal membranes, 268,
Seasons of the year in etiology of poliomyelitis
anterior acuta, 668,
Secretion, innervation for processes of, 58.
Secretions, certain centres for, in the medulla oblon-
gata, 862.
Seeligmueller, 624, 809, 814,
Sensation, disturbances of, in diseases of the spinal
cord, 66; in acute bulbar myelitis, 903; in acute
spinal meningitis, 226, 239; in anemia of the
medulla oblongata, 880; in anemia of the spinal
cord, 286; in chronic spinal meningitis, 255, 257 ;
in concussion of the spinal cord, 349; in hemiple-
gia et hemiparaplegia spinalis, 650; in hemor-
rhage in the medulla oblongata, 871; in hyper-
zemia of the spinal meninges, 203 ; in inflammation
of the spinal dura mater, 220, 224; in injuries of
the medulla oblongata, 895; in meningeal hemor-
rhage, 212; in multiple sclerosis, 484; in myelitis,
402, 428; in myelomalacia, 471; in paralysis
ascendens acuta, 739; in poliomyelitis anterior
chronica, 717; in slow compression of the cord,
828, 333; in spasmodic spinal paralysis, 627; in
spinal apoplexy, 297; in spinal irritation, 361; in
spinal nervous weakness, 373; in syringomyelia,
800 ; in tabes dorsalis, 542, 545, 547; in tumors of
ya
ir
7
INDEX. 971
the medulla oblongata, 954; in tumors of the api- '
nal cord, 753 ; in tumors of the spinal membranes,
268 ; in wounds of the spinal cord, 311, 312.
Sensory Conduction in the Medulla Oblongata, $54,
Sensory Conduction in the Spinal Cord, 35.
Septicaemia in diseases of the spinal cord, 122.
Soquin, 666,
Setchenow, 51, 52.
Sex in etiology of diseases of the spinal cord, 150; of
acute spinal meningitis, 229; of multiple sclero-
sis, 475; of myelitis, 388, 427; of paralysis ascen-
dens acuta, 735; of progressive bulbar paralysis,
909; of spinal apoplexy, 292; of spinal irritation,
£60; of spinal nervous weakness, 371; of tabes
dorsalis, 523,
Sexual excesses and irregularities in etiology of dis-
eases of the spinal cord, 147; of chronic spinal
meningitis, 253; of concussion of the spinal cord,
846; of myelitis, 388, 427; of myelomalacia, 470;
of poliomyelitis anterior chronica, 714; of spinal
irritation, 360; of spinal nervous weakness, 371;
of tabes dorsalis, 525,
Sexual functions, disturbances of, in diseases of the
spinal cord, 136; in hemiplegia et hemiparaplegia
spinalis, 653; in multiple sclerosis, 486, 503; in
myelitis, 446 ; in poliomyelitis anterior acuta, 699 ;
in spinal nervous weakness, 373 ; in tabes dorsalis,
543, 585.
Shaw, 665.
Silver, nitrate of, in diseases of the spinal cord, 190;
in multiple sclerosis, 512; in myelitis, 425, 463 ;
in poliomyelitis anterior acuta, 710; in progres-
sive bulbar paralysis, 945; in spasmodic spinal
paralysis, 645; in tabes dorsalis, 614,
Simon, 128, 222, 267.
Simon, Th., 386, 398, 748, 749, 750, 752, 754, 764, 773,
796, 797, 798.
Simple Softening of the Spinal Cord, 467.
Sinkler, Wharton, 668, 688, 710.
Siredey, 615.
Skin, affections of, in diseases of the spinal cord, 119;
in acute spinal meningitis, 242; in hemiplegia et
hemiparaplegia spinalis, 650; in inflammation of
the spinal dura mater, 224; in multiple sclerosis,
483; in myelitis, 403; in paralysis ascendens
acuta, 740; in poliomyelitis anterior acuta, 630,
693, 700; in slow compression of the cord, 328,
$30, 336 ; in spina bifida, 788; in tabes dorsalis,
540, 574, 586.
Sleeplessness in spinal nervous weakness, 374.
Slow Compression of the Cord, 319.
Small-pox in etiology of multiple sclerosis, 476;
of myelitis, 590; of paralysis ascendens acuta,
755.
Smell, disturbances of, in multiple sclerosis, 500; in
tabes dorsalis, 582,
Soden a, Taunus, baths of, in diseases of the spinal
cord, 165.
Solmon, 651, 653.
Sonnenkalb, 720.
Spaeth, 86, 58, 90, 92, 95, 519, 554, 569, 570.
Spasm in diseases of the spinal cord, 99; in spinal
irritation, £62.
Spasmodic Spinal Paralysis, 620.
Speech, centres for, in the medulla oblongata,
859.
Speech, disturbances of, in diseases of the spinal cord,
142, 143; in anemia of the medulla oblongata,
£80; in hemorrhage in the medulla oblongata,
872; in multiple sclerosis, 487, 496; in myelitis,
412, 447; in paralysis ascendens acuta, 742; in
progressive bulbar paralysis, 915, 919; in tabes
dorsalis, 563; in tumors of the medulla oblongata,
954.
Spiess, 518.
Spina Bifida, 785.
Spinal Apoplexy, 291.
Spinal Cord, Introduction to Diseases
of, 3.
ANATOMICAL INTRODUCTION, 7; bibliography, 7.
PuHyYsIoLoGicaL INTRODUCTION, 33; bibliography,
83; sensory conduction, 35; motor conduction,
87; co-ordination of movements, 39; vaso-motor
paths and centres, 42; trophic centres and paths,
44; reflex action, 46; inhibition of reflex action,
51; centres and paths for the innervation of the
viscera, 52.
GENERAL SYMPTOMATOLOGY, 66; disturbances of
sensibility, 66; diminution of sensory action,
anesthesia, 67; exaggeration of sensory action,
%3; disturbances of motility, 79; diminution of
motility, weakness, and paralysis, 79; imperfect
co-ordination of movements, ataxia, 83; various
characteristic gaits, 96; increase of motility,
spasm, 97; alteration in the velocity of the motor
conduction, 104; electric reaction of the motor
apparatus, 105; disturbances of reflex activity,
107; vaso-motor disturbances, 111; trophic dis-
turbances, 113; disturbances of the urinary and
sexual apparatus, 129; disturbances of digestion
and defecation, 138; disturbances of respiration
and circulation, 140; disturbances of the oculo-
pupillary fibres, the various cerebral nerves, and
the brain itself, 141.
GENERAL ETIOLOGY, 146; neuropathic disposition,
146; sexual excesses and irregularities, 147; in-
fluence of age and sex, 159; general disturbances
of nutrition, 151; propagation of neighboring mor-
bid processes, 151 ; exposure to cold, 151; disturb-
ances of circulation, excessive exertion and psy-
chical influences, 152; poisonings and the local
development of various infectious diseases, 153 ;
972 INDEX,
acute diseases, 153; irritation and disease of per-
ipheral organs, 154.
GENERAL DraGnosis, 155.
GENERAL THERAPEUTICS, 160; external remedies,
162; cold, 162; warmth, 163; baths, 1643 cli-
mate, 175; electricity, 178; blood-letting and de-
rivatives, 185; external frictions, 186; internal
remedies, 187; symptomatic remedies and meth-
ods, 192; general methods of life, 196. _
Spinal Cord, Diseases of Membranes of,
199.
HYPERZMIA OF THE MENINGES OF THE CORD, AND
OF THE CORD ITSELF, 199; bibliography, 199;
pathological
anatomy, 202; symptomatology, 203; diagnosis,
206 ; treatment, 207.
MENINGEAL HEMORRHAGE, 208; bibliography, 208 ;
etiology and pathogenesis, 209; pathological anat-
omy, 210; symptomatology, 211 ; course and ter-
mination, 213; diagnosis, 214; prognosis and
treatment, 215,
INFLAMMATION OF THE SPINAL DuRA Mater, 216;
bibliography, 216; Pachymeningitis Spinalis Ex-
terna, 217; pathological anatomy, 218; symp-
tomatology, 219; diagnosis, 220; prognosis and
treatment, 221; Pachymeningitis Interna, 221;
etiology and pathological anatomy, 222; symp-
tomatology, 223; diagnosis, prognosis, and treat-
ment, 225.
INFLAMMATION OF THE SPINAL PIA MATER, 226;
bibliography, 226; the acute form, 229; etiology,
229; pathological anatomy, 231; symptomatolo-
gy, 234; course, duration, termination, 244; di-
agnosis, 245; prognosis, 247; treatment, 248; the
etiology and pathogenesis, 200;
chronic form, 252; etiology, 252; pathological '
anatomy. 253; symptomatology, 2555; course, du-
ration, result, 257; diagnosis, 258; prognosis,
259; treatment, 260.
TUMORS OF THE SPINAL MEMBRANES, 2625 biblio-
graphy, 262; pathological anatomy, 264; etiolo-
gy, 268; symptomatology, 268 ; course, duration,
termination, 273; diagnosis, 274; prognosis and
treatment, 276.
Addendum. Anatomical changes in the spinal mem-
branes, without clinical significance, 277.
Spinal Cord, Diseases of, 279.
HYPERZMIA OF THE Corp, 280; general remarks,
280.
ANZMIA OF THE Corp, 281; bibliography, 281; pa-
thogenesis and etiology, 282; pathological anato-
my, 285; symptomatology, 286; course, duration,
termination, 288; diagnosis, prognosis; 289;
treatment, 290.
SPINAL APOPLEXY, 291; bibliography, 291; patho-
genesis and etiology, 292 ; pathological anatomy,
294; symptomatology, 297; course, duration,
termination, 201; diagnosis, 802; prognosis and
treatment, 304,
Wounps, £05; bibliography, 805; etiology, 306;
pathological anatomy, 308 ; symptomatology, 810 ;
course, duration, termination, 316; diagnosis and
prognosis, 317; treatment, 818.
Stow COMPRESSION OF THE Corp, 319; bibliog-
raphy, 319; etiology and pathogenesis, 320; patho-
logical anatomy, 824; symptomatology, 827;
course, duration, termination, 338; diagnosis,
389; prognosis, 341; treatment, 342. °
CONCUSSION OF THE SPINAL Corp, 344: biblio-
graphy, 344; etiology and pathogenesis, 345;
pathological anatomy, 346 ; symptomatology, 348;
diagnosis, 853; prognosis, 255 : treatment, 356.
SPINAL IRRITATION, 357; bibliography, 357; eti-
ology, 860; symptomatology, 361; course, dura-
tion, termination, 363; diagnosis, 265; vee
and treatment, 367,
SPINAL NERVOUS Westened 869; bibliography,
369; etiology, 371 ; symptomatology, 372; course,
duration, termination, 376; diagnosis, 378; Prog-
nosis, 379; treatment. 380.
MYELITIs, 382; bibliography, 382; introduction,
883; history, 385; Myelitis acuta, 387; etiology
and pathogenesis, 3888; pathological anatomy,
891; symptomatology, 402; course, duration,
termination, 414; diagnosis, 418 ; prognosis, 420 5
treatment, 422; Myelitis chronica, 426; etiology
and pathogenesis, 427; pathological anatomy,
429; symptomatology, 438; course, duration,
termination, 448; different forms of chronic my-
elitis, 449; diagnosis, 453; prognosis, 456; treat-
ment, 457.
MYELOMALACIA, 467; bibliography, 467; pathoge-
nesis, 468; pathological anatomy, 470; symptom-
atology, 470 ; diagnosis, prognosis, treatment, 471.
MULTIPLE SCLEROSIS, 472; bibliography, 472; his-
tory, 473; etiology and pathogenesis, 475; path-
ological anatomy, 477; symptomatology, 483;
course, duration, termination, 505; diagnosis,
507; treatment, 512. '
TABES DorRSALIS, 513; bibliography, 513; history,
517; etiology and pathogenesis, 522; pathological
anatomy, 531; symptomatology, 540; analysis of
symptoms, 547; course, duration, termination,
596; theory of the disease, 599; ae 603 ;
prognosis, 607 ; treatment, 608.
SPASMODIC SPINAL PARALYSIS, 620; pinitoigeslall
620; introduction and history, 621; etiology and
pathogenesis, 624; pathological anatomy, 625;
symptomatology, 627; course, duration, termina~
tion, 635; theory of the disease, 636; complica-
tions, 538; diagnosis, 642 ; prognosis, 644; treat-
ment, 645.
HEMIPLEGIA ET HEMIPARAPLEGIA cvntstuee
ae
a
“
|
|
|
|
INDEX. 973
bibliography, 646 ; history, 646; etiology and path-
ological anatomy, 648; symptomatology, 649;
pathological physiology, 654; course, duration,
termination, 660; diagnosis, 661; prognosis, 662;
treatment, 662.
PoLiomye.itis ANTERIOR Acura, 663; bibliogra-
phy, 668; history, 664; definition, 666; etiology
and pathogenesis, 667 ; pathological anatomy, 670 ;
symptomatology, 681; the poliomyelitis anterior
acuta in children, 681; the poliomyelitis anterior
acuta in the adult, 699 ; course, duration, termina-
tion, 701; diagnosis, 703; prognosis, 706; treat-
ment, 707.
Po.iomyYe itis ANTERIOR Cnronio, 712; history,
713; etiology, 714; pathological anatomy, 716;
symptomatology, 717; diagnosis, 728; prognosis,
731; treatment, 731.
PaRAtysis ASCENDENS AcuTA, 732; bibliography,
732; history, 732; etiology and pathogenesis, 735 ;
pathological anatomy, 736 ; symptomatology, 737;
diagnosis, 743; prognosis, 745; treatment, 746.
INTRAMEDULLARY Tumors, 747 ; bibliography, 747 ;
pathological anatomy, 748; etiology, 752; symp-
tomatology, 753; diagnosis, 755; prognosis and
treatment, 756.
SuCONDARY DEGENERATIONS, 757; bibliography,
%57; history, 758; etiology and pathogenesis, 759 ;
pathological anatomy, 767; symptomatology, 774;
diagnosis, 776; prognosis, 777; treatment, 778.
DEFORMITIES AND MALFORMATIONS, 779; biblio-
graphy, 779; general classifications, T79; symp-
toms of spina bifida, 7&7; diagnosis, 790; progno-
sis, 791; treatment, 791.
RaRE AND Doustrvut Diseases, 794; Syringomy-
elia, 795; bibliography, 795; pathogenesis and
pathological anatomy, 796 ; symptomatology, 800 ;
Saltatory Spasm, 801; bibliography, 801; symp-
tomatology 801; etiology, 806; treatment, 808;
Tonic Spasms, 808; bibliography, 808; symp-
tomatology, 8093, etiology, 814; treatment, 814;
Intermittent Spinal Paralysis, 814; bibliography,
814; symptomatology, 815; diagnosis, 817; treat-
ment, 817; Toxic Spinal Paralysis, 817; biblio-
graphy, 817; general remarks, 818; Paraplegia
dependent upon Idea, 819; bibliography, 819;
etiology, 819; symptomatology, 819; diagnosis,
821; treatment, 821.
Spinal cord, abnormal size of, 781.
Spinal cord, affections of, in chronic myelitis, 429 ; in
hyperemia of the spinal meninges, 202; in in-
flammation of the spinal dura mater, 222; in in-
flammation of the spinal pia mater, 254; in me-
ningeal hemorrhage, 211; in multiple sclerosis,
477; in myelitis, 391; in poliomyelitis anterior
acuta, 671; in poliomyelitis anterior chronica,
716 ; in secondary degenerations, 767 ; in spasmo-
dic spinal paralysis, 625; in syringomyelia, 800 ;
in tabes dorsalis, 531; from tumors, 748; in tu-
mors of the spinal membranes, 267; affections of,
in etiology of hemiplegia et hemiparaplegia spina-
lis, 648 ; of secondary degeneration of the cord
itself, 762; of spinal apoplexy, 293.
Spinal Cord, Anatomy of, 7.
Spinal Cord, Physiology of, 33,
Spinal Cord, Inflammation of, 382.
Spinal Infantile Paralysis of von Heine, 663.
Spinal Irritation, 257.
Spinal Nervous Weakness, 369.
Spinal Paralysis, Acute, of Adults, 663.
Spinal Paralysis, Chronic Atrophic, 712.
Spinal Paralysis, Intermittent, 814.
Spinal Paralysis of Brown-Séquard, 646,
Spinal Paralysis, Toxic, 817,
Spine, rigidity of, in acute spinal meningitis, 235.
Steiner, 204.
Steinmann, 59.
Stelnthal, 518, 546,
Stenson, 282.
Steudener, 313, 316.
Stieda, 837, 838.
Stilling, 30, 365, 844. —
Stimulants in concussion of the spinal cord, 856; in
hemorrhage in the medulla oblongata, 876; in
myelitis, 425; in paralysis ascendens acuta, 747;
in spinal irritation, 367; in spinal nervous weak-
ness, 380.
St. Moritz, baths of, in diseases of the spinal cord, 170,
Stokes, 254,
Strychnia in diseases of the spinal cord, 188; in anz-
mia of the spinal cord, 290; in concussion of the
spinal cord, 356; in myelitis, 426, 464; in myelo-
malacia, 471 ; in poliomyelitis anterior acuta, 710;
in slow compression of the cord, 343; in spinal
irritation, 368; in spinal nervous weakness, 381 ;
in tabes dorsalis, 615.
Subacute and Chronic Inflammation of the Gray An-
terior Horns, 712,
Sweating in tabes dorsalis, 589; suppression of, in
etiology of acute spinal meningitis, 231; of tabes
dorsalis, 529.
Symptomatology. See Different Diseases.
Syphilis in etiology of diseases of the spinal cord, 153;
of hemiplegia et hemiparaplegia spinalis, 649; of
myelitis, 390, 428; of paralysis ascendens acuta,
%35 ; of tabes dorsalis, 528 ; of tumors of the spinal
cord, 752; of tumors of the spinal membranes, 268.
Syphiloma of the Spinal Cord, 751.
Syphiloma of the Spinal Membranes, 266.
Syringomyelia, 795.
TABES Dorsatis, 513.
Tabes Dorsal Spasmodique of Charcot, 620,
974
Talipes a result of poliomyelitis anterior acuta,
695.
Tarchanoff, 43,
Taste, disturbances of, in multiple sclerosis, 500; in
tabes dorsalis, 582,
Taylor, 723.
Teale, J. W., 128.
Teissier, 519,
Temperature of body in diseases of the spinal cord,
127; in acute spinal meningitis, 285, 242; in
hemorrhage in the medulla oblongata, 872; in
meningeal hemorrhage, 213; in myelitis, 402; in
paralysis ascendens acuta, 740: in poliomyelitis
anterior acuta, 681, 635, 700; in tumors of the
spinal membranes, 272; in wounds of the spinal
cord, 312, 313.
Tendons, affections of, in poliomyelitis anterior acuta,
680 ; in spasmodic spinal paralysis, 62S; in tabes
dorsalis, 575.
Tenner, 283, 886.
Teplitz, baths of, in diseases of the spinal cord, 167;
in myelitis, 460.
Thiry, 861.
Thomsen, J., 809.
Thrombi and Emboli in Arteries of the Medulla Ob-
longata, 876.
Thrombosis in etiology of myelomalacia, 468,
Tibbits, 423,
Tiesler, 154.
Tirard, 882, 884.
Tobacco, poisoning by, in etiology of spinal paralysis,
818; of tabes dorsalis, 529.
Todd, 105, 518,
Tongue, affections of, in diseases of the spinal cord,
142.
Tonics in meningeal hemorrhage, 216; in myelitis,
425 ; in myelomalacia, 471; in slow compression
of the cord, 342; in spinal irritation, 367; in
spinal nervous weakness, 381.
Tonic Spasms, 808.
Topinard, 70, 71, 86, 386, 519, 523, 524, 549, 553, 556,
557, 570, 572, 580, 616.
Toxic Spinal Paralysis, 81%.
Toxic stimulation in etiology of hyperemia of the spi.
nal meninges, 201,
Traube, 210, 217, 264.
Treatment. See Different Diseases,
Troisier, 116, 649, 788.
Trophic centres and paths in the spinal cord, 44.
Trophic disturbances in diseases of the spinal cord,
113; in tabes dorsalis, 586.
Trousseau, 519, 523, 569, 585, 600, 906, 935.
Tscheschichin, 128.
Tubercle of the Medulla Oblongata, 951,
Tubercle of the Spinal Cord, 750.
Tubercle of the Spinal Membranes, 265.
INDEX
Tubercular basilar meningitis in etiology of acute spi-
nal meningitis, 230.
Tuberculosis in etiology of diseases of the spinal cord,
153; of tumors of the spinal cord, 752.
Tuberculous diathesis in etiology of tumors of the oer
nal membranes, 268,
Tuckwell, 285.
Tuengel, 750.
Tuerck, 74, 326, 386, 473, 518, 622, 758, 759, 761, 770,
773, 906.
Tumors of the Medulla Oblongata, 950,
Tumors of the Spinal Cord, 747.
Tumors of the Spinal Membranes, 262.
Tumors in etiology of hemiplegia et hemiparaplegia
spinalis, 649; of injuries of the medulla oblongata,
890; of slow compression of the cord, 320.
Tutscheck, 283, 286.
Typhoid fever in etiology of diseases of the spinal
cord, 153; of paralysis ascendens acuta, 735.
Typhus fever, in etiology of multiple sclerosis, 476 ;
of myelitis, 390; of tabes dorsalis, 528.
UNDERWOOD, 665.
Unilateral Lesion of the Spinal Cord, 646.
Urinary symptoms in diseases of the spinal cord,
132; in acute spinal meningitis, 236, 240 ; in
spinal irritation, 363,
Urine, changes in, in diseases of the spinal cord, 122,
129; in hemorrhage in the medulla oblongata,
872; in myelitis, 411; in spinal apoplexy, 299; in
tumors of the medulla oblongata, 955; retention
of, in concussion of the spinal cord, 350.
Uspensky. 59, 179, 649.
Uterine contractions, innervation for, 57.
Uterus, diseases of, in etiology of diseases of the
spinal cord, 154.
VALENTINER, 473.
Valerian in myelitis, 465.
Vanlair, 65.
Vaso-motor centre in the medulla oblongata, 861.
Vaso-motor disturbances in diseases of the spinal
cord, 111; in myelitis, 410, 443; in spinal irrita-
tion, 362; in tabes dorsalis, 586,
Vaso-motor paths and centres in the spinal cord, 42.
Venous congestion in etiology of hyperzemia of the
spinal meninges, 202,
Veratrine in myelitis, 465.
Vertebree, diseases of, in etiology of acute spinal me-
ningitis, 280; of chronic spinal meningitis, 253;
of meningeal hemorrhage, 209 ; in slow compres-
sion of the cord, 321; of tumors of the spinal
membranes, 268; injury of, in etiology of wounds
of the spinal cord, 306.
Vichy, waters of, in myelitis, 423,
Vigués, 649, 655.
f
iy
}
INDEX. 975
Virchow, 108, 184, 264, 265, 266, 278, 282, 749, 750,
951, 952.
Vix, 649, 650, 893.
Vogt, 308, 665.
Voice, disturbances of, in multiple sclerosis, 487, 497.
Voisin, 116, 389, 587, 884, 890, 891, 980.
Volkmann, 688, 693, 702, 709, 711, 712.
Vomiting in acute bulbar myelitis, 903; in acute spi-
nal meningitis, 241; in hemorrhage in the me-
dulla oblongata, 872; in poliomyelitis anterior
acuta, 686, 700; in slow compression of the cord,
837; in spinal irritation, 362; in tumors of the
medulla oblongata, 954.
Vossius, 581, 596.
Vulpian, 42, 43, 45, 109, 116, 227, 386, 468, 473, 495,
504, 519, 539, 614, 665, 666, 673, 733, 736, 759, S54,
861.
Wacusmotha, 907, 969, 930.
Wagener, E., 751.
Wagner, J., 949.
Waldmann, 527, 529, 530, 550, 611, 615, 616.
Walford, 733.
Waller, 45.
Warmbrunn, baths of, in diseases of the spinal cord,
167.
Warmth in diseases of the spinal cord, 163, 164; in
anzemia of the spinal cord, 290; in chronic spinal
meningitis, 261; in meningeal hemorrhage, 216 ;
in myelitis, 422; in poliomyelitis anterior acuta,
711; in spinal apoplexy, 805; in spinal irritation,
368.
Waters, 893.
Waters, mineral, in diseases of the spinal cord, 192;
in concussion of the spinal cord, 357 ; in myelitis,
423, 460; in progressive bulbar paralysis, 944; in
tumors of the spinal membranes, 276,
Watt, 794.
Weakness, Functional, of the Spinal Cord, 369.
Webber, 713, 716.
Weber, 230.
Weil, A., 283
Weiss, 666.
Wells, Spencer, 196,
Westphal, 48, 49, 86, 102, 266, 386, 390, 392, 417, 419,
474, 476, 505, 575, 583, 588, 626, 634, 637, 639, 733,
734, 736, 737, 739, 740, 743, 749, 750, 759, 770, 776,
797, 798, 867, 873.
Whipham, 265, 271.
Wiesbaden, baths of, in diseases of the spinal cord,
167,
Wildbad, baths of, in diseases of the spinal cord, 167 ;
in myelitis, 460,
Wilks, 266.
Willigk, 468, 879.
von Wittich, 104,
Woroschiloff, 35, 38, 39, 41, 96, 558, 657.
Wounds of the Medulla Oblongata, 887,
Wounds of the Spinal Cord, 305.
Wunderlich, 128, 190, 463, 518, 614,
Wundt, 35, 148.
Zenker, 473, 480.
von Ziemssen, 178, 231, 242, 565.
Zinc in diseases of the spinal cord, 191 ; in anemia of
the spinal cord, 290; in myelitis, 465; in spinal
irritation, 367.
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