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.•^4 8 




It is seldom in practice that we meet with diseases in their 
fully-developed, so-called "t}-pical" forms; more often we have 
to deal with patients who exhibit signs and symptoms common 
to several diseases. This volume approaches the subject of 
diagnosis of nervous diseases from the clinical standpoint, 
avoiding abstruse details of purely theoretical interest. Of the 
original lectures on which the work is based some were delivered 
at the Westminster Hospital, others to post-graduate audiences 
in London and elsewhere. 

The present edition differs considerably from the first, which 
was published two years ago. The text has been revised 
throughout and several chapters, with a number of fresh illus- 
trations, have been added. 

The subject of the work is mainly that of diagnosis ; treat- 
ment is not discussed save incidentally here and there. The 
order pursued is that in which it is convenient to study 
phenomena during the process of diagnosis. All the clinical 
illustrations are from cases which I have observed personally in 
hospital or private practice. 

I hope that the book, despite imperfections of which I am 
conscious, will continue to be useful to the advanced student and 
to the practitioner, not to replace but to supplement the text- 
books already in use. 

To my hospital colleagues I am indebted for their courtesy 

in permitting me to study many of tbeir cases. My thanks are 

due to various friends for photographs. Amongst these I would 

particularly mention Dr. James Collier {Figs. 32, 56, 81, and lOS), 

r. Lockhart Mummery (Fig. 134), Mr. Jackson Clarke (Fig. 

40), Dr. H. R. Sedgwick (Fig. 63). Dr. A. Ross Sinclair (Fig. 73). 



Dr. A. H. Watt (Fig. 157), and Dr. S. J. Aarons (Fig. 25). 
Dr. F. X. Dercum, Dr. M. Allen Starr, Mr. Bishop Harman, and 
Mr. Harold Barwell have kindly allowed me to use various 
diagrams, to which their names are attached in the text. I am 
also indebted to the publishers of the Practitioner for certain 
illustrations in the chapters on Hysteria and on Affections of 
the Sympathetic, originally published in that journal. 

Lastly, I desire to express my warmest thanks to Dr. S. A. 
Kinneir Wilson for his invaluable help and advice in the correc- 
tion of the proof-sheets, a task which in the original edition was 
kindly undertaken by Dr. A. F. Street. 


94 Hahley Street, London, W. 
November 1908. 



Anatomy and Physiology 



Anatomy and Physiology (continued) . 



Method op Case-Taking .... 






Fits and other Convulsive Phenomena . 



Involuntary Movements .... 






Disorders of Articulation .... 



Cranial Nerves 

. 110 


Cranial Nerves (continued) . 



Pain and other Abnormal Subjective Sensations . 



Abnormalities of Sensation : Hyper^esthesia, Par 

.fiSTHESiA, Anaesthesia 

. 179 


Organic Motor Paralysis of Upper Neurone Type 



Organic Motor Paralysis of Lower Neurone Type 



Recurrent and Transient Palsies .... 

. 235 





Postures and Gaits 









Affections of the Sympathetic. Angio-Neuroses . 



The Neurosf^ 



Electro-Diagnosis and Electro- Prognosis 



The Cerebro-Spinal Fluid 



Disorders of Sleep 



Intra-Cranial Tumours 




• • 



I. Sub-ungual hfemorrhat^es of the hand . 
II. Erythromelalgia 

. To face page 288 








There is no department of medicine where an accurate knowledge 
of anatomy is of greater importance than in the diagnosis of 
nervous diseases. Iiet us therefore, at the outset, recall some of 
the main points in the anatomy and physiology of the nervous 

The nervous system consists of two main divisions :—(l) the 
cerebro-spinal, comprising the brain and spinal cord, together 
with the cranial and spinal nerves, and (2) the sympathetic, 
constituted by two chains of pre-vertebral ganglia, one on each 
side of the spine. These two, the cerebro-spinal and sympathetic, 

For teaching purposes it is convenient to regard the nervous 
system as built up of nerve-cells, and their processes the nerve- 
fibres. Both are excitable. But whereas the nerve-cell has been 
commonly assumed to originate impulses as does the cell of an 
electric battery, the nerve-fibres serving merely as conductors, it is 
more than doubtful whether any impulse ever arises within a 
nerve-cell, except as the result of a transmitted impulse. Each 
nerve-fibre is made up of a bundle of extremely fine neuro- 
fibrillte which traverse the nerve-cell, entering it through one process 
and leaving it through another. In this way the nerve-cell acts 
as a convenient shunt for impulses, receiving them from one 
quarter and transmitting them to another. The nerve-cell also 
exerts a trophic infiuence over the nerve-fibre and is intimately 
concerned with its nutrition, so that the nerve-fibre degenerates 
if separated from its trophic nerve-cell. 


In a reflex motor act, which is the simplest manifestation of 
nervous energy, as for example in the plantar reflex, the impulse 
or stimulus starts from a sensory end-organ, in this instance the 
skin of the sole. The impulse travels up a sensory nerve-fibre, 
through the corresponding posterior nerve-root into the spinal 
cord, and there, through the intermediation of another inter-com- 
municating nerve-fibre and cell in the grey matter of the cord, 
it reaches an anterior comual cell. From this motor-cell an 
efiEerent impulse starts, travelling outwards along an anterior 

Ibst, ntjyr root 

Wipherat ntrye/ 



Fio. 1. — Diagram of a {Simple Spinal Reflex. 

nerve-root into a peripheral nerve and thus reaching a muscle-fibre 
in the flexor muscle of the toes. The muscle contracts and with- 
draws the sole of the foot from the original irritant. 

The accompanjdng diagram (Fig. 1) will serve to recall the chief 
components of a simple spinal reflex, such as we have just described. 

Some reflexes occur unconsciously, as for example the reflex 
contraction of the pupil when the retina is stimulated by light, 
or again, the normal movements of the stomach and intestines. 
But in other cases the afferent impulse, besides exciting a reflex 
motor action, sends part of its impulse upwards to the higher 
centres of the opposite cerebral cortex, where it produces a con- 
scious sensation. This is accomplished by means of a sensory fibre 
passing upwards in the substance of the spinal cord, as indicated 
in the other diagram (Fig. 2), through relays of nerve-cells and 


fibres in the medulla, pons, and so on, to the perceiving centre in 
the cortex. 

Moreover, a discharge of motor energy from the motor cell in 
the anterior comu can be produced not only reflexly, from below, 
but also voluntarily, from above. This is achieved by an impulse 

Sensory t 




Fig. 2. — Diagram of a Voluntary Motor Act 

descending from the cortical motor centre of the opposite side, 
through the crossed pyramidal tract down the cord to the anterior 
comual cell (see Fig. 2). A discharge can also be voluntarily 
inhibited from above. 

Confining ourselves now to the consideration of a cerebro-spinal 
reflex motor action, we must bear in mind that afferent impulses, 
on reaching the cortical sensory centres, do not necessarily produce 
a descending impulse along the pyramidal tract. If they do, this 
is simply an automatic action, or a longer variety of reflex. There 
exist in the cortex perceiving-centres which take cognisance of the 
source and nature of the stimulus, and determine whether or not any 


active notice shall be taken of it, that is to say, whether a voluntary 
(and not merely an automatic) movement shall or shall not take place. 

Some reflexes, even though associated with conscious sensory 
impressions (for example the vomiting reflex, or the sexual reflex), 
cannot be inhibited. This is possibly owing to the absence of anta- 
gonistic muscles which could prevent the reflex. But other reflexes 
can be inhibited by contracting the opposing muscles and thereby 
fixing the part which would otherwise make a reflex movement. 

Finally, by education, a motor impulse can be initiated at the 
cortical motor centre, mthout any preceding afferent impulse 
from the part to be moved. All movements in a new-bom 
infant are either reflex or automatic, and only gradually does the 
child learn to call in antagonistic muscles, and, by an effort 
of will, to inhibit reflex acts and to initiate voluntary ones. 

Certain more complicated reflexes, such as the reflex move- 
ments of respiration, have their centres in the medulla ; others, 
such as the movements of the heart and blood-vessels, have their 
lower reflex centres in the sympathetic ganglia, but can also be 
influenced by the cerebro-spinal nervous system. Others again, 
such as the movements of the stomach and intestine, can be per- 
formed independently of the central nervous system. 

Figs. 3 and 4 are diagrams of the cerebral cortex, both on its 
convex and its mesial aspect. It is unnecessary here to enumerate 
in detail the various fissures and sulci, or the different lobes and 

When we look at a brain, the first landmarks to be identified 
are the Sylvian and Rolandic fissures. The fissure of Rolando 
starts at the middle line above, from a point half an inch behind 
the mid-point between the nasion and the external occipital 
protuberance. It runs downwards and forwards, along the convex 
surface of the brain, in the direction of the anterior part of the 
horizontal limb of the Sylvian fissure, making an angle of about 67 J 
degrees, i.e, three-quarters of a right angle, with the middle line. 

These two figures also show diagrammatically our present 
views on cerebral localisation. It should be particularly observed 
that the motor areas in the pre-central convolution extend back 


as far as the Rolandic fissure but not behind it, as was formerly 
taught. Not only by experimental stimulation in anthropoid apes,^ 
and in certain cases in man, but also by histological research,^ 
it has been shown that the posterior wall of the Rolandic fissure 

Fig. 3. — Scheme of Cerebral Localisation (outer surface). 

Fio. 4. — Scheme of Cerebral Localisation (mesial surface). 

differs in structure and function from the anterior or motor wall. 
The anterior wall possesses giant pyramidal cells with no granular 

* Sherrington and Griinbaum, Trans. Path. Soc, Lond., 1902, vol. liii. 
p. 127. 

* Campbell, A. W., Histological Studies on the Localisation of Cerebral 
Function, 1905. 

Brodmann, K., Journ. f. Psychologic und Neurologic, Bd. ii. p. 80. 


layer, wbiUt the posteriot wall has a distinct granular layer with 
no giant cells (see Fig. 5). 

Another point to remember is that the different so-called motor 
areas are not sharply marked ofi fiom one another like a mosaic, 
but overlap, each area in Figs. 3 and 4 signifying that stimulation 
of that point produces the maximum movement of the particular 

Hc«4^ra>'\s' ' ".,-'■■ "^'■"' ■■""^O^fn^ 

Flu. 6. — Diagram of cellular Htructure of pre- and poBt-central convolutione 
(after Vogt). 

part mentioned. Moreover, there are minor variations in the 
extent of the various centres in different individuals. 

The chief path by which motor impulses are conducted from the 
cortical motor areas to the muscles, is the pyramidal tract, whose 
course is diagrammatically indicated in Fig. 6. From the motor 
cells in the cortex the fibres converge through the cof(ma radiata 
into the great strand of nerve-fibres between the lenticular 
nucleiis externally and the optic thalamus and caudate nucleus 
internally, namely, the internal capsule. Fig. 7 shows a horizontal 
section through the internal capsule, in which we notice that it has 
an anterior and a posterior limb, joining each other at an obtuse 
angle, the genu or knee. The motor fibres for the leg and arm 


Caudate JfiLcJeus 

LeniicularNunlenjS - - - 

Level of Sr'-Jferve 

Level oflioLciaLNerve 



MypocflossoL Nerve 

-Direct^ramidjaL THlcC 



Fig. 6.— Diagram of Pyramidal Tract and its course through the brain 

and cord. 


occupy the anterior two-thirds of the posterior limb, the fibres for 
the tongue and mouth are at the genu, those for the face just in 
front. But the order in which these different strands pass through 
the internal capsule is not quite the same as that in which they 

Fig. 7,— Horizontal bi 
positiun of the vi 
aad HorBley.) 

started from the cortex. Thus we notice that immediately behind 
the fibres for the lips we have, from before backwards, those for 
the shoulder, elbow, and fingers (not fingers, elbow, shoulder), 
then for the trunk, and lastly for the hip, knee, and toes. We 
also notice, in passing, that the pathway of the sensory fibres 
traverses the posterior part of the capsule, antl that behind them 


' again are the visual fibres. The aeriBory fibn-s probably do not 
form a separate, compact bundle, but arc partially mingled with 
[ Bome of the motor fibres for the leg. 

Before leiiving Figs, (i and 7, it is of interest to study briefly, 
with their help, the difierent effects produced by lesions of the 
pyr&midiil motor tract at various levels. 

A Jesion in or near the trwtor cortex, if moderate in size, will 

produce, according to its situation, a monoplegia of the face, arm, 

or leg, on the opposite side of the body. A somewhat larger lesion 

will produce a brachio- facial or a brachio -crural monoplegia. {We 

observe that facio-crural monoplegia without implication of the 

arm is impossible from a single lesion.) For the prwluction of a 

complete hemiplegia of face, arm, and leg there must be a very ex- 

[ tensive cortical lesion. But in the inUrruil capsule all these strands 

I are closely crowded together, so that a moderate-sized capsular 

a. can produce a complete hemiplegia, whereas a capsular lesion 

I small enough to cause a mere monoplegia is well-nigh impossible. 

If the capsular lesion be in the region of the f/enu we have 
I hemiplegia of face, arm, and leg. And moreover, from paralysis 
of the muscles which rotate the head and eyes to the opposite side, 
I the patient has " conjugate deviation " of the head and eyes 
I towards the aide of the lesion, owing to unopposed action of the 
I muscles supplied by the intact hemisphere. 

If, on the other hand, the capsular lesion be farther back along 
I the posterior limb of the capsule, the hemiplegia will affect the leg 
I much more than the arm, and the face only slightly ; whilst, owing 
I to interference with the sensory tract, which lies between the motor 
I and the visual fibres, there will now be hemiansesthesia also. 

Lastly, if the lesion be at the extreme posterior end of 

I the capsule, there will be not only hemianiesthesia but also 

fmianopia from interruption of the visual fibres. Here again 

e note that it is impossible for a single capsular lesion to produce 

lat the same time hemiplegia and hemianopia without also pro- 

I ducing hemianaesthesia. 

A lesion oj the crus cerebri will tend to implicate the third cranial 
I nerve on the side of the lesion, producing at the same time a bemi- 



plegia of face, arm, and leg on the opposite side. This so-called 
" Weber's ayndrome " is one variety of " crossed paralysis." 

A unilateral lesion of the pons at the level of exit of the facial 
nerve will produce anotbet " crossed paralysis," viz. : — facial palsy 
on the side of the lesion with hemiplegia of the arm and leg of the 
opposite side. And if at the same time the nucleus of the sixth 

FiCi. H.— DUgriLiii of Tmcl-a in the Spinal (.'unl. 

1. CrouHl pyrimlJil tnrt (ileicendliii:) Ti. l>lrec:tnriionii1 ccrphellir 

>nd »<piDU-thalsmlc trust (uucnd 111)1.) n. Vi^iitral ci^rrlivllnr trai't (f 

2. Uireat ptramldiil li " " 
U. l^itwru-lii tenia) Iri 

1:1 (Kur 



cranial nerve be implicated (which is not unusual, since the facial 
nerve hooks round the sixth nucleus within the pons), we Have 
nuclear palsy of the sixth nerve, facial palsy on the same side, 
and hemiplegia of the arm and leg on the opposite side : — the 
" Millard-Gubler syndrome." 

Unilaieral lesions of the pons or medulla behw the level of the 
facial nerve leave the face unaffected and produce only a hemiplegia 


of arm and leg. And a unilateral lesion of the spinal cord below the 
cervical enlargement will produce a monoplegia of the leg on the 
side of the lesion vrithout affection of the arm. It will also produce 
some anaesthesia of the opposite leg. Such motor paralysis of one 
leg and sensory paralysis of the other is called " Brown-Sequard 
paralysis," to which we shall return later. 

Fig. 8 is a diagram representing the tracts in the spinal cord 
of chief clinical interest. There are also other ascending and 
descending tracts of minor importance, which we have omitted 
from the diagram for the sake of simplicity. 

The pyramidal tracts are by far the most important descending 
tracts in the cord, for they convey voluntary motor impulses down- 
wards from the motor cortex towards the anterior comua. The 
pyramidal fibre does not actually join the anterior comu, but ends in 
the region of the posterior comu, whence a short intermediate con- 
necting-cell and fibre run forward, linking it to the anterior comual 
cell (see Fig. 2). Most of the voluntary motor impulses decussate 
at the lower end of the medulla and traverse the crossed pyramidal 
tract in the lateral colunm, a few nm in the direct pyramidal tract 
and cross over later within the cord itself. A few pyramidal fibres 
also run down in the homolateral pyramidal tract (which we might, 
somewhat paradoxically, call the uncrossed crossed-pyramidal tract). 
These fibres probably do not cross over, but supply motor impulses 
to the homolateral leg. 

Sensory Paths. — ^According to Head, Rivers, and Sherren,^ 
the various afferent impulses from the periphery, on their way 
towards the spinal cord, do not run indiscriminately along the 
afferent nerves but are conducted along several distinct classes of 
nerve fibres. According to these observers, conmion sensation is 
a complex affair, based on three kinds of sensibility : — 

1. Deep sensibility y a variety which takes cognisance of deep 
pressure, and which, if that pressure be excessive, is capable 
of producing a sensation of pain — " pressure-pain." Deep sensi- 
bility also includes sensations from muscles, from joints, and 
the vibration-sense (see later, p. 184). The fibres conducting deep 

1 Brain, 1905, pp. 99-115. 



sensibility run along with the muBCuUr nerves and are not de- 
stroyed by division of all the sensory nerves to the skin. 

2. ProtojxUhic cutaneous sensibility, a variety which responds 
to painful cutaneous stimuli (pricking, faiadic stimulation), also to 
extremes of cold and heat, like freezing and burning (tempcTatures 

Fia. fl.— Diagi 

TrmperaUirt a/ui Pain, 
Tactilr Strut. 

X KcnsoTy pablia ii 

of 45° C. and over, and of 10° C. and under). These protopathic 
fibres from the skin are the first to regenerate after injury to a 
cutaneous nerve, so that the protopathic sensations are the earliest 
to recover as a cutaneous nerve heals. 

3. Epicritic cutaneous sensibility, whose fibres are the slowest 
to recover after injury. This group includes the appreciation of 


light touches, of cutaneous localisation, the recognition of finer 
differences of temperature — not merely between hot and cold, 
but between warm and cool. 

These differences, it should be noted, apply only to the extra- 
spinal portion of the sensory paths, i.e. to the peripheral nerves. 

All the sensory impulses, whether conveying sensations of 
touch, temperature, or pain from the skin, sensation of active 
muscular contraction from the muscles (kinsssthetic sense), or 
sensations from the joints or bones, enter the spinal cord through 
the posterior roots, as indicated in Fig. 9. 

Once the afferent impulses enter the spinal cord, it is no longer 
a question of deep, epicritic, or protopathic sensation, they now 
become redistributed in simpler fashion. Thus all sensations of 
temperature run together in one tract, whether they reached the 
cord by the protopathic or the epicritic route : similarly all sen- 
sations of pain run together in the cord, whether they were 
protopathic or " deep " in the peripheral nerves, and so on. This is 
indicated in the following scheme. 

Paths in Spinal Cord. Paths in Pkripukral Nerves. 

Posterior Column \ rp«/.f ii« 
Lateral Column / ^»"ue 

Deep . . a Pressure. 

I fi Light Touches. 

Lateral Column 


Epicritic . \ o Differences in Size. 

(fr»»..w..«*.... / « ^« Moderate differences of Temperature, 

lemperature j ^ ^ ^ Extreme differences of Temperature. 

Protopathic-^ i, Cutoneous Pain (pricks, freezing, burns, 
i, electricity). 

B fB Pressure-Pain. 

(Muscles I wx-^_ /i Lengthening or Shortening of Muscles. 

Posterior Column^ ^^P ' ' \ 

( Joints ic I ic Joints— passive movements. 

Lateral Column Vibration A \A Vibration (tuning-fork). 

Of these various impulses, the fibres conveying sensations 
from the muscles and joints, together with the smaller part of the 
fibres for tactile sensation, ascend in the posterior column to the ' 
gracile and cuneate nuclei of the same side of the medulla. Most 
of the fibres for tactile sense, together with those for temperature 
and pain, cross in the anterior commissure to the opposite side 
(these crossed fibres not coming directly from the posterior root, 
but through the relay of another cell in the posterior horn) and 


ascend the cord in the opposite lateral column, in the spino- 
thalamic tract. Thus the lateral column conducts not only 
p}rramidal motor impulses coming down, but also spino-thalamic 
ascending impulses of touch, temperature and pain. 

The upward course of the various sensory fibres through the 
medulla and pons is somewhat complicated, and not yet entirely 
settled, but the most probable arrangement is shown in Fig. 10. 

Most of the fibres for touch cross the middle line in the spinal 
cord, as already explained, and then pass directly upwards in the 
spino-thalamic tract of the lateral column and into that part of the 
medulla called the formatio reticularis. The formatio reticularis 
leads the fibres up through the pons and cms to the optic thalamus, 
and thence they pass through the posterior limb of the internal 
capsule to the sensory cortex behind the fissure of Rolando. 

As the sensory tract traverses the pons it passes along the 
inner side of the sensory spinal root of the trigeminal nerve of the 
same side. Thus a unilateral lesion of the fonnatio reticularis 
below the exit of the fifth or trigeminal nerve will produce a 
" crossed ansesthesia," i.e. anaesthesia of the face on the side of 
the lesion, and of the arm, leg, and trunk of the opposite side. But 
higher up the pons the sensory fibres from the face also cross the 
middle line, so that a lesion of the formatio reticularis in the cms 
cerebri will now cause complete hemianesthesia of face, arm, and 
leg (see Fig. 11). 

The fibres for temperature and jxiin, entering by the 
posterior root, pass into the grey matter of the posterior cornu. 
There they start afresh and cross to the opposite side of the 
cord, ascending in the opposite lateral cohimn near the crossed 
tactile fibres. On reaching the medulla, they diverge from the 
tactile fibres and pass to the outer side of the olivary body, close 
to the lateral margin of the medulla and intermingled with the 
fibres of Gowers' tract. They then leave the region of Gowers' 
tract and pass upwards through the pons, gradually inclining to- 
wards the other sensory tracts and ultimately ascending with them 
to the optic thalamus and thence through the internal capsule to 
the cortex. Gowers' tract, now separate from the temperature 



Optic ThaUimus 

Tactile St 

Joail Srnxt 

KutaaUhtOr: Stuff 

^jMcHorRcvt — 



and pain fibres in the upper part of the pons, hooks sharply 
backwards and enters the cerebellum from above, through the 
superior peduncle. 

The sensory fibres from muscles and from bones, together with 
the uncrossed minority of tactile fibres, ascend uncrossed in the 



Fig. 11. — Course of Sensory Fibres in the Pons (Starr). 

A. T/esion causiOK right heniiaiiH^sthesia. 

B. Lesion causing " alternate heuiianaisthesia" of left face and right side of body. 

posterior column of the cord to the nucleus gracilis and nucleus 
cuneatus, the nucleus gracilis receiving the fibres from the lower 
limb, the nucleus cuneatus those from the upper limb. From these 
two nuclei, nerve fibres pass upwards, and cross the middle 
line in the internal arcuate fibres, forming the superior sensory 
decussation of the fillet (contrast this with the spinal decussation 



^B of the thermal, pain, and the majoiity of the tactile fibres). The 

^P sensory fibres from the leg, passing through the nucleus gracilis, 

cross lower down than those froai the arm, which go through the 

nucleus cuneatus. Having crossed to the opposite side and reached 

the fillet, B flattened strand of fibres, they pass upwards in that 

^L iract not far from the thermal and pain fibres. The main maaa 

^L* of the tactile fibres ascends through the crua cerebri to the optic 

^B thalamus, and passes on through the internal capsule to the sensory 

^P cortex, which lies mainly behind the Rolandic fissure.' 

^P We have still to consider another tract, which conducts sensory 

fibres for the sense of equUihrium. This tract does not commence in 

the posterior root-ganglion but arises as an "endogenous" tract 

I within the cord. Arising from the ceUs of Clarke's column at the 
base of the posterior horn, it constitutes the direct cerebellar tract 
and ascends, uncrossed, into the restiform body and cerebellum. 
Before leaving the motor and sensory tracts within the central 
nervous system it will be useful to mention the symptoms produced 
by a lesion of one lateral half of the spinal cord. Such a lesion 
is most commonly the result of a stab in the back ; less commonly it 
is produced by bullet- wounds, fractured spine, or by chronic diseases 
^^ of the spinal cord itself. The syndrome which results is known 
^m as Brown-S^quard paralysis and it will be readily understood by 
^^ reference to Figs. i> and 12, The symptoms are as follows : — 
^H (1.) On the side of the lesion we have, from interruption of the 
^H'tnotor tract, motor paralysis of the corresponding leg, with an 
^Beztenaor plantar reflex from the outset and, later on, exaggeration 
^R(>f the deep reflexes. There is a slight elevation of temperature, 

^^f • Sensory iinpulaeB run up not only to thn post-central convoliitionB, but 
klsD to the motor arena. Tliua a leBJon of the motor cortex, lipmdeB esiusmg 
a monojJopa of the corrCBpondiug limb, producer alight aiueBthesia o( the 
affected limb, with dofipjeiit sense of position in the weakened parta and 
diminiahed kinajsthetic sense in the afFei^ted mmdes. It is to be boma in 
that the pjTamidal mutor cells do not lio in the most superficial layer 
it the cortex, but are covered by e. layer of eella which am probably 
function. A striking evidence of this was afforded by a case 
Negro and Oliva. Tlieee obaorvore had the opportimity of stimulating 
t&e motor cort«i of a woman who had been trephined. They found that 
with feeble stimulation only sensory symptoms were produwid, a stronger 
Miiuulue being required to cause motor 

ating I 

that ^^M 
3tiger ^^^1 


owing to the interruption of vaso-motor fibres which descend in 
the lateral column. There is loss of sense of position on passive 
movement of the limb, due to interruption of the uncrossed fibres 
from the posterior roots below the lesion, which ascend in the 
posterior colunm. The paralysed leg is not anaesthetic, but, 
just at the level of the lesion, there is around the trunk a 
narrow zone of anaesthesia to touch, temperature, and pain, 
from severance of a few sensory fibres cut across before they 
have succeeded in crossing to the other side. Finally, there 
is a narrow zone of hypersesthesia above the ansesthetic zone, 
perhaps due to local irritation of the lowest imsevered posterior- 
root fibres in the cord, close above the lesion ; but this explana- 
tion is in dispute. 

(2.) On the side opposite to the lesion there is no motor paralysis. 
But there is loss of cutaneous sensation to temperature and pain 
(completely), and to touch (partially), in the non-paralysed lower 
limb and in the corresponding half of the trunk up to the level of 
the lesion. " Vibration sense " (tested by a tuning-fork) in the 
bones of the leg on the uninjured side is also lost, since the path 
of vibration sense in the spinal cord closely corresponds with 
that of temperature sense. There is a zone of h3rper8esthesia 
above the anaesthetic area, as on the side of the injury. Motor 
power is unimpaired, so also is the sensation of position on active 
or passive movement of the limb. 

Oerebellum. — ^The cerebellum consists of a middle lobe or 
vermis, with a lateral lobe on each side, and its cortex is 
finely folded into leaves or lamellae. Within the white matter, 
at a distance from the cortex and analogous in some respects to 
the basal ganglia of the cerebrum, there are several important 
masses of grey matter, of which the chief are the corpora derUata, 
two hollow crumpled sacs, one within each lateral lobe ; the roof 
nuclei within the middle lobe ; and the nuclei of Deiters, or accessory 
vestibular nuclei, within the pons, one on each lateral aspect. 
Deiters' nucleus has several highly important connections, with 
the cerebellar cortex, with the ocular nuclei (third and sixth), 
and with the anterior cornual cells of the same side of the 



cord, through the veatibulo-apinal tract. This centre in Deitera* 
nucleus, with its varioua connections, is probably the lower reflex j 
mechanism whereby, when we hear a sound, the head and eyes are 


promptly tiirned towards the side on which the auditory stimulus 
was received. 

Each lateral lobe has three peduncles (Fig. 13). Of these, 
the superior peduncle contains fibres derived mainly from the \ 



dentate nucleus, this nucleus in turn being connected with the 
cerebellar cortex. The fibres of the superior peduncle pass up ventral 
to the corpora quadrigemina, cross the middle line and reach the 
red nucleus in the cms cerebri of the opposite side. Starting again 
from this station, fibres run forwards along the anterior limb of 







arXabrospuial tract i: 


Ca^helUw tract 


Fig. 13. — Diagram of chief connections of Cerebellum and of Red Nucleus. 

the internal capsule, and pass to the optic thalamus and to the 
cortex of the frontal lobe. In this way the cerebellar hemisphere 
of one side is connected with the opposite side of the cerebrum, 
such connection being not a direct one, from cortex to cortex, but 
indirect, by the intermediation of intra-cerebellar and intra-cerebral 

The middle peduncle constitutes the greater part of the trans- 
verse fibres of the pons. And here again its fibres are not mere 
commissural strands nmning from one lateral lobe to the other. 


21 J 

Fibres from each lateral lobe cross the middle line, it is true, bat 1 
they end in cells in the fonnatio reticularis of the opposite side 1 
of the pons. There new fibres arise and pass up the superior | 
peduncle through the cms cerebri and internal capsule to the I 
frontal, temporal, and occipital lobea of the cerebrum. Im- ] 
portant fibres alao connect Deiters' nucleus with the correspond- 
ing aide of the cerebellar cortex in the region of the flocculus, 
conveying impulses to the cerebellum from the semicirculat ] 

The inferior peduncle or reatiform body connects the cere- 
bellum with the medulla and spinal cord. It contains the direct J 
cerebellar tract, conveying impulses of equilibration from the 1 
same side of the spinal cord, also arcuate fibres from the poa- 
terior column nuclei of both sides, and fibres from the inferior 1 
ohve of the opposite side. All these fibres are afferent, leading J 

Broadly speaking, then, each lateral half of the cerebeUum is 
in connection mainly with the cerebral hemisphere of the opposite I 
or contra-lateral side, with both sides of the medulla, and with the | 
same or homo-lateral side of the spuial cord. 

Thus the cerebellum receives impulses from various sources :- 
from the cerebrum through the superior peduncles, from the skin 1 
and muscles through the inferior peduncles, and from most of the 
cranial nerve nuclei, especially from the semicircular canals, through 
the middle peduncles. And in turn the cerebellum sends efferent 
impulsea to the cerebrum, reinforcing the general muscular tonus 
and co-ordinating the motor impulses proceeding from the I 
cerebrum. In most voluntary movements the centre of gravity of ] 
the body requires to be altered and certain muscular groups have 
to co-ordinate to maintain equilibrium. For this purpose the j 
tonus of these muscular groups has to be augmented, and this is i 
accomplished by the cerebellum, the great centre for co-ordination 
and equilibration, partly by the action of the dentate, roof, and 
embolifomi nuclei on the cerebral motor cortex, partly by the 
nuclei of Deiters and the descending vestibulo-spinal tracts to the J 
spinal cord. 


Experiments ^ have shown that although the cerebellum as a 
whole — comprising cortex and nuclei — responds to stimulation, 
the cerebellar cortex, compared with the cerebral, is relatively 
very resistant to excitation. On the other hand, the sub-cortical 
cerebellar nuclei are highly excitable, and it is probable that 
stimulation of the cerebellum produces motor phenomena mainly 
by excitation of these nuclei. If we stimulate one lateral half of 
the vermis or the lateral cerebellar hemisphere, we produce move- 
ments of the homolateral limbs and also rotation of the body 
around its own longitudinal spinal axis. Thus excitation of the 
right side of the cerebellum produces a rotation in the direction 
of unscrewing an ordinary screw (the animal's head representing 
the head of the screw). Conversely, removal or division of the 
right lateral lobe produces rotation in the reverse direction — 
namely, that of screwing in a screw — since the intact side of the 
cerebellum maintains its tonic action, and is no longer opposed 
by the afEected side whose muscles have lost their tonus (hjrpotonia). 
In such unilateral destructive lesions loss of co-ordinating influence 
also causes inco-ordination of the homolateral arm and leg, 
together with various ocular phenomena, including nystagmus, 
owing to loss of cerebellar influence on the ocular nuclei through 
Deiters' nucleus. 

Stimulation of the vermis in the middle line produces bilateral 
movements. Thus, if the posterior end of the vermis be stimu- 
lated, the animal rotates violently forwards, whilst if the anterior 
part of the vermis be stimulated, the animal rotates violently back- 
wards. Destruction of the middle lobe produces opposite effects, 
the animal tending to fall forwards from an anterior lesion of the 
vermis, and conversely. 

The movements of the trunk and limbs which result from 
stimulation of the cerebellar cortex are apparently not produced 
by direct action of the cerebellum on the spinal cord. Not only 
is there no direct tract leading downwards from the cerebellum 
into the cord but only an indirect path through Deiters' nucleus 

* Horsley and Clark, Brain, 1908, p. 4.'5. 



and the vestibulo-Bpinal tract, but Fagano ' has shown that if the 
ctmtralateral cerebral cortex be extirpated, stimulation of the 
lateral lobe of the cerebellum no longer induces movements in the 
homolateral limbs. The motor action of the cerebellar nuclei is 
exercised indirectlj, through the intermediation of the auperior 
peduncles and the cerebral cortex. 

* Rivitla di patologia jurDo*a t mmtale, 1002, p. 14S. 



Having considered the chief motor and sensory tracts within the 
central nervous system, let us now pass to the peripheral paths 
whereby the central nervous system is connected with the various 

Firstly, as to the motor system. Motor fibres starting in the 
cortex, and passing down the pyramidal tract, as already described, 
reach the nuclei of the various motor cranial nerves in the crura, 
pons, and medulla. Then, passing along the spinal cord, the 
pyramidal tract gives oft fibres to the anterior cornua at various 
levels all the way down. This portion of the motor tract, from the 
motor cortex to the extremity of the pyramidal fibres, is called 
the upper motor neurone^ and if the cortical motor cell or its axon, 
the pyramidal motor fibre, be destroyed, we have degeneration 
of the whole length of the pyramidal fibre below the level of 
the lesion, stopping short when it reaches the anterior comual 
cell. This so-called " descending degeneration " does not, as the 
name might suggest, begin at the lesion and spread downwards, 
but aftects simultaneously the whole motor fibre below the lesion, 
on the side remote from the nerve-cell which is its trophic centre. 

From each anterior comual cell a new motor fibre passes out 
of the cord along an anterior nerve-root, enters into the formation 
of a peripheral motor nerve, and thereby is conducted to a 
muscle-fibre. This lower segment of the motor path, starting at 
the anterior comual cell and ending in the muscle-fibre, is called 
the lower motor neurone. Here also, if the anterior comual cell or 
its axon, the peripheral motor nerve, be destroyed, we again have 
a " descending degeneration " of the whole fibre on the distal side 
of the point of injury, and of the muscle-fibre also. We note that 
degeneration of the upper motor neurone does not spread into the 
lower neurone, nor vice versd. It is particularly to be remembered 




that a lesion of the upper motor neurone leaves the lower reflex 
arc intact, whilst a lesion of the lower motor neurone not only 
severs the reflex arc, but also causes the muscle-fibre in that reflex 
arc to degenerate and waste away. 

Therefore in diagnosing the position of the lesion, in any given 
case of motor paralysis due to organic disease, the first question 
we must ask ourselves is whether the lesion is in the upper (cortico- 
spinal) or in the lower (spino-muscular) motor neurone. There 
is usually little difficulty in answering this question, if we bear the 
following points in mind : — 


I. MoUir Paralyaia. 
3. Sp^ticity. 

3. No muscular wueliag 

from (tisuM:). 

4. Electrical reai^tiuns normal, 

!i. Deep reflpxes present nad often 

6. Extensor pla.itar reflex (if foot 


1. Motor I'al-aiysis, 

2. Fliiccidily. 

3. Miinculiir Att'U]>]iy. 

4. ll.D.(reftctionsof degeneration^. 
O. Deep reflexes alisent or dimi- 

e. Plantar ref!e>:, if present, of 
normal flejcor type (unlias 
lesion tmralyww Hex or 
museleB tli em selves). 

Having thus recognised which motor neurone, upper or lower, is 
affected, we have then to decide at what level in the affected neurone 
the lesion is situated. To that point we shall come later (p. 203), 

Returning for a moment to the sensory fibres ; these may 
also be regarded as arranged in sensory neurones. The lowest 
sensory neurone starts from a sensory end-organ, in the skin or 
elsewhere, and extends up to the nervo-cell in the intervertebral 
/ganglion on the posterior spinal root. This ganglion-cell is the 
trophic centre for the peripheral sensory fibre, and a lesion at or 
IjelQW this cell will cause " descending degeneration " of the distal 
segment of the fibre and of the peripheral end-organ. There is, 
however, one sensory end-organ, the muscle -spindle, which is an 
exception to this rule, and docs not degenerate when the afferent 
fibre leading from it to the ganglion-cell is destroyed. The 
niuscle-spindle thus has its trophic centre within itself. 

But the ganglion-cell of the posterior root is also the trophic 
iutre for the fibre which passes upwards from it along the pofl- 


terior root and enters the posterior column of the spinal cord. 
And therefore a lesion at or above the intervertebral ganglion-cell, 
in the posterior root, or in its intra-spinal prolongation in the pos- 
terior column, will cause an " ascending degeneration " of the fibre 
through its whole course within the spinal cord. Here again this so- 
called " ascending " degeneration occurs simultaneously throughout 
the entire extent of the nerve-fibre, on the side remote from its 
trophic centre in the intervertebral ganglion ; and this degeneration 
extends as far as, but does not impUcate, the next nerve-cell whose 
axon leads upwards towards the brain. Similarly a lesion of this 
second sensory neurone causes ascending degeneration in the fibre 
of the fillet above, as far as, but not including, the optic thalamus. 
There a third neurone starts, leading up to the sensory area of the 
cerebral cortex. In the case of the ordinary sensory tract, the 
path traverses the internal capsule. In the case of an impulse 
which traverses the cerebellum, the chain of successive neurones is 
more complex, and consists, firstly of a posterior-root neurone, 
secondly of an ascending spino-cerebellar neurone, thirdly of a 
cerebello-dentate, fourthly of a dentato-thalamic, and lastly of a 
thalamo-cortical neurone. The so-called " WaUerian degeneration " 
— " ascending » or " descending " as the case may he-signifies 
that a nerve-fibre, separated from its trophic cell, degenerates on 
the side remote from that cell. 

The anterior and posterior nerve-roots join to form mixed 
nerve-trunks. These again branch and intermingle to form plexuses 
in the cervical, lumbar, and sacral regions. The distribution 
of the different nerves, motor and sensory, is represented in 
Figs. 14, 15, and 16. 

Root Lesions. — But what is perhaps less familiar, though of 
equal diagnostic importance, is the distribution of the anterior 
and posterior spinal roots. In lesions of the lower motor neurone, 
we have often to decide whether the distribution of symptoms 
points to a lesion of a peripheral nerve-trunk, such as the musculo- 
spiral or sciatic, or whether it points to a lesion of one or more 
nerve-roots before they have joined to form the trunks of a plexus. 
Thus, for example, the deltoid is frequently paralysed alone owing 


to a lesion of the circumflex 

as a result of a lesion of the anterior c 

Again, a lesion of the musculo -spiral i 

but it is never paralj'seil alone 
or anterior nerve-root. 
may produce paralvsta 

both of the supinator longus and of the extensors of the wrist and 
fingers, but these muscles are never affected together by a lesion 
of a single segment of the spinal cord or of a single anterior root, 
since their motor cells lie at different levels in the anterior comu. 
This will be readily seen on studying the tables on p. 31, which 
show the nuclear representation of muscles in the anterior comua 


at varioua levels of the spinal cord. For clinical purpoees, the 
distribution of each anterior root may be considered the same 
as that of the spinal segment from which it arises. 

In connection with the toot distribution of sensory and motor 
fibres, it is interesting to note that in each embryonic segment or 
metamere, the muscular territory (myotome) of the segment corre- 
sponds more or less closely with the cutaneous distribution 
(dermatome) and with a zone of the bony skeleton (sclerotome). 

Fia. 17. — Tronsverao sertion through upper third of thigh. 
The thick black line indicates tlie boundary between the 

£ re-axial and poat-axial reaioiiB of the limb. The fine black 
nes mark the srgiuental diatributinn. (After Bolk.) 

In the trunk this segmental or metameric arrangement is com- 
paratively easy to recognise, especially in the thorax, and even in 
the limbs, though more complex, a similar arrangement can be 
made out. Thus, aa Bolk has shown, in the limbs there is for 
every spinal segment a corresponding dermatome, myotome, and 
sclerotome, but they are subdivided into a pre-axial and a post- 
axial division in each case (see Fig. 17). 

We observe that comparatively few muscles are confined to a 
single segment, bnt that most of them are represented In two or 
more segments. If, therefore, a cord lesion be limited to one 
segment, it will cause complete paralysis of the muscles con- 
fined to that particular segment and partial paralysis of muscles 

CI 1 C! 1 « j C« ' C6 ' CB 

C7 C8 1 Thl 


w-broi'd , 1 

' Muscular Localisation 

o-bjold 1 


■ Cervical Enlarobmbnt 




Bop nMorLonim 


Tsm MlDor 










T.,v\: ^7 

"^.""l "l, "r L. "" V 1 E, |«i «. 





Mdsculab Localisation 

1 P^tfn 


Lumbo-Sacral Cord 


ObUmwr Enl. 

Add'nctor Ung 

Qiudrlcep. EiWiuor 

Tem laic. (em. 


1 TII>>A 

1 Exl«ii>.|iro 

p. b.llQOl> 



1 Kilflii«.r 


I ^G 

IIUD. Modlx. 

1 q' 


' IMronaD ■ l0D|riu> 

E«, bruvLaiKltomai 


TlbMlipHlIc 1 

riei. loDK. dlultor. 

Fle». long. h.llac. , 


SS."«,'or I..t«'n.«. 

1-1 ■ularb 1 

Venra. Brov. 

AbdacCAr bmllDcl- 

nei.brev. hill. 



Spblncler A nl eit. 

1 Le 







whose motor nuclei extend up or down into other a 

explains the apparent irregularity in the distribution and de( 

of paralysis in certain cases of infantile paralysis. 

Similarly in a case of cutaneous anuBsthesia it is important t 
distinguish between a posterior-root lesion and a lesion of a j 

pheral nerve-trunk such as the radial or ulnar The distnbutioii i 

the posterior nerve-roots is indicated diagrammaticaltv m Fig. 18J 

Paths of Special Senses —Olfactory Path —The olfacto 
nerves, about twenty on each side ansing from the under e 
of each olfactory bulb, perforate the cnhnform plate of the 
ethmoid bone and are distributed to the olfactory region of the 
nasal mucous membrane. The central olfactory tract has various 


connections, not of great clinical importance, leading to the optic 
thalamus and to other sub-cortical ganglia. It connects the 
olfactory bulb with the cortical centre for smell, situated, as we 
have already seen, in the uncinate gyrus at the tip of the temporo- 

lenoidal lobe (Fig. 4). The olfactory tract does not traverse 
the internal capsule. Each olfactory bulb is connected not only 
with the uncinate gyrus of the same aide, but also, through the 
anterior commissure, with that of the opposite side. 

Visual Path.— This is of great clinical importance. Starting 
from the retina, the visual fibres run backwards along the optic 
nerve. At the optic chiasma there is a partial decussation, so that 
the fibres from the left halves of both retinae (corresponding to the 
right halve* of the visual fields) run together in the left optic 
tract, and vice versil. The central visual impulses, from each 
macula lutea, pass into both optic tracts. The fibres of each optic 
tract run backwards, winding around the outer aide of the cms 
cerebri, to the primary optic centres, viz, : — the posterior part 
of the optic thaJaniuB, the external geniculate body, and the 
superior corpus quadrigeminum. 

From these three stations new fibres arise, forming the " optic 
radiation," passing through the internal capsule behind the 
fibres for common sensation (Fig. 7) and so reaching the cortical 
half-vision centre. This centre, mainly on the mesial aspect of 
the hemisphere, is divided into an upper and a lower part 
by the calcarine fissure (Fig. 4). Above the fissure is the cuneate 
lobe, be'ow it ia the lingual gyrus. The half-vision centre also 

[extends on to the convexity of the occipital lobe at its posterior 
extremity (Fig. 3), The calcarine fissure forms a boundary- 
line between the cortical representations of the upper and lower 
quadrants of the corresponding half of the visual field. Therefore 
a lesion of the left occipital lobe, or of the whole of the left 
cuneua and lingual gyrus, or of the fibres of the left optic radiation, 
will cause a right-sided hemiatiopia in both visual fields ; a lesion 
of the left cuneus, i.e. limited to the part above the calcarine 
fissure, will cause blindness of the right lower ijuadnn)t of both 
visual fields ; whilst if the lesion be bcfaw the left calcarine fissure, 
^ L 



in the lingual gyrus, it will produce blindness of the ri;/kl upp 
quadraiit of both fields. These are varieties of " quadianti 

—Diagram of Visual Fatba (after Violet), 
urtiwei BlindneM of rnie eye. 
„ BL'temponl Hemlinnpii. 

'.', B, HemUniipli wfth Bemrnptc Puiill KewUon. 
., with Niiminl Piiplf Kcwllou. 

». CroiHd ATnUfopLo. 

Besides the half-vision centre, there is a higher centre on ti 
surface of the occipital cortex, where a lesion, if suJ 



ciently superficial (ao as to miss the subjacent optic radiation), 
may cause, not hemianopta, but what is called " crossed ambly- 
opia." This means a concentric contraction of both visual fields, 
more marked in the eye of the side opposite to the side of the 
lesion. Such a lesion has not been conclusively demonstrated 
in gross organic disease, but crt>saed amblyopia is one of the most 
frequent symptoms in hysteria. 

Finally, in right-handed people there is in the left angular 
gyrus a centre for the storage of visual memories of written and 
printed speech. If this centre be destroyed, we have word-blind- 
ness, which may or may not be asBociat«d with right hemianopia, 
according as the subjacent optic radiations are aSected or not. 
Fig. 19 indicates diagrammatically these various fibres and centres, 
and also shows the effects upon the visual fields of lesions in various 
parts of the visual path. 

Oufitatorr PatlL^The course of the taste-fibres outside the 
brain is somewhat complex, and we shall study it again later when 
we consider the cranial nerves. It is probable that some of the 
taste impulses, chiefly those from the front of the tongue, enter the 
brain through the sensory root of the fifth cranial nerve, some 
through the gloss o-pharyngeal nerve, and some through the 
nerviis hittrmfdiits or sensory root of the facial. The cortical 
centre for tast* is in the front part of the temporal lobe, close 
to the olfactory centre (Fig. 4). The intra -cerebral course of the 
gustatory fibres is not definitely settled, but it is probable that 
they do not traveree the internal capsule. 

Auditory Path. — This is of some practical importance. Enter- 
ing the medulla in the cochlear division of the eighth nerve, 
the auditory fibres embrace the restiform body, acme passing 
along its inner side to the ventral auditory nucleus, others 
passing along its outer side to the dorsal auditory nucleus. From 
these two nuclei new fibres pass upwards towards the cortex. 
A few run up uncrossed in the fillet of the same side, but most 
of the fibres decussate and ascend in the fillet of the opposite 
side. Some end in the posterior corpus quadrigeminum, others 
go on to the corpus geniculatum externum, and finally the bulk 


of them, passing through the sub-lenticular region of the internal 
capsule behind the sensory fibres, reach the cortical auditory 
centre in the superior temporal convolution (Fig. 3), and in the 
anterior transverse temporal convolution of Heschl : — Flechsig's 
" auditory gyrus " ^ (situated on the upper surface of the temporal 
lobe, at the bottom of the Sylvian fossa, immediately behind the 
insula), with which the superior temporal is continuous. We note 
that each cortical centre receives auditory messages from both 
ears, though more extensively from the ear of the opposite side, 
and that therefore a lesion limited to one temporal lobe will not 
cause deafness. In right-handed people there is a specially 
differentiated portion of the left auditory centre where memories 
of word-sounds are stored up (Fig. 3). 

A certain amount of clinical evidence^ supports the view 
that there is a special cortical centre associated with the 
sensations of hunger and thirst. It would appear to be in 
the temporal lobe, at or near the olfactory centre. Abscesses, 
injuries and tumours in this region have been associated 
with voracious appetite and intense thirst, persisting for weeks 
or months. 

Arteries of the Brain. — ^Most cases of acute brain disease 
which we meet with in practice are the direct result of some 
vascular disease, e,g, haemorrhage, thrombosis, or embolism. It 
is therefore important to understand certain facts about the 
cerebral circulation. 

The brain is supplied by two pairs of arteries — ^the internal 
carotids and the vertebrals, as shown in Fig. 20. The two 
vertebral arteries join to form the basilar artery which runs 
forwards in the middle line along the front of the pons, supply- 
ing perforating branches to the pons and arteries to the cere- 
bellum. Between the crura cerebri the basilar divides into 
the two posterior cerebral arteries, each of which winds round 
the outer side of the cms, supplying it as it passes, and also 
giving branches to the optic thalamus and the corpora quadri- 

* Neurohgisches CentrMlatU 19()8, p. 1. 

' Stephen Paget, Essays for Students^ 1898. 



gemina. Finally it teaches and supplies the lower part of the 
teraporo-occipital cortex (Figs. 21 and 2Ia). Each posterior cerebral 
artery sends a posterior communicating artery forwards to join 
the internal carotid. 

The internal carotid, close to its termination, gives of! an 
important branch — the anterior choroid artery, which passes 
backwards to enter the descending horn of the lateral ventricle. 

The area supplied by the anterior choroid (see Figs, 21 and 21a) 
includes the posterior two-thirds of the posterior limb of the in- 
ternal capsule, part of the choroid plexiis of the lateral ventricle, 
and also the uncinate gyrus of the temporal lobe.* Finally, the 
internal carotid divides into three main branches — anterior 
cerebral, middle cerebral, and posterior communicating. The two 
anterior cerebral arteries are connected by the short anterior com- 
municating artery, thus completing the "circle of Willis." The 
anterior cerebral artery passes forward, and then, curving round 
to the top of the corpus calloaum, it turns Wckwards, parallel 

' Beovor, Brain. 1307. p. HVA 



with its fellow of the oppoait« side, between the meaial surfaces oil 
the two hemispheres. Most of the mesial surface of the cerebral ■ 
hemisphere, as far back as the paric to-occipital fbsure, is supplied 1 
by the anterior cerebral artery (Figs. 21 and '21a). It also sendsl 
branches over the edge of the hemisphere to its convex surface, 1 
supplying the anterior and mesial jmrt of the frontal lobe and a I 
small part of the parietal lobule. And at the beginning of it»l 
course, it sends a tew perforating branches inwards to the caudata I 



hatenor OreiralA 


ial fupplj of oorli 

The middle cerebral artery, or arteria fosses Syhni, is climoalli 
the most important of the three. Its main trunk passes upwardffi 
and outwards along the Sylvian iiasure to the surface of the island I 
of Reil, where it divides into its terminal branches. At ita be-^ 
g innin g it gives off numerous basal perforating arteries, which 
enter the anterior perforated space and ascend to the caudate and 
lenticular nucleus (which together constitute the corpus striatum), 
also to the optic thalamus. These branches are called lenticular, 
lenticulo -striate, and len tic ulo -optic, according to their distribu- 
tion. All these, and especially one of the lenticulo-striate arteries, .. 



', are frequently the seat of cerebral htemorrhage. The main trunk 
I of the middle cerebral runs along the Sylvian fissure, where it 
divides into four terminal branches (Figs. 21 and 21a). One goes 
to Broca'a convolution (the third inferior frontal) ; another to 
the lower two-thirda of the pre-central convolution and to the 
adjacent part of the second frontal convolution ; another to the 
post-central convolution and the adjacent superior parietal con- 
volution : and a fourth to the supra- marginal convolution, the 


T Beovor.) 

, angular convolution and the upper temporal convolutions, and 
so to the tip of the lobe on its mesial aspect. 

The cortical arteries anastomose with one another ; but not 

i'«o the perforating basal vessels. They are "terminal" arteries, 

, and do not anastomose either with each other or with the cortical 
els. Therefore if a basal artery becomes blocked by throm- 
bosis or embolism, a permanent area of necrosis results. On the 
other hand, the blocking of a cortical artery admits of a more 

1 favourable prognosis, since a collateral circulation may develop 

I and the necrotic process be arrested. 


The cerebellum is HUpplied by the anterior cerebellar and] 
au]>crior cerebellar arteries froni the basilar, and by the poste 
cerebellar artery from the vertebral, 

The sfinal cord is supplied by three main arteries, one anterioi 
and two posterior, running on the surface along the entire extenti 
of the cord. The anterior spinal artery arises from one or othttti 

Ant' Radicular 

^ — ^^ brantrtus /ivmr 
I \ bMrcostal Jtrta 

vertebral, receiving a small communicating branch from the opp« 
site vertebral. As it runs down the front of the cord, it is reinforce 
by a series of smaller vessels, derived from the intercostal i 
lumbar arteries, which enter here and there along the antericn 
roots. The anterior spinal artery sends numerous branches deeply 
along the pia mater lining the median fissure, dipping alternately 
into the right and left sidea of the fissure, and supplying the 
grey matter of the cord. The two posterior spinal arteries, onej 
on each side, also arise from the vertebral arteries and nukfl 
downwards on the back of the cord, close to the posterior r 



being reinforced by small brandies entering here and there along 
the posterior roots. Fig. 21 shows diagram mat ically the position 
of these various spinal arteries, and it should be observed that the 
grey matter and the white receive their blood-supply from different 
vessels. Moreover, hke the perforating basat arteries of the brain, 
all the spinal arteries, once they have penetrated the cord, are 
terminal arteries and do not anastomose. Therefore embolism or 
thrombosis of a spinal artery always produces an area of 

The Venona Circulation in the brain is peculiar, inasmuch as the 
direction of the blood-stream in the cortex is the same in the 
arteries as in the veins, i.e. from before backwards. The superior 
longitudinal sinus receives not only the superior cerebral veins from 
the cortex, but also some veins from the scalp, and through its 
starting-point at the foramen cfficum it receives branches from the 
nasal vein, though after childhood this foramen often becomes 
closed. Therefore when IfiTonibosis of the superior longitudinal 
tinus occurs in a marasmic child, wc expect epistaxis and distension 
of the nasal veins, together with distension of the veins of the 
scalp. Posteriorly the superior longitudinal sinus ends at the 
torcular Herophih. 

The inferior longitudinal sinus is quite small, and, like the 
superior, lies between the layers of the falx cerebri, but at its lower 
edge. It runs backwards to the anterior edge of the tentorium, 
receiving branches from the mesial surface of the hemispheres, and 
ends in the straight sinus. The straight sinus receives some 
cerebellar veins and the veins of Galen from the velum inter- 
poaitum and interior of the brain, and passes backwards either into 
the torcular Herophili or into one of the lateral sinuses. When 
the veins of Galen are thrombosed the cerebral ventricles become 
distended with fluid. 

The lateral sinuses begin at the internal occipital protuberance 
and arch outwards, one on each side, to open through the jugular 
foramen into the internal jugular vein. The sinus passes close to 
the mastoid portion of the temporal bone. Here it receives 
the superior petrosal sinus, and also emissary veins from the 


Bcalp in the mastoid region. Just before it empties into \ 
jugulftr, it receives the inferior petrosal siiiua and sonietinies tlu 
occipital aiiiiis from the torcular. IjtUeral sinus thrombosis 
well-known and dangerous complication of suppuration in 
middle ear. It is recognised by distension ot the mastoid vein 
oedema of that region, and hardness and tenderness of 
internal jugular vein. 

The cavernous sinuses lie one on each side between 

FlQ. 23.— Thro 

sphenoidal fisanre and the apex of the temporal bone, Each sinua 
receives the ophthalmic veins from the orbit and communicates 
by means of the circular sinus with its fellow of the opposite side. 
The sinua ends posteriorly by opening into the two petrosal sinuses. 
Thrombosis of the aivemous sinus is generally secondary to some 
septic condition of the orbit, naso-phar3Tix, or sphenoidal sinus. 
It is recognised by the presence of chemoais (cedema of the con- 
junctiva), proptosis (bulging forwards of the eyeball), and cedema 
of the upper lid and root of the noae (see Fig. 23). There may be 
paralysis of certain of the external ocular muscles from aSection 



of the third, fourth, or sixth nerves which he in the outer wall 
of the cavernous sinus. 

Nearly all the intra-ctauial venous blood leaves the skull by 
the internal jugular veins, so that in an infective thromboBia of 
any of the cerebral sinuses it may become necessary to ligature 
the internal jugular vein, to prevent a general pyiemia. 



In no class of maladies is a thorough examination of the patient 
of greater importance than in cases of nervous disease. One can- 
not urge too strongly the value of systematic examination, though 
it matters little what particular scheme of case-taking be adopted, 
so long as it is one which ensures that the investigation is complete, 
so that no point of importance is overlooked. Sometimes, it is 
true, we may make a diagnosis at a glance, as for example 
in paralysis agitans, or chorea. But more usually the patient 
presents symptoms or signs which are common to several diseases, 
and we have to decide which of these diseases he is suffering from. 
The chief causes of wrong diagnosis are insuj£cient examination, 
inaccurate observation, and, less commonly, false conclusions 
from correct and suj£cient facts. But if we pursue a good routine 
method of examination, gross errors of diagnosis can generally 
be avoided. 

Examination of a nervous case should not be confined to the 
nervous system alone. All the systems of the body should be 
investigated. An accomplished neurologist must be in the first 
place a sound physician. 

The value of negative as well as positive facts cannot be 
over-estimated. The neurological student should accustom him- 
self from the outset not only to chronicle deviations from the 
normal, but also, if he finds that certain other functions are 
normal, to record the fact and not to pass them over without 

As in any other case, a careful history should first be obtained. 
It is comparatively seldom that a patient, however willing he may 
be, provides us spontaneously with an accurate history of his 
case. We generally have to guide his tale by suitable questions, 
and in many cases we have to supplement the patient's accoimt 



I by mquiring for corroborative or correcting facts from the patient's 
We first inquire as to the mode of onset ol the patient's 
symptoms, whether such onset waa sudden or gradual, and, if 
gradual, the exact order in which the various aymptoma appeared. 
In the family fiistmy, inquiry should be made as to the occur- 
rence of nervous or mental disease in other members of the 
family, also as to a family history of gout, tuberculosis, cancer, 
&c. In certain cases, consanguinity of the parents should be 

t inquired for. In the account of the patient's previous hmUh, it is 
important to inquire as to syphilis, kidney disease, gout, rheumatic 
fever, or any previous nervous disease, and a note should be made 
■8 to the patient's occupation and habits of life, and as to his 
temperance in alcohol, tobacco, &c. "When inquiring about venereal 
disease, if the patient is a man, we should put our questions straight- 
I forwardly, but in female patients considerable delicacy is necessary, 
and it is advisable simply to inquire for collateral symptoms, 

»e,^., rashes, falling out of hair, sore throat and, especially in married 
women, a succession of premature or dead children. In any case 
we should never interrogate a male patient on the subject of 
venereal disease in the presence of his wife, or vice verad. 

Having thus noted the chief points in the history of the case, 
we proceed to the examination of the patient's jn-esent slate. The 
Bl following scheme will be found useful : — 

Scheme for Routine Examination of Nervous System. 

Higher Cerebral and Mental FimctioiiB. 

Intellectual funcuuns^EiMotional slat-e — Memory — H a! hi ci nations or 
del ua i a s^ IJcilirinni — Coma^Drowsi neaa — Insomnia. 

»^ta or other Abnormal Uovamente. 
Fits — TreiiioiB — Fibrillary movcmeii ta — Chorea — Atheloeis — Tic — 
Myoclonus, &c. Description of each. 
Speech and Articulation. 

Afihafiin — Is piitieiit right or left liaiided ) 
Cranial Nerves. 

1. Smell ^Anosmia — Paixiamia. 

L2. Visual acuity — Fields of vision : Hemiariopiu, int. — ColuiiivblindneRB 
— Ojihthalmoscopii: eininitiation — optic discs, atrophy, neuritis — 
retinal luomorrhagea, choroiditis, &c. 


\ Pupils : Size, shape, reaction to light (direct and consensual), and 
'I to accommoilation — External ocular movements — Ptosis — Move- 
' j ments of eyes in all directions — Convergence — Squint — Diplopia 
/ — Nystagmus. 
5. Sensation — Face : Conjunctival, nasal, and buccal mucous membranes 
Motor — masseters, temporals, pterygoids, &c. 

7. Facial muscles, upper and lower — Chorda tympuni : taste in anterior 

two-thirds of tongue — Nerve to stapedius — hy pcracousis ? 

8. Hearing : Aerial and bone conduction — Examination of meatus and 

tympanic membrane — Tinnitus — Vertigo. 

9. Taste : Posterior third of tongue — Anaesthesia of pharynx — Difficulty 

in swallowing. 

10. Palate — Recurrent laryngeal branch — Laryngoscopic examination — 

Heart, respiration, digestion ? 

11. Stemo-mastoid and Trapezius. 

12. Tongue (motor only). 

Sensory Functioxui. 

Subjective sensations : Pain : — site, character, frequency — Headache — 
Vertigo — Tingling — " Pins and Needles " — Formication, &c. 

Sensibility to touch — pain — temperature — Localisation of the spot 
touched — Vibration-sense (with tuning-fork) — Anaesthesia — Ptir- 
aesthesia — Hyperaesthesia — Tenderness on pressure over nerve- 
trunks, muscles, or skin — Joint-sense— Sense of active muscular 
contraction with different weights — Stereognosis. 

Motor FunctionB. 

Paralysis or Paresis : — In head and neck, upper limbs, diaphragm, inter- 
costals, spinal and abdominal muscles, lower limbs. 

Monoplegia — Hemiplegia — Diplegia — Paraplegia — Hemi - para- 
plegia — " Crossed paralysis," &c. 

Co-ordination : — Unsteadiness of upper or lower limbs on voluntary move- 
ment — Gait. 

Muscular Atrophy or Hyperti-ophy : Rigidity— Flaccidity — Hypotonia. 


Saperfidal. — Conjunctival, palatal, epigastric, abdominal, cremasteric, 
plantar (flexion or extension of hallux) — bulbo-cavernosus — anal. 

Deep. — Jaw, wrist, elbow, knee, ankle-jerks. Ankle-clonus — knee- 
clonus, &c. 

Organic. — Micturition — Retention — Retention with overflow incontinence 
— Intermittent incontinence — Constant paralytic dribbling — 
Defaecation — Control of sphincters — Priapism. 

Trophic FunctionB. 

Musc'los. — Electrical reactions — Faradic — Galvanic. 
Skin. — Bull* — Herpes — Bed-sores — Perforating ulcers— Glossy skin, &c. 
Joints and Bones. — Charcot's arthropathy — Spontaneous fractures — Pes 
cavus, &c. 



i&tion of Skull and Vertebral Column. 

Abnormal pRijecliima (ir liepreasions — Teudtrnssa, Ac., im ]«m ciission. 
rebro-spinal Fluid. 
NakBii-eye charactera of fluid — Microscopic exaniinatiim — Battel iolugical 

characters— Cliemical reactions, &c. 
mpathetic Nervous S^stenL 
Cervical sj-rajialhetic — Dilatjition of pupil tu shade and cocaine— Oil io- 

Bpinii! reflux — ProptOBia — ExoplillialinOB — Enoplitlialmos — Re- 

InicLir.n of upper lid— Pseud o-ptjiaia — Flu8hinn or sweating ot 

face, neck, upper extremity. 
Angio-neurosea — Raynaud's diaease— Erytlironielalgia — Angio-neutotic 

U'deinfl— Local iaed hypcridnwi" or anidrosis — Intermittent limp, 

Several points should be noticed in the foregoing echeme. We 

:m with the higher cerebral and mental functions, for this 

that if a patient be mentally obtuae, or worse, if he 

delirious, then any statement he may make is open to 

doubt, and tor our diagnosis we must rely mainly, and in cases 

of coma entirely, upon physical signs and upon the history 

supplied by the patient's friends. 

The patient's emotional state is sometimes of diagnostic signifi- 

Not only are many hysterical patienta unduly emotional, 

,t a similar condition is observed in certain cases ot disseminated 

sclerosis, where there is a tendency to smile and giggle upon slight 

provocation, whilst, on the other hand, cases ot aphasia and of 

advanced bulbar palsy are often lachrymose. 

The statements of a patient who is addicted to alcoholic in- 
imperance or to chronic poisoning with opium, cocaine or other 
must also be received with considerable scepticism. There 
a special variety of loss of memory, called Korsakow's psychosis, 
which occurs chiefly in chronic alcoholics, where the patient, 
'ho is usually a woman and the subject of peripheral neuritis 
it commonly alcoholic, but sometimes due to other causes, 
ich as arsenic, septic absorption. &«.), has a faidty conception 
time and place and a specially deficient memory for recent 
rents. Moreover she frei^uently has what ari euphemistically 
lUed " pseudo-memories," so that " the truth is not in her." 
of the toxic varieties of insanity, and is commoner in 
linen than in men. Male alcoholics seldom show Korsakow's 

, sclei 
' adva: 


psychosis, but tend rather to suffer from the more violent and 
dramatic "delirium tremens," with the tremors, acute distress, 
and hallucinations of rats, devils, &c., so familiar to the lay writer. 

Passing from the patient's mental condition, we should carefully 
observe and describe any fits, tremors, or other spontaneous 
abnormal movements that may be present. Disorders of speech 
and articulation should next be studied, and the cranial nerves 
examined in due order. 

It will be observed that, in our scheme of case-taking, sensory 
functions are investigated before motor. As a matter of experi- 
ence, this order of examination is found to be of considerable 
practical advantage. The discovery of an area of anaesthesia 
often puts us rapidly on the track of a correct diagnosis and 
enables us to select with greater ease the saUent points in the 
motor and other phenomena. 

Certain accessory methods of examination, such as the testing 
of electrical reactions and lumbar puncture, are required only 
in special circumstances, where they may throw a flood of light on 
an otherwise obscure case. Inspection, palpation, and percussion 
of the skull are of considerable value in some cases of tumour of 
the brain, especially in cases of cerebellar growths. Sometimes it 
is advisable to have the scalp shaved, in order to detect abnor- 
malities in the shape of the cranium. 

Having collected our facts, comprising the history and the 
present state of the patient, we are now in a position to make our 
diagnosis. And in the process of diagnosis we have, first of all, 
to ask ourselves — ^Is the disease an organic one, due to a gross 
irritative or destructive lesion in the nervous system, for 
example cerebral haemorrhage, alcoholic neuritis or tuberculous 
meningitis ? Or is it one of the so-called " functional " diseases, 
that is to say, without known morbid anatomy, for example 
hysteria, migraine, neurasthenia ? ^ 

If the evidence points to an organic lesion, we have then to 
ask ourselves two further questions : (1) Where is the lesion ? 

* Tho boundary-line between functional and organic diseases is not so 
definite as might at first sight be supposed. At the present day, many 



I {2) What is its pathological nature ? The answer to the first 
question, which constitutea the anatomical diagnosis, is derived 
mainly from a study of the distribution and grouping of the signs 
and symptoms. The answer to the second, constituting the paiho- 
Utgiail diagnosis, is attained mainly by a study of the history of 
the mode of onset. 

In making an anatomical diagnosis we should always endeavour 
to think of a single lesion which will account for ail the symptoms. 
Thus, for example, if a patient conies t* us with hemiplegia of the 
I left arm and leg, of the " upper motor neurone " type (see p. '2^i), 
at the same time a right-sided facial palsy of the " lower 
ODOtor neurone" type, instead of diagnosing two lesions, one 
i the right side of the brain causing left hemiplegia and another 
the right facial nerve causing right facial palsy, we prefer 
) diagnose a single lesion in the right side of the pons, imph- 
sating simultaneously the right facial nerve and the pyramidal 
ict (see Fig. fi). 
Aa an example of pathological diagnosis, suppose we have a 
Mtient with spastic paraplegia of both lower limbs and ana>stheBia 
*p to the level of the umbilicus, the anatomical position of the 
lesion is comparatively easy to fix, namely in the lower dorsal region 
of the cord, implicating both sensory and motor tracts. If the 
symptoms appeared suddenly, we think of a vascular lesion such 

tM haemorrhage or thrombosis ; if they developed within a day or 
diaonacs are HossiiiDd as functional, for no better reason than thnt in them 
no constant aniLtomical changes have yet been recognised. Id such diseasas 
aa epitepay, paralysia agitana. cxophthulmii' g<iitre. and Raynaud's disease, 
there can bo little doubt that profound molecular ciiangps enist — in the 
two former inntances in the central nervous ayatem. in the two latter 
in the aympalhetic syatem — but these phangea have not yet been reeog- 
nisod. Other diBoases again, due to poisoning by mic^robea or their toninH, 
or hy other poisons— '.?. chorea, hydrophobia, tetanus, certain varieties 
of epileptiform fit«. Ac. — are undoubtedly the result of pathological clianges 
' ~ ' IB grotipa of nerve elements. And yet, because tliese changes 

not visible histologically, they have beun classed as " functional." Even 
itself, the prototype of functional diseases, has some profouni) 
iilerlying bio-chemical change. The lorm " fwictional," then, is a eonfesaion 
of our etiological ignorance, and is by no means synonymous with " curable," 
aa the steady and progressive advance of such a diseaee as paralysis 
Bgit«ns readily shows. 




two, some inflammatory condition such as myelitis is probable ; 
whilst if they only appeared very slowly, taking many months 
to reach their present intensity, we have to think of a slowly pro- 
gressive lesion, such as a tumour. 

We must never diagnose hysteria or neurasthenia until we 
have excluded gross organic di^^se. And, finally, we should 
remember that the presence of certain hysterical or neurasthenic 
sjrmptoms does not exclude a co-existent organic lesion, nor vice 
versd. Functional and organic disease may be combined in the 
same patient, and this combination increases the diflSculty of 

V w k k » 

» « 

• • • 

• • • • 



■ We arc not infrequently called to see a patient who in found to be 
mconacious. In such cases it is of great importance to make a 
lorrect diagnosis as to the probable cause-. There are different 
* degrees of unconsciousness. For example there are conditions 
in which the patient can be roused from his unconsciousness 
by shaking, shouting, or other stimuli, as in the case of ordinary 
sleep. When this degree of unconsciousness occurs in pathological 
conditions, as in a patient stupefied by various poisons (whether 
produced within the body or introduced from without), or from 

t mechanical compression of the brain, for example by hsBmorrhage, 
we call the condition stupor. 
Coma is that degree of unconsciousness which is so deep that 
We are unable, by any ordinary stimulas, to rouse the patient. 
A deeply comatose patient does not swallow fluids placed in his 
mouth, his conjmictival reflexes are absent and his pupils in- 
sensitive to light. 

How are we to proceed when called to see a patient whom 

I we find comatose ? Firstly, we inquire into the history, as to the 
patient's previous health, whether the coma was sudden or gradual 
in onset and whether it was preceded by other symptoms, such aa 
convulsions or headache. We then examine the patient, feel the 
Bead for signs of injury, smell the breath, examine the pupils, 
noting their size, equality or inequality, and their reaction to 
light ; we hsten to the heart and note the character and frequency 
of the pulse and respirations. We note the radia! blood -pressure 
md, if possible, measiu-e it (by means of a Riva-Rocci sphygnio- 
tanomettr). We observe whether the face is symmetrical or 
, and whether there is conjugate deviation of the head and 
yea in any direction. The optic discs in certain cases should 
ex&mined. We lift the limbs in turn and let them fall. 


observing whether there is any difference between the flaccidity 
of the two sides. We also test the knee-jerks and examine the 
abdominal and plantar reflexes on both sides. Then we pass a 
catheter, draw off the urine, note its specific gravity and test 
it for albumen and for sugar. Finally we note the temperature 
in both axillflB, and in certain cases we perform lumbar puncture 
and examine the cerebro-spinal fluid. 

The first question is whether the coma is due to a general 
toxaemia, such as poisoning by alcohol or opium, ureemia, dia- 
betes, &c., or whether it is the result of same gross intra-cranial 
lesion, such as haemorrhage, meningitis, abscess, tumour, &c. 

As a general maxim we may state that, if coma be toxsemic in 
origin, practically all the signs and symptoms will be bilaterally 
symmetrical. On the contrary, most cases of gross intra-cranial 
disease being unilateral, or at least asymmetrical, there will there- 
fore be a corresponding preponderance of sjrmptoms on one side 
of the body, so that, in addition to coma, we have a number of 
unilateral signs. Let us consider these unilateral cases first. 

The commonest case is that of spontaneous cerebral hamorrha^e. 
Here the onset of imconsciousness is generally sudden ; the 
patient's face is flushed or cyanosed, his skin sweats profusely, 
he breathes stertorously, his blood-pressure is high, and his pulse 
is slow, full and bounding. All his Umbs are flaccid, but on 
comparing the two sides, we find that the flaccidity is more 
absolute on the hemiplegic side. For example, the elbow of the 
affected side can be passively flexed to a greater degree than 
that of the healthy side. The arm and leg on the paralysed 
side also fall more '' dead " than do those of the sound side 
when lifted up in turn and allowed to drop. The paralysed 
leg lies extended, whereas the healthy one tends to be semi- 
flexed. The head and eyes are often turned to one side, 
generally away from the paralysed limbs, unless the haemorrhage 
be cortical or intra-ventricular, in which cases the deviation 
may be toward the paralysed limbs, and is associated with 
other irritative phenomena, e.g. spasticity instead of flac- 
cidity. The face is asymmetrical, especially its lower part, the 



paralysed cheek flaps loosely during respiration and the mouth 
is distorted like a mark of exclamation laid on its side (!— )> as if 
[ the patient were " puffing his pipe " at the paralysed angle of the 
I mouth. The pupila are generally dilated and sometimes unequal, 
I the larger pupil being on the side of the brain lesion. In pontine 
liEemorrhage, however, the pupils are often contracted to pin- 
points. At the onset oE an ordinary apoplexy, whilst we get little 
, help from the deep reflexes, which may or may not be diminished 
or lost on the affected side, there is, from the very outset, 
an extensor plantar reflex in the toes of the hemiplegic foot, 
and all the other superficial reflexes on that side are diminished 
or absent. The akin of the abdomen can be pinched or pricked 
on the paralysed aide without eliciting an abdominal reflex — 
I (Rosenbach's sign). The temperature on the paralysed side is 
usuaUy higher than on the other, althoi^h the general temperature 
[ of the whole body falls at first. It the coma has lasted several 
I hours, the bladder becomes distended and may develop an overflow 
I incontinence. Afterwards, the temperature rises above normal, 
[ and in bad cases may go on to hyper-pyrexia. 
I Most cases of spontaneous cerebral heemorrbage occur in patients 
' past middle-age, in whom the arteries are no longer elastic and 
healthy, and there is often a history of kidney disease, with ita 
resultant cardiac hypertrophy and high-tension pulse, conditions 
particularly liable to result in the bursting of a cerebral artery. 
I The actual attack of hiemorrhage not uncommonly occurs during 
I some slight physical exertion or mental excitement, as in public 
lapeakers, such as clergymen, politicians, or after-dinner orators, 
I old men with brittle arteries, during straining at stool. In 
I most cases of intra-dural cerebral haemorrhage from whatever 
[ cause, the cerebro -spinal fluid is tiuged with blood in greater or 
I smaller amount (see later, p. '■i'-.lO). 

But cerebral haimorrhage may also, in rare cases, occur iu young 
people having healthy veaaels, as for example in a child during 
[ violent convulsions or during a paroxysm of whooping-cough, 

Ivhere the heemorrbage is commonly venous and due to passive 
Boogestion with rupture of the cortical veins, or it may occur in 





any of the so-called " bleeding diseases " — ^purpura, hsemophilia, 
leukaemia, &c. 

Cerebral hsemorrhage often occurs in cases of general paralysis 
of the insane, and in fact may be the first symptom calling 
attention to the disease. The symptoms are those already 
described, but there is usually a history of previous mental 
failure, grandiose ideas, loss of memory, attacks of emotional 
excitement, and sUght indistinctness of articulation. In the 
absence of such history, we may be unable at the time to diagnose 
anything more than the fact of a cerebral haBmorrhage. But 
afterwards, when the patient recovers from his apoplexy — ^and the 
general paralytic recovers much more rapidly than the non-insane 
patient — we can generally recognise the characteristic evidences 
of the disease, both psychical and physical. 

Coma may also be due to traumatic cerebral "compressioii," 
where there is a haemorrhage on the surface of the brain, either 
intra- or extra-dural. The signs are practically the same as in 
spontaneous apoplexy but the onset is different, for there ia a 
history of a head injury. The symptoms develop gradually, 
especially if the haemorrhage be extra-dural, beginning with local 
paralysis and perhaps localised convulsions. T}ie paralysis gradually 
increases, the patient becomes drowsy, stupid, and finally comatose, 
the blood-pressure meanwhile rising to an excessive degree. There 
may be, before the onset of coma, a " lucid interval " of several 
hours or even a whole day, during which the patient, who was 
perhaps only stunned by the original blow, recovers consciousness 
and is apparently normal. A lucid interval, when followed by 
the above symptoms, generally indicates that the haemorrhage is 
extra-dural. In intra-cranial haemorrhage cedema of the retina 
often supervenes within a few hours.^ This oxlema is more intense 
in the eye on the same side as the focal compression, and the fact 
may be of diagnostic value in obscure cases of coma following head- 
injuries. This retinal cedema rapidly subsides if the intra-cranial 
tension be relieved by operation. It is imcommon for symptoms 
of compression to come on immediately after the head injury, 

* Cushing, New York Medical JournaU January 19, 1907. 




bey do bo, they suggeat a deprefsed fracture pressing 
-he brain. This can generally be detected by examina- 
tion of the cranium. 

Pontine Haemorrhage is generally near tlie middle line, and 
therefore tends to produee bilateral symptoma. Pontine cases 

lerally (but not alwaya) have strongly contracted pupils owing 

irritaUon of the third nerve nuclei. There ia often hj^per- 
pyrexia and most cases are fata!. 

Thrombosis of the Cerebral Sinuses is a rarer cause of coma. 
Here the diagnosis rests chiefly on the history. Cases secondary 
to suppurative conditions oE the middle ear or frontal sinuses will 

■kave a corresponding history and the other signs of intra-cranial 

Ivenous obstruction. Primary thrombosis of a sinus, occurring 

Iwithout infection, as in marasmus, profound anaemia, &c., is ex- 

ssively difficult to recognise. Thrombosis of cerebral arteries, 

iducing cerebral softening, often causes hemiplegia, but its onset 

I slower than is that of hemorrhage ; it more often comes on 

>diiring ordinary sleep and ia rarely associated with coma. 

Amongst the other gross intra-cranial diseases producing coma, 
there is cerebral meningitis. Here again our diagnosis depends 
on the history. Most frequently the patient is a child. Instead of 
a history of sudden coma or of head injury we learn that there have 

tien, for some days, headache, vomiting, photophobia and head- 
traction, and often the characteristic " hydrocephalic cry." The 


child gradually becomes drowsy, apathetic, and finally comatose. 
Rigidity of the neck muscles and head-retraction persist during 
the coma (Fig. 24). Kernig*s sign is often of value. This consists 
in a reflex contraction of the hamstring muscles when an attempt 
is made to put the sacral nerve-roots on the stretch by flexing the 
hip to a right angle and at the same time extending the knee. If 
the meningitis be chiefly on the convexity of the brain, there are 
commonly convulsions preceding or accompanying the coma. On 
the other hand, if the meningitis be mainly basal, there are cranial 
nerve paralyses, especially of the ocular muscles. Examination of 
the cerebro-spinal fluid obtained by lumbar puncture gives con- 
clusive evidence in cases of suspected meningitis. Optic neuritis, if 
present, will indicate that the coma is not due to mere haemor- 
rhage, but that there is increased intra-cranial pressure, either 
due to meningitis, cerebral abscess, or possibly, if the history be a 
matter of weeks or months, to intra-cranial growths, syphilitic, 
tuberculous, or neoplastic. 

Let us now pass to the other class of cases of coma, due not to 
a gross intra-cranial lesion, but to some general toxic condition 
of the higher cerebral centres. In this group the important 
point to notice is the absence of imilateral signs. 

In the coma of opium poisoning there may be a history of 
laudanum swallowed or morphine injected hypodermically. An 
empty laudanum-bottle or a h3rpodermic-syTinge may be found 
by the patient's side when he is discovered. If laudanum has 
been taken by the mouth, its odour may be detected in the 
breath. A chemical analysis of the stomach-contents obtained 
by the stomach-tube, will also help in the diagnosis. In the 
comatose patient we notice the excessive slowness of respiration, 
the slow and feeble pulse, the cold clammy skin, and, most striking 
of all, the pupils contracted to pin-points. These sjrmptoms might 
be confused with those of pontine haemorrhage. But there is not 
the pyrexia of a pontine apoplexy, and the coma of opium is not 
so deep as that of haemorrhage. Moreover, in opium-poisoning 
the plantar reflexes are of the normal flexor type. 

The coma of acute alcoholic poisoning is not so deep as that 



I of apoplexy, for the patient can generally be ronaed, temporarily 

I at least, by energetic stimulation. The typical Btertor of apoplexy 

is not present, the pupils are dilated and react to light, and the 

corneal reflexes are preserved. Tlie temperature is subnormal, 

the breath and stomach-contents smell of alcohol, and if we mix 

H specimen of the urine with potassium -bichromate solution and 

. then allow strong sulphuric acid to flow to the bottom of the test- 

I tube, a green colour appears if alcohol be present in the urine. 

We must be careful, however, not to diagnose alcoholic poison- 

I ing simply because the patient's breath smells of alcohol. In the 

' first place, a patient with cerebral hsemorrhage may have had 

I alcohol given him, juat at the onset of his symptoms. Or secondly, 

i a patient who has been drinking alcohol may have an attack of 

apoplexy, or he may fall and sustain a head injury causing com- 

l pression. Therefore every patient with apparent alcoholic coma 

should be carefully watched for about twenty-four hours, in case 

unilateral paralysis, or inequality of the pupils should supervene. 

Post -epileptic Coma may be mistaken for apoplexy, if we do 

f not happen to know tliat the patient is epileptic. But generally 

we have the history of preceding fits, and in a chronic epileptic 

[ there may be old sears about the scalp, tongue, or face, the result of 

I injuries during previous fits. There is no preponderance of uni- 

L lateral symptoms after a general epileptic fit, nor is there inequality 

I of the pupils. The tongue may have been bitten during the fit and 

I may be still bleeding during the stage of coma. Within an hour or 

lIcHS. the epileptic recovers conaciouauesa without paralytic sequehe. 

Ursemic Coma is not uncommon, occurring as it does in 

[ patients who are the subjects of nephritis, acute or chronio. 

I The coma is usually preceded by uriemic headaches, vomiting, 

■snd convulsions, local or general. A history of previous renal 

{disease is here of great value. And there may be obvious 

■igna of renal dropsy about the face and legs. The breath often 

ihas a urinous odour, and a catheter specimen of urine will show 

albumen together with various kinds of casts, and, in acute nephritis, 

P)lood. ' But we must not forget that a patient with chronic 

renal disease, a higb-t«naion pulse and a hypertrophied heart, is 


just the one in whom cerebral haemorrhage may fairly be 
expected. Therefore in a case of coma, mere albuminuria should 
not lead us to diagnose ursBmic coma. We must always be on 
the look-out for sjmiptoms of unilateral paralysis. 

Diabetic Coma is easy to recognise, if we know that the patient 
has been suffering from diabetes. Even if there be no history 
of diabetes, examination of the urine shows the characteristic 
high specific gravity, together with the presence of sugar in large 
amount as shown by the ordinary tests The addition of a 
few drops of liq. ferri perchloridi to the urine produces a deep 
brownish-red colour, due to di-acetic acid. The " acetone " smell 
of the breath is unmistakable and occurs only in diabetes, in the 
rare condition of " delayed poisoning by anaesthetics," ^ and in the 
" cyclical or periodic vomiting " with acetonuria seen in children,'- 
both of which latter conditions are associated with acute fatty 
changes in the liver. Further, diabetic coma is not sudden in onset, 
but is commonly preceded by headache, irritability and uncon- 
trollable drowsiness, merging into profound coma with remarkably 
deep noisy breathing. The pulse is usually small and rapid, unlike 
the full, slow pulse of cerebral haemorrhage. 

Sunstroke sometimes causes coma. Here, of course, it is 
essential that there should be a history of exposure to a hot 
sun, of a previously healthy patient. Alcoholic patients are more 
liable to sunstroke than teetotalers. A patient who is comatose 
from sunstroke often has extraordinary hyperpyrexia — 108° F. 
and upwards. General convidsions may occur. 

In malarial climates we must also be prepared to meet with a 
comatose variety of pernicious malaria, where the parasites produce 
thrombosis of the smaller cortical vessels. A malarious patient may 
rapidly become comatose and die within a few hours, as happened 
to a friend of my own. In such cases the malarious history and 
the examination of the blood for the plasmodium will settle the 
diagnosis. A patient dying from cancer may become comatose 
shortly before death — ^the so-called coma carcinomatosnm. 

* Gutlirie, Clinical Journal, June 12, 1907. 

* Langmead, British Medical Journal, 1905. p. 3o0. 

COMA 59 

We need not do more than mention the terminal coma of such 
diseases aa acute yellow atrophy, or the " coma-vigil " of typhus 
and of severe enteric fever. 

Hysterical Trance, by a careless observer, might be nustaken 
for true coma. The hysterical patient, however, has neither stertor 
nor cyanosis, the breathing and heart's action are regular, 
though perhaps very faint, the pupils react to light and the patient 
generally reusts forcible opening of the eyes. Thus a young man 
of twenty-two who had sudden attacks of apparent sleep (narco- 
lepsy) coming on in the middle of meals or when playing cards, 
refused to be roused by ordinary stimuli In the form of shaking or 
shouting, but yielded at last to forcible di^:ing in the ribs. He 
passed through a stage of " grande hystt-rie " before waking up, 
and for some time afterwards had hysterical blindness and other 
hysterical stigmata. 

The hTpBotic trance may be r^arded as an artificially-induced 
form of hysteria, the result of stiggestion in a highly sensitive 



We are often consulted about patients who are said to have " fits," 
but we are seldom fortunate enough to witness an attack. If 
we do, the diagnosis presents little difficulty. More often, in 
making the diagnosis as to the nature of a fit, we have to 
depend upon the description given by the patient's friends. 

The following is a list of the chief clinical conditions in which 
convidsive phenomena occur. 



'Hysteria major. 
Hysteria minor. 
Post-epileptic hysterical attacks. 

Epilepsy major (grand mal). 

Epilepsy minor (petit mal). 

Post-epileptic automatism — " masked 

Toxic conditions : — Unumia, puer- 
peral eclampsia, alcohol, absinthe, 

. Epileptiform ( lead, &c. 

General paralysis of the insane. 

Organic brain lesions — Jacksonian 
fits, &c. 

Infantile Convulsions in ^ - 

1^ Organic. 

Stokes- Adams' disease. 


In making inquiries about convulsive phenomena, whatever 
be their nature, it is advisable to avoid using the word "fit," 
especially if we are discussing symptoms in the presence of the 
patient. It is better to refer simply to " attacks." Many 
epileptics are unaware of their own disease, and even when they 
know its nature, they dislike hearing about their " fits." 

The first point we should try to determine is whether the 



attacks are hyatencal or epileptiform. In reference to tliis the 
age and sex of the patient are often of importance. We do not 
meet with hysteria in infanta, and rarely in children below the 
age of puberty. Epilepsy ia of equal frequency in both sexes, 
whereas hysteria is twenty times commoner in females than in 
malea. Hysterical attacks in male patients are most frequent in 
lada at about the age of puberty. 

Scheme of InTeBtisation in Cases of Fits 
Eiciling cause. Nature of warning, if any. Onset, sudden or gradual. 
Scream. Injuries during fulling. Move.niciitfl, toiiii:, (clonic, (inqioaivK. 
iBUrtiug-poititi of niovcDienta, and exact order oF spread. Biting of tongue. 
^ii^turition or defcecnCiun. Colour of face, pale, Buslied, cyanosed. Pupil.s. 
I Conjunctival retlEX<^ Knue-jerka immedintdy after attack, Dumtion of 
altat'lc, After-sj-niptonii (i^onia, vomiting, lieadaclie, sleep, Sic). 

Pursuing the foregoing scheme, we should inquire whether 
there was any apparent cause for the attack, Hysterical attacks 
generally follow some emotional disturbance. Epilepsjr comes on 
without exciting cause. A warning or aura before an attack 
of epilepsy may be of the moat varied character. Perhaps 
the commonest ia the " epigastric " aura, or there may be 
an indescribable feeling of terror, subjective auditory or visual 
phenomena (visual auric being most frequently red in colour), 
unilateral tingling or twitching of the face or one of the limbs, or a 
*' dreamy " mental state (sometimes associated with subjective 
sensations of smell or taste), and so on, according to the particular 
,eorticai area whence the epileptic explosion happens to start. But 
,often the epileptic has no aura, he falls suddenly as if struck 
down by an unseen hand. On the contrary, hysterical attacks 
ttsually come on gradually, and are often preceded by the hysteri- 

" globus " or ball in the throat, or by feelings of palpitation, 
■excitement, giddiness, tingUng in the feet, &c. Sometimes at the 
onset of the attack the epileptic, as he falls, utters a weird epileptic 
cry or moan, which is not repeated. By this time he is already 
unconscious and does not hear his own cry. Frequently he injures 
himself in fallmg, especially by striking his head. Many chronic 
epileptics may be recognised by the presence of numerous scara 


on the scalp and face. The hysterical patient, on the contrary, 
never injures herself when falling. She comes down carefully, 
often on a sofa or easy-chair. She not uncommonly screams, and 
may continue to scream or shout throughout the attack. 

The nature of the movements during the attack is of importance. 
In epilepsy we have the tonic stage, in which all the voluntary 
muscles, including those of respiration, become suddenly rigid. 
The patient, therefore, falls Uke a log, and his lips and face become 
cyanosed, his pupils dilating and becoming insensitive to light. 
The tonic stage passes into the clonic, in which violent jerking 
occurs in all the voluntary muscles, at first rapid, and gradually 
becoming slower and of greater range. The eyes, which during 
the tonic stage have been drawn to one side (the side on which 
the tonic spasm was more intense), now show rapid clonic jerks 
towards that side. The face loses its cyanotic hue, air re-enters 
the lungs, and is jerked out in short puffs mixed with saliva, 
forming a froth which is not unfrequently blood-stained, since the 
jerking tongue may be bitten by the clonic movements of the jaws. 
During this stage the patient often empties the bladder and some- 
times the rectum. Within two or three minutes from their 
onset, the movements gradually cease, and the patient remains in 
a state of coma, with stertorous breathing, flaccid limbs, and 
sometimes profuse sweating, the eyes being now turned to the 
side opposite to that towards which they originally deviated, 
and the pupils being now contracted. Then, after ten minutes 
or so, the coma passes off, and the patient may vomit, or may 
wake up, perhaps with a headache, or may pass into a sound sleep. 

In a hysterical attack, on the other hand, the patient's face 
is natural in colour, never cyanosed, though later it may become 
flushed from physical exertion. The voluntary muscles are usually 
contracted, the fists clenched, the eyes tightly closed and resistant 
to opening, but if the eyes be forcibly opened the eyeballs roll 
upwards. Then, after a stage of general tremor totally unUke the 
clonic stage of epilepsy, the patient makes violent " purposive " 
movements, kicking, pushing, biting, rolling about, banging her 
head on the floor, beating her own face, pulling her hair, &c. 


iDuring this stage various groteaque postures may be assumed ; of 

I the83, the most charat^terivtic is one in which the hack is arched 

I (opisthotonos) and the patient lests on her head and heels. Or 

I there may be curving of the trunk laterally (pleurosthotonos), 

or forwards (emprosthotonos), "crucifixion" attitude, &c. The 

patient may talk, scream, or sing during the attack, which may last 

for many minutes. But throughout the attack the pupils generally 

react to Ught, and the conjunctival reflex is usually preserved. The 

hysterical patient never bites her tongue, though she may bite her 

lips or fingers, or snap at the fingers of bystanders. She never 

empties the bladder or rectum during the attack, and after it is 

■ she may or may not have any recollection of what has 

kappened, and is sometimes in a semi-dazed condition. 

The knee-jerks, during the stage of flaccid coma terminating a 
severe epileptic fit, may be temporarily abolished, but soon they 
become exaggerated, and, for a few minutes, ankle-clonus may 
«ften be elicited, and the plantar reflex may be extensor in type. 
In hysteria the deep reflexes are unaltered. 

li we bear in mind the foregoing points, the diagnosis between 
severe epileptic fit and an attack of " grande hysterie " is 
generally easy. 

Catalepsy, another variety of hysterical attack, is easily recog- 
nised by the peculiar immobility of the limbs. The patient during 
ttie attack, though not unconscious, is unable to move a muscle, 
but her limbs are plastic like those of a lay figure, and if placed 
passively in any posture, remain there. 

There are also many varieties of minor hysterical aUackfi, e.aay 
t recognition, of which the commonest consist merely in emotional 
Dutbursts of uncontrollable laughing or crying, or a feeling of a 
amp in the throat^" globus hystericus " — which causes the patient 
o swallow. 

Supposing, then, that we have come to the conclusion that 
the patient's attacks are hysterical and not epileptiform, we should 
not rest content until we have settled the further point as to whether 

(e hysterical attack was preceded by an attack of minor epilepsy 
petit mat. 


Attacks of j)€tit mal are often overlooked. It is well to 
remember that in true epilepsy (whether major or minor) the one 
essential phenomenon is not convulsions but loss of consciousness. 
In petit mal it may* be the only phenomenon, so transient, 
perhaps, that the patient does not even fall ; he simply pauses 
for an instant during conversation, looks strange, and then goes 
on with what he was saying. Or he may fall down and get 
up again immediately, a variety of epilepsy which is often mis- 
taken for syncope, but is distinguished by the suddenness of 
onset and of recovery. If we happen to observe a patient at the 
moment of his attack of petit mal, we generally notice that the 
pupils dilate and his face turns momentarily pale, the pallor being 
followed by flushing. It is immediately after such a minor attack 
that some patients go on to a post-epileptic hysterical attack, and if 
the initial epilepsy be not recognised, treatment will fail. 

Attacks of minor epilepsy are, now and then, associated with 
post-epileptic automatism, in which the patient has an attack of 
petit mal which perhaps passes unnoticed ; he then proceeds to 
perform some unusual or inappropriate act, of which he has no 
recollection afterwards. Perhaps the commonest automatic action 
is that of undressing ; or he may proceed to empty his bladder, as 
in the oft-quoted instance of the judge who did so in the comer of 
his court of justice ; or he may perform some still more complicated 
action. Thus a case of mine was that of a well-known financier 
who had several attacks of loss of memory. During one of these, 
lasting two and a half hours, he attended an important board- 
meeting and proposed certain resolutions to which, both before 
and after, he was strongly opposed. He then took a friend out to 
lunch and returned to his office. He finally woke up and asked 
his confidential clerk where he had been. The medico-legal signi- 
ficance of these cases is of importance, since such a patient, in a 
condition of post -epileptic automatism, may commit serious and 
complicated crimes, of which he has afterwards no recollection. 
This condition is sometimes called " masked " or " larval " epilepsy. 
It is possible that attacks of automatism or psychic epilepsy may 
occasionally actually replace the ordinary epileptic fit without 


an antecedent attack of prtU mat, may in fact be " epileptic equi- 
i valent*." But the more carefully such cases are observed, the 
' oftener is some incUcatitm found of minor epilepsy immediately 
before the eccentric action, in the form perhaps of initial transient 
I pallor. This was so in the case of the financier above referred to. 
\ Other cases of ambulatory automatism are hysterical in nature 
I (see later, p. 360). A previoiLS history of epilepsy, either major or 
minor, is of great diagnostic value. 

Supposing that, having excluded hysteria, we arrive at the 
conclusion that a patient's fits are epileptiform, we must still re- 
member that other conditions besides idiopathic epilepsy can pro- 
duce epileptiform fits. Thus for example fits may be of toxic 
origin. Acute alcoholic or abmithe poixoning may produce coma 
and convulsions. The history and the smell of the breath will 
usually guide us in such cases. The sudden withdrawal of 
alcohol from a chronic drnnkard is sometimes followed by 
an epileptiform fit. In the convulsions of Uad poisoning 
there are usually other signs of plumb ism, such as the 
blue line in the gums, weakness of the extensors of the wrist, 
optic neuritis, &c, Toxins produced within the body may also 
cause fits exactly similar to epilepsy, witness the uTcemic con- 
vulsions of Bright's disease and of puerperal eclampsia. In every 
case of fita appearing in a previously healthy individual, the 
urine should be tested and the optic discs examined. In the 
e of a young officer who was brought into hospital at 
Pretoria suffering from a succession of fits typically epileptic in 
character, but simply uriemic, acute nephritis was the cause. In 
, chronic renal disease, besides the cardio- vascular changes, there 
not uncommonly exists albuminuric retinitis, which is of great 
diagnostic significance. When we come to the subject of infantile 
convulsions we shall find that many of them are toxic in origin. 

Epileptiform fits may occur during the course of general paralysis 
of the insatie ; they may, in fact, be thi first symptom of the 
disease. Epileptic fits appearing for the first time in a middle- 

Iaged patient should always suggest the possibiLty of paralytic 
dementia. In such cases we look for inequality or irregularity of 


the pupils, and especially loss of the light reflex, mental changes, 
facial tremors, and slurring articulation, and a history of sjrphilis 
should be sought. Lumbar puncture may show lymphocytosis 
of the cerebro-spinal fluid, a condition which is constant in general 
paralysis but does not occur in idiopathic epilepsy. 

Epileptiform or hystero-epileptiform fits may also occur in 
psychasthenic individuals. Such patients have stigmata of psych- 
asthenia in the form of phobias, tics, obsessions, &c. (see p. 341). 
Epileptiform fits in psychasthenia, imlike true epilepsy, occur only 
after some direct exciting cause, such as physical or mental over- 
exertion, excitement, &c. The attacks, as a rule, are few in number 
and may be limited to a single one. 

Intra-cranial tumours anywhere, even deep within the substance 
of the brain, may cause general epileptiform fits, from increcised 
intra'Cranial pressure. Here we are usually guided by the cardinal 
signs of intra-cranial tumour — ^headache, vomiting, optic neuritis, &c. 

All the epileptiform fits to which we have as yet alluded have 
a bilateral general distribution, and are not succeeded by any 
localised paralysis. But when fits are produced by gross focal irrita- 
tion of the cortex their onset is a local one, and they are not 
neces^rily associated with los^ of consciousness. Such " Jack- 
sonian " fits are usually followed by weakness of the part which 
is primarily convulsed. Jacksonian fits may occur as often as 
fifty or a hundred times a day. They usually begin with a 
subjective sensory aura, such as tingling, numbness or twitching, 
localised in some particular part, e.g. the thumb or big'toe. Then 
there is tonic spasm of that part, followed by clonic jerking. 
This may remain confined to the muscles where it began, or 
it may spread to others. If it spreads, it does so by a 
deliberate march from one cortical centre to another (Fig. 3, p. 5). 
Thus a fit commencing in the big toe would occur successively 
in the ankle, knee, hip, shoulder, elbow, hand, &c., and would 
afEect the face last of all. Or a fit beginning in the elbow would 
spread vid the shoulder, hip and knee, to the toes, and simul- 
taneously vid the wrist, fingers and neck, to the face and tongue, 
as the ripples produced by dropping a stone into a pool spread 


I concentrically in ever-widening circies. A patient who has 
I Jacksonian (its may remain conscious throughout the fit and may 
I even be able to apeak, though he is usually somewhat excite<l. 
[ But if the convubion spreads to the opposite cortical area, thus 
[ becoming bilateral, consciousness is lost as the fit crosses over. 
I Jacksonian Hts are followed by local weakness and increased deep 
I leflexes in the convulsed part. Fig. 25 shows a patient during 
t localised fit in the left face, due to a gumma in the cortical facial 
I centre. Fig. 2(i shows the nmximuni voluntary movement of the 
I lace after an attack. It will be seen that the left lower face is 


Cortical g:uQiiDa of the face-centre of the rigUt cereliral cortes. 
Fis. ■:& ihowi imtieiit durini i Jukioiiliiii fit of the left live, 
rig. ^(huwi wiakiieu ol &r left Imas on volnnUry Diuvein<:l.t. 

larkedly weaker than the right. The localised paralysis j 
HoS in the reverse order from that in which the spasm t 
Bthe muscles first convulsed being the last to recover power. 

Of course, cortical lesions will produce localised motor pheno- 
mena only it they affect the motor centres in the region of the 
re-ccntral gyrus. A focal lesion of a sensory cortical area pro- 
pduces, not a motor, but a sensori/ fit. Thus disease of the tip 
Bof the temporal lobe {Fig. 4, p. .'5) causes a sudden subjective 
msBtion of smell or taste (often associated with a characteristic 
' dreamy " mental state), occipital lesions cause subjective visual 
illucinations such as flashes of light, and so on. Moreover, after 


the sensory fit it is not uncommon to find temporary sensory 
paralysis, e,g, anosmia after a temporal fit, or hemianopia after 
an occipital fit. 

A Jacksonian fit, of whatever variety, is the result of a local 
lesion in the neighbourhood either of the cortex or of its superjacent 
meninges or bones. If the lesion be in the substance of the cortex, 
not merely superficial to it, there will be some local paralysis even 
before the fit occurs. 

Localised fits may be produced by any irritative cortical lesion. 
The commonest causes are tumours, syphiUtic or otherwise, 
abscesses, meningitis of any variety, local hsomorrhages, depressed 
fractures, and so on. Localised fits may also be produced by 
svb^cortical tumours in the pre-central region. In such cases 
we observe muscular paresis in the affected limb, together with 
recurring convulsive phenomena in the limb ; but the point of 
onset of the successive fits is less constant than in a true cortical 
convulsion, and the fit begins sometimes in one, sometimes in 
another muscle-group of the affected limb.^ We should also bear 
in mind that Jacksonian fits may occur in certain cases of general 
paralysis of the insane, and sometimes even in ursemia. 

Infantile Convulsions are epileptiform attacks occurring in 
infancy. The symptoms are similar to those of true epilepsy, but 
less violent. When called to see a child with convulsions, we 
should first examine for rickets, since rickety and hereditarily 
neurotic children are especially prone to convulsions. We should 
also try to determine whether the fits are reflex, toxic, or organic 
in origin. In rickety . infants of neurotic inheritance reflex con- 
vulsions may be set up by peripheral irritation such as the cutting 
of a tooth, round-worms in the intestine (thread-worms do not 
cause convulsions), a tight prepuce, &c. Moreover, rickety children 
often have other nervous symptoms, such as tetany, laryngismus 
stridulus, and the well-known inversion of the thumbs towards 
the palms, a phenomenon which sometimes precedes a convulsion. 
Toxic conditions may produce convulsions in previously healthy 
children. Thus any acute fever such as pneumonia, measles, scarlet 

' Cf, van Valkenburg, Neurologischea CerUralblaU, 1906, p. 694. 




L with 

^K>r ai 


fever or influenza, may be ushered in by a convulsion instead of 
by a rigor as in the adult. The convulsions produced by round- 
worms may be partly toxic in origin. Ursemic convulsions occur 
in chitdren, though less often than in adults, and in cases with 
recurring convulsions the urine should always be esamined. 
Asphyxial convulsions, due to deficient oxygenation of the brain, 
occur in dyspntea from any cause, e.g. during pneumonia and 
diphtheria, during a paroxysm of whooping-cough, or in the 
cyanosis of congenital heart disease, Intra-cranial organic lesions 
may cause infantile convulsions. Thus, for example, polio-ence- 
phalitis superior, an acute inflammatory affection of the cortex, 
has a febrile onset with vomiting and convulsions, usually more 
marked on one side than on the other. After the convulsions 
have passed off, the child is often left permanently hemiplegic or 
diplegic. If the cortex of the frontal region is affected, permanent 
mental dulness may ren>ain. Local disease or injury of the bones 
or membranes may produce infantile convulsions. Convulsions 
appearing within a few hours after birtb are not unfrequently the 
result of compression of the brain by a meningeal htemorrhage. 
Meningitis, whether due to the tubercle bacillus, to s3'philiB, or 
to other organisms, may produce convulsions, not only when 
cortical, in which case convulsions appear early, but also in basal 
cases, where the fits are due to increased intra-cranial pressure. 

Epileptiform fits also occur in one variety of the Stokes-Adams' 
syndrome, a coiidition which occurs after middle life, usually in 
male patients with degenerate arteries, and is characterised 
ity paroxysmal attacks of abnormal slowness of the ventricular 

it, the rate sinking as low as twenty per minute or even less, 
together with excessive pulsation in the veins at the root of the 
neck, more rapid than the ventricular beats, and corresponding 
with the auricular contractions. Such a patient b liable to 
tyncopal attacks, to which may be superadded epileptiform fits 
IF attacks of coma without convulsions. More or less slowness of 

;e usually persists between the paroxysms, as a permanent 
phenomenon. The condition is frequently due to disease, 
syphilitic or otherwise, of the auriculo-vetitricular muscle-bundle 


of His, which connects the right auricle with the interventricular 
septum. When this bundle is diseased, heart-block ensues ; the 
auricles go on contracting normally, but the ventricle only responds 
to every second or every third stimulus. There is thus a dissocia- 
tion between auricular and ventricular rhythm.^ 

Strychnine Convulsions should never be confounded with 
epileptiform fits, since they begin with clonic spasms, and 
shortly become tonic with opisthotonos, the tonic spasms recurring 
again and again with increasing severity. A patient poisoned by 
strychnine is not unconscious. Moreover, there are periods of 
intermission, lasting for several minutes at a time, during which 
the muscles are relaxed. The tonic spasms of tetanus might be 
mistaken for strychnine-poisoning, but they have no initial clonic 
stage. The earliest symptom of tetanus is the well-known tonic 
spasm of the jaw muscles, producing " lock-jaw." To this there 
are superadded paroxysms of tonic spasm in the face {rUus 
sardonicus), trunk and limbs, with opisthotonos, somewhat like 
those of the tonic stage of strychnine-poisoning. Between the 
tetanic paroxysms there is no complete muscular relaxation as in 
strychnine-poisoning, but simply a remission in the degree of 
spasm, the jaw muscles remaining partially contracted. 

A patient suffering from rabies exhibits great mental excite- 
ment, with tonic spasm of the muscles of deglutition, especially on 
attempting to swallow liquids (hence the misnomer hydrophobia). 
The spasm may also hs induced by other stimuli such as a bright 
light or a loud sound. The spasm spreads to other muscles, 
especially those of respiration, and severe opisthotonos may super- 
vene at the end, the patient dying either of respiratory spasm 
or from syncope. Hydrophobia may be simulated by hysterical 
patients who have been bitten by a non-rabid dog, and in such cases 
globus hystericus and hysterical opisthotonos may both occur, 
but true respiratory spasm does not occur in hysterical attacks, 
though there may be hysterical rapidity of breathing. 

During an attack of tetany the posture is very characteristic. 

^ See Ashton, Norris and Lavenson, American Journal of Medical Science^ 
1907, p. 28. 


There is a bilateral tonic spasm, usually painful, of the hands and 
feet, the hand assuming a conical shape, the fingers being ex- 
, tended at the inter-phalangeal joints, slightly fiexed at the 
metacarpo-phalangeal joints and pressed together with the thumb 
usually tucked inside the fingers ; at the same time the muscles of the 
thenar and hypothenar eminences are contracted, so that the hollow 

[ of the palm is deepened. In the feet, the toes are flexed towards the 
Bole, the ankle ia dorsiflexed and the foot is sometimes inverted. 
These postures may persist during sleep. Pressure on the nerve- 
trunks of the affected limb induces a typical spasm (Trousseau's 
sign), and the muscles and nerves are unduly irritable both to fara- 
diam and to galvanism (Erb's sign). Tetany is most commonly met 
I with in rickety children (Fig. 27), in whom it is often associated 
I with laryngismus stridulus and with excessive irritability on per- 
I cussion of the facial neiVe (Chvostek's sign). But it occasionally 


occurs in adults, e,g, after extirpation of the thyroid gland, or 
rather of the parathyroids. The parathyroid glands produce an 
internal secretion which neutralises certain toxic products of 
metabolism. Tetany is, therefore, sometimes a symptom of 
parathyroid deficiency, whether arising from disease or from 
artificial removal of the gland. Tetany also occurs sometimes 
during pregnancy or lactation, and as a grave terminal symptom 
in dilatation of the stomach. This variety of tetany is probably 
toxic in origin : so also are the rare cases of tetany associated with 
congenital dilatation of the large intestine in children.^ Cataract 
is a curiously frequent concomitant of the gastric form of tetany. 
An endemic form of tetany also occurs in certain Continental 
towns, chiefly in the winter months. It is especially common 
amongst shoemakers. 

Cerebellar Pits. — Irritative lesions of the cerebellum are 
occasionally associated with cerebellar fits. These are never clonic, 
but consist of tonic spasms, sudden in onset. In unilateral cere- 
bellar disease the spasms are more marked in the homolateral 
limbs than in those of the opposite side. The face is usually 
unaffected. The homolateral limbs become rigidly adducted to 
the trunk, the contra-lateral limbs are abducted, whilst at the 
same time there is a screw-like rotation of the limbs, trunk, and 
head around their own long axes, from the side of the lesion 
towards the healthy side,^ and a deviation of the eyes towards 
the healthy side. Hughlings Jackson has described another variety 
of cerebellar fit occurring in cases of tumour of the middle lobe. 
Here also, as in tumours of the lateral lobe, the fits are tonic, not 
clonic. They consist of head-retraction with arching of the back, 
flexion of the elbows, supination of the hands, and rigid extension 
of the legs, with pointing of the toes. 

But let us not forget that epileptiform fits, cerebral in type, 
may also occur in cerebellar tumours, due either to the general 
increase of intra-cranial pressure, or to a fulminating meningitis 
superadded to an old tuberculous tumour. 

* Langmead, Lancet, Jan. 19, 1907. 

2 Grainger Stewart and Holmes, Brainy 1904. 



I Besides fits, which we have already conaidered, there are many 
I other conditions in which involuntary contractions occur in 
I tie voluntary muscles. But oiu knowledge of the mechanism 
I. of their causation is so incomplete that it is impossible 
rat present to classify them accurately. We must therefore 
I content ourselves, in the meanwhile, with referring to some of 
ftheir chief clinical varieties. 

In studj-ing involuntary movements occurring in striated 

Hiauscles, it is important to observe whether the movement is cou- 

ffined to an individual muscle or part of a muscle, or whether, on 

■ the other hand, it consists in alternate contraction of muscles and 

r of their antagonists. We should also observe whether the abnormal 

muscular contractions produce movements of a joint, or whether 

they are so localised, either to a small muscle or to part of a 

larger one, that we merely see or feel the muscle fibres contracting 

meath the skin. 

The muscular phenomenon known aa shivering or rigor is aome- 

Btimes physiological. For example, when a healthy person becomes . 

■chilled, as by prolonged swimming, he often shivers on coming 

rout of the water. The involuntary muscular contractions of 

which shivering consists are tor the purpose of producing heat 

and thereby raising the depressed body-temperature. But often 

rigors are toxic in origin, aa are those orxurring at the onset 

of certain acute fevers. Thus we have rigors in pneumonia, ague, 

influenza, scarlet fever, &c. And the rigor which sometimes follows 

catheteriaation is probably also toxic in origin, since it rarely occurs 

except when there is a raw surface in a urinary tract which is not 

aseptic. In all these toxic rigors, although the shivering patient 

has a sensation of cold, his temperature meanwhile is rising, 

and it continues to rise until the rigor stops. He has the sensa- 


tion of cold because by vasomotor action the blood is driven out 
of his skin, which is therefore cooled and is actually cold, although 
the temperatiire of the blood is raised. 

Transient flickering or quivering of a muscle, a condition known 
as myokymia (or more popularly as " live flesh "), affecting a few 
muscle-bundles of a single muscle, without producing movement 
of a joint, is not uncommon in people who are anaemic or 
out of health. It is specially conmion in the orbicularis oculi 
and in some of the larger muscles of the limbs, e,g. the deltoid and 
biceps in the upper limb, the glutei and quadriceps in the lower. 
This variety of myokymia is not associated with muscular atrophy, 
nor with any alteration of electrical excitability. It is unaffected 
by rest or by voluntary exertion, and has no serious significance. 

Sometimes, however, fibrillary movement occurs in organic 
lesions of the lower motor neurone. Thus in the muscular atrophy 
of chronic anterior poliomyelitis, of amyotrophic lateral sderosiSy and 
of some cases of syringomyelia, diseases in which the cells of the 
anterior comua are undergoing slow degeneration, there may be seen 
fibrillary or fascicular tremors in the wasting muscles. This 
quivering myokymia can often be elicited by gentle flicking, or by 
a breath of cold ai^ blown over the sldn. A precisely similar 
fibrillary tremor occurs in the wasting tongue of bulbar paralysis, 
when the degenerative process has involved the hypoglossal 
nuclei. Fibrillary tremor does not occur in the primary 
myopathies, whether atrophic or pseudo-hypertrophic in type. 
In other cases fibrillary tremor occurs in the distribution of a 
motor nerve which has begun to recover from previous paralysis. 
It is not uncommon in the face during convalescence from facial 
palsy, and sometimes it persists for months and years after 
voluntary power has returned, as in the case of a professional 
friend of my own who is otherwise perfectly well. More usually 
the myokymia passes off when motor power has been restored. 

Somewhat different in appearance is the condition known 
as myoclonus, a rare disease, characterised by paroxysms of 
sudden shock-like contractions in various muscles, lasting for 
several minutes at a time, irregular in rhythm and varying in 




rapidity from ten to fifty per minute. In alight cases the twitches 
may be insufficient to produce movements in the afiected parta. 
The muscles affected are usually those of the limbs, especially the 
lower limbs, often sjanmetrically on the two sides, but contractions 
may also occur in the trunk and even iu the face. Sometimes the 

t-tio. 28 Doverricht'H fatoily mjoclonus or " myoclouus epilepLicus" in a bny 

Bged 13. Besides (tie musclsB indiuftled by shading in the dlagraiu, the aoft 
folate was also alTected. 

diaphragm and the larynx are aSected, so that curious grunting 
Bspiratory sounds are produced. There is no muscular atrophy 
: alteration in electrical excitability. The spasms cease during 
leep. Several varieties of myoclonus have been observed ; in 
—Friedreich's paramyocUmm muUipkx, usually a disease of 
idult life — the myoclonus ceases on voluntary movement. 



Another variety is Unvemcht's family myoclonus or myochntu 
epilepCicm, in which several members of a family are affected, all 
belonging to the same generation, though the disease is not banded 
down from parent to child. In addition to the myoclonus, these 
patients have epileptiform fits, and they tend ultimately to become 
more or lese demented. Moreover, the muscular contractions in 

family myoclonuB are intensified by voluntary movement and by 
psychical excitement. Family myoclonus usually manifests itself 
in early life, often at or before puberty. Thus in a little boy of 
thirteen suffering from myoclonus affecting the muscles of the neck, 
shoulders, trunk, thighs and cremasters (see Fig. 28), the condition 
had existed since the age of four, and he had abo epileptiform 


ifita. Two elder brothers were similarly affected, both of wbom, 
■s the patient graphically put it, began to " click " at the age 
of seven. On the other hand, another patient Buffering from 
Friedreich's paramyocloima, showed no symptoms of the disease 
till the age of forty-seven. He never had fits, and at the age of 
fifty, when he came under observation, he liad myoclonic shocks 
. limited to the muscles indicated in the accompanying diagram 
K(Fig. 29). Another variety ia the nystuginus-mi/oclonus of Lenoble 
1 Aubincau, to wh!c?h we shall refer later (see p. 124). 
We next pass to the consideration of tremors. The term "tremor" 
ia applied to involuntary rhythmic oscillations of one or more parts 
of the body, resulting from the alternate contraction of muacle- 
^_gioups and of their antagonists, A simple tremor is one which 
^^hfiects a single muscle-group and its antagonists, whilst in a com- 
^^pound tremor several groups with their antagonists are in action, 
producing a complex movement, e.g. flexion and extension of the 
fingers combined with pronation and supination of the forearm. 
Tremors may be rapid or alow ; they may be diminished or increased 

I by voluntary exertion, and they generally cease during sleep. 
We must not forget that an ordinary vohmtary muscular 
movement is not the result of a continuous muscular contraction 
but ia constituted by the fusion of a rapid succession of short single 
tontractions, averaging from ten to twelve per second. In condi- 
tions of temporary fatigue or of chronic asthenia the rate of these 
muscle discharges becomes slower and less regular, so that the 
individual muscular contractions fuse less perfectly and the result 
is a very fine tremor. In emotional excitement — more often in 
states of fear than from pleasurable emotion — there may be 
^m, a fine rhythmic tremor of about eight or nine oscillations per 
^Koecond, and the same occurs in exopfuhalmic goitre. This tremor is 
^Vmade more apparent by voluntary exertion. It is best elicited by 
1 making the patient hold his hands horizontally in front of him, 
with the fingers widely spread, We can then feel the tremor even 
better than see it, by placing our own fingers lightly on the dorsum 
^L of the patient's hand. This fine tremor affects all the limbs, 
^■^uid is famiUar to the knees of many a pubhc speaker. 


Similar fine tremors also occur in certain toxic conditions. The 
tremor of chronic alcoholic poisoning is familiar to the layman, 
and when an alcohoUc patient becomes delirious and maniacal, 
his tremors are so evident that the condition is termed " delirium 
tremens." But other poisons besides alcohol produce fine 
tremors : for example, nicotine poisoning from excessive cigarette- 
smoking, also chronic poisoning by lead, mercury, chloral, ice. 

In cases of suspected alcoholism a valuable corroborative sign, 
known as QuinquaucTs sign, may often be elicited. In testing for 
this, we make the patient extend the fingers at the inter-phalangeal 
joints and press them at right angles to the palm of oiir own 
hand, which we hold in a vertical position. For the first two 
or three seconds nothing particular is noticed, but if the patient 
be a chronic alcoholic, we soon begin to feel a series of slight 
shocks, as if the phalanges of each finger were knocking, one 
against the other, trying to reach our palm. 

The tremor of paralysis agitans is generally rather coarse, 
varying in different cases from four to seven oscillations per second. 
It produces joint movements, e.g, the well-known "pill-rolling" 
movement of the thumb and fingers, flexion-extension movement 
of the wrists, pronation-supination of the forearm, flexion-extension 
of the ankle, &c. The coarser the movement, the slower is the 
rhythm. Paralysis agitans generally begins unilaterally, and may 
remain confined to one side for some time before ultimately be- 
coming bilateral, as may be seen in Figs. 30 and 31, which are taken 
from the same patient at an interval of three years. Usually the 
tremor of paralysis agitans can be temporarily controlled by 
voluntary exertion. But this is not always so, indeed cases occur in 
which voluntary movement increases the tremor. Paralysis agitans 
is always accompanied by rigidity in the affected muscles; in 
fact, rigidity may be well marked without tremor, in the so-called 
" paralysis agitans sine agitatione." An attack of ordinary 
hemiplegia occurring in a patient with paralysis agitans, arrests 
the tremor in the hemiplegic limbs, but if the hemiplegia be not 
complete or permanent, the tremor may subsequently reappear. 

Senile tremor is not unlike the tremor of paralysis agitans, 




but its onset occurs much later in life. Moreover, it begins 
bilaterally, and i* unaccompanied by the characteristic rigidity 
of Parkinson's disease. Thus in a famous old admiral it began 
at the age of eighty-four as a gentle antero-posterior tremor of 
the tongue, with a synchronous movement of the orbicularis oris. 

loth his hands had tremor and an internsseal attitude like that of 

laralysis agitans, but without rigidity. 

Fio. 111.— Piiraljsis Agitans:— 
ieii>si(i<.'u. Ihc sHnie )iatietit aa in Fig-30> 

three years later. 

In rickety children, especially during the second six months 

after birth, we sometimes observe a peculiar involuntary rotatory 

or nodding tremor of the head which usually cornea on quite 

^Bftuddenly in winter-time and is known aa spasmus nutans. It 

^■jl generally accompanied by fine, rapid nystagmus, which may be 

^Riore marked in one eye than in the other. If we fix the child's 

head, the nystagmus increases. The head movement is more often 

a lateral rotation than an antero-poaterior nodding. It stops when 

the child's eyes are closed, either voluntarily or artificially. T he 


symptom persists for six or eight weeks or longer, and then passes 
off, perhaps to return again in the following winter. It is not 
associated with any mental defect. 

Head-rolling is another variety of involuntary rhythmic move- 
ment met with in children, chiefly below the age of two years. 
Many of the patients are rickety and a large proportion have otitis 
media, latent or evident.^ The movement is more vigorous than 
that of spasmus nutans, it is unassociated with nystagmus, and it 
ceases when the child sits up, only occurring when he lies down. 

Rhythmic tremor sometimes occurs in gross brain disease. 
Thus, for example, in cases of lesions in the tegmental region 
of the pons or cms cerebri,^ affecting the rubrospinal tract 
(which descends from the red nucleus into the lateral colunm of 
the opposite side), or in lesions of the adjacent part of the oytic 
thalamus, we occasionally observe a slow rhythmic tremor of the 
limbs of the opposite side, chiefly in the hand and foot. This tremor 
is increased by excitement or voluntary movement, but ceases during 
sleep. In the diagnosis of such cases we have, besides the tremor, 
the other localising signs of a gross destructive lesion. Thus if 
the ocular nuclei (which lie dorsal to the red nucleus) be affected, 
there is ocular palsy of the nuclear tjrpe ; if the pyramidal tract 
be affected there is spastic hemiplegia ; and if the sensory tract, 
traversing the internal capsule and optic thalamus, be implicated, 
we have hemianesthesia. When a unilateral lesion of one cms 
cerebri produces oculomotor paralysis of one side with tremor of 
the opposite arm and leg, this is known as Benedikts syndrome. 
Moreover, certain lesions of the optic thalamus cause loss of emo- 
tional mobility in the opposite side of the face, with little or no 
weakness on voluntary movement. 

In many cases of tumour of the frontal lobe, there is a fine 

tremor in the upper limb when it is held horizontally forwards. 

The tremor in such cases affects the homolateral limb ; thus in a 

right-sided frontal tumour we expect tremor in the right hand. 

Let us now pass to the irregular, non-rhythmic, spontaneous 

1 Still. ClinicalJournal, Nov. 28, 190(3. 
* Holmes, Brain^ 1904. vol. xxvii. p. 327. 



niovcmeiita. Of these, ordinary " rheumatic " diorsa {urnishes 
one of the most striking examples. All aru familiar with the 
irregular, jerking, wriggling, grimacing muvementa of a choreic 
child. They may affect the face, soft palate, tongue, trimk, limbs, 
and even the muscles of respiration. The movements of the 
limbs are often more marked on one side than on the other, and 
may be confined to one side — so-called hemi-chorea. Choreic 
movements occur spontaneously but are increased by emotion or 
by voluntary movements. They cease during sleep. The muscles 
of choreic limbs have a tonus which is less than normal — 
hypotonia. A good method of eliciting choreic movements in a 
slight case of the disease, is to make the child hold both hands 
above the head, when after a few seconds slight involuntary move- 
ments appear in the fingers of one or both sides. 

Huntington's chorea is a hereditary variety of chorea which 
somes on after middle life and becomes steadily worse. It is asso- 
[ated with progressive dementia. 

Hyoscvne chorea, whose symptoms are similar to those of 
idinary chorea, occurs during acute intoxication with hyoscine, 
i is sometimes, but not invariably, associated with mild delusions. 

The movements of athetosis or " mobile spasm " are different, 
Bcurring as they do most commonly in the spastic lunbs of old 
miplegica (chielly after infantile hemiplegia). Athetosis never 
occurs in a limb which is completely paralysed but only when some 
degree of voluntary power survives. The movements are usually 
confined to the upper limb, and consist of very slow, ii-regular, twist- 
ing movements, most marked in the fingers and wrist, but in severe 
cases affecting the forearm, elbow, shoulder, and even the lower 
limb, where the most common involmitary movement is a hyper- 
extension of the great toe. Ordy in bilateral athetosis (gener- 
ally, though not always, following diplegia) do the movements 
affect the face, causing hideous grimacing. In a typical case the 
hand movements consist of slow flexion, then hyper- extension and 
spreading out of the fingers, irregularly, one after another. Com- 
bined with this, there is alternate abduction and opposition of the 
thumb, with flexion or extension at the wrist, and pronation or 


sii])inatiu(i of tin- forearm. Figs. 3'2 trO 35 an? taken from a well- 
marked case of athetosis in wliicli the nioveiiiciita affected all the 
joints of the upper limb. Athetosis ia intensified by voluntary 
movement whether of the paralysed limb or of the opposite 
unaftected hand. It cannot be controlled by voluntary effort, 
and Bometinies persists even during sleep. 

KlOS. 32 to 35.— Atbetosis in a woman af^eii a9, tliL' HiibjeiM of right-«ided 
lietiii|jleK''^ of nineteen ;eurs duration. 'I'hero wat< severe paralysis of lh« 
tieht, upper limb from tlie shouUiur dowDwarcle. The figures sboir albelOBls 
of lingers, wrist, and elbow. 

Many healthy people make automatic extension niovemonta of 
the upper limbs during the act of yawning. By the ancients 
these were termed pandiculation. Such mnvementa are often 
well seen in the paralysed limbs of a case of severe hemiplegia 
when the patient yawns or ia tickled, and the patient may harbour 
vain hopes of a return of motor power by observing extension 
movements of his paralysed fingers or elevation of the paralysed 



Unfortunately these movements are not a. hopeful sign in 
hemiplegia ; on the contrary, the more severe the lesion of the 
pyramidal tract, the more marked is the pandiculation. It does 
not occur in limbs which are the subjects of athetosis or other 
involuntary movements. Pandiculation has been ascribed by 
Bertolotti ' to irritation of the thalamic centres. 

Spontaneous movements also occur in cases of advanced 
Friedreich's ataxia, being mout marked in the head. neck, and 

II cliising Ihi 

IHilltA 111 tillgPTB 

face. They commonly consist in irregular nodding movements of 
the head or grimacing, which has been called " nystagmus of the 
face." But in Friedreich's ataxia the most outstanding feature 
is inco-ordination of voluntary movements. The absence of the 
knee-jerks, the deformity of the feet, the scoliosis, &c,, will all 
point to a correct diagnosis. 

Spontaneous movements also occur iu certain cases of tabes 
where there is severe impairment of joint-sense. The movements 
are chiefly seen in the fingers and wrists, and can best be demon- 
strated by making the patient close his eyes and hold his hands 
' Rertu iieuTologiqvr, lOOfi, p. '.>Sa 


steadily in the air with the fingers extended. In a few seconds we 
observe slow irregular flexion or extension movements of the fingers, 
which gradually assume curiously distorted attitudes, of which the 
patient is totally imaware. (See Fig. 36, also Fig. 151, p. 291, 
where similar movements have occurred in the lower limbs.) 

Again, in general paralysis of the insane, spontaneous tremors 
of an irregular type are frequently observed, even when the patient 
is at rest. They occur chiefly in the face, especially if the patient 
be emotionally excited or just about to speak. Waves of fibrillary 
tremor appear, rippling along the muscles of the lips, tongue, and 
face. Here we have other physical signs to guide us, e.g. the slur- 
ring articulation, the irregular or unequal pupils, frequently of 
Argyll-Robertson type, exaggeration or loss of the knee-jerks, the 
condition of the cerebro -spinal fluid, and the characteristic mental 

There is another great group of involuntary movements which 
includes the habit spasms, the tics, and the reflex spasms. A 
proper classification of these is well-nigh impossible, since the 
different varieties merge into each other. All are most common 
in people of " nervous " constitution, all are increased by 
emotion, and they cease during sleep. Slight degrees of habit- 
spasm may occur without any other sign of functional disease. 
Public speakers, such as clergymen, barristers, actors, and even 
medical lecturers, occasionally have little unconscious " tricks " 
of movement. A distinguished university professor has frequent 
clonic jerks of the frontales muscles, which suddenly elevate his 
eyebrows ; a popular comedian makes rapid blinking movements 
of both eyes (blepharo-spasm) when he advances towards the 
foot-lights; a young lady has clonic spasms of both platysmata 
when her neck is exposed in evening dress at dinner parties, and 
so on. Such minor degrees of habit-spasm are usually bilateral 
and occur without any local exciting cause. 

More severe varieties of habit-spasm are included under the 
term "Tic." A tic is of cortical, not reflex origin, and consists 
in the frequent explosive repetition of the same motor act — gener- 
ally a violent, irregular one, such as rapid shaking or tossing of 


the head, grimacing, wriggling of the shoulder, &c. It passes off 
I as suddenly as it comes on. Moreover, it does not interfere with 
I voluntary movements. For example, however violent a tic of the 
I right shoulder or arm may he. the patient's handwriting shows 
I no ahuormality. As Patrick ' has put it, when the impulse to tic 

can no longer be controlled, the patient takes pen from paper, 
I executes his tic and then resumes writing. At first sight, tic might 
' be confounded with chorea. But chorea does not repeat the 

Fit!. 37.— SpaBraotliu turticultis, witli accondarj byperl rojiliy of riglit 

iBme movement regularly again and again. Patients who have 
lievere tic usually show signs of mental degeneracy. This does 
rnot mean that they are necessarily deficient in intelligence. On 
I the contrary, they are often "superior degenerates," bright and 
[lively, but mentally immature, capricious, emotional, psychasthenic, 
und frequently the subjects of obsessions and various forms of 
t* phobia." The greater the psychical abnormality, the more 
■uvelerate is the tic. " Tiqueura " often have explosive articulation. 
" word -swallowing," sudden stoppage of speech, disordered re- 
spiration, echolalia (repetition of a particular word or phrase), 
or coprolalia (re^ictition of a blasphemoiis or obscene word). 

IS/MisimxIic /(irtiadlis ia one of the commonest and most severe 
• Jourml 0/ Amtriean Med. Angac, Feb, 21. i»05. 


varieties of tic. Though the movement of the head is apparently 
a unilateral one, the head being jerked constantly to one side, 
commonly to the left (see Fig. 37), it is really a bilateral affair, 
since muscles on both sides of the neck are employed to produce 
the movement, and it is sometimes combined with a backward 
jerk, a so-called retro-collic spasm. The movement may be tonic, 
clonic, or a combination of the two — tonico-clonic. The patient 
can often curb the movement by means of some antagonistic 
gesture of his own invention, e.g. by light pressure on the chin with 
his finger. Severe torticollis usually begins after middle life. At 
first occurring in paroxysms, it ultimately becomes continuous 
during waking hours, and the affected muscles become hyper- 
trophied from over-use. 

Besides idiopathic spasmodic torticollis, which comes on ap- 
parently spontaneously, certain cases have a definite exciting 
cause and should be classed, not with the tics, but with the reflex 
spasms which we shall consider presently. Thus, for example, 
we may have neuralgic torticollis,^ in which an occipital neuralgia 
or a painful tooth is followed by spasmodic torticollis, usually tonic 
in form. When the neuralgia passes off, the muscular spasm ceases 
also. Again, we may have labyrinthine torticollis,^ due to chronic 
irritation of one of the semicircular canals. In such cases the 
torticoUic spasm has the object of mitigating vertigo, which would 
occur if the head were not kept leaning over to the opposite side. 
A torticollis thus initiated may become inveterate, but some cases 
are cured by the administration of quinine. A small proportion 
of cases are examples of professional torticollis, occurring only at 
the moment of performing a special act, especially in cobblers and 
tailors, who have to turn the head and eyes to follow the needle. 
Such cases are more properly to be classed with the occupation- 
neuroses (see p. 239). Spasmus nutans, head-rolling, and other 
rhythmic movements (see p. 79), must not be confounded with 
true torticollis, in which the spasms are either tonic or irregularly 

^ Cruchet, Traite dea TorticoUs Spasmo<UqufH^ Paris, 1907. 

2 Curschmann. Deutsche Zeit/tchnft filr Nervenheilktttide^ 1907. p. 305. 



There is another group of movements which, originally excited 
by some peripheral irritation, ate classed as reflex spasma. A 
spasm, unlike a tic, begins locally, perhaps in a single muscle, 
and spreads to adjacent muscles. When the exciting stimulus 
is unilateral, the reflex ■ spasm is usually unilateral also, but 
not invariably ao, for bilateral reflex spasms also occur, as in 
tonic and clonic contraction of the orbiculares oculorura (ble- 
pliarospaam), the result of corneal or conjunctival inflammation, 
or as in the case where a vaginal caruncle or anal fissure 
produces vaginismus with bilateral adductor spasm. Of the 
unilateral reflex spasms one of the most striking is the intense 
facial spasm which occurs in severe cases of trigeminal neuralgia or 
tic douloureux, which is not a true tic but a reflex spasm, In 
this disease the patient has paroxysms of agonising pain in one or 
more divisions of the trigeminal nerve. During a paroxysm, the 
lace on the side of the pain is thrown into strong tonic con- 
traction, the eye is closed, the mouth is drawn up on the affected 
.«de, and the patient often presses his hand desperately over 
the site of pain. Only when the acute stage of the paroxysm 
passes oS do the facial muscles relax. Less severe unilateral 
fa/ml spasm, either tonic or clonic, implicating some or all of the 
facial muscles, may occur from other reflex causes, generally in the 
territory of the fifth nerve, such as a decayed tooth, a non-empted 
wisdom-tooth, a nasal polypus, &c. But unilateral facial spasm 
also occurs, leas frequently, in lesions of the facial nerve itself, 
as for example when tumours or abscesses compress the nerve. 
Sometimes it follows an attack of ordinary facial palsy, less 
commonly it may precede its onset, so that in every case of 
unilateral facial spasnv we should search for local lesions in the 
territory not only of the trigeminal but also of the facial nerve. 

Sometimes a leflex-spaam may persist as a habit-spasm, long 
after the original exciting cause has passed away. Such cases 
can usually be diagnosed by their history. For example, a lad 
iost his left arm by avulsion in a machinery accident. The stump 
was amputated at the shoulder-joint, but clonic spasms appeared 
in the trapezius and scapular muscles, and these persisted after 


all the posterior nerve-roots in that region were divided by 
operation. But other cases occur, even of unilateral spasm, with- 
out any reflex exciting cause or the history of one, and they 
are difficult to classify. Thus a lady whose menopause oc- 
curred at the age of forty-five, at the same time also lost most 
of her property through the failure of a bank. She gradually 
developed clonic spasm of the left facial muscles. At first, this 
consisted merely in a slight flickering of the lower lid for a second 
or two, every few days, but the condition gradually increased in 
severity until, when she came under observation thirteen years 
later, the spasms affected all the facial muscles on one side, be- 
ginning as a flickering movement, and then becoming tonic and 
lasting from twenty to thirty seconds at a time, the eye being 
closed, the eyebrow elevated, the angle of the mouth drawn out- 
wards, and the platysma thrown into strong contraction. In the 
intervals between attacks the face was symmetrical. Under treat- 
ment by bromides and galvanism this case became rapidly better. 
Finally, there are numberless varieties of hsrsterical spasms, 
apart from the hysterical " fits," which have already been dis- 
cussed. We can only refer to some of the commoner types. 
Thus saltatory spasm consists of a series of jumping or skipping 
movements, which occur whenever the patient assumes the erect 
posture. A similar spasm, less severe in degree, may produce 
paroxysms of trembling in the legs, as in a hysterical girl of nineteen 
with many other stigmata of hysteria, in whom the spasms ceased 
at once when she lay down. All sorts of movement, however, 
may occur in hysteria, simulating almost any kind of tremor. 
For instance, a hysterical woman of twenty-one had constant 
movements of the face, left arm, and both legs, resembling those of 
athetosis but being very much faster. In her case typical hysterical 
contractures and segmental anaesthesia of the hysterical type, 
together with the normal state of the reflexes, &c., aided in the 
diagnosis of hysteria, which disease will be further considered in a 
subsequent chapter. 



exchange ideas with our fellow-men chiefly by means of speech. 

I arbitrary code o( signals, vocal or written. These 

pials are perceived by our auditory or visual centres. Every 

■ country has its own particular code or language, which is learned 

f by each of its inhabitants. (Jestures and ruJniic movements, as 

J of communication, although international, have a very 

QJted field of usefulness as compared with speech. Two in- 

ilividuals, each ignorant of the other's language, can certainly 

' communicate with each other after a fashion by means of gestures 

alone, but they cannot express many ideas in this way, but 

only simple primitive emotions such as pleasure, anger, surprise, 

ind so on, or pantomimic imitations of certain acts. 

There are three chief classes of cases in which the functions 
[ articulate speech may be lost. Firstly, there are conditions in 
iiich the patient's higher intellectual functions are in abeyance, 
ither congenitally as in idiots, or from disease as in acquired 
mentia, coma, or in certain casei of hysteria. Such patients 
! speechless, but they are not aphasics. Secondly, there are 
cases where the higher intellectual centres are capable 
function, but the cortical speech-centres which control the 
- acts of speaking and writing, or the sensory processes of 
Kognising spoken or written words, are diseased, and yet the 
Mtient has not necessarily any paralysis of the peripheral organs of 
xh, nor is he necessarily deaf or blind. To this group the term 
W aphasia " is applied. Lastly, there are the cases where, with 
^tact intellectual functions and normal cortical speech-centres, 
lere are defects in the peripheral organs of articulation, so that 
lie patient is unable to articulate distinctly^for example, cases 
i cleft palate, post-diphtheritic palsy of the palate, facial or hypo- 



glossal paralysis, bulbar paralysis, and so on. These are affections, 
not of speech proper, but of articulation. 

Aphasia may be defined as impairment or loss of speech due 
to the loss of memory for those signs, vocal or written, by means 
of which we exchange ideas with our fellow-men. An aphasic, 
unless his higher intellectual centres are impaired, usually pre- 
serves his powers of gesture and of pantomime. Aphasia is due 
to disease, organic or functional, of certain well-defined special 
centres in or near the cortex of the brain. These cortical centres 

Fig. 38. — Diagram of left cerebral hemisphere, showing approximate 
positions of the centres concerned in speech. 

A. Auditory word-centre. \ a«.^-«-« 
V. Visual word-centre. J^ sensory. 

Sp. Vocal word-centre. i vf«»r»i. 

W. Motor centre for writing. / '*^«>^o'- 

exist on both sides of the brain, but ordinarily in right-handed 
people the speech-centres on the left side 6f the brain are pre- 

Let us consider the speech-centres somewhat more in detail. 
For the interchange of ideas two distinct processes are required — 
one sensory, the other motor. The sensory process includes the 
hearing and imderstanding of spoken words, and also the seeing and 
understanding of written or printed letters. The memories of 
words heard and seen are stored up in specialised parts of the 
auditory and visual centres, named respectively the auditory word- 
centre and the visual word-centre (Fig. 38). The auditory word- 
centre is at the upper or Sylvian surface of the temporal lobe 
(anterior transverse gyrus of Heschl, Flechsig's " auditory gyrus ") 







in the adjacent poBterior end o( the first temporal convolution : 
Slie visual word-centre ia in the angular gyriiB. Either centre may 
be diseased ; so that we have two varieties of sensory aphasia, 
viz. — auditory aphasia and visual aphasia. Then there is in 
speech the motor element, consisting of the motor act of expressing 
ilves in words, either vocally or by means of writing. The 
imories of these motor acts of vocal speech are ordinarily sup- 
'posed to be stored up at the posterior end of the inferior frontal 
(Broca's) convolution, and in the adjacent part of the pre-central 
convolution and of the insula. If this centre be destroyed, motor 
aphasia or aphemia is said to result, the patient being unable to utter 
words of which his motor memories have been destroyed. Marie, 
however, has recorded cases of destruction of Broca's convolution 
without any speech defect, and denies that it has any special im- 
portance in the mechanism of speeeh. He considers that cases of 
so-called motor aphasia are really examples of ordinary sensory 
iphasia combined with articulative difficulty (anarthria) due to a 
of the lenticular nucleus and its surrounding white matter, 
isnd maintains that isolated lesions of Broca's convolution are 
accidental and of minor significance. Earlier writers used also t« 
ideecribe a separate centre for writing (independent of the vocal 
rord-centre), a lesion of which would produce loss of the faculty 
writing — agraphia. But no case has been verified p&thologically 
in wliich a focal lesion has produced pure agraphia without affec- 
tion of vocal speech, so that the writing -centre, although it may 
be represented diagrammatical ly in a theoretical scheme of cortical 
ipeech -centres, is probably merely a part of the ordinary psycho- 
itor centre for the upper extremity. 

Fig, 30 is a scheme of the connection of the various centres 
concerned in speech. Let us first notice that the motor vocal 
word-centre is subservient to the auditory word-centre, and that 
the writing-centre is similarly subservient to the visual word- 
lire, A child learna to speak first by hearing spoken words 
then imitating them. Therefore speech at first is entirely 
iditory in origin. Later, in learning to read, the meaning of each 
ird is learned by associating the letters seen with words heard 



spoken, so that the auditory word-centre acts as the instructor of 
the visual word-centre. 

In most people, during the process of silent thought, words 
are revived primarily in the auditory word-centre, and there is 
usually a simultaneous revival of the same words in the visual 
word-centre. But in other people the revival in the visual word- 
centre comes to be of greater importance. Accordingly we may 
classify people into " auditives " and " visuals " according to their 
mode of revival of words in thought. Most of us are ** auditives." 


Fig. 39. — Diagram of Speech-Centres (after Brarawell). 

A. Auditory woni-centre. V. Visual word-centre. 

Sp. Motor vocal word-centre. W. Motor centre for writing. 

HV. Half-vision centre. 

The interrupted lines indicate possible bat less habitual routes for transmission of impulses. 

Simultaneous revival of word-images in several speech-centres 
makes our comprehension of the idea more perfect. Thus a 
diflficult concept is better imderstood if we read it aloud, because 
this involves the activity of the visual, auditory and vocal 

Aphasia commonly results from organic disease of one or more 
of the cortical speech-centres, or of the sub-cortical fibres connect- 
ing them. The most frequent organic causes are embolism, haemor- 
rhage, or thrombosis, cerebral abscesses and cerebral tumours. The 
differential diagnosis between these various conditions depends 
largely on the history ; embolism producing the symptoms suddenly, 
haemorrhage taking several minutes, thrombosis taking perhaps 



tourt), absce^ and tumours being still mon; gradual in onset. But 
also meet with cases of temporary or functional aphasia, 
Ktmotimes from mere debility or exhaustion, sometimes following 
"congestive attack" in general paralysis, or accompanying a 
Pparoxysm of migraine, or after an epileptic fit. 

In investigating a case of aphasia we should first note whether 

■the patient has other signs of gross cerebral lesion, such as 

■liemianopia, or hemiplegia, and should inquire whether he is 

■naturally right- or left-banded. Most children are taught to write 

with the right hand, whether they are right-handed or not, and 

therefore in determining tliis point we inquire with which hand 

a man draws a cork, throws a atone, &c. ; or if a woman, with 

which hand she combs her hair. 

The following seriejt of inquiries (based on Beevor'a scheme) 
(diould then be made. The capital letters in parenthesis indicate 
e parts of the brain involved in each case, 

1. Can the patient spontaneously utter intelhgible words ? 
Bp.) Note the extent of hia vocabulary. Can he pronounce all 
rorda or only a few ? Get the patient to talk spontaneously, and 
ibserve whether he talks fluently or misplaces words or syllables, 
vhether he talks in disjointed phrases, ("telegraphic" type of 
Ipeech.) or whether he talks unintelligible jargon. 

2. Can he understand words which he hoars ? (A.) Ask him 
► touch his nose, ear, eye, chin, &c., in turn, thus testing his 
iterpretation of nouns. Then ask him to smile, whistle, shut 
la eyes, &c,, thiis testing his comprehension of verbs. Some- 
lines we find that the patient executes the first command correctly, 
rot continues to repeat the same act in response to different 
ommands. A patient can sometimes sing the words and air of 
• aong. when he is unable to repeat the words in a speaking 

3. Can he understand written questions or commands which 
IB sees ? (V.) Write down and show him simple sentences, such 
B " How old are you ? " " Put out your tongue." " Give me 
cur left hand." 

i. Can he write spontaneously i (W.) If his right hand is 


paralysed, let him try with the left. Observe whether he writes 
intelligibly, whether he misplaces words or syllables, or whether he 
scribbles meaningless signs. 

5. Can he copy from printed to written letters ? (V-^W.) 
Print some word such as " Hospital " or ** Monday," and get him 
to copy this. 

6. Can he write to dictation words which he hears ? (A-^ V -^ W.) 

7. Can he pick out objects of which he hears the name ? 
(A-*V ) Place in front of him a heap of objects, such as a key, 
a shilling, a match, a pencil, and ask him to pick out each in turn. 

8. Can he repeat words heard ? (A-^Sp.) Try him first with 
simple words and phrases ; e.g. " cat," " dog," " nurse," " good- 
morning," &c. 

9. Can he name objects seen, and can he read aloud from words 
shown to him ? (V-*A-*Sp.) Point to different objects and ask 
him what they are. 

10. Does he understand gestures and pantomimic movements ? 
Without speaking to him, get him to imitate you when touching 
the nose, spreading out the fingers, protruding the tongue, &c. 

Auditory Aphasia, or Word-Deaftiess.— The patient in this 
case is not deaf, but simply word-deaf. He hears ordinary sounds 
and noises, but spoken words are not understood ; they sound to 
him like an unknown tongue. The character of the sjrmptoms 
varies according as the lesion is subcortical or cortical in position. 

(a) Subcortical, or Pure Auditory Aphasia.— This is 

extremely rare (Marie, in fact, denies its existence). Here the 
lesion simply blocks the way-in for spoken words. The patient 
therefore has word-deafness — i.e. he is unable to understand what 
is said to him ; he is also unable to repeat spoken words or to write 
from dictation. But the auditory word-centre being still intact, he 
possesses all his memories of auditory speech, and therefore 
spontaneous speech is perfect. Moreover, the visual word-centre 
being in normal working order, he is still able to read, and, as a 
matter of fact, reading is his only means of receiving messages 
from other people. 



(b) Cortical Word-Deafness. — This is much commoner than 
the other variety. Here the lesion involves the cortical centre itself, 
and the auditory memories of spoken words are obliterated. And 
therefore, in addition to the previous defects of woid-deatneas with 
inability to repeat spoken words or to write from dictation, there 
K other symptoms due to the fact that the motor speech-centre b 
> longer controlled by the auditory word-centre. Internal speech 
and thought are impaired, and ho the patient makes mistakes 
'vhether in speaking spontaneously or in reading aloud He also 
makes mistakes in writing, especially in spelling. He talks fluently 
enough, it la true, but he tends to mix up his words or syllables, 
and in a severe case may jabber unintelligible jargon. Word- 
deafness renders the patient unaware of his own errors. This, as 
we shall see. is in marked contrast with motor aphasia, where the 
pfttient recognises his own mistakes as soon as he has uttered 
If the lesion of the auditory word-centre be incomplete, 
^e word-deafnesa and resulting errors of speech are also partial. 
Tieae latter may, in a slight case, be confined to inabihty to name 
objects, i.e. nouns, the patient being still able to express abstract 
ideas. Thus a partially word-deaf patient, who is unable to name 
a knife shown him, may say, " It is for cutting." Or again, partial 
word deafness may produce simply confusion of words ; the patient 
may say one word when he means another {paraphoiiiii). It rarely 
happens that word-deafness remains permanent and complete ; the 
auditory word-centre in the opposite hemisphere generally cnm- 
'pensates, to some extent, as time goes on. 

The extent of mental disturbance in word-deafness varies accord- 
ing to whether the patient be a strong " auditive " or a strong 
"visual." In the latter case the mental impairment ismuch less than 
ui the former, and the disturbances of motor speech are but alight. 
The auditory and visual word-centres are fairly close together, 
and more than this, they are supplied by the same branch of the 
middle cerebral artery (see Fig. 21, p. -iS} ; so that it is not un- 
common for a single arterial lesion, e.g. a thrombosis, to affect both 
I centres together and to produce a combination of word-deafness 
and word -blindness. 


Visnal Apliasia, or Word-Blindness (Alexia) — in word-hlind- 
ness the patient can see, but cannot understand printed or written 
characters. They appear to him like strange hieroglyphics. He sees 
the shape of the letters, but they convey no meaning to his mind. 

Here, as in word-deafness, the symptoms vary in degree. The 
patient may be unable to recognise a single letter (letter- blindness), 
or he may be able to spell out the letters singly but unable to read 
syllables or words. Often a patient who is unable to read any 
other word, can recognise his own name. Frequently he retains 

FlO. 40. — Diagram reprationling a lesion (inilivntcil by 
wliich prodm'CH pure word bli nil nc-ss (Itjisi 
C. C. Fuslcrlor ntnniity ol cnrpiu I'ulloiiim. 

the power of recognising numbers and of doing addition, sub- 
traction, and multiplication sums. We have to recognise two 
varieties of word-bhndncss, according as the lesion is cortical or 
subcortical in position. 

(a) Subcortical, or Pure Word-Blindness. — Here the way- 
in for visual word -impression is destroyed, the visual word- 
centre remaining intact. The patient cannot understand written 
or printed words, nor can he read aloud, but he still retains 
the power of writing spontaneously and from dictation : and 
therefore he can express his thoughts perfectly in writing, but 
is unable to read what he has himself written. Inasmuch as 
a subcortical lesion, in order to produce word-blindnesa, must be 
beneath the angular gyrus and in such a position as to cut ol! the 
afferent visual impulses from both half-vision centres to the vifluiil 



^K bave 
H "ah 

word-centre in the angular gyrus, it wiL necessarily implicate the 
optic radiation to some extent. And therefore a pure or subcortical 
word-blindness is always aaaociated with hemianopia or, when 
paitial, with he mi -achromatopsia (Fig, 4'J). 

(i) Cortical Word-Blindneaa. — In this variety, in addition to 
the symptoms just descrihod. there is loss of the memories of written 
or printed words, and therefore, inasmuch as the ^Hsual word-centre, 
which controls the writing-centre, is destroyed, the patient has 
uraphia. He. is unable to write spontaneously, to copy from printed 
into written characters, or to write from dictation. If the lesion 
of the visual word-centre he partial the alexia and agraphia aie 
also incomplete, and mistakes in writing may amount simply to 
the writing of wrong words, syllables or letters — so-called " par- 

These points are illustrated by Bramwell's well-known diagram 
(Fig. .t!!), in which a lesion at the position marked 1, destroying 
fibres passing from one half-vision centre to the visual speech- 
centre, would not prcduce word -blindness. A lesion at 1, destroy- 
ing fibres passing from both half-vision centres to the visual speech- 
centre, would produce word- blindness but not agraphia, since the 
visual speech-centre is unaffected and is able to influence the 
motor writing-centre. A lesion at 2, destroying the visual speech- 
centre, would produce word-blindne^ and agraphia. A lesion at 
3 would produce agraphia (uidess the motor writing-centre could 
be brought intii action in some loundabout way), but not word- 
blindness, the visual speech -centre being intact. 

Motor Aphasia.— In this variety the patient has lost the 
power of expressing himself by spoken words. He can neither 
speak spontaneously nor can he read aloud. And yet (unless the 
motor speech -cent res on both sides of the brain are destroyed) he 
is not absolutely dumb. As Hughlings Jackson puts it, the patient 
is speechless, but as a rule not wordkss. He can usually utter 
intelligently a few words, such as "yes" and "no," by means of 
the speech-centre on the uninjured aide, and in addition he may 
have other words or phrases, moatly interjections, such aa 
oh my!" "come oul" "damnl" "by Jove!" — so-called 


" recurrent utterances " — which he - utters automatically when 
excited, or when making an effort to speak. A patient who 
has motor aphasia, unlike a word -deaf person, is conscious of his 
own errors. 

(a) Subcortical, or Pure Motor Aphasia. — Here the patient, 
though intelligent and able to understand spoken and written 
language (by means of his uninjured auditory and visual word- 
centres), cannot utter spoken language, either spontaneously by 
reading aloud or by repeating what he hears. This is because 
the way-out for spoken speech is blocked. But his mental speech 
processes are unimpaired, and if the outgoing fibres from the 
writing centre are unimpaired, he is able to express himself in 
writing, as in the scriptural case of Zacharias, the father of John 
the Baptist (St. Luke, chap, i.), and in many cases the patient 
can indicate by signs how many syllables or letters are in the 
word which he desires to speak but cannot utter. 

(b) Cortical Motor Aphasia. — This type, in which the lesion in 
supposed to be limited to the cortical motor speech-centre in the 
inferior frontal gyrus and adjacent grey matter of the iiisula and 
pre-central gyrus, is less securely established than the other varieties. 
(Marie denies its existence altogether.) The patient in this variety 
has not only all the defects of a subcortical case, which we have 
jiist considered, but, in addition, his mental processes of internal 
thought are impaired, since the co-ordination of memories of words 
spoken and written by himself is impaired. He has therefore 
difficulty in understanding complicated sentences, whether spoken 
or written. Together with difficulty in vocal speech there is often 
(though not always) associated a similar difficulty in writing — 
agraphia — proportional to the defect of speech. 

Pure isolated agraphia, without any other symptom, does not 
occur, and as we have seen, the commonest variety of agraphia 
is that due to cortical word-blindness. The study of agraphia due 
to sensory aphasia is easier than that associated with motor aphasia, 
because in sensory aphasia there is no necessary motor ])aralysis 
of the right arm or hand, whereas sometime:; in motor aphasia the 
patient has to make his attempts at writing with the left hand. 



Sucli are the chief types o( aphasia. Clinically, however, it ia 
V commoner to meet, not with pure auditory, viBual, or motor 
t aphasia, due to a small focal leaion, but with combinations of 
L these, or with total aphasia, the result of a larger destructive 
I lesion implicating several or all of the speech- centres. Such severe 
[■ aphasias, of course, produce a more profound degree of mental 
I deficiency, and inasmuch as the same artery, the middle cerebral, 
Isupplies not only the speech -centres, but also the other cortical 
Imotor areas and the corpus striatum (see Figs. 21 and 21a), total 
jAphasia is usually combined with severe right hemiplegia. 

Uarie,' whilst adniiiling tlie existence of viatial, auditory and motor 

_ tphoBia aa clinical syudroniM, dt^nies the existence uf diagrammatic visual, 

auditory and nioUir apcech -centres, and attrilnit.efi all aiihoaic phenomena to 

itit«llectiial deficiency fi-nm disiDt«g; of some part of Wi^rnicke's zone 

(which consists of tlie g}'ri aurronndiiig the exti-emities of the Sylvian and 

the parallel Gsgiirc), whic^h /one he reganis aa an intellectual area. According 

. Id Marie the eaaeiitiat fact of aphasia, of whate\'er variety, is inanfficieiit cuin- 

[ prehension of speech. He adduces evidence to Ehon- that Broi-a's convolution 

' plays no speeial part in tliu function oF HjiKecli c:!ce])t in so Far as it contains 

certain motor centres for the Face, tongue and larynx. In fact he diamrds a 

special vocal-u-ord-<:entre just as others disciird a motor cenlre for writing. 

Tlie syndi'ome of motor aphasia ia explaim^d by him as due to iutelleetual 

deficiency pltu articulalive anarthria, this latter heing due to a lesion of the 

lenticular zone (comprising the lenticular nucleus and its surrounding white 

matter). In other woula, he regards motor aphasia simply aa a sensory 

aphasia minai the pou er of speech. The intellectuid procesfies of speech in 

right-kandeil patients arc localised in the left hemisphere, wliereas unarthria 

..may be produced by a lesion of either lenticular j;one. 

But though Marie's views are reductive in their simplicity, there are 

L'Wrtain obstacles lo accepting tlicm in their entirety. Even supposing that 

■ the only real varielieM of aphasia are sensory, and that some defect of iutelli- 

rgence is present In every cose, it. geem* none the lesa proliable that visual and 

laudiLory speech-cenires do exist, and that lesions of these centres, rather than 

■e intellectual delit:ienay, are the cause of the » ell-deli tied clinical types of 

aphasia. As Uejerine has urged, we may have advanced dementia 

rom undoubted cortical disease, as in general paralysis, without any aphasia, 

■ensory or motor. It therefore seemn proliable that the diminution of 

'intelligence which is seen in aphasiu patients is due to interference with 

cortical sensorial prou^aseH, producin;; disruption of the cerebral meehanisui ot 

speech, rathei' than that the ajibaaic phenomena should lie regiirded asaecondaiy 

, it may be 

' Semaine MidicaU. 190Q, Noa. 21, 42, and t 

kto intellectual detiuit. With regard to Marie's conceptio 
a mere combinaliou oF intellectual deficiency with a 


objected that this fails to account for the presence of well-artic'ulated " re- 
current utterances" such as are present in most patients with complete motor 
aphasia. If anarthria alone were the cause of the speech-loss, it ought to 
render the articulation of all words difficult. Moreover, the cortical vocal- 
word-centre is not limited to Broca's convolution, but probably extends into 
the insula and to the neighbouring part of the pre-central gyrus. So that 
there is no insuperable difficulty in the existence of a lesion limited to Broca's 
convolution unaccompanied by aphasia. 



It is necessary to distiiigiiisli clearly between speech and articula- 
tion. Speech is a cortical function, articulation is mainly bulbar. 

Disordered articulation, or dysarthria, signifiea difficulty in per- 
[onuing the co-ordinated niuscular raovementa necessary for the 
production of the consonants and vowels which go to form syllables 
and words. 

In simple dysarthria there is no afiection of the cortical 
intres or paths which are concerned in the processes of speech 
A patient, for example, who has advanced bulbar palsy, 
even when he is unable to articulate a single word, is not, strictly 
qteaking. speechless. He is inarticulate, which is quite a different 
thing. His mental speech-processes remain normal, he can still 
express himself fluently in written speech, and he is able to under- 
stand everything he hears or sees. 

The peripheral mechanism of vocal speech is partly musical 
l(or voiced), consisting in vibration of the approximated vocal 
It ia also partly consonantal (or voiceless), consisting in 
ihe co-ordinated action of numerous muscles of the hps, tongue, 
palate, and pharynx. The term " articulation " is speciaUy applied 
to this latter, the consonantal element. 

To test a patient's power of articulation, we listen to his 
onlinary conversation, or we ask him to read aloud a passage 
<m a book or newspaper, and notice how he pronounces his 
words. Then, if he shows any abnormality in connection with 
particular consonants, we ask him to repeat " catch " words, 
chosen so as to present special difficulties, e.g. " British consti- 
tution," " bibUcal criticism," " West Register Street," " hippopo- 
Kmus," " Burgess's fish-sauce shop," &c. 
Difficulties of articulation are the result of defects, consisting 

^_ onlir 


either in paralysis or inco -ordination, of certain groups of muscles 
in the lips, tongue, palate, pharynx, or larynx. The underlying 
defect may be either in the bulbo-muscular neurones (comprising 
the pontine and medullary nuclei, the peripheral motor nerves and 
the muscles), or it may be due to supra-nuclear affections in the 
cortico-bulbar neurones, at some point between the higher speech- 
centres and the bulbar nuclei. Or it may be due to ataxia of the 
organs of speech. 

Infra-nuclear and Nuclear Affections of Articulation.— 
Articulation may be impaired as a result of paralysis of any of the 
motor nerves or nuclei supplying the articulative muscles. 

Unilateral hypoglossal paralysis (as in the case of a business man 
shown in Fig. 72, in whom this nerve was divided by a stab in the 
neck dealt by a discharged employe) produces motor paralysis 
followed by atrophy of the corresponding half of the tongue. The 
paralysed half-tongue feels to the patient as if he had a foreign 
body in his mouth. This makes his articulation clumsy, lisping and 
indistinct, especially in the case of Unguo-dental (S, Z, Th) and of 
anterior linguo-palatal consonants (T, D, L, R). But after a few days 
the patient becomes accustomed to the feeling of his palsied half- 
tongue, and his articulative difficulty to a large extent disappears. 

Facial palsy, from its affection of the lips, renders labials (P, B) 
and labio-dentals (F, V) indistinct, especially so when the palsy 
is bilateral. 

Bilateral paralysis of the palate, e.g. post-diphtheritic paralysis, 
congenital cleft palate, and syphiUtic perforation of the palate, 
all produce the same articulative difficulty, inasmuch as the nasal 
cavity cannot be shut off from the mouth. As a result the voice 
is nasal, and certain consonants are altered (B becomes M, D be- 
comes N, K becomes Ng, and so on), so that articulation as a 
whole is indistinct. This indistinctness of articulation is increased 
when the patient stoops forwards : it diminishes or even disappears 
on lying with the head thrown backwards, since in the latter 
position the soft palate tends to fall back by its own weight and 
shuts off the naso-pharynx.^ 

* Schlcsinger, Neurologieches CentralbkUt, 1906, p. 50. 




Total paralysis of the palate is also associated with difficulty 
in deglutition, especially with fluids, which during the act of swallow- 
ing regurgitate into the naso-pharynx and escape through the 
anterior narcs. 

Unilateral paralysis of the recurrent laryngeal nerve renders 
the voiee hoarse, by paralysing one vocal cord, and so inter- 
fering with the phonation of vowels, but not with the articu- 
lation of consonants. If the vagus root be affected at its point 
of exit frona the medulla, the soft palate is often paralysed 
on the same side (see later, Cranial Nerves). But unilateral 
palatal palsy, uiiUke bilateral, does not affect the articulation of 

Articulation may also become indistinct from disease of the 
bulbar nuclei — so-called glosso-labio-laryngeal paralysis, or bulbar 
paUy. In this disease there is a diffuse, progressive weakness of 
the muscles of articulation, with atrophy and fibrillary tremors of 
the muscle fibres, especially those of the tongue and lips. Articula- 
tion becomes more and more indistinct, saliva dribbles from the 
patient's trembling lips, and in advanced cases there is interfer- 
ence with swallowing and coughing. If, as is often the case, 
bulbar palsy is an upward extension of an amyotrophic lateral 
sclerosis, there may be a concomitant muscular atrophy and 
fibrillary tremor in the muscles of the upper limbs, especially 
in the intrinsic hand muscles. Owing to affection of the pyra- 
midal tracts, there is also exaggeration of the deep reflexes. 

There is a form of myopathy — the fitdo-saiiiah-humeral type 
of Landouzy and Dejcrine, in which the facial muscles are 
atrophied. This affection is a bilateral one and the patient's 
lower lip protrudes in a characteristic fashion which has been 
icd the " tapir " type of Up. He has also a peculiar " trans- 
rerae " smile. In severe cases of this disease the articulation of 
labial consonants becomes impaired just as it does in double 
facial palsy, 

Myasthenia gravis, when it affects the bulbar muscles, repro- 
jduces all the features of bulbar palsy, with this difference, thai 
iTthe paralysis varies in its degree from time to time, becoming 


accentuated by fatigue. After a period of rest a patient so 
affected may resume with normal articulation, but, if he continues 
to speak, his muscles gradually become exhausted, and his articula- 
tion becomes more and more indistinct. Not only the lips and 
tongue, but the ocular muscles, the muscles of mastication and 
various muscles of the trunk and limbs, show evidence of temporary 
paralysis or fatigue, and ultimately the patient succumbs to fatigue 
of his respiratory muscles. 

Articulative Ataxia. — There are some diseases in which articul- 
ation becomes indistinct, not from paralysis of the muscles but 
from ataxia. 

In Friedreich's ataxia, for example, the articulation becomes 
slow, thick, and clumsy, and the patient talks as if he had a 
foreign body in his mouth, so that his speech has been aptly 
termed the " hot-potato " speech. The pitch of the voice in this 
disease may vary from word to word, and in advanced cases a 
certain degree of mental feebleness is often superadded. 

In laryngeal tabes where the larynx is affected by ataxy the 
voice is tremulous, and when a tabetic patient has ataxia of 
the tongue his articulation becomes laboured. This lingual trouble 
in tabes is often associated with a peculiar constant rolling move- 
ment of the tongue on the floor of the mouth, even when the 
patient is not speaking. The patient often has an annoying 
subjective sensation in his tongue, as if it were covered with 
blotting-paper, which he tries to get rid of by the restless rolling 
of his tongue. 

Supra-nuclear, or Cortico-bulbar Affections of Articulation. 

— Articulation may be affected where the upper or cortico-nuclear 
neurones are involved. The slurring articulation of many cases of 
acute alcoholic intoxication is familiar to laymen, being especially 
marked in the pronunciation of labial and of anterior linguo-dental 
consonants. In rare instances alcoholic dysarthria persists for 
days after the alcoholic celebration. Tollmer and other French 
authorities ascribe this circumstance to cerebellar intoxication. 
Many alcoholic patients realise their own articulative difficulty, 
and in endeavouring to compensate for it, they utter certain 



I words with a deliberation and undue emphasis that betrays 
f them. 

Very similar to the alcoholic articulation is that of general 
I paralysis of the insane. But the typical general ])aralytic shows 
I also a characteristic fibrillary tremor of all the muscles around 
I the lips and nose. 

Both in acute alcoholism and in general paralysis there is 
often a tendency to choose an occasional wrong word, or to mis- 
place syllables. Such defects are not bulbar but cortical in origin. 
In the later stages of general paralysis, articulation may be t-otally 
inintelligible, reduced to a mere mumble. 

After an attack of hemiplegia, right-sided, the patient is often 
r aphasic. But even in a left-sided hemiplegia where no true 
I Bphasia exists, it is not uncommon to find a temporary change in 
I the articulation, which loses its crispness, and becomes a little 
I laboured and indistinct. This dysarthria usually passes off after a 
I few days, but sometimes persists permanently, especially if the 
■ lesion involves the lenticular nucleus. A lesion of the left lenticular 
I produces greater dysarthria than one of the right nucleus.' 

In cases where a patient has a bilateral hemiplegia we often 

Emeet with " psevdo-buJhar" paralysis. The most common history 

lie that there have been one or more hemiplegic attacks, all confined 

I to the same side, but at last the patient has an attack on the 

opposite side. This now produces, in addition to the classic signs 

wot a double hemiplegia, pseudo-bulbar [laralysis, with thick, in- 

■idistinct articulation, closely resembling that of true bulbar palsy 

I'Wid with the same dribbling of saliva, difficulty in swallowing, 

■ifioughing. &c., but without atrophy or fibrillary tremors of the 

^ected muscles. The pseudo-bulbar patient ia emotionally 

ritable ; he laughs, or more often cries, on slight provocation, 

md, unlike the subject of true bulbar paralysis, he is generally 

lomewliat deficient mentally. There is usually a history of sue 

aaive (more rarely of simultaneous) attacks of hemiplegia on 

tppoaite sides of the body. 

Dovhh athetosis is a disease which is usually congeiiitBl. It 
* Hingaxiini. SuUa tintotnalologia dtlU knonr d(l nucUo UMicolart. 1903. 



ia characterised by wild wriggling and twisting movements of all J 
the limba, chiefly ou attempted voluntary movements, and hy I 
grimacing of the face, together with spastic rigidity of the aftected I 
muscles (see Fi^. 41 aud 42). There is generally a certain degree i 
of mental deficiency. In this disease- articulation is often affected. \ 
The grimaces of the face and of the tongue muscles interfere con- 
siderably with articulation. Moreover, irregular spasmodic con- 
tractions of the diaphragm and other respiratory muscles give 1 

the voice a curiously jerky or groaning character, due to sudden ] 
interruptions of breathing. 

Patients suffering from disseminated schrosia frequently have a 
peculiar so-called "staccato" speech, in which the words are 
enunciated in a jerky mincing fashion, very difficult to describe, J 
but easy to recognise once it has been heard. This is sometimes I 
called the " scanning " speech, from its fancied resemblance to | 
the scansion of Latin or Greek verse. 

In paralysis agitans, as the disease advances, the patient's i 
voice becomes thin, feeble and reduced almost to a monotone, 


whilst his articulation, like hia gait, acquires a " festinant " char- 
acter. When speaking, he begins slowly, but towards the ends 
I of sentences or long words he tends to hurry, so that the final 
f syllables are pronounced hastily. Together with this we have the 
.characteristic "starched," expressionless face, the Parkinaonian 
I mask, conunencing unilaterally and ultimately becoming bilateral. 
Severe cases of chorea may have the articulation interfered 
Kwith, owing to sudden violent movements of the face, tongue, and 
K.^espiratory muscles. Speech becomes hesitating and jerky, and 
I in very bad cases the voice may be reduced to a whisper. 

There are also affections of articulation due to functional 
^cortical disturbances. Of these the most familiar is stammering, 
I which consists in a want of co-ordination between the vocal 

V (laryngeal) and consonantal (oral) mechanisms of speech, so that, 
I in the common type, the patient sticks at a consonant, which he 

■ often continues to repeat, over and over again, before he finally 
■.succeeds in cnmiciating the rest uf the word. He misdirects 
R his energy on the consonants, instead of touching them tightly 
l«nd passing on to the vowel sounds. Most stammerers lose their 
I stammer when they sing, their attention being then directed to 

■ the vocal part of speech. 

A rarer variety of stammerii^ is that in which the patient sticks 
I at initial vowels. This is due to temporary spasm of the false 
f Tocal cords, and the patient remains with his mouth wide open 
\ until the spasm relaxes, when his words suddenly rush forth in a 

Y hurried stream until he has no breath left. He then takes another 
I breath and the precipitate rush again occurs.' 

Many stammerers acquire various tricks, chiefly through their 

lorts to overcome the stammer. Thus extra noises may be thrown 

lin, e.g. sudden inspiratory grunting or whooping noises, or the 

Ipatient may make grimaces or curious contortions of the limbs. 

< Catbcort haa piiinttHl out that tliiB variety of atnnimeriii); is doscribed 
D ShBke«pearu'H ■■ As You Like It" (Act iii. Seenp 2) Ha follows: — 

I would tliou coiddat afaniiiier. that thou mightst pniir out tliis con- 
I out of Ihy mouth, aa wine comes out of & n arrow 'neckLid bottle, 
^Uber too much at once, or nonE< at ull. I prithee, lake tlie cork out of thy 
nith thai 1 luuy di-ink thy tiilings." 


This leads us to recall the various articulative tics or habit-spasms 
which are met with in pyschasthenic patients, either in conjunction 
with stammering or independently of it, and these may be of the 
most varied character. The patient's speech may be interrupted 
by weird pharyngeal barking or grunting noises. Or the articulation 
may be monosyllabic, a whole breath being taken for each syllable. 
Or, again, it may be jumbled up in the most extraordinary ways, 
though the " tiqueur " usually interpolates, now and then, a clearly 
articulated sentence or phrase amongst the other unintelligible 
ones. Hysterical aphonia is fairiy common, and can usually be 
recognised by the history, together with the characteristic laryngeal 
appearances. We also meet with cases of hysterical mutism, where 
the patient refuses to utter even a whispered word. 

Deaf-mutes are the patients who are populariy known as 
"deaf and dumb." A normal child learns to speak by imitating 
words which he hears, but if a child be congenitally deaf, he 
does not leam to speak, but remains deaf and dumb. Moreover, 
if he is born with normal hearing, but subsequently becomes deaf, from middle ear disease or from meningitis, should this occur 
before the age of about six years, he usually loses his power of 
speech. Deaf-mutes can generally be taught to speak again by 
the oral or " lip-reading " method, where the child imitates the 
movements of his teacher's muscles of articulation and also learns 
to phonate, though usually with a harsh, discordant voice. But 
even deaf-mutes who have never been taught to speak, usually 
make noises of some sort or other, often pharyngeal snorts and 
grunts, or spluttering labial noises, and less frequently laryngeal 
sounds. They do this especially when excited. This was the case 
with a deaf-mute who used to make weird snorting noises when 
playing football. These doubtless helped to smite terror into the 
hearts of the opposite side. The congenital deaf-mute is usually 
brighter and more clever than the acquired deaf-mute. Deaf- 
mutes generally have a wonderful command of gestures and 

The dumbness which is present in profound degrees of idiocy 
is not an articulative difficulty, but a true speech affection due to 


mal-development of the cortical speech-centres. An imbecile 
child is speechless because he has no ideas to express ; in this 
respect he differs from the deaf-mute, who is often bright and 

Certain varieties of deficient articulation are met with in 
children or in adults who are mentally more or less childish. The 
condition known as lalling consists in a want of precision in the 
pronunciation of certain consonants. Thus a patient may substitute 
the uvular R for the ordinary linguo -palatal R, or he may sub- 
stitute W for R, so that " broken reed " becomes " bwoken weed," 
Or, again, the patient may substitute Th for S and is then said to 
lUp. These last two varieties are sometimes voluntarily assumed, 
as a fashionable affectation, by young men not overburdened with 
brain power. More serious varieties of lalling are where the 
letter L is replaced by some other consonant, so that " elephant " 
may be pronounced as "edephant," "csephant," " enephant," 
"elephant," &c. Still worse is it when the patient has difficulty 
with K or G, their places being taken by T and D respectively. 

As a general rule, it may be stated that laUing on a single 
consonant does not necessarily indicate defective intellect, whereas 
lalling on many consonants, if the patient has passed the age 
of childhood, should arouse the suspicion of mental deficiency, 
although lalling is a normal stage in the process of learning to 

Finally, there is the condition known as idioglossia, where 
from difficulty in pronouncing his consonants a child retains the 
correct vowels, but substitutes other consonants and seems to 
speak a new language of his own. In the course of time the 
child usually completely outgrows this weakness. 



The recognition of cranial nerve palsies is, diagnostically, of the 
utmost importance, nor is it a matter of such difficulty as is 
conmionly imagined. 

First or Olfactory Nerves. — ^From the under surface of the 
olfactory bulb on each side there arise some twenty minute nerves 
which perforate the cribriform plate of the ethmoid to be dis- 
tributed to the upper part of the nose. To test the sense of smell, 
we direct the patient to close his eyes. We then hold aromatic 
substances, such as oil of cloves, peppermint, or asafoetida, in 
front of each nostril in turn, closing the other nostril with the 
finger. Ammonia or acetic acid must not be used to test the 
sense of smell, since these stimulate the fifth nerve (common sensa- 
tion), and may produce a pungent sensation in the nose, even 
when the sense of smell is lost. 

Anosmia, or loss of the sense of smell, is sometimes of 
diagnostic value. It may occur, for example, in congenital absence 
of the olfactory nerves, in some frontal tumours, in lesions of the 
olfactory bulb or olfactory tract, in injuries of the anterior fossa of 
the skull, and when there is atrophy of the olfactory nerves in tabes. 
It also occurs unilaterally very often in hysterical hemiplegia and 
is then associated with diminution of the other special senses on 
the hemiplegic side. But the value of anosmia as a symptom is 
lessened by the fact that numerous local obstructive conditions 
in the nose also produce loss of smell, e.g. nasal polypi or even a 
simple cold in the head. 

Parosmia, or perverted sense of smell, and various subjective 
hallucinations of smell occur not only in mental disease but also 
in gross lesions of the uncinate gyrus, which is the cortical olfactory 
centre. But here again local nasal conditions may also cause 




olfactory aenaationa, e.g. the unpleasant odour perceivpd by a 
patieiit suHeriiig from empyema of the antrum of Highmore, 
from which horribly offensive pus is escaping into the n(«e. On 
the other hand, in ozeena from chronic atrophic rhinitis, the 
offensive smeli is not perceived by the patient, though it is pain- 
fully evident to his neiglibours. 

Second, or Optic Nerve. — This contains not only visual fibres, 
but also the afferent fibres for the pupillary reflex. 

We have already referred to the course of the visual path from 
retina to cortex (Fig, 19, p. 34). In testing vision we should 
determine vUiial acuity by means of test types at a fixed distance, 
such as six metres. Using SneUen's types, of which the largest 
should be readable at sixty metres, and the sm^Uest at six metres, 
we direct the patient to read the letters from above downwards 
If his vision is norntal te will be able to read the smallest type at 
six metres. His visual acuity is then represented as V = J. But if 
he can only read down as far as the type which ought to be visible at 
thirty metres, then V= ^'g. Each eye should be tested separately, 
the test types being well illuminated and the patient standing 
with his back to the light. When the visual acuity is much im- 
paired, the patient may not see even the largest type, but can only 
count fingers at a short distance, or perhaps can only tell hght 
from darkness. 

Hemeralopia, or day-blindness, is a condition in which the power 

of vision is bad during the day or in a bright light, whilst the 

patient sees better in a dim light. The phenomenon is not un- 

I common in tobacco amblyopia, where there is usually present a 

I central scotoma for green and red. The hemeralopia is probably 

I due to the fact that a bright light rapidly fatigues the retina and 

I also, by producing pupillary contraction, causes the peripheral part 

[ of the retina to be less in use than the central, whereas in a dim 

light the pupil dilates and the unaffected peripheral portion of the 

retina comes into play. 

Nydalojiiu, or night -blindness, where the patient becomes 
almoBt blind at dusk or in u dim light, is associated with various 
renditions, of which the most interesting is congenital reliniiia 


pigmentosa, a disease easily recognised on ophtliahnoscopic exa- 
mination. It also occurs to a lesser degree in certain cases of 
" cortical " cataract, where the lenticular opacity acts as a 
permanent diaphragm. 

Colour vision is most conveniently tested by means of Holmgren's 
wools. These are thrown on a table well lit by daylight, and the 
patient is given one particular test-skein of wool which is kept 
separate from the heap, and told, not to name the colour, but to 
match it, selecting from the heap of coloured skeins all those which 
are like the test-skein, whether lighter or darker in shade. The 
patient is given a pale green test-skein. If his colour vision is 
normal, he will pick out all the pale greens correctly, but if he is 
red -green colour-blind he will select a grey or straw-coloured skein. 
Congenital red-green colour-blindness is the commonest variety. 
Yellow-blue colour-blindness is less common. If a patient be 
totally colour-blind he will confuse with the test-skein all those 
of similar brightness, no matter what their colour may be. 

The size of the fiM of vision in each eye is of great importance 
and for its accurate measurement a perimeter is required. This, 
however, is a large and expensive apparatus. For clinical purposes 
the following method is sufficient, presuming that the physician's 
own visual fields are normal. The physician sits exactly opposite 
the patient, about a yard away from him, and tests each eye 
separately. To test the patient's right eye direct him to cover up 
his left and to gaze steadily at the physician's left eye. Meanwhile 
the physician closes his own right eye and looks steadily at the 
patient's pupil, watching that the patient's eye does not wander 
from the fixation point. Then, holding his own left hand in 
a plane midway between himself and the patient, and beginning 
almost at arm's-length, he brings his hand inwards from the 
patient's ear towards the middle line, meanwhile moving his own 
fingers. If the patient's visual field is normal, he will catch sight 
of the moving fingers at the same time that the physician does so. 
If he does not, that visual field is contracted and the physician 
then brings his moving fingers inwards until the patient does catch 
sight of them. In this way we test both the upper and lower 



[quadranta of the field oa the temporal and nasal sides, in turn. 
[ we find the visual field dirainiahed in one or other eye, it is well 
) take a eareful perimetric chart. 
We may find a central scotonut or blind patch in one or both 


patient catches sight of it. Central scotoma may occur in various 
organic diseases of the optic nerve or retina, such as early optic 
atrophy, central retinal haemorrhage, &c., or it may result, in a 
minor degree, from obstruction to central vision, e.g., by central 
opacities in the lens or cornea. Such conditions are easy of re- 
cognition. Central colour scotoma to red and green (detected in a 
similar fashion with coloured objects) together with deficient visual 
acuity, is highly suggestive of tobacco amblyopia. In such cases, 
besides a history of chronic excess in tobacco, we look for corro- 
borative signs such as fine tremor of the hands, cardiac irregularity, 
cardiac pain, &c. An almost identical amblyopia may also occur 
from chronic alcoholism. 

The visual field may be concentrically contracted. This con- 
dition is sometimes due to optic atrophy, the field being reduced 
to a small area surrounding the fixation-point, so that the patient 
looks at the outer world as though through a narrow tube. More 
commonly concentric contraction of the visual field occurs in 
hysteria, the field on the hemiplegic side of the body being more 
contracted than that on the other side (Fig. 43). Less frequently 
a cortical lesion of the angular gyrus, not impUcating the sub- 
jacent optic radiation (Fig. 19), causes a similar concentric con- 
traction of both fields, more marked in the eye of the side opposite 
to that of the brain lesion. This is somewhat clumsily named 
crossed aniblyojna, but, as previously observed, it is much 
commoner in hysteria than in organic brain disease, and in 
hysteria it is frequently associated with diminution or loss of 
other special senses on the side of the more contracted field 
whose colour sense is frequently lost (achromatopsia). 

Hemianopia (Fig. 44) means blindness of half the visual field, 
right or left as the case may be, from causes other than retinal 
disease. It usually affects the visual field of both eyes, and is due 
to a lesion of the visual fibres at or behind the optic chiasma. 
Such chiasmic lesions may result from pressure by tumours, 
s)rphilitic or inflanmiatory affections of the basi-sphenoid, from 
tumours of the brain or of its membranes, and especially from 
pituitary tumours, as in acromegaly. We have already considered 


r the signs of lesiona of the optic tracts, and it is convenient here 
pto recall the effects of lesions of the optic chiasma. 

{A) If the lesion he in the central part of the chiasma. ititer- 
Ptupting the decusBating optic fibres (belonging to the nasal halves 
of both retinfe), there is blindness in the outer halt of each 
visual field: — bi-temporal kemianopia (Fig. 45), This sometimes 
occurs in pituitary tumours. 

(B) If the lesion be situated at one or other lateral extremity 
l-of the chiasma, it will interrupt merely the non -decussating fibres 

R. Optk Tnict. I. Iljillc Tr«-t. 




)iagrani of c. 

oiir!.c„r visual iibr 


mot the optic nerve and optic tract on that side, causing unilateral 
wnaml hemianopia in the corresponding eye. To produce bilateral 
l.n&sal hemianopia there must be two separate lesions, one at each 
I end of the chiasma, a condition which very seldom occurs. A 
Fteeion involving the central part of the chiasma and extending to 
m one or other side {Fig, 45, A plus B) will produce the sum of these 
I two, namely bi-temporal hemianopia plus unilateral nasal hemi- 
lanopia, i.e. total blindness of one eye with temporal hemianopia 
I of the other. 

(C) A lesion of the left optic tract behind the chiasma produces, 
already seen, hemianopia in the right halves of both fields 
f vision. 


(D) A lesion of one optic nerve simply causes blindness in the 
corresponding eye. 

In rare cases we may have a qtuidrantic hemianopia in which 
only one quadrant (instead of one-half) of both visual fields is blind. 
This is generally due to a lesion limited to part of the cortical half 
vision centre in the cuneate lobule and lingual gyrus. The calcarine 
fissure divides the half -vision centre into an upper and a lower part. 
A lesion above the calcarine fissure, t.e. in the cuneate lobule, 
causes blindness of the lower quadrant, whilst a lesion below the 
calcarine fissure, i.e. in the lingual gyrus, causes blindness of the 
upper quadrant of the corresponding half -field.* 

The optic discs and retin» should be examined with the 
ophthalmoscope in every case of nervous disease. The most im- 
portant conditions to look for are optic neuritis and optic atrophy. 
Optic neuritis occurs in numerous pathological conditions within 
the skull, especially in intra-cranial tumours and in tuberculous 
meningitis. But it also occurs in nephritis, in lead poisoning, in 
diabetes, and in severe anaemia ; and these four common conditions 
must always be excluded before we diagnose gross intra-cranial 
disease. We may also meet with optic neuritis in certain cases of 
cervical myelitis. Optic atrophy may occur primarily, as in tabes 
and disseminated sclerosis, or it may be a secondary post-neuritic 
process. Sometimes it follows a retro-hulbar neuritis, whether 
occurring spontaneously, or in disseminated sclerosis, or in chronic 
alcohol or tobacco poisoning. Pallor of the temporal halves of the 
optic discs is often an early sign of disseminated sclerosis. The 
combination of optic atrophy, blindness, and mental deficiency 
occurs in the anuiurotic family idiocy of Tay and Sachs, an affection 
of certain Jewish children, coming on in infancy. In these cases, 
on ophthalmoscopic examination there is a characteristic cherry- 
red spot seen at the macula lutea, due to local oedema and atrophy 
of the retina, whereby the vascular choroid shines through. Apart 
from optic neuritis and optic atrophy, we must be on the lookout 
for other pathological conditions of the fundus, such as choroiditis, 

1 Henschen, Le Centre cortical de la Viaion. Int'Omat. Med. Congress, 
Paris, 1900. 



albuminuric retinitis, tubercle of the choroid, occluaioti of the 
central retinal artery, retinal hiemorrhage, &c. 

It must be remembered that a patient may have severe optic 
neuritis without any impairment of vision. Optic atrophy, on the 
other hand, causes the visual field to contract concentrically to a 
greater or less extent, whilst the visual acuity diminishes and 
ultimately the eye becomes blind. The atrophy of retro-bulbar 
neuritis often produces central scotoma from affection of the papillo- 
macular bundle of optic nerve fibres. 

Third, Fonrtti, and Sixth Nerves. — It is convenient to study 
together these three nerves which, between them, innervate all 
the voluntary muscles of the eye. The distribution of each is aa 
follows : — The third nerve (oculo-motorius) supplies all the external 
ocular rauscloa except two : — the superior obhque supphed by the 
fourth nerve, and the external rectus suppUed by the sixth, it 
also supplies the voluntary part of the levator palpebral superioria 
(the involuntary port being supplied by the cervical sympathetic), 
and it contains fibres which indirectly, through the ciliary ganglion 
and short cihary nerves, supply the non-striated sphincter pupills 
and ciliary muscle. The fourth nerve (patheticus) supphes the 
superior obhque alone, the tixih nerve (abducens) the external 
rectus alone. 

Until comparatively recently, the motor nucleus for the pupil 
mWM generally considered to be located in the third nucleus, and 
■In « special part of it near its anterior end (the so-called Edinger- 
Westphal nuclei, situated close to the middle hne, one on each 
aide, consisting of stnall nerve cells embedded amongst the 
larger cells of the oculomotor nucleus). To explain the occur- 
rence of loss of the light-re6ex various theoretical lesions 
w«re utMunied, sometimes in these Edinger - Westphat nuclei 
(Bemheinu-r '), sometimes in Mcyoert's fibres leading from the 
anterior curpora quadrigemina to the supposed pupillary centra 
in the third nucleus. But against the first of these theories, 
cases have been rcconled of tumour i>f the mid-brain completely 
destroying the oculomotor nuclei and so producing ophthalmoplegia 

' V. Orw-fo'it Arckiv. 18B7. J 


(D) A lesion of one optic nerve simply causes blindness in the 
corresponding eye. 

In rare cases we may have a qtuidrantic hemianojna in which 
only one quadrant (instead of one-half) of both visual fields is blind. 
This is generally due to a lesion limited to part of the cortical half 
vision centre in the cuneate lobule and lingual gyrus. The calcarine 
fissure divides the half -vision centre into an upper and a lower part. 
A lesion above the calcarine fissure, t.e. in the cuneate lobule, 
causes blindness of the lower quadrant, whilst a lesion below the 
calcarine fissure, i,e. in the lingual gyrus, causes blindness of the 
upper quadrant of the corresponding half-field.* 

The optic discs and retinsa should be examined with the 
ophthalmoscope in every case of nervous disease. The most im- 
portant conditions to look for are optic neuritis and optic atrophy. 
Optic neuritis occurs in numerous pathological conditions within 
the skull, especially in intra-cranial tumours and in tuberculous 
meningitis. But it also occurs in nephritis, in lead poisoning, in 
diabetes, and in severe anaemia ; and these four common conditions 
must always be excluded before we diagnose gross intra-cranial 
disease. We may also meet with optic neuritis in certain cases of 
cervical myelitis. Optic atrophy may occur primarily, as in tabes 
and disseminated sclerosis, or it may be a secondary post-neuritic 
process. Sometimes it follows a retro-bulbar neuritis, whether 
occurring spontaneously, or in disseminated sclerosis, or in chronic 
alcohol or tobacco poisoning. Pallor of the temporal halves of the 
optic discs is often an early sign of disseminated sclerosis. The 
combination of optic atrophy, blindness, and mental deficiency 
occurs in the anuiurotic family idiocy of Tay and Sachs, an affection 
of certain Jewish children, coming on in infancy. In these cases, 
on ophthalmoscopic examination there is a characteristic cherry- 
red spot seen at the macula lutea, due to local oedema and atrophy 
of the retina, whereby the vascular choroid shines through. Apart 
from optic neuritis and optic atrophy, we must be on the lookout 
for other pathological conditions of the fundus, such as choroiditis, 

1 Henschen, Le Centre cortical de la Vision, Int-emat. Med. Congress, 
Paris, 1900. 


albuminuiic retinitis, tubercle of the choroid, occlusion of the | 
central retinal artery, retinal htemorrhage, &c. 

It must be remembered that a patient may have severe optio 
neuritis without any impairment of vision. Optic atrophy, on the 
other band, causes the visual field to contract concentrically to a 
greater or lees extent, whilst the visual acuity diminishes and 
ultimately the eye becomes blind. The atrophy of retro-bulbar 
neuritis often produces central scotoma from afiection of the papiUo- 
macular bundle of optic nerve fibres. 

Third, Fourth, and Sixth Nerves.— It is convenient to study 
together these three nerves which, between them, innervat« all 
the voluntary muscles of the eye. The diatribution of each is as 
follows ; — The third nerve (oculo-raotorius) supplies all the external 
ocular muscles except two : — the superior oblique supplied by the 
fourth nerve, and the external rectus supplied by the sixth. It 
also supplies the voluntary part of the levator palpebrse auperioria 
(the involuntary part being supplied by the cer^Hcal sympathetic), 
and it contains fibres which indirectly, through the ciliary ganglion 
and short ciliary nerves, supply the non-striated sphincter pupillffi 
and ciliary muscle. The fourth nerve (patheticus) supplies the 
superior oblique alone, the sixth nerve (abducens) the external 
rectus alone. 

Until comparatively recently, the motor nucleus for the pupil 
was generally considered to be located in the third nucleus, and 
in a special part of it near its anterior end (the so-called Edinger- 
Westphal nuclei, situated close to the middle line, one on each 
aide, mnsiating of smai] nerve cells embedded amongst the 
larger celb of the oculomotor nucleus). To explain the occur- 
n'nce of loss of the light-refiex various theoretical lesions 
wore assumed, sometimes in these Edinger - Wcstphal nuclei 
(BernhcimtT '), somt-times in Meynert's fibres leading from the 
anterior corpora tiuadrigemina to the supposed pupillary centre 
in the third nucleus. But against the first of these theories, 
cases have been recorded of tumour of the mid-brain completely 
dtwtmyiiig the oculomotor nuclei ami so producing opbihalmoplegia i 
' v. Orkcfa'a JrcAiv. ISUT. 


(D) A lesion of one optic nerve simply causes blindness in the 
corresponding eye. 

In rare cases we may have a qtuidrantic hemianopia in which 
only one quadrant (instead of one-half) of both visual fields is blind. 
This is generally due to a lesion limited to part of the cortical half 
vision centre in the cuneate lobule and lingual gyrus. The calcarine 
fissure divides the half -vision centre into an upper and a lower part. 
A lesion above the calcarine fissure, t.e. in the cuneate lobule, 
causes blindness of the lower quadrant, whilst a lesion below the 
calcarine fissure, t.e. in the lingual gyrus, causes blindness of the 
upper quadrant of the corresponding half -field.* 

The optic discs and retinas should be examined with the 
ophthalmoscope in every case of nervous disease. The most im- 
portant conditions to look for are optic neuritis and optic atrophy. 
Optic neuritis occurs in numerous pathological conditions within 
the skull, especially in intra-cranial tumours and in tuberculous 
meningitis. But it also occurs in nephritis, in lead poisoning, in 
diabetes, and in severe anaemia ; and these four common conditions 
must always be excluded before we diagnose gross intra-cranial 
disease. We may also meet with optic neuritis in certain cases of 
cervical myelitis. Optic atrophy may occur primarily, as in tabes 
and disseminated sclerosis, or it may be a secondary post-neuritic 
process. Sometimes it follows a retro-btJbar neuritis, whether 
occurring spontaneously, or in disseminated sclerosis, or in chronic 
alcohol or tobacco poisoning. Pallor of the temporal halves of the 
optic discs is often an early sign of disseminated sclerosis. The 
combination of optic atrophy, blindness, and mental deficiency 
occurs in the amaurotic family idiocy of Tay and Sachs, an affection 
of certain Jewish children, coming on in infancy. In these cases, 
on ophthalmoscopic examination there is a characteristic cherry- 
red spot seen at the macula lutea, due to local oedema and atrophy 
of the retina, whereby the vascular choroid shines through. Apart 
from optic neuritis and optic atrophy, we must be on the lookout 
for other pathological conditions of the fundus, such as choroiditis, 

1 Henschen, Le Centre cortical de la Vision, Int'Omat. Med. Congress, 
Paris, 1900. 

albuminuric retinitis, tubercle of the choroid, uccluBion of the 
central retinal artery, retinal hemorrhage, &c.. ' 

It must be remembered that a patient may have severe optio 
neuritis without any impairment of vision. Optic atrophy, on the 
other hand, causes the visual field to contract concentrically to a ' 
greater or less extent, whilst the visual acuity diminishes and 
ultimately the eye heoomea blind. The atrophy of retro-bulbar 
neuritis often produces central scotoma from affection of the papiUo- 
macular bundle of optic nerve fibres. 

Third, Fourth, and Sixth Nerves.— It is convenient to study 
together these three nerves which, between them, innervate all 
the voluntary niusclefi oE the eye. The distribution of each is as 
follows : — The third nerve (oculo-raotorius) supplies all the external 
ocular muscles except two : — the superior oblique suppUed by the 
fourth Derve, and the external rectus supphed by the sixth. It 
also gupplica the voluntary part of the levator palpebrse superioria 
(the involuntary part being supplied by the cervical sympathetic), 
and it contains fibres which indirectly, through the ciliary ganglion 
and short ciliary nerves, supply the non-striated sphincter pupill» 
and ciliary muscle. The fourth nerve (patheticus) supplier the 
superior obUque alone, the sixth nerve (abducens) the external 
rectus alone. 

Until comparatively recently, the motor nucleus for the pupil 
WM generally considered to be located in the third nucleus, and 
in a special part of it near its anterior end (the so-called Edingor- 
Weetpbal nuclei, situatnl close to the middle line, one on each 
side, consisting of small nerve cells embedded amongst the 
larger cells of the oculomotor nucleus). To explain the occur- 
rence of loss of the light-reflex various theoretical lesions 
wcrv assumed, sometimes in these Edinger - Westphal nuclei 
(Bemheiraer '), sometimi-s in Meynert's fibres leading from the 
anterior corpora quadrigemina to the supposed pupillary centra 
in the third nucleus. But against the first of these theories, 
coses have been recorded of tumour of the mid-brain completely 
destroying the oculomotor nuclei and so priKlueiiig ophthalmoplegia . 
■ V. atttB(e» ArtAiv, 18UT. , 


(D) A lesion of one optic nerve simply causes blindness in the 
corresponding eye. 

In rare cases we may have a quadrantic hemianopia in which 
only one quadrant (instead of one-half) of both visual fields is blind. 
This is generally due to a lesion limited to part of the cortical half 
vision centre in the cuneate lobule and lingual gyrus. The calcarine 
fissure divides the half-vision centre into an upper and a lower part. 
A lesion above the calcarine fissure, i.e. in the cuneate lobule, 
causes blindness of the lower quadrant, whilst a lesion below the 
calcarine fissure, i.e. in the lingual gyrus, causes blindness of the 
upper quadrant of the corresponding half-field.^ 

The optic discs and retinse should be examined with the 
ophthalmoscope in every case of nervous disease. The most im- 
portant conditions to look for are optic neuritis and optic atrophy. 
Optic neuritis occurs in numerous pathological conditions within 
the skull, especially in intra-cranial tumours and in tuberculous 
meningitis. But it also occurs in nephritis, in lead poisoning, in 
diabetes, and in severe ansamia ; and these four common conditions 
must always be excluded before we diagnose gross intra-cranial 
disease. We may also meet with optic neuritis in certain cases of 
cervical myelitis. Optic alraphy may occur primarily, as in tabes 
and disseminated sclerosis, or it may be a secondary post-neuritic 
process. Sometimes it follows a retro-bulbar neuritis, whether 
occurring spontaneously, or in disseminated sclerosis, or in chronic 
alcohol or tobacco poisoning. Pallor of the temporal halves of the 
optic discs is often an early sign of disseminated sclerosis. The 
combination of optic atrophy, blindness, and mental deficiency 
occurs in the amaurotic family idiocy of Tay and Sachs, an affection 
of certain Jewish children, coming on in infancy. In these cases, 
on ophthalmoscopic examination there is a characteristic cherry- 
red spot seen at the macula lutea, due to local oedema and atrophy 
of the retina, whereby the vascular choroid shines through. Apart 
from optic neuritis and optic atrophy, we must be on the lookout 
for other pathological conditions of the fundus, such as choroiditis, 

1 Henschen, Le Centre cortical de la Vision. Int^mat. Med. Congress, 
Paris, 1900. 



^H albuminuric retinitis, tubercle of the choroid, occlusion of the 
^f central retinal artery, retinal hceniorrhage, &c. 

It must be remembered that a patient may have severe optic 
neuritis without any impairment of vision. Optic atrophy, on the 
• other hand, causes the visual field to contract concentrically to a 
^b greater or less extent, whilst the visual acuity diminishes and 
^B nltimately the eye becomes blind. The atrophy of retro-bulbat 
^H neuritis oft*n produces central scotoma from affection of the papillo- 
^M macular bundle of optic nerve fibres, 

^B Third, Fourth, and Sixth NerveS' — It is convenient to study 

H together these three nerves which, between them, innervate all 

B the voluntary muscles of the eye. The distribution of each is as 

H follows :— The third nerve (oculo-motorius) supplies all the external 

^M ocular muscles except two : — the superior oblique supplied by the 

BL fourth nerve, and the external rectus supphed by the sixth. It 

also supplies the voluntary part of the levator palpebrse auperioria 

(the involuntary part being supplied by the cervical sympathetic), 

and it contains fibres which indirectly, through the ciliary ganglion 

I and short ciliary nerves, supply the non-atriated sphincter pupillee 
and cihary muscle. The fourth nerve (patheticus) aupphes the 
superior oblique alone, the sixth nerve (abducens) the external 
rectus alone. 
Until comparatively recently, the motor nucleus for the pupil 
was generally considered to be located in the third nucleus, and 
in a special part of it near its anterior end (the so-called Edinger- 
Westphal nuclei, situated close to the middle line, one on each 

[side, consisting of smaU nerve cells embedded amongst the 
larger cells of the oculomotor nucleus). To explain the occur- 
rence of loss of the light-reflex various theoretical lesions 
were assumed, sometimes in these Edinger ■ Westphal nuclei 
(Bemheimer '), sometimes in Meynert's fibres leading from the 
anterior corpora quadrigemina to the supposed pupillary centre 
in the third nucleus. But against the first of these theories, 
cases have been recorded of tmnour of the mid-brain completely 
destroying the oculomotor nuclei and so producing ophthalmoplegia 
I V. Groefe's Anhiv, 18»7. 



externa, and yet the pupillary reflex still remained (Biancone/ 
Jacobsen^). Moreover, total ophthalmoplegia, internal and ex- 
ternal, has occurred without any affection of the Edinger- 
Westphal nuclei (Monakow ^). Further, degeneration of Meynert's 
fibres has not been demonstrated, even in cases of tabes or 
general paralysis where loss of the pupillary light-reflex is one 
of the commonest clinical phenomena. Lastly, experimental 
and clinical evidence (Piltz,* Bach *) has shown that the ciliary 

Corpora, Qiujudrigendnou 

in Nucleus 

Effereftt i 

MiibUory Fibres fhmv 
Brairvto J^ihaiyGan^^un 





Fwres fronv ja vvR 


■Ext. GenjLCulalRjBodbf 

'*JII Nerve 

Ciliary GanglLorv. 
PupU/ coThstrictin^Iibres. 


Fig. 46. — Diagram of the path of the pupil-reflex (modified from Bach). 

ganglion is the peripheral motor nucleus controlling the sphincter 
pupillse, and Marina,* in a series of twenty-eight cases of tabes and 
general paralysis exhibiting the Argyll-Robertson pupil, found 
this ganglion invariably degenerated. In one of them where the 
Argyll-Robertson phenomenon was confined to one eye, the ciliary 
ganglion was degenerated on that side alone, the ganglion of the 
other side being normal. It is therefore probable that degenera- 
tion renders the ciliary ganglion inexcitable to the stimulus of 

» Rivista di Freniatria, 1899. ^ Deutsche Med. Wocheivtch., 1900. 

3 Gehim-pathologie, 4te Aufl. 1905, s. 1053. 
* Neurologischea CentrcUbkUtt 1903. * Zeitsck. fur Augenhcilkunde, 1904. 

® Annali di Necrologia, HK)I. 



[light, whereas it can still respond to the stronger stimulus of volun- 
tary impulses transmitted along the third nerve. 
The Papil. — We note the size of the pupil, both in a bright 
and in a dim light, and we observe whether the pupils are equal in 
diameter. Abnormal dilatation of the pupil (mydriasis) is often 
present in anEemia and neurasthenia, but it may occur, on one or 
both sides, in organic nervous disease. Mydriasis may be either 
paralytic, from paralysis of the sphincter pupilla;, as in disease of 
the third nerve or ciliary ganghon, or it may be irritative, as 
when due to stimulation of the dilator pupillae. It also occurs 

I when optic atrophy has caused blindness, and is then due to the 
absence of visual impressions. Myosis or abnormal contraction of 
the pupil occurs in pontine hjemorrhage, probably from irritation 
of inhibitory fibres leading from the brain to the cihary gangha.' 
It is also present in many cases of tabes, as well as in certain 
cases of disease of the cervical region of the cord (notably in 
Byringomyelia) from interruption of the pupil-dilating fibres.* 
Hyosis is also caused by iritis and by the irritation of foreign 
bodies in the cornea, and a transient myosis occurs for a day or 
80 aft«r excision of the Gasserian ganglion * {see Fig. 46). 

Variations in the size of the pupil may also be the result of 
^mydriatic drugs, either locally instilled (atropine, homatropine, 
•cocaine) or taken internally (belladonna), whilst other drugs are 
JmyoticB, either local (eserine, pilocarpine) or internal (opium, 

The outline of the pupil should be carefully examined. Some- 
mes, instead of being circular, it is oval or irregularly polygonal. 
I variations have an important diagnostic value. For if we 
K«xclude congenital malformation such as coloboma, operative pro- 
loedures such as iridectomy, and disease such as iritis and synechite, 
pthen it may be taken as a general rule that irregularity of the pupils 
signifies either tabes, general paralysis, or old syphilis, the lesion 
being either in the short ciliary nerves or in the ciliary ganglion 
itself. Ectopia pupUlw is a condition in which the pu[)il is not 

ti Bach, ZeilKhnjI /Hr Augeitkeilkundt. 1004. e. 105. 


in the centre of the iris. Sometimes it occurs in lesions of the 
mid-brain ; ^ in other cases, however, it appears to have no 
pathological significance. Irregularity of the pupil can be pro- 
duced experimentally by stimulation or division of the short 
ciliary nerves. Each eye must be tested separately, noting the 
effect on the pupil of shading and imcovering, first the same eye 
and then the opposite eye. 

The fwpiUary reflex to light should always be observed. Nor- 
mally the iris contracts when light falls on the retina, whether of 
the same eye (direct reflex) or of the opposite eye (consensual 
reflex). The light-reflex depends upon the integrity of a reflex arc, 
whose afferent limb is the peri-macular fibres of the retina and optic 
nerve, whose intermediate station is in the mid-brain and whose 
efferent limb passes through the third nerve and ciliary ganglion 
to the pupillary sphincter (Fig. 46). 

If the healthy pupil be strongly illuminated and examined with 
a magnifying lens (say x 10), we observe that it is not stationary 
but in a continuous state of fine irregular movement, slight 
alternate narrowing and widening, varying both in rhythm and 
amplitude. This normal pupillary unrest * must not be confounded 
with hippuSj which is a pathological condition consisting in rhythmic 
clonic contractions of the iris, regular in their periodicity, much 
coarser in range, and visible to the naked eye. Loss of the normal 
pupillary unrest is always pathological, and may be one of the 
earliest signs of organic affection of the reflex visual path, e.g. in 
tabes or general paral3^is. 

Loss of reaction to light occurs in optic atrophy, in paralysis 
of the third nerve, and in degeneration of the ciliary ganglion. 
Loss of the Ught-reflex with preservation of contraction during 
accommodation for near objects — ^the classic Argyll - Robertson 
phenomenon — occurs tjrpically in tabes and in general paralysis 
of the insane. Marina has shown this to be associated with de- 
generation of the ciliary ganglion. It also occurs in blindness from 
optic atrophy. In the early stages of optic atrophy the pupil of 
the affected eye may contract to light fairly well for a moment, 
but under continued exposure it dilates again, unlike a healthy 

1 S. A. K. Wilson, Brain, 1900, p. 524. 

* Hiibner, Archiv fUr Psychiatries 1900, Band 41, s. 1010. 


r pupil.' If tliia phenomenon be associated with diminution of 
[ visual acuity or with failure to distinguish between red and green 
[ in the centre of the visual field, we should be suspicious of early 
optic atrophy (even though the optic disc be normal in appear- 
ance), which in many cases is due to commencing disseminated 
sclerosis. W^fiidte's kemiopic jnipiUaTtj reaction, in certain cases 
of hemianopia. is absence of pupillary contraction when a ray of 
, light is thrown on the blind side of the retina. It signifies a lesion 
of the visual path behind the chiasma, and below or at the cor- 
pora quadrigemina. In retro -quadrigenunal hemianopia, where the 
lesion is anywhere between the corpora quadrigemina and the 
visual cortex, the pupillary reaction is normal (Fig. 19, p. 34). 

The rmdion of the pupil to accommodation is the contraction of 
the pupil which occurs when the patient converges the eyes to look 
at a near object. We test this by holding a finger close to the 
patient's face, first telling him to look at some distant object, 
and then suddenly to look at the finger. If he is blind, he 
can nevertheless converge by attempting to look at his own finger. 
In paralysis of the third nerve there is total immobility of the 
corresponding pupil, both to hght and on convergence. Loss of the 
contraction on accommodation with preservation of the light-reflex 
—a condition the converse of the Argyll -Robertson phenomenon 
— ^ia not uncommon after diphtheria, and is often accompanied 
I by other evidences of post -diphtheritic neuritis, such as paralysis 
of external ocular muscles or of the palate, loss of knee-jerks, 
, 4c, ParadoxicaX pupillary reaction is when the pupil dilates 
instead of contracting on accommodation. The reaction of the 
pupil to painful stimulation of the skin of the neck, causing the 
pupil to dilate, is important with regard to the cervical sympathetic 
(see later, p. 321). A psychical dikUation of the pupil also occurs, 
temporarily, under the influence of lively emotion. 

Let us now consider paralysis of external ocular muscles. 
To detect paralysis of the ocular muscles, having first examined 
I the pupils, noting their size and any irregularity of outline, and 
f having tested their reaction to light and on accommodation, we then 
rAsk the patient to follow our finger with his eye, making lum look 
lalternately up, down, to the right and left, and making him 
' Ounn. Brit. Med. Journal. 11107, p. 3G3. 



converge. Meanwhile we observe whether there be any squint, 
deficient movement in any direction, diplopia, or nystagmus. 

If an individual muscle is paralysed, there is diplopia, squint, 
and deficiency of movement of the affected eye towards the direct- 
ion of traction of the affected muscle. Fig. 47 is Bishop Harnian's 
diagram indicating the action of the individual muscles. A simple 
rule, worth remembering in all cases of ocular paralysis, is that the 
affected eye is displaced (by the unopposed antagonists) in a direction 
opposite to the direction of traction of the paralysed muscle, whilst 

Itf.O. ^. SupJL u. Snp^R ^ Inf.O 


tnUL httJL 





Fig. 47. — N. Bishop Harinan's chart to show (1) Movements of ocular muscles 

and (2) Position of false image in paralysis. 

1. (a) Rectangular movements. The arrows point to the direction in which the eye is turned 

by each muscle. 
(6) Rotation. Put a match, head upwards, on each of the dotted lines indicating the 
vertical meridians. Muscles that rotate eye inwards turn the match-head towards 
nose (Sup. Rectus and Sup. Oblitiue) ; those that rotate it outwards turn match in the 
opposite direction (Inf. Oblique and Inf. Rectus). 

2. Put matches on dii^^m again. The match will represent the true image. The four rays 

marked Sup. R., Inf. R, Sup. ()., and Inf. O. will represent the relative position (in 
vertical and lateral displacement and tilting) of the false image produced in paralysis 
of each of these muscles. In paralysis of Int. or Ext. Rectus the false image will run 
vertically through the correspon<ling arrow-head. 

the false image, seen by the affected eye, is displaced in the direction 
of traction of the paralysed muscle. Figs. 48 and 49 are Werner's 
well-known " memoria technica," showing the position of the false 
image in the various ocular paralyses. Fig. 48 shows the position 
of the false image in paralysis of any of the recti ; Fig. 49 in 
paralysis of the oblique muscles. For example, Fig. 48 shows 
that in diplopia from paralysis of the left inferior rectus, 

(1) the false image is on the right of the true (i.e. it is crossed) ; 

(2) the false image has its upper end inclined towards the true ; 

(3) the false image is lower than the true ; and (4) the diplopia 
occurs on downward movement of the eyes. To test diplopia we 
use a long, lighted candle, at a distance of about three yards from 

the patient, holding it, first, exactly opposite the patient and 
moving it gradually from side to side and then from above down- 
wards. One of the patient's eyes is covered with a red and the 
other with a green glass, to differentiate the two images, and the 
patient has to tell ua the relative position of the red and of the 
green candle. It is necessary to ensure that the patient keeps 
his head fixed during the process of testing. The false image is 
that seen by the paraljmed eye, the true image by the sound one. 
Diplopia is a more delicate teat than paral3rtic squint, for where 

ngi. 4S and -ti*.— Weraer's " artificial memory " for the double images in ocular 
paralyses (OpAiAaimin Rrview. 1886}. Fig. 4S showa the pusition of the 
images in paralysiii of ttie recti mnscles. Fig. 4!> io poialysis of the ubliqne 
muscleji. Tho dotted linos indicate " ful^ " imagea. the thick black lines 
" true " imagog. 

ihere ia slight paresis of an ocular muscle there may be no notice- 
able squint, and yet the diplopia may be quite appreciable to the 
patient, To detect a paralytic squint we direct the patient to follow 
_our finger, moving it laterally from side to side, and then vertically 
jUp and down, and observe whether there is deficiency of movement 
r both eyes in any particular direction or directions. 
Nystagmus is an involuntary rhythmic tremor of the eyeballs, 
generally bilateral and symmetrical. The movement consists of 
&n oscillation usually horizontal, from side to side, but sometimes 

Eical or even rotatory. Nystagmus may be either UTidvlaiory 
ire the movement* to both sides are equal in range and of 


equal speed) or rhythmic, the commoner type, where both move- 
ments are equal in range but the one is fast and the other slow. 
In most cases nystagmus occurs only when the eyes are voluntarily 
moved to an extreme degree either laterally or, less commonly, 
vertically ; in rhythmic horizontal nystagmus the rapid jerk is to 
the side towards which the eyes are directed. But sometimes, 
especially in the rotatory variety, nystagmus occurs when the eyes 
are directed straight forward. In cases where an ocular muscle 
has been paralysed but is in process of recovery, if we make the 
patient look steadily in a direction which necessitates the active 
movement of the formerly paralysed muscle, slight rhythmic 
nystagmus may develop, analogous to tremulousness of the hand 
after carrying a heavy weight. Njrstagmus occurs in various 
organic diseases, notably in disseminated sclerosis, Friedreich's 
ataxia and cerebellar disease. It is present also in certain patients 
who have become more or less blind (though in complete blindness 
the movement is more often a slow rolling of the eyes), also in 
albinism, and a well-recognised form is miner's nystagmus, due to 
persistent ocular strain in a dim light. 

Another variety is aural or vestibular nystagmus. This may be 
produced experimentally in healthy subjects by syringing the drum 
of the ear with water, either distinctly above or distinctly below 
the temperature of the body. Bdrdny^ regards this nystagmus 
as a result of convection currents in the endolymph produced by 
warming or cooling of the labyrinth. The presence of such nystag- 
mus can be used as a test of the integrity of the vestibular nerve. 

There is also a rare congenital affection known as nystagmus- 
myoclonus, in which, together with nystagmus, commonly of the 
lateral variety, there are involuntary jerking movements of the 
limbs or trunk. These movements are aggravated by cold or by 
tapping the muscles, but can be controlled by an effort of will. 
The deep reflexes are often exaggerated, and it is not unusual to 
have other co-existing deformities, such as hypospadias, flat-foot, 
facial asymmetry, persistent branchial cleft, &c.^ 

* Centralhlatt fur Augenheilkutuie^ AuguBt 11)05. 

* Lenoble and Aubiueau, Revue de Medicine^ July 10, 1906. 


Nystagmiiti can be produced ia a uoniial pt^rsciii by placing IJini on B 
I rolating sUxiI and Bpiniiing him rapidly around the long axis of his own 
I bodyj in sucIj a case, if the sluol be siiddeuly atop)>ed, a temporary arier- 
iujeU^mus n|ip«nrB, homoiital and rl]ythinio,lbe rapid phase of the nyatag- 
I iDus being in tlie opposite direction from the previous rotation. If a 
I patient who already hiia a horixoubil nyHtAgnnie be similarly revolved 
§ iround hia own luug axis, on suddenly stepping the rotaLion n-e liiid that tlte 
original nyslagmus towards the directiun oF roMtion has temporarily ceaaed 
K whilst, that in the opposite direction is exaggerated.' In such a case, the ex- 
l.perimental after-nystagnius has over-corapenaated the pre-existing nyatugmus 
I for the time. 

We are now in a position to recognise the sigoB of paralfsiB 
Fof any of the ocular nerves. In a case of complete third nerre 

r Pig. so,— Total paralysis of right third nerve from syphilitiu disease. 
Fig. Gl.^'l'hP BB.iiiC pntiont. the right eyelid lieing poBsivi-'lf lifted to show Ihc 
external strabiamus aud diliioitioii of jjupil on the panilysed aide. 

paralysia (Figs. 50 and 51) there is ptosis or drooping of the upper 

I lid, from paralysis of the levator palpehrse, with over-action 

■ of the frontalis on that side, so that the eyebrow stands higher 

Pthan normal. In hysterical ptosis (Fig. 5'2), on the other hand, 

I there is no over-action of the frontalis, nor is there in the ptosis of 

I myasthenia gravis, where the frontalis is usually partially paralysed 

8 well. In third nerve paralysis there is also external strabismus 

I irom imopposed action of the external rectus, and there is inabiUty 

' CoBsirer aiid Loeaer. NtMroIogiaeAea Ocntralblatt. IU08. s, 2fi2. 



to move the- eye upwards, directly downwards, or directly inwards,,, 
although a ahght downward and inward movement can be execut«d i 
by the superior oblique The pupil is dilated owing to paralysis of the I 
sphincter iridia, and does not contract either to light or on attempted J 

FlO. 52.— Ciue of lett-Biiled byetcritnU pioaia iu a. woman of 23. showing 
absence of frtinCalii over-actioD on piuolyeed side. Tho area on Che left 
aide of the head, neuk, trunk and ahooldec, within the black lino, was 
totally aiinsthetic to all forms of atimult. There was losu of smell anil taste 
on the left side : contraction of the left vianal lield and diminution of 
bearing in the left ear. The fignre also shows the presence of ''dermo- 
Brnphisin." The patient's name having been traced on the ohesC with the 
head of a pin, a bard, cord-like pnttern was produced, capable of being 

accommodation. Complete paralysis of the third nerve is leaaj 
common than is a partial paralysis, affecting one or more muscles. 
Paralysis of the Fourth Nerve causes impairment of the 
downward and inward wheel -rotation of the eye around its 
an tero- posterior axis by the superior obhque. The deficii 




of movement is difficult to see, and the paralysis is recognised 
mainly by the characU'ristic diplopia which occurs when the patient 
gazes in the direction in which the superior oblique ought to come 
into action, i.e. downwards and inwards. When the patient looks 
horizontally forwaids or upwards there ia no diplopia. But when he 
looks downwards and inwards, diplopia appears, the false image 
standifig lower than the true, and having its upper end tilted 
towards the other (Fig, 49). The false image also appears to the 
patient nearer to him than the true, the reason for which is 

Kig. fi3 shows the normal n 
Pig. S3a ithow» attempted i 
nrreated at the iiiid-posilion. 

obscure. Moreover the patient feels giddy, especially when he 
looks downwariia, as in walking downstairs, and he habitually 
inchnes his head forward and towards the sound aide. 

Paralysis of the Sixth Nerve is particularly easy to recognise. 
There is merely paralysis of the external rectus, with inability to 
turn the eye outwards beyond the raid-point, all other move- 
ments being normal (Figs. M and Ma), and there is diplopia on 
looking outwards. In old cases in which contraction of the non- 
paralysed internal rectus has supervened, an internal strabismus 


Sometimes an external ocular muscle ia attacked by rheumatic 
'jayoaitis, which causes an ocular palsy of benign form. The muscle 
■jaoat frequently thus afEected is the external rectus. 

Ocular paralyses differ in type according aa they are due to 


a supra-nuclear lesion (between the second frontal gyrus and the 
ocular nuclei), a nuclear lesion in the mid-brain, or an infra-nuclear 
lesion of the individual nerves such as we have just described. 

Ocular paralysis from a sapra-nuclear lesion never attacks a 
sin^ ocular muscle or even a single eye. On the contrary, assoc- 
iated muscles of both eyes are affected. The common type of 
paralysis from a destructive lesion at or above the internal ^psule 
is one in which the patient loses the power of turning both eyes 
towards the contra-lateral side. Therefore the unopposed anta- 
gonists draw both eyes over towards the side of the lesion ; this is 
called conjugate detnation. In certain cases of conjugate deviation, 
although the patient can no longer turn his eyes voluntarily to 
one side, say the right, he can do so reflexly by fixing some object 
directly in front with his eyes, this object being then moved to- 
wards the right or the patient's head being passively rotated to 
the left.* Curiously enough, conjugate deviation upwards or 
downwards does not occur from a paraljrtic lesion of the internal 
capsule, unless a bilateral lesion is present. In supra-nuclear 
lesions reflex nystagmus is still preserved. Bar&ny ^ has shown that 
reflex nystagmus can be produced in normal individuals in two 
ways. Firstly, there is optic nystagmus^ produced by making the 
patient watch a rapidly-moving landscape when looking out of the 
window of a railway carriage, or by making him watch a series of 
vertical bars on a horizontally revolving cylinder. Secondly, there 
is vestibular nystagmus, produced either by rapid rotation of the 
individual on a revolving chair (rotation to the right producing 
horizontal nystagmus to the left and vice versd), or by syringing 
the ear with cold water (stimulation of the right ear producing 
nystagmus, partly horizontal but mainly rotatory, to the left and 
vice versd). If the vestibular nerve 'be diseased, reflex vestibular 
n)n3tagmus is abolished.^ 

Shew demotion of the eyes occurs in certain lesions of the 
lateral lobe of the cerebellum or of its middle peduncle. Thus in 
a woman with a fatal haemorrhage in the right half of the cere- 

* liMf\w^\\ovfsV.y, MUnchener medizinische Wochenachrijt^ 1903, s. lOfjO. 

• BArAny, ibid,, 1907, 8. 1072. 



' bellum and pons, the right eye was directed downwards and 
inwards, and the left eye upwards and outwards. 

A nuclear lesion of the third, fourth, or sixth nuclei in the floor 
of the Sylvian aqueduct may be partial or complete, and the tj^e 
of ocular palsy which results is called nuclear ophthalmoplegia. 
In some cases the fibres for the ciliary ganglia or the ganglia them- 
selves or short ciliary nerves to the internal ocular musciea (iris 
and cihary muscle) are alone affected, and not the external muBcles 
of the globe. The result ia ophthalmoplegia iniema, in which the 
pupils are dilated and immobile both to light and on convergence. 
This condition may be unilateral or bilateral, according as the ciliary 
gangha or short ciUary nerves are afiected on one or both sides. 
It often occurs as a transient result of post-diphtheritic neuritis. 
Ophlhalmoplegia externa is a nuclear disease of the Sylvian aqueduct 
affecting numerous external ocular muscles, generally of both eyes 
and often symmetrically. A fairly common type is where the 
power of upward rotation of the eyes is lost, lateral movements 
being still possible. Ophthalmoplegia externa usually occurs alone, 
leas commonly it is associated with the internal variety. When both 
vaiietiea are combined we have total oplU/udtnoplegia, in which 
the eyes are fixed and motionless, the pupils being immobile, 
both varieties of reflex nystagmus (optic and vestibular) being 
lost, and the patient can look in any particular direction only 
by facing his head that way en bloc. Nuclear ophthalmoplegia, 
especially external ophthalmoplegia, may be associated with motor 
paralysis of the limbs if the lesion extends ventrally and impli- 
cates one or other pyramidal tract, or it may be associated with 
involuntary tremors if the lesion affects the red nucleus or rubro- 
spinal tract (Fig. 13, p. 2(J). 

Sometimes it is possible to differentiate between a nuclear and 
an infra-nuclear ocular lesion. In the case of paralysis of the sixth 
nudeue in the pons, there is not merely weakness of the external 
rectus of the same side, as in paralysis of the sixth nerve trunk, 
but in addition the internal rectus of the opposite eye is paralysed, 
BO that conjugate movement of both eyes towards the affected 

L side ia impaired. The weakness of the contralateral internal 


rectus is only in connection with its associated movement with 
the external rectus of the homolateral eye. This is proved by 
the fact that, in paralysis limited to the sixth nucleus, both 
internal recti can still act normally during convergence. Again, 
since the facia] motor root loops round the sixth nucleus within 
the pons, a lesion of the sixth nucleus is not infrequently 
accompanied by facial paralysis on the same side. 

With regard to the diagnosis between nuclear and infra-nuclear 
paraljrsis of the third nerve, if in a doubtful case the orbicularis 
oculi is foimd to be affected together with the external ocular 
muscles, then the lesion is in the region of the nucleus, since the 
orbicularis is innervated by a group of cells which are in anatomical 
proximity to the oculomotor nucleus (but which really belong to 
the facial). 

MendePs theory* assumed that these cells belonged to the oculomotor 
nucleus and reached the orbiculares through the facial, but Bishop Hai man - 
lias shown that all the facial muscles, from orbicularis oculi downwards, are 
innervated from the group of cells comprising the facial nucleus, the upper 
end of this group extending as high as the oculomotor, and the lower end 
reaching to the level of the hypoglossal. 

Sometimes transient ocular palsy afifects the third nerve in 
whole or in part, recurring in the same eye without apparent 
cause at intervals of weeks or months, and clearing up com- 
pletely between the attacks. This condition, known as Charcot's 
migraine ophtalmopUgique, is generaUy associated with headache, 
most intense in the eye and forehead of the affected side, and 
with vomiting. Its pathology is obscure ; probably some cases 
are due to an inflammatory affection of the meninges at the point 
where the third nerve pierces them to enter the sphenoidal fissure. 
This is all the more probable inasmuch as the first division of the 
fifth nerve, which traverses the sphenoidal fissure, is often simul- 
taneously affected, with the result that there is blunting of sensa- 
tion in its area of distribution. 

Now and then we meet with congenital ptosis, in which there 
is paralysis of the superior rectus and levator palpebrse superioris 

* IntemcUional Med. Congress, Washington, 1887, vol. 5. p. 311. 
* Transcictions of OphthalmologiccU Society, 1903, p. 350. 



of one eye. In aonie of these cases, although the patient cannot 
raise Lis upper lid voluntarily, yet, curiously enough, the lid is 
jerked up when certain jaw movements are made, particularly when 
the patient throws into action the external pterygoid muscle of the 
same side, in depressing the lower jaw towards the opposite side. 

This so-called " jaw-winking " movement has been shown by 
Harman to be the survival of a movement in fishes whereby, when 
the mouth is opened for breathing or eating, the gill swings open. 
In man the pterygoid and orbicularis oculi muBcles are homologous 

Grtal AuruTidur 

Km, .'i 4.— Cutaneous supply uf hoad (modifli 

with the deep and superficial nniscles of the branchial arch of the 
fish's spiracle, and when the one is contracted the other t«nds to 
relax and " the weak levator, taking advantage of the quiescence 
of its too powerful opponent, lifts the eyelid." 

Jaw-winking movementa generally disappear before adult life. 

The Fifth or Trigeminal Nerre has a most extensive distri- 
bution, the main points of which are as follows : — The nerve 
consists of two distinct parts, sensory and motor. The sensory root, 
the one on which is the Gasst^rian ganglion, divides below the 
ganglion into three divisions, of which the first two are entirely 
sensory. The motor root courses beneath the Gasserian ganglion. 



and tlien joins the thiid division, which thus becomes a mixed 

The pTiA or ophthalmic division passes through the sphenoidal 
fissure into the orbit and supplies the eyeball and lachrymal gland, 
the conjunctiva (except that of the lower lid), the skin of the fore- 
head and scalp up to the vertex (Fig. !i4), the mesial part of the 
skin of the nose, and the mucous membrane of the upper part of 
the naaal cavity. It also contains efferent pupil-dilating fibres 

OLtsio -pfujryngtai 

derived from the cervical sympathetic, joining it at the Gasserian 
ganglion, and going to the iris (Fig. 46). 

The ^tsmd or superior maxiUary division passes through the 
foramen rotundum across the spheno-maxillary fossa to the infra- 
orbital canal. In the spheno-maxillary fossa it is connected with 
Ueckel's gangUon, which gives of[ amongst other branches the 
Vidian nerve. This latter runs backwards to join the facial nerve, 
the posterior end of the Vidian being named the great superficial 
petrosal (Fig. 55). The superior maxillary division supplies the 
skin of the upper lip, the side of the nose and adjacent part of the 
cheek, the lower eyelid and part of the temple. It also supplies the 


conjunctiva of the lower Ud, the upper teeth, the mucous membrane 
of the upper lip, the upper part of the cheek, upper jaw, uvulft, 
tonsil, naao-pharynx, middle ear and lower part of nasal cavity. It 
also contains some taste fibres to which we shall refer presently. 

The third or inferior maxillary division is a mixed nerve. It 
emerges ihrougli the foramen ovale. The motor fibres supply the 
raasseter, temporal, and both pterygoid muscles, also the tensor 
tympani, mylo-hyoid and anterior belly of the digastric. The 
sensory fibres supply the skin of the posterior part of the temple 
and adjacent part of the pinna, the anterior and upper wall of the 
external auditory meatus, as far as and including the anterior 
part of the drum, part of the cheek, the lower lip and chin, also the 
lower teeth and gums, the tongue (aa far back as the circumvallate 
papilla), floor of mouth, inner surface of cheek, and salivary glands. 

The Coarse of the Taste Fibres is a complicated one 
and still much disputed ' (Fig. 5.^). Those for the anterior two- 
thirds of the tongue are contained in the lingual nerve — a branch 
of the third division. But they do not run straight up from the 
lingual into the fifth nerve. They leave the lingual, course along 
the chorda tympani. and reach the facial within the Fallopian aque- 
duct. They run in the facial aa far as the geniculate ganglion, 
where some pass ofl along the great superficial petrosal to Meckel's 
ganghon, ultimately rejoining the fifth nerve through its second 
division. Other taste-fibres leave the geniculate ganglion to 
enter the nervua intermcdiua, passing thence to the glosso- 
pharyngeal nucleus. 

The taate fibres for the posterior third of the tongue and the 
palat«, which are supplied by the gloss o-pharyngeal nerve, pro- 
bably ent«r the brain through the gtosso-pharynge^al. They do 
not join the fifth nerve, since division of the fifth nerve by the 
operation of removal of the Gasserian ganglion causes impairment 
of taste only in the anterior two-thirds of the tongue, and not 
constantly in that. Taste is not abolished in fifth nerve paisy, 
as was formerly thought, for in several cases of my own I 


> Ciiahing, John» Hopkins Hoapilal Baltclin 

vin. 1907, p. 219. 

my own I have ^^A 
U4-I45. Davie*. ^^| 



lound that the patient, though unable to feel the contact of f 

or other objects on one side, still retained acute sensf ot taste at*| 

the back of the tongue. 

To examine the aenae of taste we direct the patient to protrude 
the tongue, and we lub on it various substances such as sugar, salt, 
quinine, and <itric acid, preferably in white powders, which the 
patient cannot distinguish at sight one from the other. The patient 
must keep his tongue protruded throughout each test, and as 

Fiu. 5S.— I'aialjfiH of L-/I ilnr,: -. 

l(M)km|{ upwnriis aud upciiing tin 
left side with deSuient upcrard 
the deTialion of the lower jan ' 
indicates area of E 

..f Rhjhi f,jtl, iiprvL'. The- imtieiu is 
jaw. Sbowiog dil&tjitlon of pupil on 
lOTement of left eye. Also showioff 
iwards tbe righb side. The black lioe 
e right side of Che face. 

Boon as he feels a taste he should make a sign and also determinel 
in his mind what the taste is, before taking the tongue in. It Vi- 
convenient to have a card with the following words printed ( 
it; — "sweet," sour," "bitter," "salt," "coppery." The patiei 
can then point with his finger to indicate which taste he per-] 
ceives. It he be allowed to pull the tongue in while waiting fof^ 
the sensation to arrive, fallacies may occur owing to muvementi'.J 
of the tongue and the flow of saliva carrying the substance I 
other parts. To map out exactly an area of loss of taste (u^eiinajfa 
the most accurate method is to use a weak galvanic current with a 
wire electrode, which produces a coppery or metallic taste. 



When the fifth nerve is totaUy paralysed there is anEBSthesia of 
the corresponding half of the face and scalp, not extending as far 
as the angle of the jaw, this part being supplied by the cervical 
plexus (Fig. 54). The cornea and conjunctiva on the affected 
side are anaesthetic, and also the mucous membrane of the corre- 
sponding side of the nose, mouth, part of the soft palate and tongue, 
as far back as the circumvallate papillie which, with the area behind, 
are innervated by the glosso-pharyngeal. This defect extends 
exactly to the middle line, and therefore the patient when drink- 
ing feels as if the cup were broken. Food tends to collect within 
the ansBsthetic cheek, the buccinator muscle being anEesthetic, 
though its motor power is unaffected. Taste is impaired in 
the anterior two-thirds of the tongue, but does not remain totally 
lost. The trigeminal nerve has also sensory fibres for the facial 
muscles. Hence there is a degree of awkwardness and apparent 
weakness of the face — a pseudo-facial palsy, due to loss of the 
sense of active muscular contraction, AH the muscles auppbed 
by the motor root undergo atropliic paralysis and develop 
the electrical reactions of degeneration. There is hollowing of 
the temporal fosaa above the zygoma, and wasting of the 
maaaeter below it, so that the zygoma becomes abnormally 
prominent. Wlien the patient clenches his teeth, neither the 
temporal nor the masseter can be felt to harden as on the 
normal side, and when he opens his mouth the mandible is pushed 
over towards the paralysed aide (Fig. 56) This is owing to paralysis 
of the external pterygoid, which fails to draw the condyle forwards 
on the affected side. The deflected mandible carries with it the 
tongue, but there is no real deviation of the tongue, when measured 
from the middle line of the lower incisors. It is stated that paralysis 
of ihe tensor tympani causes a difficulty in hearing notes of low 
pitch, but this is not easy to determine. Secretion of tears on the 
paralysed side is diminished, as is also the secretion of nasal mucus 
and of saliva. Consequently these mucous membranes become 
abnormally dry, and may show secondary trophic changes. Thus 
stimulation of the nasal mucous membrane by snufi no longer 
causes sneezing. Smell at first ia unimpaired, but later, from 





dryness and secondary trophic changes in the Schneiderian mem- 
brane, there may be anosmia in the affected nostril. ThftJ 
corneal and the lachrymal reSex are lost, also the palatal reflex, and< 
the tongue on the paralysed side becomes excessively furred, pro- 
bably because on the anscathetic side there is deficient friction by 
food. The teeth on the paralysed side are aniesthetic and tend to 
drop out ; this has been ascribed to a trophic change, but more 
probably it is mainly traumatic, the patient biting clumsily with 


his aneeathetic teeth. It used to be stated that neuro-patalytio 
keratitis occurred in total trigeminal palsy, owing to trophic changes. 
But this is not invariably so ; when it does occur, it appears to be 1 
due to the presence of a special bacillus ' in the ana?8thetic eye, [ 
where, moreover, there is a deficiency of lachrymal, secretion, 1 
Further, if the anaathetic lids be kept closed by a suture, keratitul 
does not occur, even though the special bacillus be present. 

There is another disease which occurs in the territory of tlwij 

' Duvies and Hull. Brilieh Mfdiral Joiimal. lUOW. p. 72. 



fifth nerve, viz., progresaive fiicial hemiatrophy. This disease, whieh 
commences in early life— usually before puberty, and more often 
in females than in males — shows itself first in the skin of the 
face, either near the orbit or over the upper or lower jaw, gradually 
spreading over the whole face on one aide. The akin becomes 
thinned from atrophy of its papillary layer, the aubcutaneous fat 
disappears, and thus the affected side of the face becomes wrinkled 
and furrowed, in marked contrast with the healthy aide. Later 
the subjacent muscles, cartilages, and bones become atrophic, but 
without motor paralysis or reaction of degeneration. The corre- 
sponding side of the tongue (Figs. 58 and 147), and occasionally 
that of the soft palate, also becomes wasted. But the hemi- atrophied 
tongue, when protruded, comes out straight, unlike that of a caae 
of atrophy from hypoglossal palsy (Fig. 72, p. 160). The hair on 
the affected side of the face may fall out or become white, and the 
sebaceous glands may atrophy. The scalp is rarely affected. There 
is no ansDsthesia. The area of this disease corresponds accurately 
with that of the distribution of the fifth nerve, and in certain cases 
pathological changes have been found either in the nerve itself or 
in its nucleus of origin. Thus Mendel found signs of neuritis in 
the nerve, together with changes in the spinal root of the fifth 
within the medulla, while more recently Loebl and Wieae! ' found 
an interstitial neuritis of the Gasserian ganglion and of the parts 
distal to it. Removal of the Gasserian ganglion does not prodi 

' DttUecht ZtitKhrill fi'T NervenlKtlkunde. 1904, Bd. 27, b. 355. 


CRANIAL NERVES {continued) 

Of all the peripheral nerves in the body, cranial or spinal, the 
Seventh or Facial nerve is by far the most frequently paralysed, 
hence the importance of knowing its anatomical course and dis- 
tribution. Like the trigeminal, it is a mixed nerve, possessing a 
motor root — ^the facial nerve proper, and a sensory root — ^the 
nervus intermedins of Wrisberg. These two roots meet at the 
geniculate ganglion. 

Let us first consider the motor root. Arising from a nucleus 
situated mainly in the lower part of the pons, but some of whose 
cells (namely those for the orbicularis oculi), extend as high as 
the nucleus of the third nerve, and others (namely those for the 
orbicularis oris), are as low as the hypoglossal nucleus, the motor 
root of the facial pursues a tortuous course. Firstly, within the 
substance of the pons, it forms a loop which hooks round the nucleus 
of the sixth nerve. Then, leaving the ventral surface of the 
medulla, it enters the internal auditory meatus, and passes along 
a winding bony canal in the temporal bone — the aqueduct of 
Fallopius. Li the upper part of this canal it traverses a swelling, the 
geniculate ganglton, which is joined by the sensory root or portio 
intermedia of Wrisberg, also by the great superficial petrosal nerve 
from Meckel's ganglion, and by the small superficial petrosal from 
the otic ganglion (see Fig. 55). The geniculate ganglion is similar 
in structure to a posterior root ganglion and is sensory in function. 
Inflammation of this ganglion is accompanied by herpes of the 
external auditory canal and adjacent part of the auricle, exactly 
analogous to herpes zoster^ (see Fig. 54, p. 131). Within the 
aqueduct the facial gives off a branch to the stapedius, and, lower 
down, the chorda tympani leaves it to join the lingual nerve. It 

* J. Ramsay Hunt, JoumcU of Nervous and Mental Diaeasesy 1907, p. 73. 




^H then emerges from the skull through the stylo-mastoid foramen 
^m giving off a posterior auricular branch to the muscles of the pinna 
^M and to the occipital belly of the occipito- frontalis. The main 
^H trunk then divides into its terminal branches supplying all the 
^H muscles of the face (except the levator palpebral superioris) from 
^H the frontalis above to the platysma below. It also supplies the 
^V etylo-hyoid and posterior hplly nf the diKastrip. 






Ceac of Icfl-siiled tucial palej. Fig. SI) at rest. Fig. 110 on »,tieuipt to 
oloBO eyoa and reiraot angles of month. 

Although the facial nerve is largely motor, the geniculate ganglion 
a a sensory ganglion. The facial also contains certain secretory 
ibres, whilst the taste-fibrea of the chorda tympani accompany the 
motor portion of the nerve in part of its course. Thus lesions at 
.ifferent levels can be diatingiushed one from the other. 

1 . If the facial nerve is affected after Us exit from the ati/lo-mastovi 
oramen, e.g. hy cold, or by injuries or tumours in that region, the 
■eault (BeU'8 Paralysis) is complete palsy of that side of the face, 
ffhich is therefore asymmetrical at rest, and the asymmetry is 
xaggerated on voluntary movement. The patient ha« neither 



emotional nor voluntary movement of the affected side (Figs. 59 
and 60). 

The furrows of the forehead are wiped out, and the patient 
cannot wrinkle the brow nor frown on that side. The eye is more 
widely open on the affected side and cannot be shut. The tears 
run down the cheek instead of into the lachrymal duct, and may 
produce excoriation of the skin or eczema. When the patient 
tries to shut the eye he merely rolls the eyeball upwards and 
outwards, or upwards and inwards, sometimes with a zig-zag 
movement, until the cornea passes under cover of the upper lid. 
An additional sign pointed out by Dutemps and Cestan ^ is as 
follows : — ^When the patient looks down and then attempts to shut 
both eyes slowly, the upper lid on the paralysed side is seen to 
move up a little, owing to contraction of the levator palpebrse, 
which normally acts synergically with the orbicularis but is now 
no longer antagonised by it. 

This inabiUty to close the eye allows the entrance of foreign 
bodies, and consequently conduces to conjunctivitis. The con- 
junctival reflex is abolished, and the regular involuntary bUnking 
of health no longer occurs on the paralysed side. The eye brims 
over with tears, so that vision on the affected side is rendered less 
acute. Curiously enough, though the eye cannot be shut during 
waking hours, during sleep it often closes almost completely, 
probably from relaxation of the levator palpebraD. 

The tip of the nose is drawn somewhat towards the sound side, 
the naso-labial fold on the affected side is flattened out, the ala nasi 
sinks in and shows no active movement, voluntary or respiratory, 
though it may flap loosely during forcible nasal breathing. The 
mouth is drawn towards the sound side, but on the affected side its 
angle droops and saliva dribbles from it. When the patient smiles 
or shows the upper teeth, the healthy side moves alone ; he cannot 
whistle, and the articidation of labial consonants is impaired. 
During mastication food accumulates between the teeth and the 
paralysed cheek. The patient often bites his cheek or lower Up, and 
during forcible blowing expiration the paralysed cheek flaps loosely. 

* Journal de NeurologiCy 1904, p. 48 


Voluntary movement of the integument by the platyama, as in 
forcible depression of the chin against resistance, is abolished or the 

rears >^ 


afiected side. In those patients who were previously able to move 

'the ear voluntarily, that power is also lost. All the paralysed muscles 

gradually develop the electrical reactions of degeneration. The 

affected side of the face generally sweats less than the healthy side. 

2. If the lesion be within the FaUojrian aqueduct below the 
geniculate ganglion, it produces all the above symptoms, and, in 
addition, from implication of the chorda t3niipani, there is loss 
of taste (and sometimes slightly of common sensation) in the 
anterior two-thirds of the tongue on the affected side, and also 
occasionally abnormal subjective sensations of taste, and sometimes 
diminution or excess of submaxillary and subUngual saliva. The 
deficiency of taste and of saliva may cause this part of the tongue to 
be abnormally furred up to the middle Une. If there be paraljrsis 
of the nerve to the stapedius, there is hyperacousis or painful 
sensitiveness to musical notes of low pitch (presuming that the 
auditory apparatus is not affected), and the patient can no longer 
produce the subjective noise in the ear, which we normally hear 
on attempting very forcibly to innervate the facial muscles, espe- 
cially the orbicularis palpebrarum. 

3. If the motor root of the nerve be affected between its 
emergence from the pons and the geniculate ganglion^ it produces 
the same symptoms as in Bell's paralysis, but without affection of 
taste in the front of the tongue. And since disease in this region 
almost invariably implicates the auditory nerve, there is usually 
deafness also. If the auditory nerve chances to escape, hyperacousis 
will occur from stapedius paralysis. Many cases have deficiency 
of tears on the affected side. Most cases of basal intra-cranial 
disease present general symptoms also, such as headache, giddiness 
and vomiting. 

4. If the lesion of the motor root be within the substance of the 
pons, facial palsy residts as in Bell's paralysis, but taste and hearing 
are unaffected. There is, however, usually an accompanying 
paralysis of the sixth nerve or its nucleus, since the facial motor 
root hooks round the sixth nucleus within the pons. 

Paralysis of the soft j^alate used to be included in the symptoms of a 
lesion of the facial nerve at or above the geniculate ganglion. But the 




weight of evidence goes to girove that tlie fneiul has no share in Llie innerva- ^^| 
lion of the i«ljite. ChvrBli.k,' in 18S3, puLIishcd a msp of aarwmia «( the ^H 
fftPinl iierve in wliich [wnilysis nf tlie jmlnte liad been okiwn-i'd, but that ^^H 
was bffore the tiays of the Mnrclii method, and it is impossible to b« sure ^^M 
tluit the lower roots of the vagiis were undefteiiemted. In his case there was ^H 
atso a catuxT in t]ic tongue. ^^H 

Slight casea oE facial palsy, whether due to cold, middle-ear ^^| 
affection, compression, or other causes, may recover completely ^^H 

in one or two weeks. More severe cases last from two to eight ^^M 
months before recovery begins. Or the palsy may remain perma- ^^| 





I'la. U2. vio. ka. 

C-isi- nf Ir-ft-Midtxl fuciiil p.lay witli mil tract iir.'. Fig. •■,2 shows poaition at reHt. 

Fig. «2a 9I111W8 inaxiiiiiirii vol 1111 tiiry movement. 

nent. In severe caaej, where improvement does not begin lor 

comes on as voluntary power reappears. The mouth, becomes 
drawn back again towards the paralysed side, the palpebral fissure 
instead of being wider, is narrower than on (he healthy side, and 
bhe na8<»-labial and other furrows not only reappear, but become 
exaggerated. The result is that, when at rest, the healthy side may 
jeem the weaker of the two. though when voluntary movement 
' Wiener Meditinitchr Prcnat, 1883, a. 3*. 




takes place it is easy to aee which is the affected side (see Figs. I 
*'2 and 62a). Together with thia contracture there is always. 1 
in the spastic musclea a tendency to over-action, imperfect i 
recovery being associated with imperfect control. One variety ol I 
facial hemi-spasm results (see p. 87). Thus, on closing the eye | 
on the affected side, the angle of the mouth becomes drawn out- 
TftrcU ; or again, oa ahtrmag the upper teeth, the eye becomes'] 


Fig. HD. — Bilateral facial paliiT, iilcohoUc in origiii. OMOcialed with perlplienit ■ 
neuntia of upper and lower limbs, | 

Vig. I!3,<. — Maximaui voiuatary movcuienl of faoo, on attempt to close the 
ejnf aiirl to retract angles of mouth. 

closed. Sudden flickers of involuntary fibrillary tremors may 
sometimes be seen on the afiected side. The spastic facial muscles 
can also be made to contract reflexly by tapping lightly over the 
point of emergence of the most accessible branch of the fifth, viz., 
the supraorbital nerve.' 

Secondary contracture occurs only in cases of incomplete rej 
covery. During the stage of total paralysis, when no impulses ami 
reaching the muscles, they are quite flaccid. The development t 
contracture indicates that muscular regeneration has been imperfee 




Bilateral facial palay is rare. It may be due either to intra- 
extra-cranial causes, the commonest intra-cranial cause being 
gummatous basal meningitis. Of the extra-cranial causes, the 
most important are double otitis media, cold, and post -diphtheritic 
paralysis. Alcohohc paralysis rarely attacks the facial nerve, but 
when it does, the a&ection ia bilateral, as in the case of the 
man shown in Figs. 63 and 63a, who also had typical alcoholic 
neuritis of the limbs. 

In bilateral facial palsy there is no aaymmetry of the face, but 
it hangs Uke a fixed expreasionless mask, incapable of evincing 
the slightest emotion. 

Bilateral facial weakness also onmrs in the " facio-scapulo- 
humeral " type of myopathy, to which we shall refer in a later 

Nerras Intermediua of Wriaberg, or Sensory Eoot of the 
Facial. — Between the facial motor root and the audit(}ry nerve 
at the floor of the cranial cavity, and entering the internal auditory 
meatus along with them, there is a slender fasciculus, known as the 
rportio itiiermedia. The fibres of this nerve are remarkably small 
calibre. Their trophic centre is in the cells of the geniculate 
iglion. Centrally the fibres run into the bulb, alongside the 
fibres of the auditory nerve, to join a nucleus closely connected 
with that of the glosso-pharyngeal. Peripherally from the 
geniculate ganglion fibres run along the great and small super- 
ficial petrosal nerves ; others along the trunk of the facial, in 
the chorda tympani. The nervus intermedins probably conveys 
ite impulses upwards to the brain, by way of the glosso- 
laryngeal nucleus (Fig. (il, p. HI). And it appears to contain 
efferent fibres which join the submaxillary ganglion. Inflam- 
tion of the getiiculate ganglion, analogous to inflammation of 
posterior root ganglion in herpes zoster, as Hunt has 
linted out, produces characteristic symptoms. These consist 
pain and herpes of the auricle and external auditory canal. 
the inflammation be intense enough to implicate the motor 
ibres of the facial there ie facial palsy also, with loss of taste in 
chorda tympani distribution. If the auditory nerve be 


implicated there is vertigo, tinnitus, deafness and even nausea 
and vomiting. 

The Eighth or Auditory Nerve comprises cochlear fibres for 
the function of hearing, and vestibular fibres which supply the semi- 
circular canals and constitute the most important nerve of 
equilibration, informing us of the position of our head in space. 
Afiections of the cochlear fibres produce auditory phenomena, 
while disease of the vestibular fibres causes one form of vertigo, 
though vertigo and other auditory symptoms often result not only 
from disease of the labyrinth or vestibular fibres, but from 
afiections of the middle or even of the outer ear. 

The chief symptoms referable to the auditory nerve are deaf- 
ness, tinnitus, and vertigo. 

In a patient who is apparently deaf, we should always, before 
proceeding to test the hearing, examine the external auditory 
meatus, to make sure that it is not blocked, e.g. by wax. We 
then test aerial conduction by the ticking of a watch, the 
patient's eyes being shut and one ear closed while the other 
is being tested. Holding the watch at some distance from 
the ear, we slowly bring it nearer until the patient can just detect 
the tick. If there is dea&ess, we have to determine whether 
this is due to middle-ear disease or to affection of the labyrinth 
or auditory nerve. The tuning-fork tests help us here. Normally 
a vibrating tuning-fork, preferably C^ ( = 256 vibrations per second) 
placed on the vertex or centre of the forehead is heard equally in 
both ears (Weber's test). If placed on the mastoid process, we 
wait till it is no longer heard through the bone, and find normally 
that it is still audible when held close to the external meatus (Rinne's 
test). If the middle ear be diseased, or if the outer ear be blocked 
up, there is loss of aerial conduction, but bone-conduction is still 
preserved. The tuning-fork on the vertex is then heard louder on 
the affected side (" positive- Weber,") and Rinne's test is negative, 
i.e. the tuning-fork is no longer heard aerially after fading away on 
bone-conduction. But if the deafness be due to affection of the 
internal ear or of the auditory nerve — so-called " nerve -deafness," 
a tuning-fork on the vertex is not heard on the affected side 



(" negative- Weber "), whilst as a, rule there is "positive-Rinne," 

though not always. In deafness from chronic middle-ear catarrh, 
the hearing is generally better in the midst of a noise {e.g. in an 
omnibus or railway carriage), than in a quiet place, whereas in 
nerve-deafness the reverse is the case, Additional localising 
evidence may also be obtained from the other concomitant 
symptoms. Thus gross disease of the auditory nerve within the 
skull, f.g. in a case of lateral extra-cerebellar tumour, is often 
accompanied by facial paralysis, though this conjunction is of 
value only when middle-ear disease can be excluded. On the 
other band, disease of the lab3Tinth is often associated with tinnitus 
or vertigo, and labyrinthine deafness is specially characterised by 
loss of perception for high-pitched tones, as tested by Gallon's 
whistle. Disease of the auditory nuclei within the pons may be 
associated with weakness of the motor facial nerve of the same 
side and paralysis ot the opposite arm and leg. 

Tinnitus, or ringing in the ears, is a subjective symptom. It 
signifies irritation of some part of the auditory apparatus. The 
term does not include elaborate auditory hallucinations of cortical 
origin, such as distinct melodies or voices uttering intelligible 
words. The nature of the sound in tinnitus varies in different 
cases; for example, it may be buzzing, hissing, or whiatUng. 
Broadly speaking, we recognise two main kinds of tinnitus — the 
pulsating and the continuous. Pulsating sounds, synchronous with 
the pulse, occur in a few intra-cranial aneurisms (sometimes 
audible by the phj'sician on auscultation of the skull), but are also 
not infrequent in simple neurasthenia in the " silent watches of the 
night." Curious " clicking " sounds in the ear may result from 
clonic spasm of the tensor tympani muscle. CojUinuous sounds 
may be of high or low pitch. We should always notice whether 
they are increased or diminished by the recumbent posture. Low- 
pitched continuous tinnitus may be the result of venous 
hypereemia, in which case it is aggravated by recumbency, or 
of simple anscmia, which is relieved by lying down. Nitrite 
of amyl a^ravates tinnitus when due to hypereemia and relieves 

when due to anaemia, High-pitched continuous tinnitus is 


generally due to labyrinthine stimulation, either from outer or 
middle-ear affection (perhaps merely wax or water in the external 
meatus, an obstructed Eustachian tube, or an indrawn tympanic 
membrane), or from actual labyrinthine disease. It is also caused 
by certain drugs, notably by quinine and salicylates. Such drugs 
induce deafness as well as tinnitus, and the tinnitus may persist 
for weeks after the deafness has cleared up. Pulsating tinnitus 
due to arterial congestion can often be arrested temporarily by 
compression of the vertebral artery supplying the labyrinth, or of 
the carotid supplying the external or middle ear.^ 

Vertigo, or giddiness, is the peculiar disagreeable sensation 
which results if our sense of secure equilibration is disturbed. The 
process of equiUbration is a muscular act, where all the muscles are 
innervated, of course, by the cerebral cortex, this latter being again 
largely influenced by the cerebellum. The cerebellum is a co- 
ordinating centre for equiUbration. It receives afferent impulses 
from various sources, of which the semicircular canals of the inner 
ear are by far the most important, the others coming from the skin 
of those parts on which the body happens to be resting, from the 
muscles and joints concerned in maintaining our balance, and from 
the muscles of the head and eyes concerned in looking towards sur- 
rounding objects. Each half of the cerebellum exercises a co- 
ordinating influence, through the corresponding superior cerebellar 
peduncle, upon the contra-lateral cerebral cortex. 

Giddiness is often accompanied by a feeUng of movement 
either in the patient himself (subjective vertigo) or in external 
objects (objective vertigo). Severe giddiness usually produces 
the motor phenomenon of reeUng or staggering. 

Vertigo may result from affection either of the higher cerebral 
centres or of the co-ordinating cerebellar centres, or from affection 
of any of the afferent paths to which we have already referred. 
Severe vertigo is often accompanied by nausea and vomiting, as in 

Vertigo may occur in healthy people. Thus, for example, a 
galvanic current of 10 to 15 milliamp^res passed transversely 

1 Dundas Grant, Brit. Med. Journal, Dec. 24, 1887. 



through the head produces a variety of giddine-ss probably due to 
labyrinthine stimulation. In this the patient tends to fall to- 
wards the side of the positive pole, and his head and eyes are also 
rotated in that direction, accompanied by a rotatory nystagmus, 
until the moment of stopping the current, when he tends to fall to- 
wards the side of the negative pole. Rapid rotation of the body 
round its own axis, as in waltzing, or rapid changes in our position 
in space, as in swinging, produce giddiness which is probably due to 
variations in the pressure of the endolymph within the semicircular 
canals. Some people feel giddy when stepping unexpectedly from 
a firm surface on to a piece of boggy turf, or, as in a famous 
Edinburgh street, on to a piece of indiarubber pavement, this 
variety of vertigo being due to deficient sense of resistance con- 
veyed from the skin of the soles and from the muscles and joints 
of the lower limbs. The giddiness produced by standing near the 
edge of a cliff or of a high tower is most probably due to loss of 
muscular impression from the ocular muscles. Ordinarily we have 
surrounding objects at or above our own level with which to 
compare our position in space, and if such objects are absent 
vertigo may result. 

Vertigo is also associated with various pathological conditions. 
Among the intra-cranial causes we may mention blows on the 
head (this variety is often relieved by repeated small doses, about 
B*ff grain, of perchloride of mercury),^ and sudden cerebral ancsmia or 
hyjterwmia. A distinguished member of the medical profession 
who was the subject of aortic regurgitation used to have attacks of 
intense vertigo if he took a saline aperient. Probably in his case 
the withdrawal of a considerable amount of fluid from the circula- 
tion rendered the brain ansemic — hence the vertigo. It was alwaj-s 
relieved by the recumbent i)Osture, while cardiac tonics and the 
avoidance of hydragogue cathartics prevented its recurrence. 
Vertigo from cerebral hyperemia is very common in women about 
the menopause, also in the art«rio-si;leroKis of chronic renal disease. 
In the latter class, relief is often obtained by the administration of 
iodides. It is still more marked in many cases of cerebral hferaor- 
> Diiiidns Oriuit, Clinical Journal, Oct. B. IH07. 


rhage or thrombosis, of which it may be a premonitory signal. 
Giddiness in old people with atheromatous arteries, if it be 
associated with headache, and especially if there be no sign of 
labyrinthine disease, should always be regarded with caution. 
Intra-cranial tumours may cause giddiness by raising the general 
pressure within the skull, and cerebellar tumours are especially 
associated with vertigo, even apart from increased intra-cranial 
pressure. IrUra-cerebellar tumours of the lateral lobe produce a 
vertigo in which the subjective sense of rotation of the body is in 
the same direction as that of the apparent movement of surrounding 
objects, t.6. away from the side of the lesion. In extra-cerebellar 
tumours, while external objects appear to move away from the side 
of the lesion, the sense of subjective rotation is reversed, i.e. to- 
wards the side of the lesion. 

A characteristic form of vertigo has also been described by 
Bruns,^ and confirmed by various other observers.^ It is pro- 
duced by the presence of a cysticercus in the fourth verUride, 
Sometimes the worm is anchored to the ependjrma, sometimes it 
is swinmiing free. The patient, who otherwise shows no sign 
of intra-cranial organic disease, has paroxysms of violent vertigo, 
chiefly on sudden movement of the head, either active or pas- 
sive, causing a temporary shifting of the position of the worm. 
He also has attacks of occipito-frontal headache with vomiting ; 
his gait is tottering and unsteady, and glycosuria is not uncom- 
monly present. There may be intervals during which he is ap- 
parently well, and the case may be mistaken for hysteria. Death 
usually occurs suddenly from respiratory paralysis. 

Vertigo is associated with certain degenerative diseases, notably 
with disseminated sclerosis. Vertigo is frequently the "aura " 
of an epileptic fit, or may accompany the headache of an attack 
of migraine. A hereditary family form of giddiness has also 
been described. 

Toxic vertigo from alcohol or tobacco is a familiar type, and 
to the toxic class we may also refer cases produced by gastric 

» Centralblatt far Neurologie, 1902, p. 5G5. 
2 Osterwald, Neurologischea CerUraB)kUt, 190G, s. 2G5. 


disorder, by constipation, and by some cases of intestinal parasites, 
though in the last instance a reflex element may also be present. 
Giddiness is often present in neurasthenic and hysterical patients, , 
in whom it may be elicited by the shghtest exciting cause, for 
example by rectal examination. 

OcuUtT vertigo occurs in cases of paralysis of any ot the external 
ocular muscles, and is associated with diplopia. The visual field 
being erroneously projected, the patient judges wrongly as to 
the relation of his body to what he sees, " Objects appear to be 
in certain positions where the patient's feet, as a matter of fact, 
fail to find them " (Hughlings Jackson). The giddiness in such 
cases is not due directly to the diplopia, for it persists when the 
sound eye is covered. The condition can be imitated in health by 
closing one eye and displacing the other eye inwards by pressure 
with the finger, when if the subject tries to walk along a straight 
line his gait becomes very unsteady. 

But in the vast majority of cases vertigo is associated with 
some disorder of the ear. It may result from wax, or foreign 
bodies in tlie meatus, or it may supervene during ear -syringing, 
especially if there is a perforation of the drum. The pathological 
cause may also be in the middle ear, as in otitis media, obstruc- 
tion of the Eustachian tube, or merely from sneezing or blowing 
the nose, also from spasm of the tensor tympani muscle. 

Lastly, there is what is known as Hinibn's disease, or laby- 
rinthine vertigo. This has three main classes of symptoms; 
firstly, giddiness and reeling, due to affection of the semicircular 
canals ; secondly, deafness and tiimitus, due to aftection of the , 
auditory fibres ; and thirdly, associated bulbar phenomena such as 
nausea and vomiting, cardiac failure, cold clammy sweat, &c., due ' 
to afiection of adjacent medullary centres. 

The vertigo of Meniere's disease is paroxysmal, and comes on 
with such suddenness that the patient may fall to the ground as 
if struck down by an unseen hand. In other cases he reels, but 
has time to clutch at some neighbouring object to prevent him- 
self from falling. The giddiness lasts somet'mes for hours; 
slighter attacks may pass of! in a few minutes. It is increased 


by movement, and the slightest attempt to raise the head may 
induce vomiting. The direction in which the patient falls is 
usually forwards or towards one side, and commonly away from 
the side of the affected ear. Not infrequently nystagmoid jerks 
of the eyes occur during the attack, and double vision has also 
been observed. The vertigo is frequently accompanied or followed 
by headache, nausea and vomiting, lasting sometimes for hours. 
Together with these there are characteristic auditory phenomena, 
generally a sudden loud noise, usually unilateral. There is 
also deafness, more or less complete, on the same side as the 
tinnitus, with diminution or loss of bone-conduction. A certain 
degree of deafness remains between the attacks, but is rarely 

Such sjrmptoms, occurring with apoplectiform suddenness, 
constitute the typical picture of Meniere's disease. But frequently 
the paroxysms are much sUghter, and unassociated with nausea 
or vomiting, so that the patient may simply have sudden transient 
giddiness. But the attacks tend to recur ; rarely does a patient 
escape with a single attack. The intervals between them vary ; 
they may gradually decrease in frequency, or may progressively 
increase until after successive attacks the deafness becomes 
absolute. The vertigo then usually ceases. 

Meniere's disease is distinguished from epileptic vertigo by the 
coexistence of vertigo with tinnitus and deafness. Loss of con- 
sciousness, which is the rule in epilepsy, is rare in labyrinthine 
vertigo. Labyrinthine vertigo often yields to small doses (J to 1 
grain) of quinine. From cerebral haemorrhage or thrombosis it is 
distinguished by the presence of auditory phenomena, and by the 
absence of signs of a focal brain lesion. The pathology of Meniere's 
syndrome is obscure. Meniere himself described a hsemorrhagic 
effusion in the inner ear. But as Arthur Cheatle^ has lumin- 
ously suggested, the phenomena are in many respects closely 
analogous to those of glaucoma, and may possibly be due to a 
sudden rise of tension in the endolyn:ph or perilymph, whether 
produced by haemorrhage or other causes in the labyrinth or by 

* Archives of Otohay, vol. xxvi., 1897, p 185. 



sclerosis of the middle ear, whereby the jenpstrn ovalis and fenestra 
rotunda become fixed, thereby depriving the inner ear of safety- 
valves which normally permit of compensation for suddpn changes 
in labyrinthine pressure. 

No case of isolated palsy of the Ninth or Olosso-pliaryngeal 
Nerve has yet been observed in man, so that its exact 
functions are not completely determined. We know that it sup- 
plies taste-fibres to the posterior third of the tongue and to the 
soft palate. It probably also suppltes the taste buds which exist 
on the epiglottis and on the arj^enoid cartilage. The glosso- 
pharyngeal is also a nerve of common sensation for the back of the 
tongue, part of the soft pa!at« and upper part of the pharynx, 
whilst it has motor fibres for the middle constrictor of the pharynx, 
and for the stylopharyngeus. 

Paralysis of the nerve causes anaisthesia of the back of the 
tongue and pharynx, difficulty in swallowing and deficient taste 
in the posterior third of the tongue. In animals where this nerve 
has been divided experimentally, the pharynx and oesophagus 
remain tonically contracted, owing to paralysis of the inhibitory 
fibres contained in the glosso- pharyngeal. 

The Tenth Neire, Vagus, or PneumogaBtric Nerve, according 
to modern nomenclature, is held to include those roots which used 
to be called the " bulbar part of the spinal accessory." Nowadays 
the term " spinal acce.s8ory " is limited to the spinal part of the 
accessorius which arises from an entirely separate nucleus, whereas 
the old " bulbar part " is derived from, and belongs to, a con- 
tinuation of the vagus nucleus (nucleus ambiguus) in the medulla. 

The vagus has a most extensive distribution. It supplies the 
pharynx, larynx, oesophagus, heart, lungs, stomach, and partly 
even the intestines and spleen. By its auricular branch it also 
supplies part of the skin of the outer ear. Its pulmonary fibres 
are motor for the bronchial muscles and sensory for tlie respiratory 
passages. The vagus is both motor and sensory for the tpsophagiis, 
sensory for the stomach, and partly motor for the stomach and 
intestines. Its lowest roots of origin are those which are of the 
[ greatest diagnostic importance, for they contain motor fibres 


for the levator palati and the larynx, together with inhibitory! 
fibres for the heart. With the exception of the crico-thyroid 
muacle, which ia innervated by the superior laryngeal brancfaj 
all the laryngeal miiacles are supplied through the inferior 

recurrent laryngeal nerve. 

The symptoms of vagus paralysis vary according to the site^ 
of the lesion. Intra-cranial lesions may affect all its roots of origin, 
or may attack the upper or the lower roots alone. In the latter 
case there is often a concomitant affection of the adjacent 
hypoglossal nerve. 

flG. (H. — Paralysis of Ihe riji-lit sk1e of tlie jialale. Tlie pntient it sajing 
" All." and tlie patati- is piillvl up towards tlie left aide. The arrow 
pointfl to tbe contre of the Qvula. 

If the whole of one vagus trunk be affected, there is unilateral 1 
paralysis of the palate and larjmx, together with anaathesia of the } 
larynx on the affected aide. The only way to recognise a unilateral | 
paralysis of the palate is to watch the movement of its median 1 
raphe when the patient utters a long " Ah." Normally the raph£ 4 
rises straight up. But if one side of the palate be paralysed, the J 
healthy side alone pulls upwards and the raphe deviates to the ] 
sound side, forming a characteristic dimple (Fig. (}4}. 

If both vagi be paralysed, there is tachycardia and irregularity J 
of the heart, from paralysis of the cardio-inhibitory fibres. Thert 
is also slowness and irregularity of respiration. These do i 
occur in unilateral vagus palsy. Gastric symptoms have also bean^ 
observed even in unilateral cases, such as gastric dilatation, vomit- 1 
ing, gastric pain, and loss of the sensations of himger and thirst. 

Of all these symptoms, the moat constant and easiest to j 



recc^niae are ttc afTectton of the soft palate and the laryngeal 
palsy. Paralysis of the recurrent laryngeal nerve may occur 
alone. The commonest cause is aortic aneuriam, which frequently 
compresses the nerve on the left side. Mediastinal growths 

may also compress it, or its paralysis may even be the result 
of mitral stenosis, wherehy the left auricle may compress the nerve 
directly against the pulmonary artery, or the auricle may force 

Fio. 6a. — Org^nnta larirngcal paralyBCE {BbtwcII). 
I. Left uliliiolnr ptnlyiii. tlurtiig Intplnllon, 

11, LeK ■iHlucCor ]iani]y>lt, ilnrinu phnnillini. 
lit. LeK ni-urrenl bmigijal iMnlytk rliirlnE InipirXioli. 

IV. I«ft. recnrrciit liryiiireiil iMnlynU, ilurlng iihunsLlon. 

the left bronchus upwards and compress the nerve against 
the aortic arch,' In recurreni laryngeal parali/sis the vocal 
cord on the affected side is immobile, fixed in the cadaveric 
position, i.e. midway between abduction and adduction, and the 
voice is generally hoarse though not absent, since during pbonation 
the healthy cord can cross the middle hue to meet the paralysed 
one. If bolh recurrent larytigeah be paral3raed, both vocal cords are 
motionless and in the cadaveric position, and pbonation is impossible 
" FriBFliaiier, WittKr Klia. Wtxhtngchrill, Det. 28, 1B05. 



RJnce the cords cannot be brought together. There is no stridor 
except on deep inspiration. 

It is here convenient to recall some of the chief diagnostic 
features of laryngeal palsies (Figs. 65 and CO.) Abductor palsy, 
unilateral or bilateral, is always organic, and is often the earUest 
sign of a commencing recurrent laryngeal nerve affection. In um- 
hUeral abductor palsy the voice is unaffected, but on laryngoscopic 

examination the paralysed cord is seen to be immobile during 
inspiration, not moving outwards like its healthy fellow. On 
phonation the corda meet normally. In bikUeral abductor palsy 
the voice is also unaffected, since both cords come together on 
phonation. But since they do not move outwards during inspira- 
tion, but on the contrary are sucked together, inspiration is 
laboured and stridulous, and the patient is in danger, since the 
slightest swelling of the cords may completely block the glottis. 
Paralysis of the internal thyro-ari/tenoid muscle, which occurs in 
some cases of early bulbar paralysis, is characterised by an oval 

^H^ instead 
^^P tion, ov 



instead of a linear appearance of the glottis on attempted phona- 
tion, owing to loss of the support of these musclea. The voice is 
therefore hoarse, but abduction and adduction are otherwise 
unaffected. Adductor paralyais is always bilateral and generally 
hysterical. It is common in hysterical aphonia. The patient 
loses her voice, often suddenly, and talks in a whisper. There 

\e pMIi 

Paralysis oC ri^lil spinal ai 
ownwnrd ami outwnrd •lliplanment nt ihe right acDpii 
ha luicnil imtlincB ol lh« neck. On tbe Mnil>Kd ndr t 
usnli «<3ipulin; on the niimiBl ihlii hy tho trii[>« 
iltenipling lodcpteH Ihehesrl igalnBl: — 
Urno-nuutuld, Iheri ■- '" '■• ■ 

i« right 

is no stridor, and on inspiration the cords move normally out- 
wards. But on attempted phonation they do not reach the 
middle line. The condition often disappears suddenly, sometimes 
as a result of the process of laryngoscopy, or of the application 
of strong faradic shocks to the larynx. 

The Eleventh or Spinal Accessory Nerve is distributed to the 
I stemo-mastoid and to part of tlie trapezius. It is exclusively a 
I motor nerve. When it is paralysed, there is paralysis and atrophy 
I of the sterno- mastoid, which no longer stands out on rotation of 
\ the head to the opposite shoulder, nor on depressing the head against 


resistance {Figs. 67 and G8). The paralysis of the trapezius variesi 
in degree according to the extent to which the muscle is supplied! 
by the spinal accessory and by the cervical plexus reBpectivcly. I 
Ordinarily the uppermost fibres of the trapezius are ijinervated by J 
the spinal accessory, whilst the middle fibres of the muscle are aup-f 
plied by the third and fourth cervical nerves, and the lowest fibreflj 
of all by the spinal accessory. When the trapezius ia paralysed]! 


FlO. Gl!.— Faralysia of right t^piiial ftccesaory nerie, aliowinjc downwarrt 
anri outward dinplaceiuonc of scapufa. Owing (o absence of 
the tmpeilus, the rhomboid oiuKcles on the right. bUIv biive become 

the outline of the neck is altered, owing to the levator angi 
scapulae having become subcutaneous, and there ia a characteiiatia 
deformity of the angle of the shoulder resulting from the displace 
ment of the scapula (Fig. 69). The scapula on the paralysed sidi 
ia displaced downwards and outwards, and rotated outwards, so j 
that its inner border instead of being parallel with the spine, is 
inclined from below upwards and outwards. When the patient 
braces his shoulders back, the scapula i* imperfectly approximated 
to the middle line, and the rhomboids on the paralysed aide i 
visible subcutaneously (Figs. 70 and 71). 

The Twelfth or Hypoglossal Nerve ia also entirely motor i 



function. Immediately after its exit from the skuU it receives 
amongst other connections a smalt commum'cating branch from the 
cervical sympathetic. The hypoglossal supplies all the intrinsic 
muscles of the corresponding hall of the tongue. Outside the skull 
it ia joined by branches from the first and second cervical nerves, 
and from these two nerves the depressors of the hyoid bone are 
supplied, through the descendens hypoglmsi. 

The symptoms of hypoglossal paralysis are very characteristic 
(Fig. 72), The corresponding half of the tongue is atrophie-d 
and vmnkled. When the tongue is protruded the healthy side 
causes the tip to be pushed round to the paralysed side in a sickle- 
shaped curve. If the nerve is divided suddenly, by accident or 
operation, the patient feels for a few days as if the paralysed half 
of the tongue were a foreign body, interfering with articulation 
and mastication. But this sensation soon passes off as the patient 
becomes accustomed ta his hypoglossal palsy. 

If the lesion of the hj-poglossal be extra-cranial, after it has 


received the small communicating branch from the cervicirffl 
sympathetic, we may sometimes observe vaso-motor changes in thAl 
atrophied aide of the tongue. In two of my cases where the twelfth I 
was divided intentionally for the purpose of facio- hypoglossal I 
anastomosis, the tongue was pale on the paralysed side. From I 

Fio. 72. — Paralysis of right hypoglossal uerve frgra a stab-wound below 
the jaw. Bbowing atroph; oF corrcGponding bolf of tongue and 
marked deviation to the right whan protrudKil. 

unilateral paralysis of the hyoid depressors, the larynx may I 
pulled over towards the sound aide during swallowing. 

The hypoglossal nucleus within the medulla, as we havel 
already mentioned, is closely connected with the lowest cells of thA^fl 
facial nucleus, viz., those which supply the orbicularis oris. 
Hence in lesions in the neighbourhood of the hypoglossal nucleus, 
the muscles of the Hps are paralysed together with those of the 
tongue. This weakness of lips and tongue in nuclear lesi 



generally bilateral, owing to the close proximity of the hypoglossal 
nuclei to the middle line. 

Intra-cranial lesions of the hypoglossal nerve, e.g. from a patch ' 
of Bvphilitic nieningitis, verv frequently involve other cranial nerves , 


Flo. 73-— ParalysimjfBpinal ncccEsorj and hypoglossal on riKlitaiilf, allowing 
(lowiiwur'l anil outward tlUplacement of right ihoulder. nisa auuplij' 
of right half of tongue with deviation to ibe right on protrunioo. 

in the neighbourhood. One of the commonest multiple palsies 
IB that which produces hemiatrophy of the tongue, paralyma of the 
trapezius and stern o-majitold, and paralysis of the vocal cord and 
soft palate, all on the same side (Fig, 73). This is the result of a 
lesion implicating the twelfth, the eleventh, and the lowest roots of 
the tenth nerve. 



There is, perhaps, no sjrmptom for which we are more frequently 
consulted than that of pain. And for its satisfactory treatment 
the underlying cause must first be determined — sometimes no 
easy matter. 

With the exception of cases where pain arises in a healthy 
individual from some unduly strong stimulus, pain is always patho- 
logical. The vast majority of pains are due to irritation of some 
peripheral sensory nerve or of a posterior root. Less commonly 
pain may be due to abnormal sensitiveness of the cortical centres, 
and is functional in origin. Stimulation of the surface of the brain 
gives rise to no pain, but the meninges are exquisitely sensitive, 
the cerebral membranes being innervated by the trigeminal nerve. 
Intra-cranial diseases therefore probably cause pain chiefly through 
the intermediation of the sensitive meninges. It is possible, how- 
ever, that the pain in some cases of syringomyeUa may not be 
of meningeal origin, but due to actual distension of the syringo- 
myelic cavity by the fluid within, though against this view is the 
fact that pain is a late phenomenon in this disease. 

Spontaneous sensations of discomfort vary in degree and in 
kind. Milder varieties, not amounting to actual pain, are classed 
as dyssesthesise. They include such symptoms as spontaneous 
tingling, " pins and needles," dulness, itching, flushing, &c., whilst 
among the more severe varieties are the intense and agonising 
pains of tic douloureux, angina pectoris, renal or biliary colic, or 
the lightning-pains of tabes. 

In the diagnosis of the cause of any particular dysaesthesia or 
pain, there is one invariable rule we should always follow, 
namely, to make a careful local examination of the part of 
the body to which the abnormal sensation is referred. Only in 



163 ' 

this way can we escape gross errors, such, for example, as that of 
mistaking the pain of herpes zoater for that of pleurisy. In 
every local pain we should first search for a local cause, whether 
in the skin, muacles, bones, joints, glands, or other subjacent 
structures. Pain due to local disease ia usually more or leas 
continuous, and accompanied by objective phenomena such as 
redness of the skin, swelling or tenderness of the diseased tissues, 
rigidity of joints, and so on- The painful cramps of tetanus, 
rabies, and Htrychnia-poisoning are easily recognised and need 
not be further described. 

Some pains are generalised all over the body, for example, the 
pains of acute illnesses such as influenza, smallpox, and other 
fevers of rapid onset. In such cases the elevation of tempera- 
ture, the presence, perhaps, of a rash, and usually the occurrence 
of other similar cases in epidemic form, all help us in the 

Intractable paroxysmal pains of hemiplegic distribution, in the . 
face, trunk and limbs, so-called hemiplegia dolorosa, are highly 
suggestive of a lesion localised in the optic thalamus.' In such 
thalamic lesions there is also he mi -anaesthesia of the affected limbs 
and face, together with spontaneous choreiform or athetoid move- 
ments and also hemi-ataxy on voluntary movement. These cases 
of hemiplegia dolorosa must be carefully distinguished from the 
joint pains which are not uncommon in ordinary chronic hemi- 
plegia, which are due to secondary arthritic changes and are usu- 
ally alleviated by massage, hydro -t he ra[»utics and a uti -rheumatic 

Most cases of pain or discomfort, however, are localise! to 
some more definite area, and therefore for diagnostic purposes 
the moat convenient plan of studying pains and other subjective 
sensations is by considering the different parts of the body in turn. 

Headache. — Cephalalgia. — A diagnosis of "headache" alone 
is never sufficient. Headache ia not a disease, but merely a 

When a patieut complains of headache, local causes should i 
' DcjoriiiB unil Huusiiy, Rtvac nturoUxjiqur, lOOS. No. 12. 


first of all be excluded. Amongst the commonest heal extra-cranial 
causes we should bear in mind rheumatic affection of the occipito- 
frontalis muscle, with its diffuse tenderness on brushing the 
hair, and with aggravation of pain on movement of the scalp. 
This is often relieved promptly by hot applications. Erysipelas is 
accompanied by local redness, heat and oedema, and by fever. 
Periostitis of the pericranium causes tenderness on pressure and is 
often syphilitic in origin, in which case the pain is commonly worse 
at nights. 

Headaches from local causes in the cranial bones are most 
commonly due to inflammation of the mucous membrane lining the 
various air-cells, e.g. the mastoid, frontal, or ethmoidal cells, or even 
to an ordinary coryza. Here the previous history of the case, 
together ¥nth the local examination, will serve to indicate the 
cause. Less frequently caries of the bones or local exostoses 
may be present. Carious teeth often cause headache, referred 
especially to the temporal region. 

Gross irUra-cranial disease may produce intense headache, either 
from local affection of the meninges as in the various forms of 
meningitis (syphilitic, tuberculous, or pyogenic), or from general 
increase of intra-cranial pressure, as in diffuse meningitis, intra- 
cranial abscess, gumma, or tumours. Headaches of intra-cranial 
origin are often associated with the other classic signs of increased 
intra-cranial pressure, especially with vomiting and optic neuritis. 
In every case of obscure headache we should make a careful 
ophthalmoscopic examination. The position of the headache does 
not necessarily correspond with that of the tumour. Tumours of 
the posterior fossa produce the most severe headache. 

Then there are the headaches which result from abnormalities 
of the intra-cranial circulation, especially from aiterial hyperaemia, 
as in renal disease or in suppressed menstruation, or temporarily 
from drugs such as nitrite of amyl, erythrol tetranitrate, or alcohol. 
Hyperaemia produces a throbbing pain, sometimes associated with 
giddiness, tinnitus, affection of vision, and a tendency to attacks 
of epistaxis. The venous hyperajmia of severe cardiac disease or 
of emphysema may also produce headache, which is aggravated 


by coughing. The headache of anremia ia {trobably mainly toxic I 
in origin, rather than due to actual deficiency in the supply of blood 
to the head, 

Certain caaes of hemiplegia are preceded, for days or even for 
weeks, by headaphe. Thia is especially common in cerebral tkrom- 
bosis, where a premonitory headache is of considerable diagnostic 
value. The onset of a cerebral htEmoTthage is often coincident with 
a headache. Therefore if an elderly man complains of headaches 
and bleeding from the nose, we should be cautious in checking 
epistaxis which may act as a aafety-valve, and may save him 
from an attack of cerebral haemorrhage. 

There is another group of headaches which arc produced by 
peripheral irritation in various parts of the body. Thus, for 
example, visceral irritation may cause headache, as 
uterine diseases, or in the headaches from which so many i 
suffer at the menstrual periods, and frequently also throughout the 
menopause. In some people the swallowuig of an ice causes sudden 
frontal headache, when the ice reaches the stomach. This is a 
typical " reflex " gastric headache. Every autumn we come across 
cases of "gun headache" amongst sportsmen, the result not 
simply of the auditory stimulus of the noise of the gun, but due 
partly to the shock of repeated recoils of the weapon. Ocular 
headaches are fairly trecinent, sometimes the result of disease such 
as glaucoma or iritis, but much more commonly arising from errors 
of refraction, especially hypermetropia and astigmatism. Even 
apart from this, headache may result from prolonged eye-strain, 
e.g. after sight-seeing in picture-galleries, being commoner in 
people who have some error of refraction. 

A large group of headaches are toxic in origin, the toxins 
altering the intra-cranial circulation, usually in the direction of 
raising the blood -pressure. The onset of certain infective fevers 
is associated with headache, for example in smallpox and influenza 
(commonly associated with pain in the back), in enteric fever 
associated with dyspeptic symptoms, in scarlatina, pneumonia, Ac. 
In Buch cases the temperature, the characteristic rash, and the 
other signs and symptoms will guide us. Poisoning by toxifl 


substances is also the main cause of the headache of dyspepsia, 
whether it be the familiar " Katzen-jammer " — the bursting 
morning-headache and nausea following a joyous alcoholic evening 
(this headache, by the way, can often be relieved by a 20-grain 
dose of calcium lactate), or the headache of chronic dyspepsia, 
especially when associated with a constipated intestine. Headaches 
also result from poisoning with carbonic oxide, carbonic acid, 
and other respiratory sewage in ill-ventilated rooms or at crowded 
meetings. Other poisons, again, are autogenetic in origin, as are 
the headaches of gout, uraemia and diabetes. 

Sunstroke causes acute diffuse headache. Severe cases are 
often accompanied by other symptoms such as delirium, hyper- 
pjrrexia and coma. Neurasthenia and exhaustion, whether from 
overwork, from excessive study or from other excesses, are often 
associated with headache, frontal, occipital, or circular {douleur en 
casque). The post-epileptic headache following a fit is sometimes 
severe and may be associated with vomiting. 

Bilateral headaches are most commonly toxic. The headache 
of djTspepsia is usually referred to the frontal region, that of 
constipation to the occiput, whilst vertical headaches are most 
commonly due to anaemia or to debiUty. Some cases of con- 
cussion of the brain are followed by obstinate headaches, recurring 
for many months. These, I believe, are sometimes partly toxic 
in origin, a smaller amount of toxin being eflBcient in producing 
headache after concussion than in the case of a healthy individual, 
whilst in other instances the headaches occur on sUght mental 
exertion, especially where the patient has been allowed to return 
to work prematurely. Hence the importance of complete physical 
and mental rest after a severe head injury, even in the absence 
of signs of an organic lesion. 

Most of the headaches to which we have referred are bilateral 
or mesial in situation. Let us now consider a different group — 
the unilateral or circumscribed pains. 

Sometimes these are due to local disease of the scalp, peri- 
cranium or skull, in which case local examination will generally 
reveal the cause. Or they may result from intra-cranial disease, 



for example, meningitis, abscess, gumma or tumour. If the under- ' 
lying disease be near the surface of the skull, the site of the pain 
sometimes corresponda with that of the diaeasG. But this ia by 
no means always the case. I remember a striking case of right- 
sided cerebellar tumour where the pain was confined to the left 
supra,orbital region. The growth was diagnosed and successfully 

Some headaches are associated with great pallor of the face 
— apparently due to vaso-niotor spasm of the cerebral vessels, often 
relieved by inhalation of amyl nitrite. Others are associated 
with arterial hyperEemia, throbbing arteries, and a flushed face. 
These are sometimes promptly reheved by compression of the 
carotid artery on the corresponding side. Such angio- neurotic 
headaches are rarely bilateral. 

A very acute circumscribed variety of headache is known 
as the clavus hystericus, an agonising pain usually referred to the 
vertex, as if a nail were pressing into the brain. It occurs in 
certain cases of hysteria and neurtisthenia. It is unassociated with 
any other evidences of intra-cranial disease, and its very intensity 
leads us to be suspicious as to its true nature. 

The pain of aick-headache or migratjie (hemicrania), with its 
parox3^mal attacks occurring at intervals of days or weeks, the 
patient during the intervals being free from headache, is usually 
easy of recognition. Migraine is a family disease which generally 
appears in childhood and recurs throughout the strenuous period 
of life, tending to disappear in old age. The pain of migraine is 
often alleviated by pressure on the common carotid artery of 
the corresponding side, but reappears when the pressure is removed. 
This headache generally culminates in vomiting, and is some- 
times preceded by a visual aura in the form of a scintillating 
scotoma, consisting of a blind area in one half of the visual field, 
on the side opposite to that of the unilateral headache, the blind 
area being bounded at its periphery by a luminous zig-zag coloured 
spectrum. This scotoma not infrequently develops into a tempo- 
rary total heniianopia. The headache of migraine is generally 
unilateral, and is referred to the side contra -lateral to that of the 



visual phenomena. Thus if the visual sensations are in the left 
side of the visual fields, the headache is right-sided, and vice versd. 
Less commonly a migrainous attack may be preceded by a non- 
visual aura of some sort, e.g., by a subjective sensation of tingling 
in one hand spreading slowly up the arm to the face and tongue, 
and followed by headache on the opposite side of the head. If 
the tingling be right-sided there may be slight transitory aphasia. 
This variety of migraine is distinguished from a minor epilepti- 
form attack by the greater intensity and unilateral limitation of 
the migrainous headache, by the slow, deliberate march of the 
migrainous aura, lasting perhaps for many minutes, by the absence 
of unconsciousness, by the absence of clonic movements, and by the 
fact, pointed out by Gowers,^ that the premonitory tingling of 
migraine may spread bilaterally to the tongue and lips, whereas 
in an epileptiform attack, if the aura spreads to the tongue or face, 
it remains unilateral. Migraine and epilepsy may alternate in 
the same patient. Migraine (yphtalmoflegique is a rarer variety, 
in which, in addition to hemicranial pain, there is transient paralysis 
of the third nerve on the same side as the headache, with ptosis, 
external strabismus, mydriasis, &c. 

We now pass to pains in the* region of the trigeminal nerve. 
Of these tic douloureux is the most agonising pain from which 
a patient can suffer. The pain rarely attacks all three divisions 
of the nerve, but is usually confined to one division (especially 
the supraorbital), or it may attack two adjacent divisions. The 
disease is hardly ever bilateral except in cases of diabetes. The 
patient has paroxysms of intolerable agonising pain in the area 
of the affected division. During the attack, the face is often 
thrown into strong involuntary tonic spasm on the affected side, 
there is excessive lachrymation, and sometimes secretion of nasal 
mucus and saliva, all on the affected side. Not only do parox3^ms 
occur spontaneously, but the slightest stimuli often suffice to 
induce an attack, and therefore the patient avoids chewing food 
on the affected side. I have known cases in which it was impossible 
for the patient to wash his face for weeks at a time, lest an attack 

1 British MedicalJoumal, Dec. 3, 1900. 


shouM be thereby precipitated. Inveterate trigeminal neuralgia 
Bometimes drivea the patient to anicidc. 

Apart from these, there are numerous varieties of more localised 
paroxysmal neuralgic pains referred to individual branches of the 
trigeminal nerve, and associated with "tender points" over their 
foramina of exit. lu such local neuralgias, and In tic douloureux 
it«eU, we ahould always search carefully for some local exciting 
cause in the mouth, nose, ear, or eye. A carious or inflamed tooth 
may cause neuralgia in the whole of the corresponding division of 
the fifth nerve, and the dental surgeon by extracting it will relieve 
the condition. But we must beware of extracting sound teeth 
simply because the patient refers neuralgic pain to them. Some- 
times an abnormally- placed tooth, though healthy in itself, may 
cause neuralgia. Thus a lady of fifty-eight had a constant burn- 
ing pain along the right side of her tongue for eight years, together 
with a feeling of numbness in the area of the second division 
of the fiftii nerve. This had been vainly treated by numerous 
drugs, whilst all the time the real exciting cause lay in an 
imperfectly -erupted lower wisdom-tooth on the corresponding 
side, the date of the pain coinciding with the first appearance of 
the tooth. Antral disease, nasal polypi, and other local lesions 
may all cause localised neuralgias. If, in addition, the patient 
be anfemic or gouty, the tendency to neuralgia is increased. But 
auEemia or gout alone will not cause a local neuralgia. Some 
local determining cause must also be present, though it is some- 
times difficult to discover, Syphilitic basal meningitis or gumma, 
implicating the fifth nerve in the floor of the skull, may 
cause trigeminal neuralgia. Such cases usually show other 
evidences of intra-cranial disease, and we should look for signs of 
involvement of the sensory or motor root (see page Viii). If such 
lesions last any considerable time, they tend to produce some 
anaesthesia of the affected nerve-area. Localised aniesthesia will 
suggest an organic neuritis rather than a mere neuralgia. 

Let us now consider the various pains which may be met with 
i in the tnmk. Firstly, there are the various root-pains, due 
I to irritation of the corresponding posterior root or roots in the 


affected area. Sometimes such root irritation is due to disease 
of the spinal meninges (tubercle, syphilis, or tumour), to osteo- 
arthritis, caries or tumours of the spinal column, or to intra- thoracic 
aneurisms and new growths. Bone pains in the spine sire associated 
with local tenderness and rigidity. If we see a patient supporting 
his head with both hands owing to pain in the neck, this is almost 
pathognomonic of disease of the cervical vertebraB. Root-pain 
conmiencing unilaterally and later becoming bilateral is practically 
pathognomonic of a tumour of the spinal meninges. These pains 
when due to organic lesions of the roots, are not infrequently 
associated ¥nth a degree of hyperaesthesia or ansBsthesia of the 
painful area — ancBsthesia dolorosa. If the spinal cord be com- 
pressed or infiltrated by the same lesion as that which im- 
plicates the posterior roots, we have evidence of sensory or 
motor paralysis of the parts below the lesion, with the usual 
changes in the reflexes, &c. The girdle-pains of tabes are due 
to affection of the corresponding posterior roots. Tabetic girdle- 
pains vary in degree from the sensation of a narrow constrict- 
ing cord to one of a broad cuirass enveloping a large part of the 
trunk. Such a cuirass often feels incomplete either in front or 
behind (Fig. 78, p. 193). Root-pains may also occur in some 
cases of disseminated sclerosis (sclerosis multiplex dolorosa), and 
unless this fact be borne in mind a false diagnosis of spinal tumour 
may be made.^ Another root-pain is that associated with herpes 
zoster, which is a disease of the posterior root-ganglion. Herpetic 
pain is practically always unilateral, and may either precede or 
succeed the eruption of the herpetic vesicles. It may last for 
months after the vesicles have disappeared. The pain of herpes 
is often so sharp that it may be mistaken for that of pleurisy, from 
which it is distinguished by auscultation. Herpes zoster is often 
accompanied by a lymphocytosis of the cerebro-spinal fluid. 
Pleurodynia is a pain in one or more intercostal spaces, due to 
a " rheumatic " myalgia of some of the intercostal muscles. It 
somewhat resembles the pain of pleurisy, but is easily distinguished 
by the local tenderness on digital pressure and by the absence of 

* Frankl-Hochwart, Neurologiaches CerUralblaU, 1906, a. 973. 



friction-sounds on auscultation. There is also a very common 
tnmk-pain which we meet with in people who are neurasthenic or 
debilitated. It is a deep boring pain, usually below the inferior 
angle of one or other scapula. It is more diffuse and less 
superficial than the pain of herpes, and it has none oE the physical 
signs of pleurisy or pleurojynia. The pain of traumatic neur- 
asthenia, especially after a railway or other accident (" railway 
spine "), may simulate that of organic spinal lesions, especially 
when a h3^terical paraplegia coexists. But the diagnosis can 
usually be made by noting the excessive hyperaaatheaia of the spine, 
the absence of signs of organic disease and the presence of various 
hysterical "* stigmata " (see later, p. 3-17). Mammary neuralgia 
or mastodynia also occurs in hysterical and neurasthenic patients, 
and must be distinguished from disease of the gland by means of 
physical examination. 

We have also to bear in mind the various rejected pains 
which may occur in visceral diseases. Thus, for example, in 
pericarditis there may be precordial or epigastric pain. In aortitis 
pain may be referred to the upper three intercostal spaces on 
the right side. Physical examination will dear up the diagnosis 
in cases of aneurism and of mediastinal growths. One of the 
most severe of all trunk pains is the well-known anifina pectoris. 
This is a paroxysmal suffocative pain, or feeling of intolerable 
oppression in the region of the heart, often radiating down one or 
both arms, but especially down the left arm. It is commonest 
in male patients at or after middle life, and is usually, though not 
invariably, associated with evidence of vascular degeneration. It 
has to be distinguished from toxic or neuralgic angina, so-called 
" pseudo-angina," a similar but much less serious affection, met 
with most commonly in young girls, in women who have been 
lactating too long, or in patients before middle life who smoke 
tobacco or drink tea to excess. 

Irritation of the sensory nerves at the cardiac end of the stomach, 
by abnormal acids or other irritants, may cause burning pain, 
usually referred to the seventh left chondro -sternal junction, and 
sometimes also to the left interscapular region. Such gastric pains 


are associated with other dyspeptic symptoms to which we need 
not here refer further. As regards the situation of reflected pains 
in diseases of various parts of the gastro-intestinal tract, it is useful 
to bear in mind Mackenzie's rule,^ that pain due to affections of 
the digestive tract is referred across the middle line of the abdomen, 
in regularly descending areas as we pass from the stomach towards 
the large intestine. Thus the epigastrium is the region for gastric 
pains (disease at the cardiac end causing pain higher up than 
pyloric affections), the umbilical area is the region for pains of 
the small intestine, the hypogastric area the site of pains 
due to the large intestine. A striking experimental corroboration 
of this can be obtained at any time by taking a sharp purgative 
drug. When the familiar colicky pains appear, they are felt first 
in the region of the umbilicus, but soon they descend lower and 
lower, and when they arrive close above the pubes, the call for 
evacuation of the bowel becomes " urgent and imperative." 

To discuss fully the various causes of acute abdominal pain 
would require many chapters of description. We have to bear 
in mind not only diseases of the gastro-intestinal tract, in the 
form of catarrh, ulcer, muscular spasm, &c., but also perforations 
of various hollow . viscera, the stomach, gall-bladder, intestines 
(including the vermiform appendix), rupture of a pyo-salpinx 
or of a tubal pregnancy, biUary or renal colic, acute pancreatitis, 
torsion of an ovarian pedicle, &c. In every instance, not only 
should we carefully examine the whole abdomen, but we should, 
if necessary, examine the pelvis, per rectum or per vaginam, and 
investigate the urine and dejecta. 

Apart from acute renal colic, a floating kidney is a fairly common 
cause of diffuse abdominal pain, especially in poorly-nourished 
women with lax abdominal walls. Here again, local examination 
of the abdomen will reveal the cause. 

Before leaving the subject of abdominal pains, we must 
not fail to recall the familiar crises of tabes dorsalis : — gastric 
crises associated with pain and vomiting, intestinal crises associated 
with colic and diarrhoea, diaphragmatic crises with hiccough, 

* Brain, 1901, vol. xxv. p. 373. 


173 ' 

^^u bladder crises, &c. All these may closely simulate the pain of 
^^B acute abdominal disease. But the history u( the caee, together 
^^K with an investigation of the pupils, knee- and ankle-jerks, and 
^^M the other phenomena of tabes, will usually save us from error. 
^H Lumbago, or pain in the lumbar muBcles. a variety of 

^H myalgia, i» usually easily recognised. The pain is intensified 
^H by active muscular contraction and also by passive stretching, 
^H caused for instance by the stooping posture. It is also associated 
^H with tenderness on pressure. Lu mho -abdominal neuralgia, on 
^H the other hand, is a diffuse and more superficial pain, not confined 
^^M to the lumbar region but spreading forwards to the front of 
^^m the abdomen, and sometimes to the groin, genitals or gluteal 
^H region. It is paroxysmal, and during the paroxysm there may 
^H be cramp-like spasms of the abdominal muscles or of the cremaster. 
^H It is associated with the '' tender points " of a true neuralgia, 
^H these being situated over the vertebral spines, the iliac creata. the 
^H linea alba, inguinal canal, scrotum or labium. Sacral pain is often 
^^1 due to uterine disease, as In the famlhar uterine dysmenorrhoea 
^^1 or the well-known pains of labour. 

^^P Coccygodyiiia or neuralgic pain in the region of the coccyx, is 
^^P practically confined to the female sex. The pain may be spon- 
^^B taneouB, or it may be induced by sitting or walking or by the con- 
^^H traction of any of the mus:^le3 attached to the coccyx, e.g. during 
^^m defecation. It is often associated with local tenderness. Before 
^^m making a diagnosis of mere neuralgia, local disease of the 
^H coc«yx or of adjacent structures must always be excluded by 
^H local examination, both externally and jier rectum. 
^H Pains in the Limbs. — Brachial neuralgia, generally a uni- 

^^ lateral affection, is referred, as a rule, to the whole area of distribu- 
tion of the plexus, namely to the lower part of the neck, the 
shoulder and the whole upper limbj being most intense in the 

t proximal part of the limb. It is rare to meet with neuralgia 
confined to an individual nerve-area, such as that of the median 
or ulnar, except in cases of local injury or disease of the nerve- 
trunliB. The pain of brachial neuralgia is aggravated by move- 
ment of the limb, which feeh heavy and numb, though there la no 


paralysis. The " tender points " are over the nerve-trunks, such 
as the musculo-spiral, circumflex, median or uhiar nerves. 

If ansBsthesia or trophic changes be superadded, we probably 
have to do with structural changes in the nerve-trunk, that is, 
with a neuritis, not a mere neuralgia. In every case of brachial 
neuralgia we must carefully examine the nerve-trunks in their 
entire course, to exclude the possibiUty of organic lesions com- 
pressing or infiltrating the nerves. In addition to pain, brachial 
neuritis often produces weakness and atrophy of the corre- 
sponding muscles, and impairment or perversion of cutaneous 

Analogous to brachial neuralgia and neuritis in the upper limb, 
we have in the lower Umb sciatica, a term which includes sciatic 
neuralgia and sciatic neuritis. In every case of so-called sciatica 
we have to decide which of these two is present. In sciatic 
neuralgia there is usually a dull aching pain, more or less constant, 
in the back of the thigh, with occasional paroxysms of darting or 
boring pain, generally from above downwards, along the course 
of the sciatic nerve. Any movement of the limb whereby the 
nerve is mad^ tense, or any local pressure as from sitting on a hard 
chair, brings on a paroxysm. Therefore the patient habitually 
keeps the hip and knee slightly flexed on the aflected side, so as 
to relax the nerve. It is not uncommon to find a slight degree 
of scoliosis in the lumbar region, the concavity being towards the 
sound side. The '* tender points " a e over the posterior iUac spine, 
the sciatic notch, the popliteal space, the peroneal nerve below the 
head of the fibula, and behind the malleoli. Passive stretching of 
the nerve increases the pain, for example by flexion of the hip with 
the knee extended. Blunting of sensation in the peroneal or pos- 
terior tibial area is unconmion and indicates an organic neuritis or 
perineuritis, as also do any alterations in the electrical reactions 
of the muscles, or any considerable degree of muscular atrophy. 
In sciatic neuritis the temperature of the limb is generally lower 
than on the healthy side. The ankle- jerks should always be 
tested on both sides. In sciatic neuritis the jerk may be 
diminished or lost, whereas in neuralgia it remains normal. In 



both affections we may observe exaggeration of the cremasteric 
reflex on the affected aide. 

Meralgm parcBslhetica is a variety of neuralgia occurring in the 
area of distribution of the external cutaneous nerve of the thigh. 
It consists in parsesthesia or actual pain in the outer aspect of one 
thigh, The pain is often induced by standing or walking, possibly 
owing to stretching of the fascia lata. It is sometimes associated 
with flat-foot on the same side. Here, as in brachial or sciatic 
pain, the presence of an area of impaired sensation would indicate 
a neuritis rather than a neuralgia. 

In rare cases we may find neuralgia in the area of the anterior 
crural or of the obturator nerve, and this may be symptomatic of 
an intra-pelvic tumour, or of an obturator hernia. 

The pains of brachial or sciatic neuralgia and neuritis, and of 
meralgia pancsthetica, are unilateral. Let us now consider the 
bilateral pains which may be met with in the limbs. 

Bilateral pains should always suggest to our minds either a 
toxic cause attacking the peripheral nervous structures of both 
limbs, or some central disease of the spina! meninges aflecting the 
posterior roots bilaterally, or again some angio- neurotic condition 
such as Raynaud's disease, erythromelalgia, or intermittent limp. 

Pains in the muscles or joints are a common symptom in. people 
who work under compressed air, as in divers or workers in deeply 
sunk caissons, whether under ground or under water. The 
symptoms of caisson disease, or "decompression paraplegia," are 
most likely to occur when the worker ascends too abruptly to the 
ordinary atmosphere. All such workers ought to pass through 
a "decompression-chamber," where the atmospheric pressure is 
gradually reduced to normal. If this be not done, bubbles of 
nitrogen are set free in the blood and may either form emboli 
in the arterioles of the central nervous system with consequent 
small foci of necrosis, or the nitrogen may effervesce out of the 
capillaries into the nervous tissues, especially into the substance of 
the spinal cord. Capillary haemorrhages may also occur. Clinically 
in such cases not only have we severe pains in the limbs but 
there may also be antesthesia and paraplegia of spinal type, and 



such paralysis may be permanent. Slighter cases clear up quickly, 
if the air-extravasation has been merely from the capillaries with- 
out air-embolism of the arterioles. 

The lightning pains of tabes may be unilateral or bilateral. 
They are commoner in the legs than in the anns, since tabes is a 
disease which commonly begins in the posterior root-fibres of the 
lumbo-sacral region. These pains are variously described by the 
patient as stabbing, burning, tearing, or bursting, and are commonly 
associated with local hypersesthesia of the skin. They are frequently 
mistaken for rheumatic pains, and all the more so inasmuch as 
they often coincide with changes in the weather. 

Tight " tourniquet " pains around the lower limbs, in broad 
zones rather than narrow, are sometimes an early and persistent 
symptom in disease of the lumbo-sacral region of the cord. They 
are due to irritation of the posterior roots, and may also occur in 
tabes. Root-pains also occur, though less commonly, in certain 
cases of multiple sclerosis. 

The root-pains of tumour or inflammation of the spinal men- 
inges, or of spinal caries, are more or less constant, with paroxys- 
mal exacerbations. Inflanmiatory affections of the meninges are 
usually bilateral from the outset, with corresponding bilateral pains. 
But in cases of meningeal tumour the pains are generally unilateral 
at first, and become bilateral as the disease spreads to the opposite 
side. The level of the pains in meningeal disease varies with the 
level of the affected posterior roots. Thus in cervical meningitis, 
tumour or caries, there is pain in the neck, spreading down one or 
both arms along the corresponding root-areas ; in thoracic cases 
the pain is around the trunk, and in lumbar or sacral cases it is in 
various parts of the lower limbs. Meningeal pain is often asso- 
ciated with local hypersDsthesia corresponding to the uppermost 
roots affected, and with tonic spasms of the muscles at that level. 
If the meningeal lesion affects the cord within, whether by com- 
pression or by infiltration, there will be in addition to root-pains the 
other signs of organic cord disease — so-called paraplegia dolorosa, 
with its anaesthesia, motor weakness and alterations of reflexes 
below the level of the lesion. Inflammatory, tuberculous and 



syphilitic affections of the spinal meninges are always associated 
with cellular changes in the cerebro-apinal fluid (see p. 396). 

Affections of the peripheral nervea may also produce pain. 
Thus in peripheral neuritis there is not only pain, with hypertesthesia 
of the skin of the feet and hands, but there is intense muscular 
tenderness on pressure, together with a degree of tactile aniesthesia, 
and in severe cases muscular paralj^is and muscular atrophy, 
accompanied by the reactions of degeneration. 

Pains localised in single nerve-areas should always lead us to 
examine the nerve-trunk in its entire extent. Tubercula dolorosa 
are multiple growths (usually n euro -fibromata) in the connective 
tissue of the nerve-trunks, many of them forming little subcutaneous 
nodules easily palpable and exquisitely tender, others less accea- 
eible in the deeper nerve-trunks, causing referred pains in the 
particular nerve areas. If these growths not merely irritate but 
interrupt the nerve-fibres within the nerve -trunks, there may 
in rare cases be areas of anffisthesia. Clinically we seldom find 
motor paralysis from such growths, except as a result of pressure 
, on the spinal cord or base of the brain by a neuroma on one of the 
spinal or cranial nerve-roots. 

It is convenient here to refer to erythro melalgia, where there are 
cyanosis and pain in one or both feet in the dependent posture, 
relieved by elevating the limb : to Raynaud's disease, which may be 
associated not only with local pallor, cyanosis or gangrene, but also 
with subjective sensations of tingling or pain ; and to intermittent 
limp, when the patient after a few steps becomes unable to walk 
farther, owing to intolerable pain in the muscles of the leg. To 
these conditions we shall return later, when studying the ner- 
vous affections of the vascular system. 

Paroxysmal spontaneous pain in the periphery of a limb, 
ascending towards the trunk, sometimes occur? as a variety of sen- 
sory fit in gross disease of the cortical sensory area« in the contra- 
lateral post-centra! gyrus. Thus in one case of my own, where 
there was a focal lesion of the left post-central gyrus, the earliest 
L symptom was paroxysmal pain in the right ffngers and hand.' 
' Ri'view 0/ Nturot. and Paychiatry, 1908, p. 379. 


Finally, we should refer to the group of pains met with in 
hysteria and neurasthenia. These are more often areas of hyper- 
sesthesia than of spontaneous pain. They are specially common 
in the neighbourhood of joints, whose slightest movement causes 
intense pain. In other cases the muscles are apparently hyper- 
sensitive, so that any attempt at movement of the limb, active 
or passive, causes an illusion of pain — so-called akinesia algera. 
But the history of the case, in which there has often been a pre- 
ceding local injury, the absence of signs of structural disease, 
local or central, and the presence of other hysterical or neurasthenic 
phenomena, will aid us in our diagnosis. It may be necessary 
to give a general anaesthetic, in order to eliminate gross local 
organic disease. 



We have already considered the anatomical course of the chief 
sensory paths from the periphery to the perceiving centres in the 
brain (Chapter I.). Let us now proceed to consider the methods 
of clinical investigation of the various forma of sensation. 

All parts of the surface of the body are not equally sensitive. 
Thus the tip of the tongue, the lips, the finger-tips, in the order 
mentionetl, are most sensitive to cutaneous impression, whilst 
other parts such as the dorsal aspect of the trunk, the upper arm, 
and the calf of the leg, are least sensitive. These difierences de- 
pend on various factors, such as thickness of epithelium, relative 
abundance of sensory end-organs, &c., into which we need not 
enter more minutely here. 

All Borte of ingenious apparatus have been devised for the 
accurate measurement of minute differences in sensibiUty to touch, 
pressure, pain, temperature, and so on. But for clinical diagnosis. 
we should avoid complicated apparatus and content ourselves 
with the simplest possible methods which, while accurate enough 
for practical purposes, do not impose too great a strain on the 
patient's attention nor demand too high a degree of intelligence 
on his part. 

The most important varieties of sensory stimuli which we 
employ in testing a patient's sensory functions are Ught touches, 
pin-pricks, cold and hot objects, all of which refer to aUaneous 
sensations. We have also to consider other sensations, such as 
joint-sensation {or sense of position on passive movement), active 
mtude-sensation (kinesthetic sense, or sense of active muscular 
contraction) and, lastly, the vibralion sensation produced when a 
sounding tuning-fork is placed over the subcutaneous surface of 


a bone or upon a finger-nail. There are other varieties of sensory 
stimuli, such as electro-cutaneous sensibility (which is generally, 
but not always, parallel in intensity with the pain-sense), and 
there is the sensation of pressure and appreciation of differences 
of pressure, &c. But these, though physiologically interesting, are 
of minor clinical value. 

There is perhaps no better criterion of neurological dexterity 
than the accuracy with which an observer can map out aress of 
diminution or loss of sensation on the one hand, or of perverted 
or exalted sensation on the other. Both experience and patience 
are required, in order to obtain trustworthy results. 

Inasmuch as we are largely dependent on the intelligence and 
goodwill of our patient for accurate answers, we must as far as 
possible try to eliminate all distracting outside factors. Therefore 
we direct the patient to close his eyes when we are testing 
sensation, so that his attention may not be diverted by 
watching what is being done. We must also be careful not 
to weary a patient by too prolonged examination, lest as 
he gets tired or impatient his answers become inaccurate. The 
simpler our methods of examination, the better are our results 
likely to be. We have also to contend with wide variations in 
the intelligence of different patients, in their education, and in 
their attentiveness ; this latter may be modified by pain, by 
anxiety, or by psychical deficiencies. Sometimes we have to 
deal with deliberate attempts on the part of the patient to mislead 
us. Fortimately, patients who simulate disease generally make 
blunders so gross as to prevent an erroneous diagnosis on the 
part of a careful observer. 

Clinical Investigation of Sensation.— At the start, the 
patient's eyes should be closed, or some object should be inter- 
posed between his eyes and that part of the body which is being 
tested. We then proceed to test the various cutaneous sensations — 
touch, pain and temperature, separately and in turn. 

Touch is tested by means of some soft light object, such as a 
tuft of cotton-wool, a feather, or by gentle pulling or stroking of 
the hairs. Loss of sensation in the hairs is called "tricho- 



' Pressure is tested by means of a pencil or other 
blimt object ; if such pressure be steadily increased a " deep " 
Bensation of pain is ultimately produced. CiUnne&us j>ain is 
tested by a sharp needle ; cold by blowing on the skin, or by a cold 
object such as a metal spoon or a test-tube containing ice-cold 
water ; k&U by breathing on the akin or by a warm object such 
as a test-tube containing hot water. 

Each variety of sensation should be examined separately, before 
passing on to the next kind of stimulus, and the results should 
be recorded on an outline-chait of the body. In mapping out 
areas of abnormal sensation, it is useful to have a skin-pencil with 
which to mark the patient's skin, before copying the result on 
our chart. 

An important practical point in mapping out areas of amesthesia, 
is to begin within the aniesthetic area, and to work towards the 
normal skin, not in the reverse direction. It ia easier for a patient 
to recognise the moment when he first feels a sensation than for 
him to observe when he (iret loses it. On the other hand, in 
mapping out areas of hyperesthesia or of parcesthesia, we should 
work from normal skin towards the hyper-testhetic area, asking 
the patient to call out es soon as his sensation changes. 

In setting about the examination of the sensory functions, we 
usually begin with that of touch. The patient's eyes being closed, 
we touch him lightly on both sides of the fac« simultaneously 
and observe not only whether he feels the touches, but whether 
they are equally distinct on the two sides. We then touch sym- 
metrical spots on the neck, shoulders, hands, trunk, and lower limbs. 
We next proceed to do the same with hght needle-pricks, then 
with cold and with warm objects. If the patient has an area of 
diminished or altered sensibility, we generally discover it by this 
method. When we find an area of abnormality, we proceed to 
map it out carefully, making separate observations for touch, 
pain, and temperature, and noting whether the areas coincide 
or overlap. 

Besides noting whether a patient feels a stimulus, for instance a 
tactile one, we should also notice whether he localises it accurately. 


This is accomplished by asking him to place his finger on the spot 
where he was touched, for instance, the dorsum of the hand. A 
normal individual can do this accurately to within a fraction of an 
inch. But in certain varieties of anaesthesia, the patient, whilst 
able to tell that he has been touched, makes an error of several 
inches in localisation. This is called " atopognosis." Horsley^ 
has shown that errors in the localisation of cutaneous impressions 
are, in cases of cortical lesions, always in a proximal direction, i.e. 
the patient refers the stimulus to a point higher up the limb. 
Sometimes the patient, when touched on one side of the body, 
feels the sensation at the corresponding spot on the opposite 
side. This is termed " allocheiria," and occurs chiefly in certain 
cases of hysteria. 

When testing pain, we sometimes find that though the patient 
correctly perceives and localises the stimulus, there is an abnormally 
long interval of time, perhaps amounting to several seconds, 
between the stimulus and the patient's perception of pain. This 
is called " delayed sensation," and is met with chiefly in cases of 

When charting areas of very slight cutaneous anaesthesia, it 
is often diflScult, despite the utmost care as regards our stimuli, 
to obtain an exact outline of the area of altered sensibility. Changes 
in the quality of sensations may exist which are undetectable 
even by cotton-wool touches. Nevertheless the patient, if he 
tests his own skin, may be conscious of an abnormality too delicate 
to be discovered by another person on objective examination. 
But if we have a specially intelligent patient and get him to explore 
his anaesthetic area by stroking with his own finger, indicating 
where he perceives a line of transition between normal and abnormal, 
it is often possible for him, by such " auto-exploration," to map 
out the area of altered sensibility with great accuracy.^ 

So much for cutaneous sensations. But there are other forms 
of sensation which are of clinical importance. Joint-sense is tested 
by moving a joint passively into various positions backwards and 

» Brain, 1906, p. 137. 
* Trotter and Da vies, Rev. of Neurol, and Paych., 1907, p. 761. 



forwards, then holding it fixed in a certain position, such aa that 
of ac mi -flexion, and asking the patient to imitate exactly that 
position with the IJmb of the opposite side. It not infrequently 
happens that when a patient is in doubt as to the position of hia 
joint, he begins to make slight voluntary movements of the joint 
before answering. These must not be permitted, since he thereby 
gaina information as to the position of the limb, not from hia joint- 
sense but through an entirely different sense, viz., the kinfesthetic 
sense or sense of active muscular contraction. 

To teat this kinwslkeiic 8«we, we notice whether the patient, when 
raising his limbs, can detect differences in the weights of objects 
of similar size, for example a shilling and a sovereign, either 
placed in hia hand, or hung in a sling over his hand or foot. For 
this purpose we sometimes employ a series of leather or wooden 
balls of equal size, loaded with different weights. Normally, 
according to Weber's law, a healthy individual should detect an 
increase of one-third in the weights of two successive objects. 
Tabes is the disease in which this sense of active muscular con- 
traction is most markedly diminished, and where the joint-sense 
is notably impaired also. The loss of these two senses is probably 
the main factor in the production of tabetic ataxy. 

We purposely avoid using the term " muscular sense," for 
several reasons. Firstly, it is ambiguous, since it has been used to 
include two entirely different senses :^joint-sense and kina«thetic 
sense. Moreover, it might also be confounded with a third sense, 
the antmbilUy of mttschs to pressure with the fingers. Normally 
such pressure, if moderate in degree, is painless ; but in certain 
diseases, as in peripheral neuritis, in the various forma of myositis, 
and in the abdominal muscles superficial to an area of peritonitis, 
the muscles become exquisitely tender to the lightest pressure. 
On the other hand, it is common to find in tabes that severe com- 
pression of the muscles and tendons, for example of the leg 
muscles, and especially of the tendo Achillis, is painless. This 
muscle and tendon analgesia is often present in early stages of 
the disease, 

It is sometimes of value to observe the patient's power of re- 


cognising, without seeing them, the forms of solid objects placed 
in his hand — so-called stereognostic perception. Normally a patient 
should be able to recognise familiar objects such as a key, a coin, 
or a chain. But in some cases the patient, though able to feel 
the presence of some object, cannot describe its form and qualities, 
without seeing it. Such ** astereognosis " may be due to impair- 
ment of sensation either from peripheral disease, from thalamic 
lesions, or from disease in the cortical centres. 

Lastly, there is the vibration-sense (pallsesthesia, or " osseous 

sense ") described originally by Egge:. This 
is tested by means of a low-pitched tuning- 
fork, which is set into vibration and placed 
upon the subcutaneous surface of a bone. 
In normal individuals a characteristic vibratile 
thrill is felt. But in certain diseases involv- 
ing the posterior roots, such as tabes, or in 
transverse lesions of the spinal cord, the 
vibration-sense may be lost in the bones 

Kio.74.-Tabes with loss «o"esponding to the affected roots (Fig. 74). 
of vibration-sense in Loss of this sense may be the earliest form of 

bones of lower limbs, .i • • ^ i • • . i i 

pelvis, lumbar, and auflBsthesia m root-lesions as m tabes, where 
ThT'^n^^wUh^^oss ^^ sometimes precedes cutaneous anaesthesia, 
of vibration-sense are In Brown-Sequard paralysis vibration-sense 

shaded black. , . , 

is lost, together with the temperature sense, 
on the side opposite to that of the muscular paralysis (see 
Figs. 9 and 12). But the vibration-sense is not an exclusive 
property of bones, though bones are most strikingly sensitive ; it 
can be perceived in other tissues, notably in the nails, which are 
closely connected with the periosteum, and even in the connective- 
tissues, though in them less intensely. 

Excessive sensitiveness to normal stimuli is termed hyperces- 
thesia. Such hypcraesthesia is usually accompanied by a degree 
of discomfort or even pain, even though a stimulus be used which 
is ordinarily painless. The term parcesthesia, or perversion of 
sensation, signifies that an ordinary stimulus evokes an unusual 
sensation, as for example a feeling of tingling when the skin is 



touched, or a feeling of acute pain when moderate cold is applied. 
Under the head of parEeathesia) we may also include such pheno- 
mena as multiple sensations (polyasthesia), allocheiria, &c. 

Strictly speakin", diminution of sensation should be designated 
hypo-CBsthesia, and the term anEeathesia should he reserved for total 
loss of sensation. It is usual, however, to speak of "slight," 
" moderate," and " total " anesthesia. When only one form of 
cutaneous antesthesia is referred to, we sometimes find it con- 
venient to talk of tactilf anteslhesia, of analgesia or loss of pain- 
sense, and of therttio-ancesthesia or loss of temperature-sense 
Dissociated an<Fsthesia is where some forms of sensation, such as 
tactile sense, are normal, whilst in the same area others, such 
as pain and temperature -sense, are lost. This occurs especially 
in syringomyelia and in the Brown-S^quard syndrome. 

We speak of hemi-an<Bslhesia where one-half of the body, right 
or left, is affected, and of para-aiuEsthesia where both legs or both 
arms are aflected owing to a lesion of the spinal cord or to a 
symmetrical affection of the posterior roota. We also speak of 
radial, ulnar, peroneal anJEsthesia, Sec, where the sensory loss 
corresponds to the distribution of a single peripheral nerve, 

Hypersesthesia. — Universal hyperieathesia is rare. It is 
chiefly met with in hysteria, but also occurs in other affections, as 
in strychnia -poisoning, where the slightest touch may suffice to 
evoke a violent spasm. Hemi-hypereesthesia is chiefly found in 
neurasthenic and hysterical patients and may be associated with 
other hysterical " stigmata." Thus I remember the case of a 
soldier with traumatic hysteria who had hemi-hyi)enP8thesia, 
accompanied by abnormal widening of the visual field and by 
increased acuity of smell, taste, and hearing, aU on the hyper- 
(esthetic side of the body. 

In the thalamic syndrome, liemi-hypertEsthesia to temperature 
and pain sometimes coexists with hemi-ana«theeia to tactile stimuli 
and with impairment of joint sense, lose of osseous sense and 
astereognosis in the affected limbs. 

Hyperaisthesia in more or less symmetrical root-areas of the 
trunk or limbs, due to irritation of the posterior roots, is not 


uncommon in diseases causing pressure on the spinal cord or its 
meninges, as in caries or tumours of the spine. Here the hyper- 
sesthesia corresponds to the area supplied by the uppermost root 
involved, and is usually associated with anaesthesia and motor 
weakness in the parts below. 

Odd irregular areas of hypersesthesia are amongst the 
conmionest stigmata of hysteria, and do not correspond either to 
root-areas or to the distribution of peripheral nerves. Tender 
areas are particularly conmion over hysterical joints and over 
certain vertebral spines in hysteria, and we frequently notice that 
the lightest touches cause severe pain, whereas, when the patient's 
attention is diverted, deep pressure on the same spot may be 
painless. Pressure on such tender spots may sometimes excite a 
hysterical attack — " hysterogenic " areas— and in other cases may 
restrain or stop an attack — " hysterofrenic " areas. To this 
subject we shall return when discussing the diagnosis of hysteria. 

Next in frequency after hysterical hyperaesthesia are the areas 
of cutaneous hyperaesthesia in tabes. Tactile hyperaesthesia is 
specially common in the areas where lightning pains are felt, and 
like these pains it may be one of the earliest evidences of the 
disease. Thus a patient with incipient tabes, for years before 
he reached the stage of ataxia, was so hyperaesthetic around the 
trunk that it was agony for him to pull his shirt on, or to sponge 
his body when bathing. Tabetic h3q)eraesthesia may occur not 
only on the trunk but also on the limbs, and even on the face. 
Hyperaesthesia is specially frequent round the orbits in cases 
of tabetic ocular palsies. 

Hyperaesthesia in the areas of peripheral nerves occurs in the 
true neuralgias, as in trigeminal neuralgia, where the neuralgic 
area is often exquisitely tender, especially over the foramina of 
exit of the various branches. The patient may be unable to 
wash his face for weeks at a time, since the lightest touches 
induce a paroxysm of neuralgia. Localised hjrperaesthesia some- 
times precedes the eruption of herpes zoster, and may persist for 
weeks or months after the eruption has passed away. Lastly, 
we may mention the hyperaesthesia of the hands and feet in 



multiple neuritis, where there is oft*n preaent a degree of aneesthesia. 
The coexistence of hyperalgesia to light preaaure with ansBstheBia ^ 
tn light touches is very characteristic of alcoholic neuritis. 

FlQ. 75.— Uolvoraal aiutstheslu ia n hyslcritAl patient. SterillMd 
lafsty-pins have been pushed through the skin on both sideg. 
UyatDiical contractare of IcfC baud is ulso preseot. 

Parse sthesia, or perverted sensation, has much the same diag- 
nostic significance as hyperfeathesia. It may also be mentioned 
that when a peripheral cutaneous nerve is in process of recovery 
after an injury, there is often a stage of partesthesia through 
which the skin passes before normal sensation ia restored. 

!ry ^ 


Anaesthesia. — ^Universal anaesthesia of the skin and accessible 
mucous membranes to all forms of stimuli is exceedingly rare, 
occurring only in hysteria. Fig. 75 shows such a case in a girl, in 
whom it was possible to push pins through the skin on both 
sides of the body without causing pain. 

Hemi-anaesthesia always indicates a central affection. In every 
case of hemi-ansesthesia we must determine whether the disease is 
functional or organic, and if organic, at what level in the sensory 
tract the lesion is situated, whether in the cortex, internal capsule, 
or lower down. 

Hysterical hemi-ancesthesia is conma.oner than organic. It varies 
in degree, from total anaesthesia down to the slightest degree of 
comparative blimting of sensation, only discoverable on com- 
parison of the two sides. Not unconma.only it tends towards the 
" segmental " type, and it is frequently accompanied by other 
hysterical stigmata, especially by blunting of the special senses on 
the hemi-anaesthetic side, particularly by concentric contraction 
of the visual field, and by other features which we shall study 
later. We should remember that hysteria sometimes coexists 
with organic disease, thereby compUcating the diagnosis. 

Organic hemi-ancBsthesia may also vary in its degree, from slight 
to severe anaesthesia ; but it is never absolute in degree as in some 
cases of hysteria. It is generally more marked on the limbs 
than on the trunk or face, and more intense at the periphery of 
a limb than at its proximal end. It is never marked off by a 
sharp line running across the limb, as in the " segmental " 
anaesthesia of hysteria, but fades gradually in intensity as we 
pass from the hand to the shoulder. A degree of atopognosis is 
always present in organic hemi-anaesthesia. The special senses 
are unaffected (their paths probably do not traverse the internal 
capsule), with one exception, namely that of vision, in cases where 
the lesion implicates the optic radiations. But here again we get 
a homonymous hemianopia, unlike the hysterical contraction of 
the visual field to which we shall refer later. 

If we find that a hemi-anaesthesia is organic in origin, we have 
then to determine whether the lesion is cortical in situation or 



whether it ia lower, in the internal capsule, optic thalamus, or else- 
where. In cortical hemi-antestheaia the other aigna of cortical 
disease will aid the diagnosis. The presence of monoplegia rather 
than hemiplegia, or the occurrence perhaps of Jacksonian fits, will 
point to a cortical localisation, rememhering that the cortical 
motor areas are also partly sensory. Cortical anteathesia is leaa 
profound than capsular, and ia most distinct at the periphery of 
the affected limh. Indeed, in cortical antesthesia it is the rule for 
the trunk to be little or not at all affected. Marked astereognosia 
and atopogncsis with but slight tactile and motor loss will also 
point to a cortical lesion, probably in the upper parietal region. 

Capsular homi-anBesthesia (which, by the way, is generally the 
result of a lesion not actually in the capsule but in the jwstero- 
external part of the optic thalamus), is never monoplegic in type 
but always affects the entire half of the body, including the trunk, 
Hemi-ansstheaia from a thalamic lesion, as we have seen, is 
associated with paroxysmal pains of intolerable severity in the 
affected limbs and side of the face, and sometimes with hemi- 
hypertesthesia to pain and temperature. The thalamic syndrome 
alao includes hemi-ataxy of the limbs and spontaneous choreiform 
or athetoid movements. The deep reflexes are unaffected, and 
the plantar reflex rcmaina of the normal flexor type, since the 
pyranudal motor path ia intact. Such cases often have a history 
of transient motor hemiplepa at the onset, but this motor weakness 
rapidly disappears and ia succeeded by paroxysmal paina in the 
he mi -anesthetic limbs and face. The intensity of capsular or 
thalamic ana<8theBia is deeper than in cortical caaea, but not so 
markedly intenaified at the periphery of the limbs. It is aaaociated 
with hemianopia if the lesion extend backwards, or with motor 
hemiplegia, moat marked in the leg (but not a monoplegia), if 
the lesion extend forward into the pyramidal motor path. 

We may also have hemi- anesthesia from organic lesions of the 
aenaory path below the level of the optic thalamus ; in fact, at 
any level above the sensory (fUlet) decussation in the medulla. 
Such lesions, although uncommon, can be correctly localised 
by the coexistence of other signs. Thus a unilateral lesion 


in the dorsai aspect of the pans, implicating the trigeminal nerve or 
nucleus, together with the remainder of the sensory fibres belonging 
to the other side of the body, will cause a crossed hemi-anoBsthesiay 
i,e. anaesthesia of the face on the side of the lesion, and of the arm, 
trunk, and leg on the opposite side (Fig. 11, p. 16). A lesion of 
the sensory path in the medulla below the level of the trigeminal 
nerve, must be more widespread laterally to produce a com- 
plete hemi-ansesthesia, since the path for temperature and pain 
is here at some distance from the tactile path (Fig. 10, p. 15). 

Anaesthesia also occurs in certain lesions of the spinal cord. We 
should note, however, that there are many cord diseases in which 
anaesthesia is absent, such as progressive muscular atrophy, 
amyotrophic lateral sclerosis and acute anterior poliomyelitis. 
Disseminated sclerosis is also a disease in which sensory changes are 
frequently absent. But if the spinal cord be destroyed or divided 
at a certain transverse level, whether by trauma or by disease 
such as acute softening, whereby sensory as well as motor paths are 
interrupted, all the sensory impressions ascending in the posterior 
and lateral columns (Figs. 8 and 9, pp. 10 and 12) will be lost 
below the level of the lesion. We then have a para-ancesthesia, the 
upper limit of which corresponds with that of the highest sensory 
root affected. And since in many of these cases there are irritative 
or inflammatory processes affecting the roots immediately above the 
area of destruction, it not unfrequently happens that there is a 
narrow zone of paraesthesia or of hyperaesthesia immediately 
above the anaesthetic area. In cases where the cord is gradually 
compressed by progressive disease in the meninges or vertebrae, 
there is usually a progressive paraplegia with the usual 
alteration of reflexes. Here anaesthesia appears late in the dis- 
ease, being preceded by spontaneous subjective sensations or dys- 
CBsthesicBy after which hyperaesthesia appears, and last of all 
anaesthesia. The anaesthesia of a total transverse lesion implicates 
all forms of sensation, both superficial and deep. 

When a cord lesion is incomplete in its transverse extent, certain 
forms of sensation may escape. Thus unilateral lesions of the cord 
produce Brown-S^quard paralysis. Most conunonly this is the result 



of a stab or buUet-woimd, but it may also be caused by softeningB 
or growths. Or a lesion which was originally more extensive, e.g. 
a hffimorrliage, may clear up so aa to becorae a unilateral one. In 
the typical Brown-Sequard syndrome, as will be seen from Figs. 9 
and 12, there are on the side of the lesion the well-known motor 
and vaso-motor paralyses, together with loss of sensation in the 
joints and muscles, whilst on the opposite side there ia thermo- 
anaathesia, loss of vibration-sense, analgesia and some tactile anses- 
theaia. In thermo-anfesthesia from cord lesions, the areas of 
anaesthesia to cold and to heat are sometimes co-extensive. But 
this is not always so ; sensibility to heat may be abolished without 
loss of sensibility to cold, or vice versd, or the areas of loss to heat 
and to cold may differ widely in extent. If the lesion be above 
the lumbar enlargement, as is generally the case, the motor 
paralysis is of the upper neurone type, with spasticity, increased 
deep reflexes and an extensor type of plantar reflex. If, as some- 
times happens in stab-wounds, the lesion destroys the moat lateral 
region of the cord but does not quite 
reach the middle line, thereby sparing 
the postero -internal column, the deep 
structures on the side of the lesion 
preserve their sensibiUty. In any case, 
on the side of the lesion, a narrow zone 
of antesthesia exists, corresponding to 
the posterior root-fibres cut across at 
the level of the lesion. And above the 
anRSthesia there is a zone of hyper- 
ECfithesia from irritative root-changes. 

Dissociated ancBsthesia, often without 
motor paraplegia, is characteristic of 
disease in the region of the posterior comua of the cord or in 
the substantia gelatinosa of the medulla, as in syringomyelia 
and syringobulbia, where there are analgesia and thermo-anass- 
thesia, with loss of vibration-sense, corresponding to the area 
of spinal cord affected, whilst tactile sensation remains unim- 
paired (see Fig. 76). The patient often burns his fingers accidentally 

Fig. 76.— Syrinffoinyelift, indi- 
cnting area oi tbcrmo-anaBa- 
thesia and analgesia in tlie 
patieat shown in fig. 77. 



without pain, and he may develop painless whitlows — so-calledij 
Morgan's disease. He may also have spontaneous joint disinte 
tions, with fractures and osteophytic or destructive changes in tbl 
ends of the bones. In most cases of syringomyelia there i 
is some atrophy of the anterior cornua ; we should therefore bafl 
on the look-out for a coexisting muscular atrophy of spinal typ^ J 
involving especially the small muscles of the hands. If tlwl 
pyramidal tracts become involved in syringomyelia, a spastasl 

Flo. 77.— Sjtmguuij 

paraplegia b superadded, and sooner or later a degree of Bcolioaia>, 
or even kypho-scoliosis develops {Fig. 77). 

But unilateral cord lesions and syringomyeha are not the only 
diseases which produce dissociated antcsthesia. A small lesion 
such as an area of softening or of new growth, in the potUo-cen^Uar 
angle of the pons at the level of the auditory nerve, will cause 
deafness of the same aide with analgesia and thermo-ana^thesia 
ol the opposite side, tactile sensation being unaffected. If the 
cerebellar peduncle be involved, there will be cerebellar phenomena 
also, such as we have already studied. 

Tabd,ic anesthesia is the commonest of all organic antesthesice. 
In this disease the sensory loss tends to follow fairly closely the 




distribution of the posterior roots affected by the tabetic process. 
Thus it is commoner in the lower limbs than in the upper. Joint- 
sense and vibration-sense usually become impaired earlier than 
cutaneous sensations, whilst analgesia precedes tactile anesthesia. 
In the upper limbs the fingers on the ulnar side of the hand are 
usually affected earlier than the other digits, and there is often 
a strip of analgesia running longitudin- 
ally along the inner side of the whole 
upper Umb, corresponding to the eighth 
cervical and first thoracic roots (Fig. 78). 
In many tabetics the ulnar neive behind 
the elbow loses its normal sensitiveness 
on pressure — Biernacki's sign. And on 
the trunk it is common to find a broad 
zone of analgesia, and sometimes of 
tactile antesthesia as well, the upper 
border of which is at the 

second ribs in front. This zone is often ginlle-teeling (jotted 
incomplete laterally or posteriorly, just 
as the subjective "cuirass" sensation 
may be. Analgesia of the glans penis 
is another early sign of tabes, also loss 
of the normal tenderness of the testicle 
on pressure. Tendinous analgesia, on pinching the tendo AchilUs 
(Ahadie's s*gn), is also present in the majority of tabetic patients. 
But tabetic anesthesia is not always sharply limited to root 
areas, and we should seek for confirmatory evidence of the disease 
in the pupils, deep reflexes, cerebro -spinal fluid, &c. 

Aiuesthesia in peripheral nerve palsies of sensory or mixed 
nerve-trunks, is of course confined to the distribution of the 
affected nerve or nerves. If a cutaneous nerve be paralysed we 
have loss of " epicritic " and " protopathic " cutaneous sensa- 
tions, whilst the .deep sensibility in muscles, bones and tendons 
still preserved (see p. 12). If a mixed nerve-trunk be 
paralysed, muscular paralysis with atrophy is added to anssthesia, 
^ both cutaneous and deep, and the diagnosis, as a rule, presents 

hypencstbeiiB below the 
ouirKS. paMiiiK up between 
llsliniElBpostenorly (croBses ). 
AnalgL'sio HTeos (horizontal 
gbniling) In upper limbs (Cg 
and Tb, roots) Htid in lower 
limbs (L,, L), and S, roots). 



DO difficulties. It most be bone in nund that as a mixed nerve 
lecovera from its paralysis, sensation osually returns before motor 
power and piotopathic sensation before epicdtic. The amesthesta 
following an attack of herpes zoster sometimes lasts for a consider- 
able time after the emption has disappeared. In the anaesthesia 
of multiple neuritis, whether resulting from alcohol, diphtheria, 
diabetes, septic poisoning, or other causes, the disease is generally 


Fio. 79.— Froi 
nenritia, (bowing " (tlor 
" Eock " areas of atneslbes 

Fig. SO.-Fi 
peripberal neuritis, ehowinf; 
"glove" and "stocking" areas 
of cutaneouB paraslbeaia. 

bilateral and symmetrical, affecting bands or feet or both. Sub- 
jective tingling sensations usually precede the aniEsthesia, whicli 
is of the " glove " and " sock " variety, not marked oft sharply 
as in the " segmental " ansathesia of hysteria, but shading of! 
gradually at the upper margin (see Figs. 79 and 80). Most cases 
have also some superadded motor weakness in the form of drop- 
foot and drop-wrist. Lead paralysis difiers from ordinary peri- 
pheral neuritis in being entirely a motor paby. free from sensory 



In the investigation of the various motor palsies, apart from those 
aSecting the cranial nen-e^ which we have already studied, we 
should proceed in a definite order. 

We commence by inspection of the palsied limb or limbs, noting 
the posture of the limb, the presence or absence of local mus- 
cular atrophy or hypertrophy, the existence of pathological swell- 
ings, &c. We then proceed to palpation of the bones and joints, 
following their outlines and testing their range of passive move- 
ment, so as to discover whether the deficiency of active movement 
may not be due to ntechanical causes, such as fractures, disloca- 
tions, ankyloses, adhesions or inflammations of bones or joints, 
and so on. Thus in the c&se of a semi-comatose lady, whom I saw 
within a few hours after a carriage accident, there was apparent 
inability to move the left arm or leg. This might have suggested 
a lesion of the right cerebrum producing hemiplegia, but a pre- 
liminary investigation of the bones showed that the left femur and 
left clavicle were broken. It was therefore unnecessary to diagnose 
an intra-cranial lesion of the pyramidal tract, especially as the 
plantar reflexes were normal on both sides. The result proved 
the correctness of this view. 

We should also observe whether the muscles of the affected 
part are rigid, stiff and spastic, or whether they are loose, relaxed 
and flaccid. 

Lastly, we proceed to investigate the patient's powers of volun- 
tary movement of the affected limb. In doing this, it is 
not enough to tell the patient in general terms, to "move the 
arm," and so on. We should test each joint and each movement 
separately, fixing the proximal part of the hmb and instructing 
I the patient to perform various movements: — flexion, extension,* 


rotation inwards and outwards, &c., separately and distinctly. 
Thus, for example, when we direct a patient to pronate his fore- 
arm, we must fix the humerus and see that he does not abduct 
the shoulder to make up for deficiency in pronation. To 
determine whether a particular muscle is taking part in a move- 
ment or not, sometimes requires very close observation, not 
only by inspection but by palpation of the muscle or of its 
tendon. But, as Beevor has remarked,^ the physician '' must 
avoid the error of assuming that the tightening of a tendon from 
the stretching of a passive muscle is evidence of contraction of 
the muscle." 

Suppose that a particular movement of a limb is deficient, 
we estimate the deficiency in different ways, according to its degree. 
If the weakness ia slight, we detect it by interposing some resist- 
ance, so as to load the muscles. This is accomplished either by 
means of weights, or, in the case of the hand, by making the 
patient squeeze our hand or compress an oval spring-dynamometer, 
or, in the case of the leg, by holding the limb down and making 
him elevate it against resistance. 

If the weakness is more marked, it can be detected without 
loading the muscles. The weight of the distal part of the limb 
may already be too much for the muscles to lift, as for example in 
cases of drop-wrist and drop-foot, due to weakness of the ex- 
tensors of the wrist and dorsiflexors of the foot. But even in 
these, a minimal degree of voluntary contraction may perhaps 
still be present, and can still be detected by placing the limb pas- 
sively in such a posture that its own weight is no longer a factor, 
e,g, by testing the extensors of the wrist with the forearm midway 
between pronation and supination, or testing the movements of 
the elbow by passively abducting the upper arm and getting the 
patient to flex and extend his elbow in a horizontal plane. Or we 
may even observe the limb when it is supported on all sides by 
water, as in a warm bath. In this way we may detect minimal 
movements. And in such cases we watch carefully, not only for 
movement of the joint, but for contraction of the tendons of the 

* Croonian Lectures^ 1904, p. 4. 



muscles concerned. These latter may sometimes be felt to con- 
tract, when they are too feeble to overcome the inertia of the 

By inspection and palpation we also note whether in the affected 
limb the muscles are normal in volume and firmness, whether some 
are enlarged and stronger than asynH^tt/pertTOphy — or whether 
some are diminished in size — atToph;/, so that there is flattening, 
or even hollowing, in place of the normal muscular contour. In 
some cases, an apparent increase in volume is accompanied by 
weakness of the enlarged muscles — so-called ■pseudo-hypertrophy. 

If a muscle is atrophied, \ta electrical reactions, both to 
faradic shocks and to the continuous galvanic current, should be 
investigated. The reactions may be normal, or they may be 
merely quantitatively diminished. Or they may be qualitatively 
altered, as in the " reactions of degeneration " (see later, p. 383). 
Or they may be " mixed." where some fibres of the muscle are 
normal, whilst others intermingled with them are degenerated. 

Reaction of a muscle to direct- percussion is sometimes of value. 
This phenomenon consists in a contraction of the whole bundle 
of muscle-fibres in their entire length. Response to direct 
mechanical excitation often persists when the deep reflexes are 
lost; thus, for example, when the knee-jerk is absent in tabes 
or peripheral neuritis, the quadriceps still responds to direct tapping. 
In most cases of lower motor neurone lesion, this mechanical 
iirUability oj the muscle- fibres is increased but the contraction ifl 
more flickering than in a healthy muscle. In muscular dystrophy, 
the mechanical irritability is lost in the affected muscles. In 
cerUtn patiente, especially on percussing the pectorals or other 
flat muscles of the chest, we may observe a wave of contraction 
dashing outwards suddenly in both directions from the point 
of percussion, longitudinally along the muscular fibres, and imme- 
diately followed by a temporary small muscular swelling at 
the point of percussion. This phenomenon is called myoidema 
it ia common in pulmonary tuberculosis, but occurs also in many 
other wasting conditions not associated v^th muscular paralysis, 
and need not detain us further. 

any ^J 



The term paralysis, when appUed to voluntary muscles, 
signifies loss of the power of voluntary contraction, due to inter- 
ruption, functional or organic, in any part of the motor path, from 
the cerebral cortex down to and including the muscle-fibre. This 
latter part of the definition is necessary so as to exclude such 
cases as ankylosed joints, where movement is impossible from 
mechanical reasons without true paralysis. Strictly speaking, 
paralysis is total loss of voluntary motor power, lesser degrees of 
impairment being called pkresis. But we often employ the 
term paralysis to include partial as well as complete loss of 

The distribution of motor weakness differs according to the 
site of the lesion of the motor path. Thus in a imilateral 
brain lesion, there is usually paraljrsis of one side of the body, 
including the face, trunk, and hmbs. This is termed hemi- 
plegia, A bilateral cerebral lesion produces diplegia or double 
hemiplegia, the limbs on both sides of the body being affected. 
Paralysis of a single limb resulting from a cerebral lesion is 
termed cerebral monoplegia. Spinal or peripheral monoplegia is 
less common. 

Paralysis of the Umbs resulting from a lesion of the spinal cord 
is most commonly bilateral — paraplegia — and usually affects the 
legs alone; but if the lesion be in the cervical region, it affects 
both arms and legs. It must be distinguished from a cerebral 
diplegia. In rare cases both arms may be paralysed from a spinal 
lesion, with Uttle or no affection of the legs ; this is brachial 
paraplegia. A unilateral spinal lesion may also cause a mono- 
plegia, but this is uncommon. The term crossed or alternate 
hemiplegia means that as a result of a single lesion there is 
paralysis of some parts on the right side and of others on the 
left. For example, a lesion in the right side of the pons at the 
level of the facial nerve will cause paralysis of the right side of the 
face and of the left arm and leg. There are, of course, other 
varieties of crossed paralysis. 

When paralysis is due to a lesion of a peripheral nerve, it 
may either be asymmetrical, when the motor weakness is limited 



to one or more nerve-tninka, as in most traumatic nerve-palaiea, 
or more commonly it ia bilateral and symmetrical, as in the various 
forms of toxic neuritis, affecting either the upper or lower or all 
four limba. 

If paralysis be due to primary affection of the muscles 
themselves, as in the myopathies, its distribution ia usually bilateral, 
and it affects all four limbs and sometimes even the face. 

We must remember that it is not uncommon to meet with 
multiple lesions in a single case ; yet, in diagnosis, it should always 
be our endeavour to try to account for all the symptoms by a 
single lesion. 

Suppose, then, that a patient is suffering from motor paralysis, 
(mechanical impediments having been excluded), the ^st ques- 
tion is— Is the paralysis functional or organic? If it is organic, 
we proceed to the further questions — Where is the lesion situated ? 
(anatomical diagnosis), and what is its nature ? (pathological 

Ia the Paralysis Functional or Organic ?— Sometimes the 
distinction between functional and organic motor paralysis ia 
easy ; at other times it is a matter of considerable difficulty, 
cases of early disseminated sclerosis being particularly liable 
to be mistaken for hysteria ; moreover, it is possible to have 
a combination of functional and organic disease in the same 

More detailed consideration of the diagnostic features of 
hysteria will be postponed till a later chaptar (see p. 343), and we 
shall only here refer to some of the main features which enable us 
to decide that a case is organic rather than functional. Firstly, the 
history of the case . often guides us ; for instance, functional 
paralysis frequently follows an emotional shock or a prolonged 
mental strain, whereas traumatism, as in railway accidents, is 
equally liable to cause functional or organic disease. 

There are two classes of signs and symptoms which point 
to functional rather than to organic disease — firstly, the absencs 
of characteristic signs of organic disease, and secondly, the 
presence of certain phenomena peculiar to functional disease. 


Muscular atrophy, while much less frequent in functional than 
in organic palsies, is not pathognomonic of organic disease. 
Thus Fig. 195 (p. 361) shows a case of hysterical monoplegia 
with eictensive muscular atrophy, a rare combination. But 
the electrical reactions of degeneration never occur in functional 
paralysis. Their presence signifies undoubted organic disease, 
somewhere in the spino-muscular neurone. Paralysis of a single 
muscle is pathognomonic of organic disease; it never occurs in 
functional paralysis, which affects whole muscle-groups or, to 
speak more accurately, whole movements. To sum up then, 
the diagnosis between functional and organic paralysis is easy if 
the organic palsy is of the lower motor neurone type. It is 
chiefly when the organic lesion is in the upper or cortico-spinal 
neurone that difficulty is Uable to occur, i.e. in cases where there 
is Uttle or no muscular atrophy, and where the electrical re- 
actions are normal. In such cases the presence or absence of 
other hysterical stigmata is of great value. 

A valuable sign of organic as contrasted with hysterical hemi- 
plegia is Babinski's combined flexion of the hip and trunky a 
phenomenon almost invariably present in organic cases. To eUcit 
this the patient Ues flat on his back on a smooth hard surface, such 
as a table or the floor, with his arms crossed in front of his 
chest and the legs not allowed to touch each other. We then 
ask him to sit up without using his arms. As he does so, the 
organically paralysed lower limb becomes flexed at the hip and the 
heel is raised from the surface. Meanwhile the shoulder on the 
healthy side is carried forwards, as if to counterpoise the contra- 
lateral lower Umb. In hysterical hemiplegia this sign is absent, and 
the hysterically paralysed limb remains unraised. Another useful 
test to distinguish between organic and functional paralysis is the 
phenomenon of Grasset and Gaussd^ which is also confined to 
organic cases. This consists in inabiUty on the part of the organically 
hemiplegic patient to raise hoth lower limbs simultaneously from the 
surface when lying down as before, although he is still able to lift 
either lower limb separately. The reason for this peculiarity is that 

^ Revue neuroloyiquc, 1^5, p. 881. 



in organic hemiplegia the patient, when he tries to lift both lower 
limbe at once, is unable to fix the pelvis. In testing for this sign, 
we must be careful to see that the two legs do not touch each 
other, since the patient often t«nds involuntarily to help up the 
paralysed limb by means of the sound one. Of course, the sign is 
only present in cases of incomplete hemiplegia. Another way of 
showing the same phenomenon is to direct the patient to raise the 
lower limb of the paralysed side and hold it in the air. If we now 
grasp the sound leg and raise it up, the other hmb at once falls 
down again, because the pelvis cannot be steadied by the muscles 
on the paralysed side. On the other hand, if the patient first 
raises the sound leg and we then passively lift the paralysed one, 
the sound limb still remains in the air, the pelvis remaining fixed by 
the non-paralysed muscles of the healthy side. In hysteria there 
is no such difference between the separate and the simultaneous 
raising of the legs. 

In some cases of spastic paraplegia the rigidity of the lower 
limbs is of diagnostic value. Thus when we passively lift one 
lower limb off the bed and find that the other lower limb is 
thereby lifted up as well, we may be practically certain that the 
rigidity and paralysis are orgamc and not functional. 

A careful study of the reflexes is also of the utmost importance. 
The presence of an extensor plantar reflex in a patient beyond 
the age of infancy is pathognomonic of organic disease (see later, 
p. 301). The deep reflexes, whilst they may be e.xaggerated 
both in functional and in organic paralysis, are usuaUy normal 
in functional cases. True ankle -clonus of organic disease is 
generally readily distinguished from the " pseudo-clonus " of 
functional disease. Absence of the deep reflexes may occur in 
organic, never in functional disease. 

Incontinence of the bladder and rectum is not uncommon in 
organic diseases of the spinal cord and brain, but practically never 
occurs in functional paraplegia. 

Where is the Org^anic Lesion ? — Suppose we have come to 

I the conclusion that the patient's motor paralysis is organic in type, 

we have to ask ourselves at what point in the motor path the 


lesion is situated. First, we must decide whether the lesion is in 
the upper (cortico-spinal), or in the lower (nucleo-muscular) motor 
neurone. The distinctive characters of these two types are as 
follows : — 


Upper (cortico-spmal) Neurone. Lower (spino-muscular) Neurone. 
Supra-Nuclear Paralysis. Nuclear and Infira-Nuclear 


1. Diffuse muscle-groups affected, 1. Individual muscles may beaffected. 

never individual muscles. 

2. Spasticity of paralysed muscles. 2. Flaccidity of paralysed muscles. 

3. No muscular atrophy, excej)t from 3. Atrophy of paralysed muscles. 


4. Electrical reactions normal. 4. Reactions of degeneration. 

6. Deep reflexes in paralysed limbs 5. Deep reflexes of paralysed muscles 

present, and usually increased. diminished, nud often absent. 

6. If foot affected, plantar reflex ex- 6. Plaiitiir reflex, if present, is of 
tensor in type. normal flexor type, (unless 

flexors of toes are themselves 


Let us consider some of these points more in detail. Paralysis 
due to an upper neurone lesion never affects an individual muscle, 
but always a diffuse muscular group. The converse, however, is 
not true, and we must remember that even a lower neurone lesion 
may produce a diffuse paralysis, where a series of adjacent nerves 
or nuclei are affected. But if individual muscles are picked 
out by paralysis, the adjoining or intermingled muscles being 
perfectly normal, the cause is certainly a nuclear or infra-nuclear 

Spasticity of the paralysed muscle^ in supra-nuclear lesions 
does not set in immediately after the onset of a sudden lesion, 
but usually develops gradually in the course of from one to 
three months. Thus in a typical supra-nuclear lesion, as for 
example in apoplexy, there is an initial period of flaccidity, 
gradually replaced by the so-called "late rigidity." The degree 
of this spasticity varies in different cases. We estimate it by 
moving the patient's joints passively, and comparing their resistance 
with that of a healthy limb. 

In an upper neurone lesion, the muscles of the paralysed limb, 


in the vast majority of caaea, undergo no appreciable atrophy, 
save perhaps to a very slight degree from disuse. But there 
are occasional exceptions to this rule, as in some cases of 
hemiplegia which are associated with muscular atrophy, chiefly in 
the region of the shoulder or in the intrinsic muscles of the hand. 
Such atrophies are often (but not always) secondary to arthritic 
changes in the joints. But however intense the amyotrophy of 
hemiplegia may be, the electrical reactions of degeneration are 
never present. Degenerative reactions, (commonly referred to as 
"R.D.,") are pathognomonic of a nuclear or infra-nuclear lesion. 
Not that R.D. are necessarily present in every lower neurone 
lesion, for a slight lesion of a nerve-trunk may produce muscular 
palsy without R.D.. and in many nuclear lesions, for example 
in progressive muscular atrophy, the reactions in the affected 
muscles are mixed, 6wing to the fact that degenerated and 
healthy muscle-fibres are intermingled in the same muscle, the 
former giving R.D., the latter being normal in reaction. Again, 
in the motor weakness occurring in the different varieties of 
myopathy, there is simple diminution both to faradism and 
galvanism, but no true R.D., even in the most advanced cases. 
The reflexes in upper and lower neurone lesions will be dealt with 
more fully in a later chapter (p. 299). 

With reference to the differential diagnosis between an upper 
and a lower neurone lesion, it will be observed that no single sign 
of the six we have mentioned is pathognomonic, yet the sum of the 
various points usually enables us without difficulty to settle with 
which of the two neurones we have to deal. Sometimes there ia a 
combined lesion of upper and lower neurones, as in a transverse 
myelitis or a myelomalacia. Here the phenomena at the level of 
the lesion will be of a flaccid, lower neurone type, due to destruc- 
tion of the anterior coniua and anterior roots, whilst below that 
level there is a spastic paraplegia of cortico-spinal type, from 
interruption of the pyramidal tracts. 

Motor Palsies of Upper Neurone Type.— The signs and 
symptoms vary according to the level at which the cortico- 
spinal tract is damaged. The following are the chief sites at 


which a lesion may occur, and the diagnostic signs of each 
(see Fig. 6, p. 7). 

A cortical lesion in the pre-central convolution is often 
localised to a single limb and is more Ukely to produce a mono- 
plegia than a hemiplegia, since only a very eictensive cortical 
lesion would produce a complete hemiplegia, affecting face, arm 
and leg. What we usually find is either a pure monoplegia — crural, 
brachial, or facial, or, if the lesion be somewhat larger, an associ- 
ated monoplegia — brachio-crural, or facio-brachial. Cortical motor 
paralysis is commonly associated with local epileptiform attacks of 
the paralysed Umb, because disease may irritate the cortex in 
addition to paralysing it. The monoplegic Umb frequently shows 
a cortical type of anaesthesia, which, as we have already seen, is 
slight in degree, more marked at the periphery of the limb, and 
often transient in duration. 

A strictly locaUsed subcortical lesion is often indistinguishable 
from a cortical one, save by the absence of irritative epileptiform 
phenomena ; and in many cases the lesion is both cortical and 

A lesion in the motor path at the level of the internal capsule, 
inasmuch as all the pyramidal fibres have by this time converged 
to form a compact strand, produces no longer a monoplegia but a 
complete hemiplegia, affecting face, arm and leg. There are no 
Jacksonian convulsions as in a cortical lesion. If the capsular 
lesion extends backwards from the motor into the sensory tract, or 
into the optic thalamus, there may be a coexistent hemi-ansesthesia, 
but this is not common. A thalamic lesion is sometimes asso- 
ciated with hemi-athetosis of the hemiplegic side; this athetosis 
does not appear immediately after an attack of apoplexy, but 
develops gradually in the course of many weeks. A still more 
extensive lesion, extending backwards along the capsule from the 
motor tract, through the sensory path and into the optic radiations, 
will cause hemiplegia, hemi-ansosthesia and hemianopia. 

A lesion in the cms cerebri is recognised by the coexistence 
of third nerve palsy on one side, with hemiplegia of the opposite 
face, arm and leg, usually most marked in the face. This variety 


of alternate paralysis is tmown as Weber's syndrome {aee Fig. 81). I 
The third nerve palsy is often incomplete. When the lesion , 
extends into the tegmentum and implicates the neighbourhood of 
the red nucleus, it may produce a unilateral tremor or a hemi- 
ataxy of the hemiplegic aide, combined, as before, with a third 
nerve affection on the side of the brain lesion ; this combination 

Kio. 81.— Iicaion of t,ft cms cerebri—" \V('bi:r"s syndrome." Patient is 
looking upwanla and attempting to i^how the t«eth on both sides. 
There in dilatatioti of the lefl pufiil and paraljaia of the k/l superior 
reel us, tt^ether with beiujplcf^ia of tlie riyAC face, arm and leg. 

is known as BenediJcts syndrome. If the lesion extends outwards 
BO as to implicate the optic tract as it winds round the outer side 
of the cms, there may be superadded a hemianopia. 

As we come downwards along the pyramidal tract into the 
pons and medulla, the type of hemiplegia changes ; there is no 
longer third nerve palsy, but on reaching the level of the facial 
nerve, another variety of alternate hemiplegia appears. This 
consists of facial palsy, peripheral in type, on the aide of the lesion, 
tf^ther with hemiplegia of the arm and leg on the opposite side, 
the so-called Millard-GubleT syndrome. Other cranial nerves on the 
I side of the pontine or bulbar lesion, for example, the trigemitial, 


the sixth, or the hypoglossal, roay be affected together with 
the pjnramidal tract, and, as in the Millard-Gubler syndrome, 
may co-exist with hemiplegia of the opposite arm and leg, but 
such cases are rare. As they descend through the medulla the 
pjnramidal tracts of opposite sides converge and eventually lie 
so close together that at this level a strictly unilateral lesion 
seldom occurs, there being usually damage to both pyramidal 
tracts aifecting the limbs of both sides, though perhaps in unequal 
degree. And together with this, there are " bulbar " symptoms 
— disorders of articulation, phonation, or deglutition, from impli- 
cation of the tenth, eleventh, and twelfth cranial nerves or nuclei. 

The diagnosis of motor paralysis due to lesions of the pyramidal 
tract within the cord depends on the level of the lesion. The 
two pjnramidal tracts decussate at the lower end of the medulla 
oblongata, so that a unilateral lesion of the spinal cord pro- 
duces a homolateral instead of a contralateral motor paralysis. 
If the lesion be in the cervical region, the arm and leg on the 
corresponding side will be affected; but if it be situated 
below the cervical enlargement, the leg on the side of the lesion 
suffers alone. A primary unilateral lesion of the cord generally 
interrupts not only motor but sensory paths, and produces 
the well-known Brown-Sequard paralysis, to which reference has 
already been made. 

Bilateral motor paralysis of upper neurone type is due to bi- 
lateral lesions, which may be situated either in the brain or in the 
spinal cord. When both pjnramidal tracts are affected within the 
brain (and the commonest cause is a double focus of softening, in 
the posterior part of the lenticular nucleus, though less commonly 
the lesions are cortical or subcortical) a double hemiplegia is 
the result. In these cases of double-hemiplegia or diplegia, there 
are, besides the signs of hemiplegia on both sides (frequently 
unequal in degree), what are known as " pseudo-bulbar " pheno- 
mena. In pseudo-bulbar paralysis, the symptoms of which we 
have already studied (p. 105), it is uncommon for the two attacks 
of hemiplegia to occur simultaneously on the two sides ; they more 
usually occur successively, and it is only after the hemiplegia has 

become bilateral that the pseudo-bulbar symptoms appear. 
patients are generally excessively emotional, tending on i 
provocation to laugh or. more frequently, to weep with a peculiar 
" spastic " wail, and an unnatural slowness oE oxpressional 

Bilateral pyramidal lesions within the spinal eord produce para- I 
plegia, affecting all four limbs if the lesion be above the cervical I 
enlargement, but affecting the lower Umbs alone if the lesion be | 
below the cervical region ; it is commonly of the ordinary I 
spastic type, with increased deep reflexes. If the sensory 
tracts be interrupted by the same lesion as that which has affected 
the motor tracts, we have superadded an ansDsthesia whose upi>cr 
limit corresponds to that of the highest affected segment. 
Such cases of combined sensory and motor paralysis usually have 
loss of control of the sphincters. If the cord lesion Ik aulTiciently 
extensive to implicate the anterior cornua, there will be muscular 
atrophy, localised to the segment affect«d, i.e. at the upper 
boundary of the spastic paraple^^ia. is important to 
remembpr that if the lesion of the cord be one which completely 
divides it {e.g. a stab or bullet-wound), so that there is no coii- 
oectioTi between the cord-segments above and below the lesion, 
the paraplegia is then flaccid in tvpe and the deep reflexes are I 
absent in the paralysed hmbs. The plantar reflexes, however, J 
persist and are of the extensor type, be the lesion complete or | 

The <iifferentifll diagnosis between tumours arising within the 1 
spinal cord and thoee growing from without, is sometimes I 
difficult. In extra- medullary tumours, arising from the | 
nerve-roots or meninges on the posterior aspect of the cord, 
root-pains, unilateral or bilateral, usually precede the signs of 
transverse cord lesion, viz., paraplegia with affection of sensa- 
tion, increased deep reflexes, Ac. But if the extra-meduUarjr I 
growth 8tart« in front of the cord, root-pains are absent or lat«. 
If the anterior roots be involved, muscular atrophy of inot dis* 
tribution is a valuable focal sign. Spontaneous reflex spasmi 
of the lower Umfaa are commoner in extra-medullary than in ' 


intra-medullary growths. An extra-medullary tumour situated 
laterally sometimes compresses the cord so as to produce an 
incomplete Brown-S(5quard syndrome. Thus in one case of my 
own, where an endothelioma was removed from the first thoracic 
root on the right side, the patient had asymmetrical spastic 
paraplegia, more marked in the right leg, together with impair- 
ment of thermal and pain sense in the left leg and left side of the 

The tendency is to localise a spinal tumour below its actual 
level. Sometimes valuable indications are provided by studying 
the vibration sense of the vertebral spines, this sensibility often 
being lost below the level of the growth. 

Sometimes the lesion is not horizontal, but higher on one side 
than the other, and then the upper limit of the anaesthesia will be 
correspondingly unjBven on the two sides, and the distribution of 
muscular atrophy from anterior cornual destruction correspond- 
ingly asymmetrical. 

We also meet with cases of bilateral spastic paraplegia without 
any affection of sensation. Such cases may be examples of 
slowly-progressive primary lateral sclerosis, a rare disease, or what 
is more usual, of amyotrophic lateral sclerosis, where the signs of 
a progressive muscular atrophy are superadded to rigidity of the 
lower limbs with increased deep reflexes. A pure motor paraplegia 
is more frequently due to disseminated sclerosis, to an imper- 
fectly recovered transverse myelitis, or to some other vascular 
lesion, as thrombosis or haemorrhage, in which the sensory func- 
tions have subsequently become restored, the motor tracts re- 
maining permanently sclerosed. The history of the case is 
sufficient to distinguish these diseases. 

Sjnringomyelia, when it affects the pjnramidal tracts, may also 
produce a spastic type of paraplegia ; but it is readily recognised 
by the accompanjdng characteristic dissociated anaesthesia, to 
which we have already referred (p. 191), and frequently by the 
coexistence of atrophic changes in the bones, joints, and muscles, 
muscular atrophy occurring when the anterior cornua are implicated 
in the gliomatous process. 



Motor Palsies of Lower Neurone Type.— Here, as in upper 
neurone leaiona, the signs and symptoms differ according to the 
level at which the spi no-muscular neurone is diseased- The moat 
important diagnostic fact, for localising purposes, is the presence 
or absence of sensory phenomena. If, in a lower neurone motor 
paby, sensory changes are present, we have to do with a lesion 
of a mixed nerve, that is, of a nerve containing sensory as well 
as motor fibres. If, on the other hand, sensory changes are absent 
throughout the course of the disease, the spi no-muscular neurone 
is probably affected, either before it is joined by the sensory fibres 
(i.e. the lesion la in the anterior cornu or anterior nei-ve-root), or 
after it has parted company with them {i.e. the lesion is in a 
purely motor nerve-branch or in the muscle itself). 

A lesion of the aiUerior ctmtu within the cord (as of its homo- 
logue in the motor nuclei of the bulb) is unassociated with any 
sensory paralysis, and therefore produces a pure motor palsy of 
the corresponding muscle fibres. A lesion of the anterior nerve-root, 
emerging from the anterior cornu, produces identical signs, and is 
often indistinguishable from an intra-spinal nuclear lesion. In 
nuclear or anterior-root lesions, therefore, we find pure motor palsy, 
of lower neurone type, unasaooiated with any sensory change. The 
commonest examples of such lesions are acute anterior poUo-myeUtis 
(infantile paralysis of spinal typo), chronic anterior polio -myelitis 
(progressive muscular atrophy), and certain types of lead paralysis. 
^L Landry's paralysis is a pure motor paralysis of the whole spino- 
us muscular neurone, to wliich we shall refer presently. A nuclear or 
^H anterior-root lesion is further characterised by the " root " dia- 
^B tribution of the motor paralysis, so that in this respect it differs 
^ft irom the paralysis due to a lesion of a peripheral nerve (see Tables 



of Root Distribution, p. 31). Lesions of peripheral mixed n 
are always associated, at the onset at least, with sensory changes. 
In the case of lesions of peripheral purely motor ner\'e8 {e.g. the 
nerve of Bell to the serratus magnns), the distribution q( the 
motor palsy b totally unlike that of a nuclear or anterior root 

To distinguish between a nuclear and an anterior root lea 


ia sometimes difficult, and nuty in some instances be impoasifaj 
The coexistence of spastic phenomena corresponding to lower p 
of the cord points to an intra-spinal lesion, and indicates a < 
existing lesion of the adjacent pyramidal tract. Total escape \ 
the pyramidal tract, on the other hand, would suggest an ante 
root lesion, though not necessarily so, since acute anterior j 
myelitis does not affect the pyramidal tract. Another point whi 
may sometimes help us is the subsequent course of the diaeaBaS 


if the paralysed miiaclea recover, this is in favour of an extra- 
medullary anterior root lesion rather than an affection of the 
anterior cornu, inasmuch aa regeneration of nerve-fibres only oceurs 
in extra-spinal lesions, an intra-spinal lesion of the grey matter 
heing irreparable. 

A pure anterior cornual lesion, with its absence of cutaneous 
aniosthesia, can only be confounded with a lesion either in a purely 
motor nerve, or with one in the rauacle-fibres themselves. The 
history of the onset of the disease is of great importance, so also 

is the exact distribution of the muscular paralysis. The two chief 
diseases limited to the anterior coniua are infantile paralysis and 
progressive muscular atrophy. Acute imlerwr polto-myelitu or in- 
fantile spinal paralysis has a sudden onset, generally febrile. 
A lai^e number of muscles, sometimes in all four limbs, may be 
paralysed at the beginning. But in a week or so most of the 
paralysis clears up, leaving a residuum, almost always unilateral, of 
paralysed muscles which undergo rapid wasting. There is no exag- 
geration of tendon reflexes below the level of the lesion, since 
the pyramidal tract is unaffected. Figs. 82, 83, and S4 are examplem 
of cases of old infantile paralysis, showing the extreme degree of i 


wtnfkj vUch wiki, aad if At dNB*« aeema in duUbood. aa 
H tooat often tkecaae, tfaembwqDnft rait of ^rowtk in tlie Kadb. 
Ciromie tadenar fobhwufeUtit, or pt ugitaMt e »™»l»r atinphy, 
kM • f*^— '. nwfioai tmmA. It ocean abiMt alwmn m adults 
■ad. thoa^ b^gbuuag waHabaaMj, gHiwwMy becoaxa bOateraL 
It aMflOf ■bowa HmU fint in the aaall intitMc muscles 
of the haada (Vif. 85) ; idotp rarvlj h bq^ in the sboolder 

no. 84.— CM lofuitile paralvais (acnte anterior pollo-myeliUB). 
Paraljoln And atropbj of all the mnsclcs below the elbow, 
witli cictTpliiiD uf supiuutor longuE. 

iiiiiHclut. In this disease we observe fibrillary worm-like tremors 
ill the wasting muscles, whoae electrical reactions are a mixture of 
R.D. with hcHlthy reactions. This ia because here and thcro in 
bh« (liscaacil area a healthy anterior comusl cell survives, together 
with its corresponding healthy muscle- fibre. If the adjacent 
[lyraiiiidal tracts be sclerosed, we have amyotrophic lateral sclerosis, 
in which the deep refiesea are exaggerated and the plantar re- 
flexes extensor in type. 


There is a rare infantile variety of progressive muscular 
atrophy — Werdnig- Hoffmann type— due to degeneration of the 
anterior corrnia. The disease begins in infancy, often during the 
firet few months after birth. The muscles of the lower limbs 
are attacked first, producing weakness and wasting, though the 
atrophy may bo masked by subcutaneous fat. The knee-jerks 
disappear and the atrophied muscles lose their electrical excitability. 

Fio. HH.—Vtogi 

The disease gradually spreads upwards to the medulla and is fatal, 
with bulbar symptoms, in from one to six years. 

There is another peculiar form of muscular atrophy which is 
hereditary and runs in families, known from its distribution as 
Tooth's " -peroneal " tyjje, or as the progressive neuritio amyotrophy of 
Charcot and Marie. It conies on in childhood, commencing in the 
distal muscles of the limbs, more often the lower limbs and the 
peroneal muscles, and gradually producing weakness with 
tractiires. Talipes equino-varus appears, for which tenotomy i 

II 1 M<tt»^l».^lW[iiil]ikJtt»Ii^l 

> m a, t-tk^Ammm b f^ (S. Idpi 4« art 


^-..(•Uarie r..Jh, 

mu^ ■■-"-■ .- . . L ■ •■ _ r _ -■ i . ■ 
ibot uui clav-liaxrfi in youog pt-ople ai¥ ^Ituoat patfaof 
The dueMe hardly ever extends to the muacka of Uie 
or sbouidera. Tbe facial and trunk muacles aho eacap 
uttereating to note that when alt the mu9cl«« below the 1 
panljned, the patient may still be able to walk alone. th< 
Uw gait '» high-stepping from drop-foot. This was so in both \ 



patients here figured. The deep reflexes are lost in the atrophied 
muscles, Thua in the little boy (Fig. 85) the ankle-jerks were 
lost, whilst the knee-jerks remained brisk, since the thigh muscles 
were unafiected ; in the girl {Fig. 88) the knee-jerks and ankle- 
jerks were both lost. Pathologically 
the disease is associated with atrophy 
of the anterior corniial cells, whilst 
the anterior nerve-roots are saiil to be 
healthy.' But there is marked de- 
generation in the intru-niuacular nerve- 
ftbree of the affected musciea. There 
also a curious degeneration in the 
posterior columns, closely resembling 
that of tabe^ dorsalis. 

A lesion of a spinal nerve after 
the union of its anterior with its 
posterior root, but above the point 
where it divides into branches to form 
lexuses or individual nerves, is charac- 
terLied by a combination oE motor and 
sensory paralysis, the distribution of 
which is not according to peripheral 
nerves, but according to root areas, 
motor and sensory {see Tables of 
Muscular Localisation, p. 31, also Fig. 
18, p. 32). Tims, for example, Fig. m 
is the photograph of a sailor who 
received a violent blow on the right 
side of his neck from an iron winch. 
This produced paralysis of the deltoid, 

supra- and infra -spinatus, biceps, brachialis anticua, and supina- 
tores longuB and brevis, together with an area of cutaneous 
anaasthesia along the outer side of the whole upper limb, from 
the shoulder to the hand. All this would be difhcult of expli 
tion on the theory of multiple injuries to the numerous peripheral 
■ U^jerine nail Amiiuiil-Delille, Hevut neuroliyique, ttiOil. p. 1 

Hi. 83. — Peroneal lype cif 
muscular atrophy (Cliunxit- 
Maric - Tooth). SbowinK 
ntropliy ot intriiinlc inuscleH 
of bands. 


iiervea which supply these various parts. But the motor distrij 
bution is that of the fifth cervical root, whilst the aneestheaia <] 
the hand corresponds to the fifth and a small part of the hxI 

Fm. 89 Case oS rupture of Cg root in a sailor aged 29. There ale 

atropbjand {Miralysis of deltoid, supra, and infra-Bpiuatas, bic^. 
braoiiiulis anricuB, and giipinatoreH loDgus and bruvis, together witb 
anvatbuHia along the outer side of the limb, from tbe neck to the 
thumb and index (in tbe area itidiunted by black line]. The Ugure 
Bbowa the alropby of the deltoid with downward displacement of 
Ihu limb at tbe sboulder- joint. 

root, and as a matter of fact this lesion was subsequently verified!-! 
by operation. 

Lesions of peripheral mixed nerves, when complete, are usualljrl 
easy of diagnosis, inasmuch as there are paralysis and atrophy oil 
all the muscles supplied by the particular nerve, together withJ 
antesthesia in the area of its cutaneous distribution. It ia un-l 



□eceSBary to diacuaa the signs of paralysis of all the various 
mixed nerves. The question is one of anatomy. Let us 
select one or two illustrative examples. Ulnar paralysis afiects 
certain muscles of the hand and forearm, of which the moat 

Kigs. llOnmi !il. -Ulnar |ur 
internal tonrjyle of lUe 

important diagnostically are the interossei and the two ulnar 
luoihricales. Owing to paralysis of the interossei, extension of the 
interphalangeal joints is impaired, especially in the two ulnar 
fingers whose lumbricales are also afiected. Ansesthesia of one and 
a half fingers and of the corresponding part of the hand in also 
present (see Figs. 90 and 91, which are taken from a case where 
the nerve was out by the bursting of a soda-water bottle). In c 
standing cases, the unopposetl common extensor of the I 


MMki^uii ttmtngtmn aad pcaibm a daw-kuid. t&is far the nine 

r^awjQ b^ine tuost tvideai in tlie two olna; filers. Tbe hvpo- 

thenar eminence also becomes flattened and the palm hollow 
«i that the flexor tendons become visible beneath the skin. 
Kigs. 9i and 1'3 are from a case of division of the sciatic nei 


'219 , 

from a buUet-wouiiil in che thigh in a young soldier. It shows how 
at! the muscles below the knee are atrophied and paralysed, the 
hamstring muscles having escaped, since the nerve was divided 
below the level of the hamstring branches. Besides the muscular 
atrophy with the usual drop-foot, we have ansesthesia in the 
areas of the peroneal, musculo -cutaneous, anterior tibial, short 
saphenous and both plantar nerves. 

As a mixed nerve recovers, sensation returns more rapidly 

KiG. 04.— ParetyaiB of serrslTis mDgnuB on rjglit side. The polieiit Is 
lidiiing liolli urms horiiontally foiwards. T be lower flbrea of the 
trapviiiis are also panilfBed. 

than motor power, and protopathic sensation earlier than epicritic. 

We must therefore be prepared to find that in a long-standing case 

the sensory loss is less complete than in a recent one, or it may 

happen that sensation is quite restored when motor power has not , 

yet returned. This rule, however, is by no means invariable. 

As an example of paralysis of a pure motor nerve, we may 

select the posterior thoracic, or nerve of Bell, which supplies the 

aerratUB magnus. Fig. 94 is from such a case, and it shows I 

characteristic " winging " of the scapula when the patient 1 

his arms horizontally forwards. 



When a pure motor paralysis of lower motor neurone typ 
recovers, this indicates that it must have been of extra-meduUnrj 
origin, Bince regeneration of nerve-fibres does not occur within thi 
central nervous system. 

Besides such lesions of individual nerve -trunks, we have ala 
to bear in mind the so-called mtiUiple or feriphend neurilis — a verj 
common disease, affecting the mixed nerves aynunetrically aoM 
both sides, sometimes in the arms, sometimes in the legs, some-rV 
times in all four limbs, and even also other nerves such as those ( 

Via. !>;..— Alcohulic heuriUs wilh drop-wrisL 

the soft palate, diaphragm, and so on. Such neuritis, when a&ectinj 
mixed nerves, is easy of diagnosis. The distribution of the sensoryl 
and motor abnormalities is characteristic. The patient has subjec- 
tive tinghng feelings in the hands and feet, and on examination wefl 
find diminution of sensation to light touches in the " stocking " 
and " glove " areas of the limbs, often with extreme hypetsBsthesia J 
of the soles to pressure. Moreover, the muscles of the limbs arc 
exquisitely tender on being grasped. The motor paralysb, of thi 
lower motor neurone type, specially affects the anterior tibial aiu 
peroneal groups in the legs, producing drop-foot, and the extenaon j 
of the wrists and fingers, producing drop-wrist (Fig, OS).,! 
The coninionest causes of multiple neuritis are chronic poisoniatf 


by alcohol, arsenic {specially associated with cutaneous eruptiono^ J 
the diphtheritic poison, beri-beri (associated with ccdema of the 
Umba and of certain serous cavities), diabetes, aepticiemia, and 
other poisons. Lead neuritis is a peculiar form which practically 
never attacks the sensory fibres. The upper limbs are generally 
affected, the muscles attacked being the extensors of the fingers 
and wrists, producing wrist-drop. The long extensors of the 
thumb become paralysed later, the extensor oasis nieta carpi 
pollicifl remaining unaffected. The supinator iongus usually 
escapes, so that the disease contrasts with musculo -spiral 
paralysis, with which it might be confused on superficial examina- 
tion. The blue line on the gums and other signs of plumbium 
also aid us in the diagnosis. 

Sometimes the lower motor neurones are paralysed in their 
entire extent, from anterior cornu to periphery, the disease com- 
mencing in the lowest spinal roots and spreading upwards towards 
the bulbar motor neurones. This affection, known as acute aacend- 
ing paralysis, or Landri/'s paralysis, might be confounded with an 
ordinary peripheral neuritis wore it not for the absence of sensory 
changes. The para]3rsis, commencing in the legs, and spreading up 
the trunk to the arms, is of the usual flaccid type with loss of 
reflexes. There is no time for muscular atrophy or reactions of 
degeneration to develop, and if the respiratory muscles become 
paralysed the patient dies, generally within a week from the onset. 
The sphincters remain unaffected. Various organisms have been 
cultivated from the cerebro-spinal fluid and from the peri-dural 
tissues in such cases. The spleen is frequently enlarged, as in 
certain other infective disorders. 

Before leaving the subject of nerve lesions of lower motor 
neurone type, we must refer to lesions of the crturfd equina, 
the mass of nerve-roots, lumbar, sacral and coccygeal, contained 
within the lowest part of the spinal theca. According to the 
roots affected, anterior or posterior, we have motor and sensory 
symptoms, both distributed in "root" fashion, not according to 
peripheral nerves. The clinical picture varies according to the 
level of the lesion. When the whole cauda is involved, we I 


paralysis (of lower motor neurone type) of all the muscles of the 
lower limbs, together with anaesthesia below the folds of the groins 
in front, including the genitals, and below the upper part of the 
buttocks behind, together with loss of control of the bladder and 
rectum. If the first, second, and third lumbar roots escape, the 
anaesthesia is less extensive (Fig. 18, p. 32), sparing the upper 
part of the thighs. If the third lumbar roots escape, thereby 
sparing the quadriceps, the motor paralysis is correspondingly less, 
and the knee-jerks survive, though there is still paralysis of the 
glutei and hamstrings and of all the muscles below the knees, with 
loss of ankle-jerks and paralysis of bladder and rectum as before. 
If the lesion be lower still, the area of paralysis, motor and 
sensory, is correspondingly diminished. Below the second sacral 
roots there is no paralysis of the lower limbs, but there is a char- 
acteristic *' saddle-shaped " area of anaesthesia on the buttocks, 
perineum, scrotum and penis, with a small strip running from 
the perineum down the postero-internal aspect of the thighs. 
Here also the bladder and rectum are imcontrolled, and the anal 
reflexes are lost, but there is no motor weakness of the lower 
limbs, and all the reflexes of the lower limbs are normal. And so 
on, the area of paralysis diminishing as we descend, until when 
there is a lesion of the fourth and fifth sacral and the coccygeal 
roots, the only signs are paralysis of the levator ani, with 
anaesthesia of the anus and perineum, the sphincter ani remaining 

The chief difficulty in the diagnosis of lesions in this region 
is to distinguish between a lesion of the cauda and one of the 
contis meduUaris — that part of the spinal cord which extends 
below the third sacral segment. In both cases the motor power 
of the legs is unaffected, and there is anaesthesia of the " saddle " 
area, with loss of sexual power and of control of bladder and rectum. 
Cauda lesions, however, are more often gradual in onset than conus 
affections, and are usually accompanied by intense sacral " root " 
pains, and the ultimate anaesthesia of a cauda affection is fre- 
quently preceded by cutaneous hyperaesthesia. A bed-sore is 
»oner in a medullary lesion than in a cauda lesion. Finally 



any " dissociation " of anfestheaia, such as analgesia or therm- 
anfesthesia without tactile ansesthesia, points to a medullary lesion. 
It both Cauda and conus are included in the same disease, the 
Cauda symptoms mask the others. 

Let us now turn to motor palsies resulting from affections within 
the muscles themselves. Some of these are really the effect of 
diseases of the intra-musciilar fibrous tissue. This is the case in 
acute myositis where there is an interstitial inflammation withiu 
the muscle, often with a good deal of eilusion, so that any 
sudden movement causes acute pain ; tenderness on pressure 
is also present. Lumbago an<l the famihar " stiff neck " are 
common varieties, and their diagnosis usually presents no diffi- 
Ity. Trichiniasis is a disease in which the muscle-fibrea are 
invaded by the trichina spiralis worm. Here there is a history of 
the patient havuig eaten some meat, usually pork, which turns out 
f o have been trichinosed. Within a day or two he develops gastro- 
intestmal symptoms and becomes feverish, with widespread 
muscular pains, rigidity, and stiffness, especially in the muscles 
of the limbs. In severe cases the pharynx, tongue, diaphragm, 
■and even the laryngeal muscles may become affected. Together 
with this, there is a pecuhar oxlcma of the face and eyelids, spread- 
ing thence to the limbs, and sometimes to the serous cavities. The 
blood contains a marked excess of eosinophiie leucocytes, and the 
temperature is raised. The symptoms last usually four or five 

Sometimes, when a patient has had bis forearm fractured and 
put up in splints, the bandages may be applied too tightly and 
the blood-supply of the muscles is interfered with by the pressure. 
As a result there are swelling and pain in the hand, and unless 
the bandage.s be lotisened, ischtemic paralsrsis (v. Volkmtnn) may 
develop. This is a variety of myositis. At first the muscles ol 
the forearm swell from tEiematous effusion ; later they become 
Jlhrunken, hard, and contractured by interstitial fibrous tissue, 
ihe fingers being in a flexed position (see Fig. 96). Active move- 
■aents are lost, and even passive movements are painful. The 
pardness and stiU'ness of the muscles and the absence of R.D., 



together with the normal condition of sensation, aufiice, with tlM 
history of the caae, to distinguish it from a ueuritia. 

But we also meet with cases of muscular weakness and atroph] 
localised in certain muscles, where the motor nerves and nuclei 
are healthy, but the muscle fibres themselves are primarily diseased. 
This group of diseases is called muscular dystrophy, idiopathic 
muscular atrophy, or n 

Clinically we recognise t' 
casea in which i 

, or myopathy. ^^^H 

ecognise two main classes of myopathy : — (1) ^('(■l^^^l 
all the affected muscles waste from the outBet-j^^^f 


. which certain muscles uiiderso a false enlarsre- ' 

and (2) those iii which certain muscles undergo a false enlarge- 
ment before they ultimately become smaller — so-called pseudo- 
hypertrophic paralysis. But there is really no essential diSetent 
between these two varieties, Even in pseud o-hypertrophi( 
certain muscles undergo atrophy from the beginning, whilst 
the others atrophy and enlargement may be combined in vai 

Muscular dy3tr<iphy is a congenital disease. Not that 
symptoms appear at birth, for the child is usually bom apparently 
healthy. The age of onset of noticeable symptoms varies from 
two to sixty years, though most cases occur in childhood or youth. 

The chief distinguishing features between myopathic atrophies 
and nmscular atrophies of nuclear origin, spinal or bulbar, are aa 
follows ; — The age of onset is earlier, as a ride, in myopathy tl 


lat i^^l 


,t t^^l 






^H iu progressive niusculur atrophy or 

^H pathy often runs in families ; progtua 

^1 The muscles affected are different i 

^H sive muscular atrophy and amyotrop 

^ most commonly begins in the am 

tacking muscle-groups corresponding 

myopathy the larger muscles are 

small muscles of the hands escape. 

tends to spread up to the hulbar 

paralysis. Myopathy does not ca 

1 that in one type of myopathy — the 

is affected, and that in pseudo-hji 

are sometimes enlarged ; but myop 

the tongue, and never the larj-ux 

diseased muscles may be enlarged, 

whilst others are wasted. En- 

in nuclear disease. When a myo- 
pathic muscle voluntarily con- 
tracts, we may sometimes notice 
a ball - shaped swelling in the 
middle of the muscle, especially 
in the deltoid or quadriceps, which 
is due to the fact that the dys- 
trophy is most marked at the 
■ extremities of the muscles. Fib- 
rillary tremors, which are so 
1 common in progressive muscular 
atrophy, are rare in myopathy. 
Lastly, in myopathy, unlike ,, 
amyotrophic lateral sclerosis, the 

^1 deep reflexes are never increased. 

^Kln fact, in myopathy the knee-jerk 

^Bof the quadiiceps. 

^H The pseudo-hypertrophic variety 

^■in childhood. It is the most rapidly 


amyotrophic sclerosis. Myo- 
sive muscular atrophy does not 
n the two cases. In progres- 
hie lateral sclerosis, the wasting 
ill niiiacles of the hands, at- 

to segments of the cord. In 
generally aSected. whilst the 

Amyotrophic lateral sclerosis 
lucJei. and to produce bulbar 
ise bulbar palsy. It is true 

Landouzy-Dejerine — the face 

ertropbic cases the masseters 

thic palsy hardly ever afEects 

In myopathy anme of the 

[ia.thy. Fruiit vic'« , sluiwiiij; tu. 
l;irgtuii:nt. uf oalvus iiml 1 liiyh-s. 

may disappear from wasting 

of myopathy generally begins 
progressive form of myopathy, 




and in most caaes the jiatieiit dies before attuiiiing adult age. 

are affected four or five times as often as girls. Tlie cases tend to 

run in families, and to select patients of the same aex in each family. 
Thus we often find several brothers affected whilst the aistera escape. 

But though the females generally escape themselves, they tend to 
transmit the disease to their male offspring, so that antecedent 
cases in a family are always on the mother's side. Children of 
the same woman by different husbands may sufler from the 


disease. It is therefore unwise to nmrry a widow, however young 
and charming, who has a pseudo-hypertrophic child. The aymptoma 
of pseudo-hypertrophic paralj-sis are entirely motor. The first 
symptom which ia noticed is that tlie child falls easily, gets up with 
difficulty, and cannot nm or jump like other children. This weak- 
ness gradually increases until in a few years the patient becomes 
unable to stand or even to ait up ia bed. The arms become weak 
later than the legs. Figs. 97 to lOO show two such patieuts. In 
them we notice the characteristic " pot-belly " and the lordosis when 

L'W, HllOwillg 

standing. The gait is wide-based and waddling, somewhat like that 
of the comic-opera sailor, and there ia often a high-atepping action 
to clear the toes from the ground. But most characteristic of all 
is the way in which the patient rises from the fioor when placed 
flat on his back. He first rolls round and gets on to his hands and 
knees. Then, keeping his feet wide apart, he drags his hands along 
the floor towards his feet until the knees are straightened. Then 
he shifts his hand.'j up to his knees and proceeds to extend the hip- 
joints by climbing up his thighs. When he has reached the upright 
position, he leans his trunk backwards to keep the hips extended. 



II pseudo-liypurtropliic myopathy certain muscles are specui 
enlarged and hard— e.g. the calf nmacles and the infra-spiiu 
Other muscles may also Iwcome enlarged — e.(j. the quadric« 
glutei, deltoid, biceps, and triceps. On the other hand, eert 


juvenile tjpe. 

other muscles waste from the first, without any initial stage of 
enlargement. Thus the latissimus dorsi, teres major, and lower 
fibres of the pectoralis major are often absent, so tliat the folds of 
the axillai are poorly marked, and if we lift up the child by the 
axillffi he slips through our grasp. 

The enlarged muscles ultimately shrink and become smaller. 



Ab the calf muscles shorten, they produce a talipes equinua which 
still further hampers the walking powers. When the patient 
becomes bedridden, the contractures rapidly attain an extreme 
degree. As the quadriceps wastes, the knee-jerk disappears. 

Primary atrophic myopathy is a less common type, and owing 
to absence of muscular enlargement, it is more likely to be coniuaed 
with progressive muscular atrophy of spinal origin. At least three 


Vm. 102, — ih>iiii|ili>, Erb'a juvenile type. Palient 

i[irli,i\ 1 Pill 11 L'.^ Ill hm: 111 standing posture. 

varieties have been recognised, according to the muscles which are 
first attacked. Thus we have (a) Erb's juvenile type, affecting 
the muscles of the shoulders and upper arms ; (b) Landouzy and 
Dejerine's faciw-scapulo-humeral type, where the atrophy begins 
in the face ; (c) a type beginning in the lower limbs, chiefly in the 
anterior thigh muscles. 

In these atrophic varieties there is no striking preference for 
boys ; both sexes are equally liable. The age of onset too is 
a little later, commonly between 15 and 35 years, except in facial 
cases, where the atrophy may come on in early childhood. 



III Erb's juvenile ti/pe the atrophy begins in the large 
of the upper arnia and shoulders, especially the biceps, tricepa, and 
supinator longua. Figs. 101, 102, and lO:} are from such a patient, 
aged 47, who was a professional " living skeleton " in a travelliiig 
" freak " show. In his case the wasting was first noticed at the age 
of 19. In some instances, as in this particular case, the arms 
and legs are attacked about the same time. Or the disease i 

begin in the arms and spread to the legs. The deltoids and api 
often escape, even when the hicepa and supinator longua are 
wasted, the condition in this respect differing from cases of spinal 
origin ; and the forearm muscles, except the supinator longus, 
generally escape too. From weakness of the glutei and quadrii 
the patient when rising to the standing posture may Lave to 
up his legs, as does a pseudo -hypertrophic case. 

The Indo-soapith-humeral variety of Landouzy-Dejerine com- 
mences in early life, the facial muscles being earliest afiected. 
orbicularcs oculomni and oris are weak, so that thc' jiatient < 

)ngu B, I 


close his eyes tightly nor blow out his cheeks (see Figs. 104 and 
105), His lower lip droops and projectfl forwards, and his mouth 







habitually liangs opi.'ii. Theaiuile is peculiarly traiisverac and liaa 
' forced " look, the angles of the mouth being drawn outwards 
but not upwards. The tongue, ocular and jaw muscles are un- 


affected. Later the disease spreads to the scapular and upper-a 
muscles, and finally to the apiual muscles and lower limbs. 
A tliird type of the disease, of which Figs. 106 and 107 i 


Fio. l{)fi. — Muscular djHirophy ; type bottinning in lower limb*, but 
having advanced to upper limUi. Pntiunt prusaiiig hanilii to- 
getlier, to show atropliy of grealer fwrlion of pectoral miisules. 
Intrinsic muacles of Landg unaifectuil, 

an example, begins in the legs, and attacks the amis later, 
this patient the legs became weak at the age of 12. When sbi 
came under observation at the age of 2S she was still able to h 
her arms, which were (jontractured at the elbows, for knitting a 


to feed herself, though shu was no longBr capahle of walking, owing 
to claw- foot. 

Other Varieties of Muscular Wasting.— Wasting of muscles 
sometimes ctccura as a secondary phenomenon in other diseases, 
where there is nn implication of tho spino-muflcnlar motor nemime. 

Thus the muBoles may become small from disuse, as may be seen 
in a limb whieh, owing to a fracture, has been confioed for several 
weeks in splints. Disease of a joint is generally accompanied by 
well-marked atrophy of the surrounding muscles. This arthritic 
muscular wasting specially affects the extensor muscles of the joint 
— for extimple, the (juadriccps in disease of the knee-joint, the 
interoBsei in osteo-arthritis of the hands, the deltoid in disease 
of the shoulder- joint. A degree of muscular wasting also occun J 
in the paralysed hmbs in ordinary hemiplegia. Part of this may [ 


be the result of disuse, but there are other cases where the degree 
of wasting is excessive, and disproportionate to the paralysis. 
Lastly, we may meet with marked wasting of muscles in rare cases 
of hysterical paralysis (see Fig. 195, p. 361). But all these 
muscular wastings can be distinguished from that due to disease 
of the lower motor neurone by the absence of electrical reactions 
of degeneration. 



There are certain forms of motor paralysis which come and go. 
They tend to recur again and again, ami in the intervals between 
his attacks tlie patient is able to execute all voluntary movements 
in a nonnal or almost normal fashion. 

Of these diseases myasthenia graTis is the most serious, In 
myasthenia certain muscles become infiltrated with deposits of 
small round celb resembling lymphocytes, especially the striated 
muscles innervated by the upper cranial nerves, though some- 
times the muscles of the limbs and trunk, and even the respiratory 
muscles, may become affected. The disease is characterised by 
the fact that the patient becomes, after very moderate e.-certion 
of the affected muscles, abnormally easily fatigued, and the affected 
muscles are, for the time, paralysed. The patient wakes up in 
the morning practically normal, but as the day goes on, cer- 
tain muscles gradually become paralysed. Perhaps the muscles 
most often affected are the levators of the upper Hda. Thus 
ptosis appears, often of unequal degi'ee on the two sides {see Fig, 108), 
To this may be superadded an external ophthalmoplegia, gener- 
ally incomplete. The facial muscles also become weak, and the 
patient has a peculiar " nasal " form of smile, in which the angles 
of the mouth are drawn upwards but very slightly outwards. The 
masseters and other masticatory muscles may also be affected, so 
that the patient cannot chew more than a few mouthfuls. The 
palate, tongue, and larynx may all be implicated, producing for 
the time the phenomena of bulbar palsy. In fact, the disease 
was formerly named " asthenic bulbar paralysis." To correct his 
ptosis, the patient may tilt his head backwards. But sometimes 
the neck muscles are affected, so that the head falls loosely back- - 
wards or forwards. In the limbs it is chiefly the large proximal 



muscles which are affected. But the moat characteristic featiU 
is the tranaitoriness of the paralysis, and its recurrence i 
slight exertion. Thus the patient can walk a short distance, bo! 
soon has to stop ; he may speak a few sentences, and then 1 
voice becomes weak and his articulation indistinct. In thq 
affected muscles, the electrical reactions are altered and we liam 
the "myasthenic reaction." Faradif shocks applied to thi 

— Mj'aEthGiiui gravis iti a man of ;i]j. Miirked woakness at 
ctcrs and of loner facial muscles ; also rigbt-sideii ptosis. 

The patient is making a maximum effort to clench the jans 

and show the teeth. 

muBoIes at first produce bri.«k contractions, but on repeated stimu'J 
latiun the faradic excitability temporarily disappears. In contra 
to true bulbar palsy, there is no muscular atrophy as a niU^fl 
although in very severe cases, slight wasting may supervene,^* 
The reflexes, deep and superficial, together with the sphincters, area 
unaffected. If the respiratory muscles become severely affectedyfl 
the patient may die from respiratory failure. 

o E. IjC'vi, Rivietn di /mlnlDfii 

■irntal'-. ItlltU, p. J60. 


TfaoniBen's disease or "myotonia consenita," is a rare coiigeuital 

affection of the voluntary muscifs, which appears to he due to 
their poaseaaiiig an excessive proportion of undifferentiated sareo- 
plasm and muacle -nuclei, and relatively too small a proportion of 
the anisotropic or fibrillar elenieiit. This latter contracts briBkly, 
whereas sarcoplasm contracts very slowly. In Thomsen'a disease, 
whenever the patient atarta to perform a voluntary movement, 
his musclofl are thrown into a state of tonic spasm, which gradu- 
ally passes off, the muscles slowly becoming supple, until at length 
he can perform the movement, say that of walking, in a normal 
fashion. But if he stops and starts again, or if he tries to hurry 
his original speed, this stiffness reappears, and has again to be, 
aa it were, worked off. The lower hmbs are most commonly 
affected, but other musclea may also show the phenomena. Thus 
the patient's eyes may remain temporarily firmly closed after a 
cough or sneeze, his mouth may remain open after a yawn, and 
n. The sensory functions and the reflexes are unaffected. But 
the affected muscles have a characteristic reaction to electrical 
stimulation. Their excitability is increased to both faradism 
and galvanism. To galvanism KCC is equal to ACC (instead of 
being greater, as in health), and the contraction set up, whether 
by galvanism or by faradism, ia remarkably persiateut, lasting for 
a time after the stimulus has ceased. 

Enlenberg's disease or "paramyotonia congenita," is a family 
affection somewhat like Thomsen'a disease, in which a tonic spasm 
appears in certain voluntary muscles, more particularly in the face, 
so that the patient is unable, for a quarter of an hour or longer, 
to open his eye-s or to speak. Less often the muscles of the 
limbs are affected. The condition, however, differs from Thomsen'a 
disease in its immediate exciting cause. The tonic spasm of 
Eulenberg's disease is excited not by exertion but by cold, and 
i generally relieved by warmth. The two diseases, however, are 
closely allied, and have been observed coincidently in members of 
the same family.' 

Another interesting variety of transient paralysis is known 
■ Delprat. DtuUcht med. Woehrntehrt/t. 1R93, ». ISH. 


as intermittent limp or ''dysbasia angio-sclerotica" ("clau- 
dication intermittente " of Charcot, or the " intermittirendes 
Hinken " of German authors). An analogous condition in horses, 
known as " spring-halt," has been familiar to veterinary surgeons 
for many years. The patient is most commonly a man of middle 
age, sometimes of gouty constitution, and very often has been an 
inveterate tobacco-smoker. The symptoms are very character- 
istic. At rest he feels no disability. But when he begins to walk, 
though he starts off normally, he soon begins to feel his legs tired, 
heavy, and painful. A cramp-like pain appears and gradually 
becomes intolerable, making him limp ; and if he perseveres with 
his attempt, he finally becomes, for the time, totally unable to 
walk a single step. He rests, the pain and weakness pass off, 
only to return when he starts to walk afresh. If we examine such 
a patient during a paroxysm of temporary incapacity, we find 
his feet and legs cold, and perhaps purple or mottled red. But 
what is most characteristic of all is that the pulse in the feet, in 
the posterior tibial or the dorsalis pedis artery, is absent or nearly so. 
There are no sensory changes, the reflexes are normal, and, except 
during the paroxysms, the motor power of the limbs is unimpaired. 
All these phenomena appear to be the result of a temporary spasm 
of the arteries of the limb (the arteries themselves being frequently 
already narrowed by arterio-sclerosis), so that during walking 
an increased blood-supply to the muscles is not forthcoming, 
hence there result temporary anaemia, pain and weakness in the 
affected muscles. In rare instances similar phenomena have been 
observed in the arms. 

Rare cases have also been observed where a hemiplegia, 
partial or complete, sometimes accompanied by aphasia, occurs 
in an elderly patient, indistinguishable at first from an ordinary 
cerebral haemorrhage or thrombosis. But within a few hours 
all the hemiplegic phenomena suddenly disappear, leaving the 
patient perfectly normal. The patient may have a series of such 
attacks of transient hemiplegia at intervals of days, weeks or 
months. For over three years I watched the case of an elderly 
cabman who had numerous attacks of left hemiplegia lasting for 


a day or bo, leaving liim absolutely well in the intervals. Another 
case of mine was in a vigorous busineBS man. aj^ed fifty-one, who 
had frequent attacks of temporary aphasia with right hemiplegia. 
Similar casas havo also been recorded by Grasaet' and by Lang- 
will.* Such cases may be termed angio-apaatic hemiplegia, and are 
probably due to temporary spasm of one middle cerebral artery, 
analogous to the spasm of peripheral vessels in intermittent limp. 
They must be carefully distinguished from the transient hemi- 
plegia which is not uncommon in general paralysis of the insane. 

Amongst the transient paralyses we must also bear in mind the 
various craft-palsies, professional cramps, or occupation nearoses, in 
which the limb is normal for all motor actions except one particular 
movement — often, unfortunately, the one on whicli the patient's 
livelihood depends. The commonest variety is the so-called writer's 
cramp or scrivener's palsy, though we also meet with similar con- 
ditions in the cramp of pianists, viohnista, telegraphists, typists, 
tailor's cutters, haii- cutters, hammer- men, cow- mi liters, watch- 
makers, harpists, cigarette -makers, sempstresses, and so on. The 
cramp comes on, not during the period when the sufferer is learning 
his occupation, but after he has become an expert and requires 
to perform the particular skilled movement repeatedly for prolonged 
periods. For all other movements except that particular one, the 
limb is normal. Thus in writer's cramp the patient can use 
his hand normally for piano-plaj^ing or for grasping and using a 
heavy tool, This is because the weakness is not due to muscular 
but to cerebral fatigue. A professional cramp does not appear in 
its fully developed form at first, but passes through different stages 
of severity. In the slightest variety there is simply a degree of 
Btiffneas or spasm in performing the act, with a subjective sensation 
of pain and of intense mental discomfort and fatigue. In other cases 
a temporary paralysis appears when the_patient attempts to write, 
so that the pen can no longer be held in the hand. In still more 
severe cases tremor is superadded to spasm in the affected muscles. 
The di^nosis is easy, inasmuch as the phenomena, whether spastic 


or paralytic or perhaps a combination of both, only supervene when 
the one skilled motor action is performed, and the same muscles 
can be used for all other actions without pain, spasm or weakness. 

There is also a curious hereditary disease known as "family 
periodic paralysis." This malady may run through several suc- 
cessive generations of the same family, attacking one or more 
members of the same generation. Males and females are both 
liable. The patient, who is otherwise apparently healthy, has 
attacks of flaccid paralysis of all four limbs, recurring irregularly 
without apparent exciting cause. The duration of a paroxysm 
varies from two or three days down to a few hours. The attacks 
generally come on during the night when the patient is in bed. 
He wakes up and finds himself more or less widely paralysed. 
First the legs are afEected, later the arms, and last of all the 
muscles of the trunk and neck. The cranial nerves usually escape. 
In the limbs the paralysis starts proximally and the distal parts 
are affected last, so that the patient may still be able to move 
his toes and fingers when he has lost all power in the hips and 
shoulders. In severe cases the intercostal muscles may also be 
paralysed. Most striking of all is the fact that during these 
paroxysms of flaccid palsy the affected muscles, for the time, lose 
their excitability to faradic, galvanic, or mechanical stimulation, 
and all the reflexes in the affected limbs disappear. Sensation is 
unimpaired and the sphincters are unaffected. An additional point 
is that during the paroxysm, the left ventricle becomes temporarily 
dilated, as can be proved by percussion and occasionally by the 
appearance of a systolic mitral bruit. The muscular paralysis 
passes off in the reverse order to that in which it came on. The 
toes and fingers recover before the proximal muscles, and the 
muscles earliest attacked are the last to recover. TKe patient 
then remains apparently normal until his next attack, weeks or 
months later. 

Sudden attacks of hemiplegia may also occur in general 
paralysis of the insane, constituting a variety of so-called " con- 
gestive attacks." But although the patient may recover rapidly 
from his hemiplegia, often within a few days, he is not a normal 



dividual, for careful physical examination will always reveal 
■ avideuces o£ the diBease, mental or physical, e.g. facial tremors, 
) pupillary changes, or, most constant of all. lymphocytosis of the 
\ cere bro -spin a! fluid. 

Amongst other transient affections we may mention those 
of muscular cramp and of tetany. The conditions ate easily 
I recognised, and may temporarily interfere with the movements 
' of the affected limbs. Both are painful affectiona, tetany being 
\ most commonly seen in infants, whilst cramp is most often met 
with in healthy adolescents or adults who have been performing 
I some unwonted prolonged muscular effort, Cramp is abo a 
I. distressing symptom in cholera, in some cases of diabetes, and 
L occasionally in exophthalmic goitre. Tetany is generally bilateral, 
I and has a characteristic posture of the hands and feet (see Fig. 
[27, p. 71). 

Occasionally we see patients who complain that their lege 
I suddenly give way in the street, causing them to fall. This may 
Lbe due to various causes. For example, it is a not uncommon 
i symptom in tabes. The tabetic patient often has hypotonia of 
I the muscles about the knees and also deficient joint-sense, a com- 
bination of phenomena which may make him fall unexpectedly. 
In such a case the condition of the deep reflexes, the state of the 
pupils, and the other phenomena of tabes render the diagnosis 
easy. Other cases of sudden falling are due to minor epilepsy, 
where the patient has an attack of momentary unconsciousness 
^^ during which he falls, but recovers consciousness at once and gets 
^^■up again, not knowing why he has fallen. Here the diagnosis 
^^pwill depend on the observation of other epileptiform attacks, major 
or minor. We should particularly inquire for the occurrence of 
sudden pallor of the face or flxity of ejcpression, indicating a passing 
attack of petit mal, too slight, perhaps, to produce a fall. 
^^^ In other cases, again, we have to do with sudden vertigo, 
^^Aa in Meniere's disease, causing the patient to fall. Such cases 
^^Blre recognised by the concomitant auditory phenomena (see p. 151) , 
^^Hmd by the fact that they are not associated with loss of 


Sudden weakness of a limb may occur in hysteria, especially 
after some emotional shock. Hysterical paralysis may persist 
for variable periods of time, varying from a few hours to 
many weeks or months. The paralysis not uncommonly 
recovers as suddenly as it came on, sometimes under emotional 
or religious excitement, under hypnotic suggestion, or under 
energetic stimulation, electric or thermal, for example, that of 
a Pacquelin cautery. Hysterical paralysis never attacks a single 
muscle, but always a group of muscles. It is never accom- 
panied by reactions of degeneration, no matter how much the 
hysterical Umb may be wasted. We diagnose hysteria by a 
process of exclusion, noting not only the absence of certain signs 
of orgai^c disease, but looking also for the presence of various 
hysterical " stigmata," to which we shall refer later. 

But we must not forget that in many cases of apparently 
hysterical and transient paralysis in young women, the patient 
after one or more of such attacks may afterwards develop the 
signs of diflseminated sclerosis. The onset of disseminated sclerosis 
may be indistinguishable from an attack of hysterical paralysis, 
the weakness of the limb in both diseases may be transient and 
may apparently clear up completely for a time. But a series of 
such attacks should always raise in our minds the suspicion of an 
underlying disseminated sclerosis and should make us give a guarded 
prognosis, especially if the patient has had more than one attack 
of weakness, not necessarily in the same limb. We should pay 
particular attention to the state of the optic discs. Early optic 
atrophy will exclude mere hysteria, so also will an extensor 
plantar reflex or anything approaching a true nystagmus. In 
fact, the disease which is most often wrongly diagnosed as hysteria 
is disseminated sclerosis. 



A NEWLY-BORN child cannot co-ordinate the movements of its 
limbs. Certain co-ordinated vital actions, such as sucking, swallow- 
ing, respiration, &c., are performed well from birth, but in an 
infant's limbs the movements are mostly of an aimless restless 
character, with the exception, perhaps, of grasping movements of 
the hands. And even these latter difEer from the co-ordinated 
grasp of later life, inasmuch as the infant's thumb is hardly used 
at all for opposition, and the flexion movement of the fingers 
occurs chiefly when some object comes in contact with the hand, 
the movement being reflex rather than voluntary. 

The child only learns after long practice to use its muscles in 
such a fashion as to produce properly co-ordinated movements of 
the limbs. Walking, writing, swimming, the playing of any game, 
are all performed awkwardly at first. Skill is at last attained 
by frequent repetition, and once a co-ordinated action has been 
thoroughly learned, the effort for its performance becomes in- 
finitesimal, so that in time it is performed more or less auto- 

Every co-ordinated action involves contraction not only of the 
so-called prime-movers but of their antagonists, and if these two 
groups are not properly balanced, the attempted movement is 
awkward and jerky. This condition occurs in a number of diseases 
and is termed ataxia or incoordination. This means clumsiness, 
unsteadiness, or awkwardness in the performance of movements in 
a non-paralysed patient who was previously able to execute these 
movements in normal fashion. 

In testing for ataxia of the upper limbs, we ask the patient 
to perform such an action as picking up a small object, say 
a pin, from a smooth surface. If he is ataxic, he fumbles 



during the attempt, or may perhaps pounce on the object in a 
sudden, jerky fashion. Another useful test is to ask the patient 
to lift a brimming glass of water to his lips and notice whether 
he spills it. Or we may ask him to touch rapidly the tip of his 
nose with each index finger in succession. If he is ataxic, his 
finger misses his nose by a greater or smaller interval, or, on 
reaching it, the finger shows additional oscillatory movements. 
Other good tests for ataxia are to make the patient button or 
unbutton his coat or collar, or to write with a fine-pointed pen. 
In every case, we should observe whether the unsteadiness is 
increased or unchanged when the patient shuts his eyes. Slight 
degrees of ataxia due to sensory impairment may be noticed 
only when the patient is deprived of the help of his visual 

In the case of the lower Umbs we detect moderately severe 
ataxia by observing the patient's gait, asking him to walk 
** heel-and-toe " along a straight line, then to turn sharply and 
come back. In well-marked locomotor ataxia the gait is broad - 
based, the feet are lifted too high and the heels are brought down 
with a stamp. In cerebellar disease, on the other hand, the 
patient reels or lurches along, being especially imsteady when 
turning round (see later, " Postures and Gaits "). To detect 
ataxia of a single lower limb, we Ask the patient to place one heel 
on the opposite knee, or to trace with one foot a circle or some 
other pattern on the floor, or we ask him when lying down to 
touch with his toe our own finger held in the air. And here also, 
in ataxia of the lower limbs, we should always note whether the 
patient's unsteadiness is increased or unchanged by shutting the 
eyes. In tabetic ataxia of the lower Umbs, the unsteadiness is 
increased when the eyes are shut. Romberg^s sign consists in the 
tendency of a patient, who can stand steadily with the eyes open, 
to fall when he closes them. Thus an early sign of tabes is the 
so-called " wash-basin " sign, where the patient falls into his 
basin when washing his face. A minor degree of Romberg's sign 
can often be detected in the earlier stages of tabes, where the 
patient is still able to stand with the eyes shut, but the tendons 



on the dorsum of the foot are seen to exhibit irregular restlesa i 
contractions, the so^alled " danse dea tendons." 

Ataxia of the bulbar muacles has already been referred to (aee 
Dysarthria, p. 104). As to ataxia of the nmsclea of the tnmk, 
ita diagnostic significance is less than that of the limbs, inasmuch < 
as by the time that the trunk mnaclea are recognisably ataxic, the 1 
limbs already show very marked niiateadineas. Ataxia of the 
head and tnink muaclea is evidenced by swaying movements when I 
the patient sits up. 

Having detected ataxia in the movements of any limb, we must ' 
always determine the condition of the sensory impulses from that 
limb, testing not only the various forms of cutaneous aensibihty 
but also the deep sensations, especially the kintesthetic sense and, 
still more important, the joint-sense. Finally, we must determine , 
the condition of the deep reflexes, noting their exaggeration aa in 
diaseminated sclerosis, or their abolition as in tabes or in Friedreich's 
ataxia. We also note the type of plantar reflexes. 

The commonest variety of ataxia is that due to deficiency of J 
peripheral impreaaions^not ao much from the skin aa from the j 
deeper structures, the muscles ami joints. Thus in lesions of peri- ' 
pheral sensory nerves an antesthetic limb is often ataxic. Division J 
of the iposterior roots of the brachial plexua, the anterior roots re- 
maining intact, causes marked ataxia of the upper limb. In tact j 
auch a patient may be totally unable to move the limb if his eyee i] 
are cloaed, so that he no longer has the guiding influence of visioi 
Degeneration of the posterior roots and posterior columns, i 
in b^tex, produces marked ataxia. A tabetic patient is ataxic 1 
because of deficiency of afferent impressions, more especiallj' from ] 
his muscles and from his joints. If the muscle-tonua is lost and ] 
the muscles are hypotonic, as in many cases of tabes, the patient I 
has, as it were, to " pull in the slack " before the rausclea come ] 
into proper play, thereby making the movement jerky, inharmonious, 
and flail-like. Joint-sense being impaired, he ha^ to perform | 
a maximal movement in order to get the sensation of having I 
moved the joint at all. Thus in walking when he lifts his leg, 
owing to want of proper joint-sense, he throws the limb up with J 


abnormal suddenness and to an unnecessary height in order to 
gain the sensation of flexion of the joint. He then stamps 
it down with excessive emphasis to make sure that it really 
is extended. Such a patient with ataxia of sensory origin com- 
pensates for the deficiency of sensory impressions from his limbs 
by means of his vision. When watching his partially anaesthetic 
limbs, he can control them better. Hence if he closes his eyes, 
the regulating influence of vision is lost and he becomes much 
more ataxic. This is the probable explanation of Romberg's 
sign in tabes. 

Ataxia similar to that of tabes also occurs in other organic 
cord lesions impUcating the posterior columns, as for instance in 
tumours or chronic sclerosis of the posterior columns, whether com- 
bined or not with lateral sclerosis — e.g. some cases of disseminated 
sclerosis or spinal sj^hilis. In such diseases the other signs and 
symptoms guide us to a correct diagnosis. 

Ataxia combined with spasticity occurs in the early stage of 
subacute combined degeneration of the spinal cord, generally a 
disease of middle life. This disease occurs chiefly in conditions of 
profound anaemia. In the first stage of the malady there are loss 
of joint-sense and subjective sensations of tingling, &c., in the 
lower limbs, not unlike tabes, but with increased knee-jerks and 
extensor plantar reflexes. After lasting for weeks or months the 
disease then changes its type, and in this second stage the spastic 
paraplegia becomes severe and marked anaesthesia develops in 
the lower limbs and trimk. Lastly, and usually abruptly, within 
a few days the type changes once more, and there is a terminal 
stage of flaccid paraplegia lasting a few weeks, with absolute 
anaesthesia of the lower limbs and trunk, loss of the knee-jerks, 
the plantar reflexes remaining extensor in type. The paralj^ed 
muscles rapidly waste and lose their faradic excitability. The 
bladder and rectum are uncontrolled and the lower limbs become 
oedematous. The whole disease from start to finish lasts about 
two or three years. 

But a patient may be ataxic when all his peripheral sensations 
are normal. This occurs in the different varieties of cerebellar 


'ataxia. Let us take, for example, Friedreicfi's ataxia, a develop- 
mental diaeaae affecting mainly the afferent tracts in the cord 
leading upwards to the cerebellum, which is the centre for automatic 
co-ordination. In Friedreich's ataxia the patient becomes ataxic, 

FlC. 101!.— Friedrokh'B ataxia. Sbowing sccliosifi. 
an in tabes, but with the cutaneous and joint-sense intact. The 
ataxia is unaffected by closing the eyes. The age o( the patient, 
who is commonly an adolescent, the presence o£ scoliosis, of 
manus cava, and of pes cavus (Figs. 109 and 110), the aormal 



pupillary reactions. t.liP presence of nystagmus, tlie absence < 
lightning pains or of bladder trouble, all serve to distinguish this 
disease from tabes, though in both diseases the deep reflexes are 
absent. The plantar reflexes in tabes are flexor iji type, 
in Friedreich's ataxia they are of the extensor variety. 

Kia. 110. — Friedreich's ataiiia. ijLonin^ pui- cavus aad ojaiius ca 

Ataxia also occurs in certain localised lesions of the medul 
obloitgata. Thus, for example, a uniUtcral lesion may interrupt 
the fibres of the direct cerebellar tract and thereby interfere with 
co-ordination of the homolateral lirabB, Such a lesion, which 
usually interrupts at the same time the fibres of Gowers' trac^ 3 
may extend inwards to implicate the inter-olivary arcuate fibresj 
and the fillet, together with the nuclei of the lower cranial n 


It produces a characteristic syndrome, known as the unilateral 
huJhaf syndrome of Bdhinski and Nageotte} The symptoms are as 
follows : — ^From interruption of the cerebellar afferent fibres there 
is ataxia of the homolateral limbs. From interference with the 
tract for pain and temperature we have analgesia and therm- 
ansesthesia of the opposite side of the body (see Fig. 10, p. 15). 
From interference with the oculo-pupillary centre in the bulb there 
is myosis and pseudo-ptosis (see later, "Cervical Sympathetic 
Paralysis," p. 320), and there may be difficulty of deglutition due 
to affection of the cranial nerve nuclei. If the lesion extends 
forwards to implicate the pyramid of the same side, there is 
hemiplegia of the contra-lateral arm and leg. 

Marie*s hereditary cerebellar ataxia is somewhat similar to 
Friedreich's ataxia, but there is no loss of knee-jerks, and the age 
of onset is somewhat later. Cerebellar ataxia also occurs in 
cerebellar tumours, in vascular lesions of the cerebellum, in dis- 
seminated sclerosis affecting the cerebellum or its peduncles, in 
cerebellar abscess, in encephalitis of the cerebellar cortex, a disease 
of febrile onset which is sometimes met with in children, and it 
occurs occasionally in old age as the result of a primary senile atrophy 
of the cerebellar cortex, especially affecting the Purkinje cells. ^ 

Cerebellar ataxia differs in several important respects from the 
ataxia due to deficient afferent impressions. It is chiefly evidenced 
in the cerebellar gait, which has a staggering, reeling character, 
like that of a drimken man, but without the stamping of the true 
tabetic. We recognise several factors in the production of cere- 
bellar ataxia. Part of the ataxia, especially that of the trunk 
muscles, is due to vertigo, the patient being unsteady in his gait 
because he feels giddy. A cerebellar gait therefore occurs in many 
cases of labyrinthine disease. If a cerebellar patient lies down, 
his vertigo is diminished and there being no longer any effort re- 
quired to maintain equilibrium, his movements are much less un- 
steady. Another factor in cerebellar ataxia is the existence of 
the muscular hypotonia which we often meet with in cerebellar 

^ Uevxie ncuroloyiquet 1902, p. 358. 
^ Rossi, Nouvelle Icotwgraphie de la Salp(}lritre, No. 1, 1907. 


disease ; this hypotonia, in unilateral cerebellar lesions, is more 
marked in the limbs of the affected side. The third and most 
important factor in cerebellar ataxia is the want of the co-ordinat- 
ing influence of the cerebellum on the cerebral motor cortex. This 
connection is a crossed one, the right cerebellum being connected 
with the left cerebral cortex, vid the right superior cerebellar 
peduncle and the left red nucleus. Some tumours of the 
frontal lobe are associated with cerebellar ataxia, probably owing 
to indirect interference with the functions of the contra-lateral side 
of the cerebellum. True cerebellar ataxia, unlike the ataxia of 
tabes dorsalis, is uninfluenced by closure of the eyes. 

Ataxia also occurs in some affections of the higher cerebral 
centres. For example there are certain toxic affections in which 
the patient becomes ataxic. The most familiar variety is 
that of acute alcoholic intoxication. Part of this ataxia may 
possibly be due to cerebellar intoxication, but a large part of it 
is cerebral, as evidenced by the " mental ataxia," the disordered 
articulation, &c. The temporary ataxia of fatigue, of writer's 
cramp and of other occupation-neuroses is also probably of cerebral 
origin, so also is the transient ataxia which sometimes follows 
enteric fever or other exanthemata. 

There are certain diseases of the cerebral cortex, in which ataxia 
is distinct. In chorea the patient not only exhibits spontaneous 
involuntary movements, but he also has distinct ataxia on volun- 
tary movement. In organic monoplegia or hemiplegia, especially 
when slight in degree and amounting merely to paresis, distinct 
ataxia often exists in the paretic Umbs. Hemi-ataxia is one of 
the characteristic phenomena in lesions of the optic thalamus. In 
such cases the limbs on the side contra -lateral to the lesion are 
not only ataxic but also partially anaesthetic with loss of 
joint-sense, whilst spontaneous pains in the affected limbs are 
commonly present. Sometimes ataxia of the limbs precedes an 
attack of hemiplegia — pre-Jiemiplegic ataxia, especially in threatened 
softening from arterial thrombosis. More often the ataxia appears 
during convalescence from a slight hemiplegic attack — post- 
hemiplegic ataxia, where the patient has to learn the process of 



r co-ordination again in his paretic limbs. This form of ataxia muat 
I be distinguished from athetosis, the involuntary alow writhing 
movements of the limbs which occurs in old and severe cases o£ 
hemiplegia, eapecially of infantile hemiplegia. 

Ataxia is one nf the most striking signs of disseminated 

sclerosis, where the unsteadiness of the Umbs is often associated 

• with a superadded coarse oscillatory tremor— the so-called inten- 

I tion-tremor. How much of the unsteadiness in disseminated 

|:BclerosiB is due to cerebral and how much to cerebellar disease 

Fit is difficult to say in any individual case. The tremor of 

hemiplegic distribution which is observed in the limbs in cases 

of lesions of the red nucleus or rubro-sptTuil tract (see p. 80) is 

present at rest, but becomes exaggerated on voluntary movements, 

I rendering them ataxic. In tliis respect it contrasts with the 

r tremor of paralysis agitana, which can usually be controlled to 

[ permit of the performance of a voluntary movement. 

Finally we may meet with ataxia of the most varied types 

V in hysteria. Here the aSection is probably one which impli- 

Icatea the highest psychical centres. Tlie diagnosis of hysterical 

I ataxia rests on the presence of other stigmata of hysteria, to- 

[gether with the absence of evidence of organic disease. Some- 

I times hysterical ataxia is associated with " cortical " anEesthesia 

■ of the affected limb. In such a case the patient may be able 

^to move the limb normally with her eyes open, but when they 

closed ataxia appears. This does not necessarily occur 

pin every hysterically anffisthetic limb, for in many cases profound 

ansesthesia may be present without ataxia. The diagnosis of 

hysterical ataxia, however, seldom presents much difficulty to a 

careful observer. The disease which is most often mistaken for 

hysteria is disseminated sclerosis in its earlier stages, In both 

diseases we may have a history of transient weakness of a limb, 

apparently clearing up completely for a time. But in disseminated 

sclerosis there are evidences of organic disease ui the form of 

pallor of the optic discs, nystagmus, alterations of the abdominal 

L and plantar reflexes, sphincter trouble, and so on. 



Postures. — In health the posture of the body and of its various 
members is determined partly by gravity, partly by the relative 
strength of the muscles at the various joints. Therefore, 
inasmuch as the flexor muscles of our limbs are usually more 
powerful than the extensors, the ordinary posture of the limbs 
at rest is one of slight flexion. This is easily verified by 
observing a sleeping child. In the erect attitude the muscles 
of special importance in maintaining equilibrium are the ex- 
tensors of the hips and knees ; whilst in standing on one foot 
the peronei are of particular importance by inclining the whole 
lower limb outwards from the ankle up, and bringing the centre of 
gravity over the foot. The minor varieties of posture in difEerent 
healthy individuals, which we learn to recognise as part of each 
man's personal characteristics, are largely the result of differ- 
ences not only in muscularity but of habit. The pose of a 
powerful, muscular man is widely different from that of a thin, 
debilitated invalid. Moreover, if from exercise or want of exercise, 
certain groups of muscles are more or less developed than the 
normal, the posture is further modified, even in health. For 
example, we all know the characteristic straddling gait of the 
professional jockey. 

Similar principles apply to those cases of organic disease where 
certain muscles or groups of muscles are affected by paralysis. 
Paralysed limbs gradually assume characteristic postures, and these 
postures of organic disease are not matters of haphazard, but are 
determined by anatomical rules. 

Firstly, if the muscular paralysis be the result of a lotver motor 
neurone lesion, in the anterior cornua, anterior nerve-roots, nerve 
trunks or muscle-fibres, the paralysed muscles become wasted. 



Their unopposed iion- paralysed antagonists slowly become con- 
tracted, and fix the limb in a. eertain definite posture which 
ia best demonstrated if the patient tries to throw the paralysed 
muscles into action, in which caae the antagonists contract alone. 
For example, Fig. HI is a photograph of a woman who had 

i localised lesion in the anterior cornua of the cord at the level 
{ the fifth cervical segment, Amongst the chief muscled supplied 
r the anterior comua at that level are the deltoid, biceps and 
nipinatora. These muacles underwent atrophy and iheir unopposed 
ntagonista became contracted. As a result we see that from 
Mralysis of the deltoid and contraction of its opponents the shoulder 



is adducteil, similarly from paralysis oE the biceps the etbow | 
extended by its opponents, and from paralysis of the supinata 
the forearm is hyperpronated by their antagoniata. This posture I 
characteristic of a cord lesion at the fifth cervical aegment. 

Fig. 1 12 shows the posture assumed in a ease of paralysis of t 
external popliteal nerve. This nerve was divided by a bullet 

wound in an officer's right leg. In addition to anEcsthesia corre- 
sponding to the cutaneous distribution of the nerve, the figure 
shows the presence of foot-drop due to paralysis of the anterior tibial 
group of muscles, with unopposed contraction of the calf mu£ 
Here, of course, the action of gravity is a factor as well, the weig 
of the foot tending to increase the foot-drop. 

Fig. 113 shows the posture in a case of paralysis of ' 
musculo -spiral nerve. The patient is trying to extend both 1 
wrists. f)n the paralysed side we notice the atrophy of 



supinator longus and the paralysis o{ the extensors of the wriat 
and fingers, aiso the characteristic swelling on the dorsum of the 
hand, probably bursal in origin, which appears in long-standing 
cases of drop- wrist. 

Secondly, if the paralysis be due to an upper motor neurone 
lesion, the law which determines the posture is diflerent. We no 
longer have atrophic paralysis, limited to a i)articular muscle or 
muscles as in a lower motor neurone lesion. Instead, there 
gradually develnpes a spastic paralj'sis, in which all the muscles 

Mliuwing ciroji-i 

of the affected limb or segment of a limb are more or less paralysed. 
The muscles which are normally more powerful are therefore 
placed at an advantage during the process of spastic contracture, 
and a posture results which is an exaggeration of the normal attitude 
at rest, so that, for example, in s chronic henuplegia the familiar 
posture of the upper limb is that of flejiion with pronation, that of 
the lower limb being one of slight flexion at the hip and knee, 
with exten.sion and inversion of the ankle, and a tendency to 
dorsiflexion of the toes (see Figs. 114 and 115), 

This spastic posture in hemiplegia does not come on at once. J 
There is an initial flaccid stage, lasting several weeks or evenj 



tiiontha, Ijefore thi^ iipaatic rigidity sets in. (In a amall numbf 
of cases the heniiplegtu may remain permanently flaccid.) But 
even during this flaccid stage the postures of the heniiplegic limbs 
are often diflerent from those of the unaffected side at rest. Ono ] 
of the most characteristic signs is an apparent broadening of thffl 

Cime of loft-sided infantile humipltgia in a piitient agtd 7 j-cmrs. (Jnaet 
of hemiplegia Ave years [ireviously. Shovi'in;; [losturc of limbs. In 
Fig. 114 Dote al.Leloais of left fiu^'crh. In Fig. lin nnte inversion 
□F anklo and drawtng up of lioeU 

lower limb (Heilbronncr's ' " breites Bein "). Ttiia consists in an 
outward rotation of the lower hinb at the hip-joint, due to ite 
own weight when in the recumbent posture (analogous to the 
displacement which occurs in fracture of the neck of the femur): 
The tliigh, therefore, when looked at from the front, appears broadi 
' Deulnclie ZtiUchn'JI /iir NerrrnkeiUitiule. B»l. 2H, 1904, b. i. 



than on the healthy side. Moreover, the flaccid paralj'sed niiiscles 
fall back by their own weight, and on tranavetae section the thigh 
formB a flattened oval instead of an approximate circle as on the 
healthy side. This apparent broadening of the paralysed thigh can 

be well seen if the patient be seated on s hard, flat Bi;at. It does 
not occur in hysterical hemiplegia. 


Lviri^ loiiljiiiiiliiiiil Mil of nolun. 

In functional paralysis the conditions are different. Hystoro. 
it la often said, may simulate organic disease— thus we inay have 
functional hemiplegia, paraplegia, or monoplegia. But if wo 
examine carefully we usually fmd that this similarity is more or 



leas rough and inaccurate. And why ? Because hysterical coul 
tractures are not governed bj- anatomical rules ensuring the pn 
ponde ranee of the stronger muscles. Hysterica! contractu 
usually present some points in which they differ from the posturail 
of genuine organic lesious. Figs. ll'> and 117 are from a c 


Fm. 1 19.— Left-EJiloii lijaLutiwil lit;iiiii)ltnia with glossa-liibial Epaam 
on protrusion ot tongue. The left apper limb was also rigidly con- 
tracted at tbe Hhoulder and el bow, the band being flaccid. 

functional hemiplegia, in which the contracture alone waa enouj 
to distinguish it from an organic case. Instead of the usual flexedi J 
and pronated posture of the upper limb, we observe that the elbow 1 
and wrist are extended, the forearm is supinated, and the fmgen J 
are half-bent in a hook-Uke fashion, whilst in the lower limb t 
inveraion of the ankle ia overdone, out of aU proportion to thttl 


ordinary equinus position. The contracture in this pntlent I 
appeared suddenly, as ia so often the case in hysteria, unlike the , 
gradual development of an organic contracture. Fig. 118 shows a 
peculiar contracture of the soles in another case of hysterical para- 
plegia, in which the feet had a fold running longitudinally along 
the Boles, totally unlike any organic contracture. 

FlO, 120. — H jper-exlenBlon oi Kiiees ina'case of tabes — "genu rwufnodnn." 

Fig. 119 shows a case of left-sided hysterical henuplegia, in 
which the contracture of the upper limb differs from that of 
organic disease ; for whilst the shoulder, elbow, and wrist are rigid, 
the fingers are flaccid — a combination which does not occur in 
organic hemiplegia. We also observe that this patient has gloaao- 
labial hemispasm. When she protrudes her tongue it deviates 
considerably to the paralysed side, whereas in most cases of orcanio 
. hemiplegia, if there is tongue deviation, it is usually towards 



the unaffected side. But what is still more important to not| 
is that, when the tongue is protruded, the face on the paralyse 
side goes into a state of apasm, so that the left naao-labial fold i 
deeper than on the healthy side, a condition which is the revei 
of what we find in organic hemiplegia. Ghssn-lahial hsmisfi 
such as this is not a comnion sign, but when it occurs it i 
pathognomonic of hysteria. 

Hysterical contracturos often, but not always, disappear dui 
sleep or during deep ansestheaia. If the contracture has persiste 

for months, adhesions may form in the joints, so that even undM 
an auKsthetic the contracture may not completely relax, and ' 
may have to break down the adhesions forcibly. 

The postures of organic paralyses, then, whether supra- 
iiifra-nuclear, are definite and comparatively simple, being govemec 
by the anatomical rules we have mentioned. Hysterical eoB*l 
traetures, on the other band, being under no such restrictionajj 
may assume the most varied and weird appearances, examples 
which might be multiplied indefinitely. 

In many cases of tabes doroalis there is marked deficiency (^1 


muscular tonus, a condition known as h/potonia. This slackness of j 
the muscles has a remarkable influence on the patient's postures. 

Thus, for example, hypotonia of the peronei increases the difficulty 
of standing, since whenever the patient lifts one leg, the other f 
fixed leg is no longer pulled outwards as in health to hrinfj the 

centre of gravity over the fixed fdot. Wlieii the hamstrings and ] 
sural muscles behind the knee are hypotonic (see Fig. 120), the ' 
joint becomes hyper extended in the erect posture— the so-called ] 
" genu recurvatum " — unlike the knee-joint of a healthy individual, j 
in which, however strongly the knee be extended, theie always t6-4 


mains a concavity behind. Thia hypotonia of the popliteal muaclettl 
produces another very characteristic sign of tabes, which 
that when the patient lies in bed with the knee extended, thafl 
heel can be passively raised whilst the back of the knee re-^l 
mains in contact with the bed {see Fig. 121). Hypotor 
the muscles of the trunk and lower Umbs in tabes may permit^ 
of the patient assuming the most extraordinary postures without 
pain^ — ^posturea which are impossible to any ordinary individual 
who is not a professionally trained contortionist (see Figa. 122, 
123 and 124). 

Amyotonia congenita (sometimes, though lesa aptly, called 

myatonia cuvgenita) is a condition of extreme flaccidity of the 
muscles, which are soft and lax on palpation. When thrown into 
voluntary contraction they do not harden like ordinary muscles, 
and it may be impossible by palpation to distinguish them from 
the subcutaneous tissues. The joints are flail-like, and can be 
placed in all sorts of fantastic postures. There is no true motor 
paralysis, although voluntary movements are devoid of vigour.. 
The electric excitability is diminished both to faradism and to 
galvanism, but without polar changes. The deep reflexes ara 
absent, whilst the cutaneous and organic reflexes are normal. 
The condition is a congenital one, closely allied to myopathy, witl^i 



wluch it IB sometimeB combined. The phenomena are usually i 
detected within the first twelve monthB after birth. I 

Gaits. — ^Unlike some of the lower animala — for example, the 
chicken or the Iamb — the human infant at birth cannot stand or 
walk. It is not until the child reaches the age of about eighteen 
months that he begins to walk. First he learns to stand, and then 
after repeated efforts he succeeds in walking. During the process 
of learning, he reels and falls about just Uke an adult with cerebellar 

We do not al! of us walk exactly in the same fashion. Even 
healthy indiWduals show minor differences in gait. An old man 
walks differently from a youth, a soldier differently from a 
sailor, and a woman advanced in pregnancy differently from a 
maiden. The wearing of ordinary boots with artificial heels 
also modifies the gait, so that in health the first part of the 
boot to show signs of wear is usually the back of the heel on the 
outer side. Ladies' high-heeled boots modify the gait still more, 
throwing the weight of the body unduly forwards towards the 
heads of the metatarsal bones. 

When testing the gait in cases of nervous disease it is advisable 
to have the patient's lower limbs well exposed, and without boots. 
To get a good view of the limbs it is well to have a minimum 
of clothing on the patient. A good plan is to have the patient 
clad in some light garment like a shirt, whose tail is pulled for- 
wards between the legs from behind and pinned in front, thereby 
leaving the upper limbs free. We ask the patient to walk straight 
away from us towards some given point, then to turn round and 
come back, 

In a 7iormal gait the limbs are moved forward easily, the feet 
neither scraping the ground whilst being lifted, nor being unduly 
stamped down as they descend. The forward-moving or " active " 
leg is the one which carries the weight of the body. The trunk and 
pelvis therefore lean a little towards the corresponding side during 
the " active " phase of each limb. This trunk movement is attained 
partly by the action of the gluteal muscles, partly by the a 
lumbar muscles of the same side. A short, thick-set person with 



a broad ppivis tends to have a "waddling" gait, as the weight 
of his trunk is shifted across from one side to the othery 
When the ghitual muacles are weak, the patient watJdlai 
excessively, in his efforts to throw hia wciaht to each aid( 

The gait ia altered in various diseases. Thus it may becom 
spastic, ataxic, reeling, hifjli -stepping, and so on. 

A ejxistic gait occura in lesions of the pyramidal tract — ttX 
uxample, lii hemiplegia, in diplegia, and in spastic paraplegia. In 
organic hemiplegia the active forward-projection of the limb is 
especially difficult on the paralysed aide, and the weight of the body 
has to be carried forwards by the aid of the other aide pi 
gravity, unlike the normal gait where the weight is carried entire 
by the " active " advancing leg. Thus when the hemiplegic li 



onght to be in the " active " phase, it is not properly flexed at 
the knee or ankle, nor is it actively pushed forwards but merely 
dangles forward like a pendulum, not directly forwards, but swing- 
ing in a circular fashion round the opposite hip as on a pivot. 
When the " active " phase of the non-paralysed Umb occurs, the 
hemiplegic foot (owing to weakneaa of the peronei and dorsiflexora 
of the ankle, with over-action of the invertors and calf muscles) 
stays on the ground too long, thereby scraping the front part of 
the foot, especially the ball of the great toe; the stride of the 
paralysed limb is therefore shorter than on the healthy side. In a 
case of 8-pastic diplegia, or double hemiplegia, the patient is unable 
to project either leg forwards in the ordinary way, but has to jerk 
each forwards in turn with a circular awing, so that, in a well- 
marked case, not only does the patient take abnormally short steps, 
catching the ball of each foot on the ground, but from the circular 
Bwiog of the limbs, together with tbeir adductor spasm, they cross 
alternately in front of each other, producing the cross-legged or 
"scissor " gait (see Fig. 125). Meanwhile the trunk and upper hmbs 
make violent jerky movements, swinging the body from one side to 
the other. In ordinary spastic parapletjiH from cord disease, there 
is not the cross-legged gait of diplegia, but the patient moves 
stiffly along, taking abnormally short steps, the front part of the 
feet clinging to the ground, thus wearing out the toes of the boots. 
Meanwhile the tendency to ankle-clonua causes a " trepidation " of 
the whole body in severe cases, from tremor of the feet. Such 
a patient stumbles over the slightest obstacles. 

The gaits of h;/sUria are of the most varied types. For example, 
in hysterical hemiplegia, the patient often pushes the paralysed 
foot along the ground as if on a skate, or drags it helplessly along 
with its dorsum resting on the ground, as seen in Fig. 126. 
li this is bilateral, the patient is totally unable to walk or 
stand. Or the foot may be held in a position of talipes 
calcaneus, or the patient may walk on the outer border of the 
foot (see Fig. 127) when walking, even when no such posture is 
present at rest ; or one lower limb may be acutely flexed at the 
lup and knee, so that the patient has to use crutches. 


Or again, tlie patient may liave a zigzag gait, or tie i 
throw one leg about with s wild Sourish before bringing it to t 
ground, or may suddenly kneel down every tew steps — these ai| 
ties of gait. AsUisia-abasia ia the term applied to a condition m" 
which a hysterical patient ia unable to stand or walk, although 
capable in the recumbent poature of performing all movements of 
the lower limbs normally. The varieties of hysterical gaits are 
practically unlimited, but every one of them differs in some'] 
respect from the gait of organic disease. 

The side-gaii (Schiiller's " Flankengaiig ") is a useful means ofj 
diagnosing between organic and hysterical hemiplegia. To test it,.! 
the patient is placed on a line and made to move along it side*! 
ways in a given definite direction — aay, towards the right, 
normal individual during this movement, first leans his trunk toM 
the left, then balancing his weight on the left leg, he hfts the 
right from the ground, abducts it by a muscular effort, brings the 
tnmk erect again, puts down the right foot, last of all lifting the 
left leg, adducting it and placing it alongside the right. How iij 



F thia performed in organic hemiplegia ? We find that the hemi- 
' plegic patifMit moves sideways towards the paralysed side well, 
but badly towards the healthy aide, so that in right-sided hemi- 
plegia the patient, when going sideways towards the right moves 
normally, bnt when going towards the left he drags his right 
leg in the movement of adduction. Tliis difference in the side- 
gait on the two sides in organic hemiplegia is often quite evident 
when the forward gait shows very little abnormality. To show 
the phenomenon properly, the patient must not be too severely 

at byiiteri<^l monoptegiu oF riglit leg. 

paralysed to stand or walk, nor must he have shortening of the 
limb, as in old infantile hemiplegia. These two exceptions, how- 
ever, are readily recognised by other signs. In hysterical hemi- 
plegia the side-gait is impaired on both sides, not merely on 
the healthy side. 

An ataxic gait is seen most typically in tabes dorsalis ; but it 
occurs also to a lesser degree in other diseases imphoating the 
posterior columns of the cord — for example, in Friedreich's ataxia, 
in chronic menii^o-myelitis, or in tumours of the posterior columns, 
' also in ataxic paraplegia or postero- lateral sclerosis, whether due 
to disseminated sclerosis or to other causes. Of all these, the 


tabetic gait is the most characteristic. In this there is no motor 
weakness of the Umbs, but they are characteristically unsteady. 
The patient walks on too broad a base, with his legs unduly wide 
apart. He lifts them suddenly and violently, raising them too high, 
then bangs them down forcibly in flail-like fashion, stamping the 
heels on the ground. He tries to guide his tottering course by 
watching the ground. Therefore if his eyes be shut, or if he 
be in the dark, and especially if he narrows his base by placing 
the feet close together, he tends to fall. In slight cases of tabetic 
ataxia, when the patient is in this position, he may not actually 
fall, but we can see the tendons on the dorsum of the feet actively 
in movement, in the effort to preserve the balance. With this gait 
we usually have absence of the knee- and ankle-jerks, Argyll- 
Robertson pupils, and various other signs, such as lightning pains, 
ansesthesise, crises, and lymphocytosis of the cerebro-spinal fluid. In 
Friedreich's atcma the patient is commonly an adolescent, and 
though the knee- and ankle-jerks are absent, as in tabes, the pupils 
react normally, there are no lightning pains nor crises, and we 
usually find nystagmus, scoUosis, pes-cavus, and a peculiar affec- 
tion of articulation. In ataxic paraplegia or postero-lateral sclerosis, 
where the lateral columns are implicated as well as the posterior, 
the patient is ataxic, but with increased knee-jerks, possibly 
ankle-clonus, and usually an extensor type of plantar reflex. 

A reeling or titubaiing gait is one of the commonest signs of 
cerebellar disease, although it is also met with in severe vertigo 
of any variety, whether from alcohoUc intoxication, from ear 
disease, from diplopia, or other cause. In cerebellar disease the 
patient staggers along, with an occasional sudden lurch to one 
or other side, but neither lifting his feet too high nor stamping 
them down, as in tabes. Not uncommonly the cerebellar patient 
has a tendency to stagger persistently in some particular direction, 
depending on the position of the cerebellar lesion — thus he may 
tend to fall forwards, backwards, or to one side. As a rule, he 
manages to pull himself up after he has deviated one or two steps 
from his straight course. In some cases of unilateral tumour of the 
cerebellimi the posture of the head is altered, the ear being tilted 


f towards the shoulder on the side opposite to the lesion, and the 

face turned slightly in the reverse direction, i.e. towards the side 

of the lesion. This is well seen in Fig. 128, which represents a 

woman who had a tumour originating from the meninges over the 

I right petrous bone, and invading the right lateral lobe of the 

f cerebellum. This growth was successfully localised and removed, 

! but the patient unfortunately dieil shortly after. This " cerebellar 

ir ariaing frou 

' attitude," however, although common in lateral lobe tumours, is 

not constant in its direction. For example, cases have been 

recorded where the lateral tilting of the head was towards the 

side of the lesion, and the rotation of the face to the opposite 

I wde. Possibly these differences are associated with the intra- 

I or extra-cere be liar origin of the growth, 

A hiifh-stepping gait occurs in patients who have foot-drop. 
I Such a patient, to clear his foot from the ground, lifts the leg 
I too high, flinging the ankle up as it were, instead of actively 
[ doraiflexing it. This gait occurs typically in paripheral neuritis , 



also in mttsnUar dystrophies, and occasionally in lesions of ' 
aiuda et/mna or lower part of the lumbosacral regiwi of the spinal 
cord. It also occurs unilaterally in paralysis of the external poji- 
lileal nerve. The gait and posture of muscular dystrophy also 
possess other characteristic features. Thus from weakness of the 
gluteal muscles the patient in the erect 
posture arches his back, in order to kee 
the hips extended (see Fig. 123); this pro 
duces lordosis and " pot-belly." Furthffl! 
the weakness of the glutei, as already ex-T^ 
plained, causes a waddling gait, the lega^ 
being planted wide apart ; and as we have 
already seen, the mode of rising from the 
ground in such cases is pathognomoi 
Such a patient when placed on the ground ■ 
and told to get up rolls round on his face, J 
then gets on his hands and knees. Then. I 
to get on his feet, he extends the kneea, ,, 
and suddenly, pressing his hands on one | 
knee after the otuer, proceeds to extend J 
the hips and straighten the spLne hy I 
"climbing up" his own thighs until hej 
reaches the erect posture. 

The posture and gait of paralysis agitaiu 
are diagnostic, so much so, that patieatel 
have a strong family resemblance (see Figs. I 
130 and 131). In a well-marked case the' 
patient stands with the trunk stooping 
Kio. I2fl.— Muscular dys- forwards, the face appearing "starched" 
sZSiLg brfosf.."' '^" aiid expressionless-the so-called " Parkin- 
sonian mask," in which there is little i 
no emotional play of features. The upper Umbs are slightJy 
abducted at the shoulders, semi-flexed at the elbo^vs, sUghtl/'-l 
extended, at the wrists, flexed at the metacarpo- phalangeal joints^ J 
and extended at the inter-phalangeal joints, as if holding 
pen — the " interosseal " attitude — and very often they show tlia!l 

postuhes and gaits 2 

bnuliar rhythmic, " pi]l-ro)ling " tremor. The tremor may affect 
the proximal jointa as weU, and even the lower limbs, face, jaw, 
palate, and tongue. All the voluntary movements of the trunk 
and limbs are slow and stiff, the upper limbs no longer "swing" 
as the patient walks (in unilateral cases this loss of swing is con- 
fined to the arm of the affected side), and the gait is " featinant.'* 
The patient moves forward with short, shuffling steps, and when he 
turns, his trunk moves slowly en masse, as if made of glass, 
whilst his steps in walking tend to get faster and faster, as if he 

KiG. 130.— ParaljaiH agit an s— bilateral, 

~ were " chasing his own centre of gravity." This is called " pro- 

. pulsion." Still more frequently do we observe " retropulsion," in 
which the patient, when puUed gently from behind, tends to run 
backwards with short, hasty steps. This retropulsion may some- 
times he induced even by the act of looking upwards. A slighter 

1 degree of this same posture and gait is not uncommon in simple 

I old age. 

The gait in chorea is sometimes peculiar, partly owing to a 

» degree of ataxia, partly from the presence of additional irregular 
involuntary movements. Hometimes one foot seems as if it were 

I momentarily entangled by an invisible obstacle, which holds the 
child back for an instant, the patient then hastily resumes his 


forward progress; or his knee may give way suddenly, cauaio 
him to fall. 

Many chronic epileptics have a peculiar slouching posture ani 
gait, the posture of the hands, as Spratling ' has pointed oatj 
being specially characteristic. The fingers are habitually flexedJ 

KlCJ, 131.— Paralysis ayilans— bilaleral. 

and the wrists bent to a right angle, and the patient ofte 
has a marked forward stoop of the shoulders. 

Various deformities produce abnormalities of gait and postuiefl 
If, for example, one lower limb is shortened from disease of thi 
bones or joints, from malformations such as coxa vara, or ( 
genital dislocation of hip, or from infantile paralysis, the | 
becomes correspondingly altered. 

1 New York Maiical .J;t>mal. WMi, p. M4I1. 



Tbb central nervous system exerciser & profound influence on the 
nutrition of all the tissues. There is, however, no evidence of 
the existence of special nen'es whose function ia trophic and 

r trophic only. The control over nutrition which the nervous system 
I is probably exercised in & complex fashion, in which 
there are several factors involved. Striated muscles, for example, 
undergo atrophy when the cells of the corresponding motor nucleus 
in the cord or medulla are destroyed, or when the motor nerve- 
fibre leading from the nerve-cell to the muscle-fibre ia interrupted. 
The rctult is muscular atrophy, the different varieties of which we 
have already studied (se3 p. 203). Afferent nerve-fibres conveying 

, sensory impressions, whether conscious or subconscious, have also 
a profound influence upon tissue-nutrition, especially upon that 
of the skin and its appendages. Therefore in amesthetic areas 
trivial injuries are liable to produce destructive tissue-changes. 
Lastly, the central nervous system indirectly influences the tisaues 
through their blood-supply, by means of its connections with the 
sympathetic vasomotor system. The sympathetic system may 

I also be disordered primarily, apart from the central nervous system, 
not only in gross lesions of the sympathetic chain, but also in 
the so-called angio- neuroses. 
Excluding, then, the muscular atrophies and the angio -neuroses, 
which are studied elsewhere, let us direct our attention to certain 
trophic disorders which are associated more or less directly with 
affections of the cerebro-apinal nervous system. Trophic disorders 
may bo distributed widely all over the body, or they may be 
limited to certain circumscribed areas corresponding to a peri- 
pheral nerve, to a posterior root, or to some division of the spinal 
cord or brain. 


Generalised Trophic Disorders. — Of these, one of the best 
examples is the well-known anorexia nervosa. In this affection, 
without evidence of structural disease of any organ, the patient 
(generally a young woman) loses appetite and becomes pro- 
gressively emaciated, often to a profound degree. The condition 
sometimes follows a shock, physical or mental, perhaps an affaire 
du cosur, though in other instances we can find no apparent 
exciting cause. In diagnosing this condition, we have first to 
exclude other conditions, such as diabetes, tuberculosis, and 
malignant disease, which commonly produce emaciation. The 
patient generally exhibits certain " stigmata " of functional 
disease. Of these stigmata the most frequent is a hemi- 
anaBsthesia, usually slight in degree and generally left-sided (see 
later, p. 350). 

In marked contrast to this is the rare affection known as 
adiposis dolorosa, or Dercum's disease. It occurs chiefly in middle- 
aged women, many of the patients being alcoholic or syphilitic. 
The patient is diffusely obese, and, in addition, she has localised 
fatty lumps in the subcutaneous tissue, forming large pendulous 
swellings, chiefly on the limbs and trunk. These swellings may 
be symmetrical or asymmetrical. They appear and steadily 
increase in size, consisting of fat and of an embryonic form of 
connective tissue. The arms are most frequently the sites of 
the swellings, which are usually tender on pressure and may 
have spontaneous pains. Certain areas, however, such as the 
hands, feet, and face, are always spared. The nerve-trunks are 
tender, and there may be areas of blunting or loss of cutaneous 
sensibility. Sometimes the thyroid gland is indurated, but the 
patient has none of the mental or physical features of myxoEdema. 

A curiotis condition of the bones results from hjrpertrophy or 
functional over-activity of the pituitary gland.^ Hyper-secretion 

^ Acromegaly cannot be ascribed, as was formerly thought, to deficient 
pituitary secretion, for as Tcmiburini emd Modena have pointed out {Rivista 
aperimerUale di Freniatria, 1903, fasc. 3 and 4), experimental destruction of 
the gland does not cause acromegaly, nor do malignant growths, nor tuber- 
culous disecuse of the gland produce it, but only conditions such as hyper- 
trophy or adenoma. 


275 ( 

by this gland appears to set free in the body certain abnormal 
substances whose action is to cause ati extraordinary growth of 
bony tissues. If the disease sets in before the age at which the 
epiphyses have become joined, the bones grow enormously in all 
their dimensions, and the result is gigantism. But if the aSection 

lnt^g■lly uf ei^ht yciirs' due 

begins after the epiphyses have united, the overgrowth of the 
bones is confined to their ends, producing acromegaly. 

The phenomena of acromegaly are very characteristic (se 
Figs. Ki2 and 133). There is a progressive enlargement of the 
bones and soft parts, most marked in the hands and feet, but 
also aflecting other parts, notably the skull and face. The skull ■ 


becomes enlarged and thickened, all its bony ridges are ex- 
aggerated ; the margins of the orbits, the cheek-bones, and most 
striking of all, the lower jaw, become enlarged. The mandible 
becomes prognathous, the lower teeth biting in front of the 
upper, instead of vice versd, and the teeth become widely separ- 
ated. The soft parts also share in the hypertrophy. The lower 
lip, the tongue, uvula, tonsils, and the cartilages of the ears, all 
become enlarged, and the skin of the face becomes thick and coarse. 
The hands and feet increase in size (not the nails), so that the 
patient requires gloves and shoes several sizes larger than before 
Spinal curvature is also present, usually a cervical kyphosis, and 
the thorax, pelvis, and even the external genitals become enlarged. 
Glycosuria is a fairly common complication. In female patients 
amenorrhoea occurs. In addition to these phenomena the patient 
complains of severe headaches, owing to the intra-cranial pituitary 
tumour. This tumour, from its position in the sella turcica, fre- 
quently encroaches on the adjacent optic chiasma, and then there 
is produced a corresponding affection of the visual fields (see p. 115), 
usually commencing as a bi-temporal hemianopia, which may, as 
the disease advances, progress to complete blindness. 

Apart, however, from pituitary disease which strictly speak- 
ing, although intra-cranial, is not primarily a nervous disorder, 
we sometimes have widespread overgrowth of the tissues, confined 
to one-half of the body and probably of cerebral origin. Fig. 134 
represents such a patient with left-sided hemi-hypertrophy, in whom 
all the bones of the left side (as verified by skiagrams), including 
those of the face, Umbs, pelvis and thorax, together with the soft 
tissues of the face, tonsil, tongue, and testicle, were larger than 
on the right side. But the right side of the cranium, and pro- 
bably also the right side of the brain, was larger than the left. 

Passing next to trophic disorders of more Umited distribution, 
it is convenient to discuss them in certain groups. 

Bilateral thrombosis of the arteries of the corpora striata, and 
especially of the lenticular nuclei — a not uncommon occurrence 
in fatal poisoning by sewer gas — produces what Dana ^ has called 

^ Journal of Nervous and Mental Disease, 1908, p. 65. 



the " corpus strialum syndrome,'" in which, in addition to coma 
(with perhaps hemiplegia or diplegia from a&ection of the ad- 
jacent pyramidal patlis), there is a gangrenous condition of the 
skin and sometimea of the lungs as well. 

Trophic Changes in the Skin and its Appendages.— ff/ossy 

I ia a condition met with chieHy in the hands, in certain oases 
of long-standing peripheral nerve palsies, whether traumatic or 
neuritic in origin. It is also a frequent accompaniment of osteo- 
arthritis, not only in the ordinary " rheumatoid " variety, but also 
in the arthritis which comes on in hemiplegic limbs. The skin 
of the fingers becomes thinned and atrophic, with a peculiar smooth, 
shiny surface. The nails in many cases are altered, being longi- 
tudinally striated and exceatiively curved from side to side. The 


finger-pads are wasted and the finger-tips taper to a point, as i 
seen in Fig. 135, which is taken from a case of right-aided brachia 

Perforating ulcers occur most typically in tabes doraahs. Then 
are generally situated on the foot, on its plantar anrface, eapeci&llj' 
at the metatarao-phalangeal joint of the great or little toe. They ' 
may also occur under the heel or imder the terminal phalanx of 
the hallux. Kath ulcer begina aa a thickening of the epidermis, 
like a corn. Suppuration occurs under this, ami the pua finds— 

Km. I3S.— itiKli 

ikin ami iii|itriiig linger-l 

its way out through a small opening in the centre {Fig. 136)J 
A narrow sinus is thus formed which increases in depth until i 
may extend into the joint beneath, which is often disorganised,] 
and carious bone may be felt at the bottom. Sometimes the ulcerJ 
heals up under treatment. The tabetic perforating nicer is j 
leas. Somewhat aimilar trophic ulcers are met with i 
cases of spina Infida occulta and also in syringomyelia, but in t 
latter disease they are commoner in the hands. Diabetic t 
la alao occasionally associated with perforating ulcers of the feet^l 
a minor variety of diabetic gangrene. In leprous neuritis j 
forating ulcers are not infrequent, though it is commoner t^l 


have a still more extenBive loss of tissue, whole phalanges 
dropping from the fingers and toes. Painless whUlowa — in so- ] 
called " Morvan's disease," a sub-variety of syringomyelia, are 
found at the finger-tips. These whitlows are sometimea the result 
of trivial injuries which in a normal individual would not produce 
any serious results. In other coses the explanation is found in 
the absence of sensibihty to temperature and pain, which is 

FIO. laii.— PorfrjiTidu^ iiluors in lnb>:s. 

characteristic of the disease, so that the patient burns the fingen " 
painlessly and produces blisters and even areas of sloughing. 

In certain cases of tabes there may be a perforating ulcer in 
the mouth. First the teeth become loosened and fall out, then 
the alveolar margin of the jaw is absorbed, and if the upper jaw 
be a&ected a perforation into the nasal cavity may be established, 

lierpea zoster is a very typical example of a trophic cutaneous 
disorder wliich has a direct nervous origin, viz., inflammation or J 


thromboBia of the corresponding posterior root ganglion. In thi 
affection a crop of vesicles appear, which are distributed in i 
definite metanieric area, corresponding to the posterior 
whose ganglion is diseased. In the case of facial herpes it is tlu 
Qaaserian ganglion which is inSamed, in whole or in part, whili 
herpes of the external auditory canal is associated with in^ 

HerpCB zoster la area of flflh Herpes zoster— the same pnllent as in J 

dorsalroot. Second day after Fig. 137. Bniption surroqiida the I 

appearance of eruption. nipple, and thence extends iawarda I 

Sammation oE the geniculate ganglion. The herpetic vesiclesj 
usually become pustular and subsequently permanent scars may! 
remain. Herpes is sometimes preceded, for a day or two, byprB-.] 
herpetic pain in the area where the eruption is about to appear ^ J 
and not infrequently the eruption is followed by prolonged and J 
intractable post-herpetic neuralgia. Figs. 137 and 138 are from afl 
typical case of herpes in the area of the fifth thoracic root.] 
Sometimes herpes develops in the course of diseases of thaS 


vertebrse or of the spinal meiiiiiges. Such an occurrence aignifieB I 
that the morbid pTOceaa has attacked the corresponding posterior j 
root ganglion or ganglia. Even in simple herpes zoster we can I 
sometimes elicit Kernig's sign' (see p. 5fi). 

Bed-nores result from inflammatory and destructive changes in I 
the skin and underlying tissues of bedridden patients, whether i 
in cases merely enfeebled by prolonged illness (especially in enteric I 
fever) or, more commonly, m severe organic paralysis, such i 
hemiplegia or paraplegia. Most bed-sores, occurring as they do 
at the sites of pressure, can be prevented by careful nursing, by 
kG«ping the patient's akin acrupidously clean and dry, by placing 
him on a water-bed, and by hardening the epidermis by local | 
applications of methylated spirit. But sometimes in spite of the j 
most assiduous nursing, bed-sores may develop mthin a few days ' 
or even within a few hours of an initial paraplegia or hemiplegia. 
This so-called actde decubitus is of grave omen. 

The commonest site for a bed-sore in a hemiplegic patient is I 
over the great trochanter on the paralysed side. In paraplegia 
from cord lesions, e.g. acute myelitis, the bed-sore commonly forma 
over the middle of the sacrum (Fig. 139). A bed-sore commences 
as an area of redness of the skin, bullie then develop and burst, 
leaving an ulcerating or sloughing surface beneath. The sloughing j 
process may extend down to the periosteum and bones, and in i 
sacral decubitus the infection may extend into the vertebral 
canal, producing a fatal cere bro- spinal meningitis, septic organisms 
gaining access not only from the skin, but from the intestinal dis- 
charges. Bed-sores are also met with in advanced cases oi . 
bedridden dementia, even where there is no paralysis. In these ] 
patients, as in cases of prolonged fever, the sores develop i 
the pressure points, viz. the heels, hips, backs of the scapula J 
and even on the inner sides o[ the knees. We also meet with \ 
excoriations of the skin, which may amount to bed-sores, 

' TliJB fact, together with the trequeiit. o 
cereViro-Bpinal fluid, Hhowa that in lierpei zoBter tlie put 
neceaaarily limited to the ponlerior root-gunglion, but ii 
diftusad meningeal irritation. 

Bilheza, AmhivaiginiraUi de Med.. Ffb. 27. 190<i. 

of lymphoeytosie of the 1 
ilogical process is not 1 
uirt of a more widoljr ] 


casea of violent chorea, where the patient knocks his limbi 
against surrounding objects. 

Before leaving the subject of destructive trophic lesions of thej 
skin, we must mention sijmmetric-n] gangrene, a localised gangrenaB 

Fio. 130.— Loiubo-Buonil luynlicU witli saeral be<i-soro or rtBeubilns. 
Showing acrophy and paruljsis ot muaclea below left Icneit. The 
Hinall chart on the right Indicates tliecoexiatmgarua of anieatbesia. 

chiefly occurring in the tips of the fingers and toea, and precedeo 
by pains or parEcsthesite of the parte. But to this, the most sevei 
phase of RajTiaud's disease, we shall refer again when we coii- 
aider the angio-neurosea. 

The commonest points of incidence of rodetd nkers, especialiJ 


on the face, as Cheatle ' has shown, are at the positions where 
the various branches of the trigeminal nerve becomes cutaneous, 
especially over the points of emergence of the infra- orbital, infra- 
trochiear, temporo-malar and lachrymal nerves, and also with 
particular frequency at the inner canthus of the eye and at the 
angle where the a!a nasi joins the cheek. He has also shown 
that these spota are the favourite points of incidence of 
leucoderma and scleroderma. The precise significance of these 
facts is still obscure, but Cheatle has recorded the curious fact 
that rodent ulcers are frequently limited to the distribution of 
normal nerve-areas and that the spread of a rodent ulcer ceases 
abruptly when it reaches a cutaneous area which has become 
denervated by division of its sensory nerves. 

There arc other trophic lesions unaccompanied by necrosis or 
ulceration, and consisting in local changes affecting one or more ele- 
ments of the akin or subcutaneous tissues, whether in the direction of 
atrophy or of hypertrophy. Perhaps the most typical examples of 
this variety are scleroiierma, leucoderma, and cutaneous naivi. 
Scleroderma is a disease in which the skin becomes abnormally hard 
and fibrous. The condition may be diffuse or circumscribed. In 
the rarer diffuse variety, large areas of skin, usually symmetrical, 
and especially in the upper limbs, become hard and rigid, losing 
their elasticity so that the affected skin can no longer be pinched 
up with the fingers. Sometimes there ia a prehminary ccdematous 
stage. As the disease advances, the sclerotic process may extend 
to deeper structures such as tendons, and this, with the rigidit)' of 
the skin, limits the movements of the joints and may produce 
permanent deformities. If the fingers are affected, they become 
tapering at the tips and permanently flexed. If the face is affected, 
it becomes immobile and mask-like. Circumscribed scleroderma, or 
morphata, is the commoner variety, where small patches of skin 
become hard, white and ivory-like, the distribution of the patchee 
being somewhat similar to those of herpes zoster— 
raerical, in the area of a posterior root, or of one of the division| 
of the trigeminal nerve on the face. 

' Bril. Med. Journal. April 29. JfiOS, 


I^eucodertna, or disappe-arance of pigment from circiimacribetfB 
patches oE skin, is alxo commonly distributed, more or leas^ 
in nerve-areas. The patch of absolute pallor has a pigraenteM 
edge where it joins the normal skin, and it tends to spreaol 
slowly along the particular area. This disease, of course, is mosfn 
striking when it affects patients of sallow complexion or of dark-^ 







Cungenitttl itTiuc'iiHia ,if lUi-tttTiierip ciistriljiiliuii. j 

skinned race. Leucoderma also occurs in the niaculo-antesthetifl 
type of leprosy, where the leucodermic patches are often red and 
hypersesthetic at the edges and aneesthetic in the centre. 

Figs. 140 and 141 represent a little girl aged eight, in who« 
patches of warty growths were distributed metamerically on the 
limbs and trunk. 

Congenital ctdaneous navi — " port-wiue stains "—are also cent 
mouty distributed in root areas on the trunk or in the trigeminai 



distribution on the face. The trigeminal area ia affected with 
special frequency, one, two, or all three divisionB of the trigeminal 
being mapped out, more or leas accurately. It is an interesting 
fact that a cutaneous naivus on the face may be associated 
with hypertrophy of the subjacent deep tissues, with enlargement 
of the eyeball, and even with a nsevoid condition of th». 

285 ^B 


ninal I 

iSting ^H 
iated ^^^ 
ment ^^H 


n R^i'klmghui. 

[1 iLgnl 38. 

I nasal mucous membrane and of the dura mater on the correspond- 
ing side, all of which structures are innervated by the trigeminal 
nerve. More than this, cases of nsevi s of the face may be asso- 
ciated with recurrent epistaxis from the nsevoid nasal mucosa, and 
aometimes they develop sudden infantile hemiplegia with epilepti- 
form convulsions, due to aub-dural htcmorrhage from the dural 



* Cuihing, Journal of American Med. Aieocialian, iOOB. p. 178. 


Large neuro- fibromata — ao-caUed plexi/onn neuroma or dt^ 
phantiaxis mrvonnn — are more commoD on the trigeminal nerve^l 
especially in its upper divifiions, than on any other nerve of the! 
body. Such a tumour is generally part of a more widespreadl 
a5ection known as von ReckltnijkaiisejCs disease (see Figs. 142, 143).l 
In this disease we find, in a complete case, neuro -fibromata, often! 
of fairly large size, forming painless swellings on the face or 
where, together with multiple soft fibromata forming sessile or I 
pedunculated growths (known as molluscum fibrosum) and also! 
patches of cutaneous pigmentation distributed more or less da-J^ 
finitely in nerve areas. The ncuro-fibroraata of von Reckling-J 

Fig. 144.— Case of tsbcs nilli Ioeh ot liair in area oE L) and Sj ro 
hausen's disease do not cause, symptoms except by accidenta 
mechanical compression of adjacent structures. The disease oftenfl 
appears in childhood and remains stationary for many years, when.l 
it may suddenly resume its spread, new tumours cropping out all I 
over the body. 

Various cutaneous lesions are present in many cases of arscniailm 
neuntis. A brownish macular pigmentation of the skin is, oCfl 
course, common in chronic arsenical poisoning, without neuritis. I 
But in arsenical neuritis we frequently obse.rve special cutaneouBfl 
aSections, such as glossy skin, herpes zoster, falling of the hair, \ 
and most cliaracteristic of all, hyperkeratosis of the palms aadl 
soles, where the epidermis becomes much thickened and tends t 
desquamate. In addition to these skin lesions, we have thi 
ordinary signs of a peripheral neuritis, such as drop-wiist, drop- 
foot, &c. 



There is a rare trophic afTection of the skin, described by I 
Gowers as focal 'panatrophy, in which certain eircuinscHbed areas 1 
of the face, trunk, or limbs, varying in size from the diameter I 
of a cherry to that of an orange, undergo local atrophy of all the 
subcutaneous tissues down to the bone, the akin becoming also . 
slightly thinned. These patches look like subcutaneous c 

!iil %>i tlm right 

tions, and although trophic in origin, they do not correspond to 
(gular nerve-areas but are quite irregularly distributed. 
Trophic changes are sometimes present in the hair. Hyper- 
trichosis, or excessive growth of the hair, is met with most fre- 
quently on " hairy moles," which arc, moreover, excessively 
pigmented in the skin as well. It is important to remember 
a hairy mole in the lumbo -sacral region is often an indication 
spina bifida occuUa. Local hypertrichosis also occurs occasional 

M- that ^J 
m a ^^1 
ionally ^^| 



in other nerve-aroas. The liair may also be affected in various way«] 
in other nervoua affections. Well- authenticated cases have been ^ 
recorded of hUmcking of the hair of the scalp within a few houre, 
as a result of profound emotion. It is not uncommon to meet I 
with patches of whitened hair in nerve-areaa which have been i 
the site of severe neuralgia. Even in the ordinary greyneas of 
advancing years, and in the idiopathic premature greyness of 

ei^pondiog side 

youth, as Cheatlo ' has pointed out, the maximum greyneaa | 
often appears in nerve-areas in the scalp and beard. There ; 
a variety of localised alopecia where the hair falls out suddenly 
in a certain nerve area. Fig. 144 is from a case of tabes where 
there was a curious absence of hair in certain root-areas in the 
legs. Many cases of exophthalmic goitre, as Wabh pointed out,' 
have a band of alopecia at the frontal end of the scalp. Woj 


Sub-nngual tuBmofrhageB In a womiitt aged 42 in whom, eighteen 
month* Sifter an attaolc of left hemiplegia, there ooonrred acute iwoUing 
anil ledneaa of the leEt band, Co a lesBer degree in the left foot, and, 
a, few daT* later, in the right little finger. The affected Bnger-tipg 
became deepl7 cyanosed, bulln developed on the affected hand, and 
wen followed b; desquamation. 

The drawing sbowa the condition two and a half months later, the 
nails having grown to soiae cil«nt. The left band was hotter than the 
right, and perspired more freely. 



probably referable, as we have already seen, to a leaion of I 
the trigeminal ner\'e or nucleus. Not only is the skin on the I 
aSected aide of the face atrophied and wrinkled, but the boneSnJ 
and especially the lower jaw, become smaller (Figs. 146 and H7U 

Fio. IW,— Olil iiifaiii.ile liemiplcgiB. Fio. l.itJ.— Olclpoliomyelicia antorlorai 

lefii-ititlcii, with airesLed i^roivlh of terior acuiA. Paralyaia and atropb, 

limbb, of biceps, triceps, and deltoid on lett 

sifle, with arrested growth of humernc 

Still more rarely, we meet with cases of facial liemi-kypertrophy, 
where the bones and soft parts of one side of the face become pro- 
greaeively larger. la the case shown in Fig. 148, the enlargement J 
of the face followed an injury to the forehead in childhood t 
the side which afterwards became enlarged. 

It is not uncommon to find atrophic changes in the bones < 
paralysed Umbs. In paralytic affections of children, whether < 


the upper neurone type, aa in infantile hemiplegia (Fig. H9}, or of 
the lower neurone type, aa in acute arUerior ■poliomyelitis {Fig. 150), 
the bones of the paralysed limb become arrested in their growth 
and are smaller in all their dimensions than are the healthy limba. 
Even in some cases of hemiplegia in aduUs the bones of the , 

paralysed limbs become excessively brittle. I have known a case 
of hemiplegia in a middle-aged woman where moderate passive 
movements under an anteathetic, during an attempt to break down 
adhesions in the hip-joint of the hemiplegic side, caused a fracture 
of the neck of the femur. The brittleness of the bones in certain 
insane jxaienta and their liability to fractures on trivial injurieH 
are well known. Moreover, there is a rare disease known as ' 


idiopathic jragilUas ossium, where the patient, otherwise healthy, I 
may fracture his bones £rom minimal accidents, as, for example,- 1 
where a lad fractured his humerus by throwing a cricket-bail. I 
Similar spontaneous fractures also occur in certain caaes of tabettM 
and of syringomyelia, but in these two diaeaaes the fractures arH 

musulusi.f lofl. hacil. 

painless, so that the patient may continue to use the fractured I 
Umb in a faahion impossible to a normal individual. 

Trophic change-s in joints — the so-called arthropathies, are mat I 
with most typically in tabes (constituting Charcot's joint), iu 
ayringomyelia, and in some cases of leprosy. The large joints 
are generally those affected, the knee and the tar so- metatarsal joint 
being the joints moat commonly attacked in tabes {Fig. 151), the 
shoulder in syringomyelia* (Figs, 152 to 153), But in tabes even j 


the smaller joints may occasionally be affected, as in the patient 
shown in Fig. 15fi, where the terminal joint of the thumb was thus J 

diseaaed. Female tabetics seem to be relatively more liable than 
male patients to osteopathies and arthropathies. The exciting cause 
of a tabetic arthropathy is often some trivial traumatism, such as 

a twist 01 sprain in a joint in which the sense of pain is diminished \ 
or lost, hence the greater frequency of tabetic arthropathies 
in the lower Umbs. The joint swells painlessly, and rapid de- 
structive changes occur in its articular surfaces, which become 
eroded and may disappear, together with a considerable part of j 
the adjacent bone. Fractures of the articular ends arc common, j 

both in tabetic and in syringnniyelic joints. The ligaments 

Fw. J.'i". — Tiiljolio arlliropatlij- of lefl tbuuib. 

become lax and the joint abnormally mobile, so that in ' 
knee we may be able to protluce lateral passive movementfl 




or even to bend tlie joint into all sorts of curious positions 
(Fig. 157). The joint is sometinieB distended with a glairy 
gelatinous fluid, which may be blood-stained. In the later stages 
this fluid may be reabsorbed, throwing into relief the deformity 
of the boiiea (Fig. lo8). But the changes in such arthropathies are 
not entirely destructive. Osteopliytic outgrowths are often formed 

'7.— Tubollo nrlhropalby ol[tits. 

in the peri -articular tissues, causing irregular thickening of the 
bones, and producing little islands of new bone amongst the j 
tissues around the joint. These can bo readily detected on palpa- 
tion and verified by skiagrams {Figs. 159 and 160). 

Joint aSections of a different kind are met with in some casea j 
of chronic hemiplegia. The joints of the paralysed Umbs, two or j 
three weeks after the hemiplegic attack, become swollen and ' 
deformed. But, imlike the tabetic and syringomyelic arthropathies. 


hemiplegic joint-affoctiona are acutely painful. Moreover, tin 
changes in lieniiplegic joints are not destructive but more ofl 


the nature of a subacute oateo-arthritis, with pain and rigidit] 
oil passive movements and with a tendency to the formation < 
fibrous adhe-sioiis within the joint and to thiekening of tlu 


joint capsule. When the fingers are affected, they lose their 
normal outline and become clumsy -looking and " sauaagy " in 
appearance. Together with this hemiplegic arthritis it is not 
uncommon to have a degree of muscular wasting, but without 
electrical reactions of degeneration. 

Finally, we must bear in mind that certain hysterical patients 
complain of joint-pains, usually mono-articuJar, which may more 

KiG. mo.— X-rav plnitQgra|ili of labctio nrtbropathj hE knee, froiu 
patient abnwn in Fig. t.'il. Showiog ()isnp[>enranGc: of nrtluiitar 
Burfaoes and presunui! oF booy rteposil.- [n peri -articular tissues. 

or leas closely simulate organic joint disease. The patient is 
commonly a young woman who, after some local injury to the 
joint, or after some emotion, or perhaps from being acquainted 
with another patient who has joint disease, suddenly complains 
of intense joint-pain, together with cutaneous hypericsthesia in 
that region. The joint is rigid and resistant to passive move- 
ment, and if the condition has persisted, as is sometimes the 
case, for'weeks or months, fibrous adhesions may form. But 
there is no true swelling of the joint when compared with the 


corresponding limb of the opposite side, though a false appearance 
of swelling may appear to be present owing to disuse-atrophy of 
the adjacent muscles. The presence of other hysterical " stigmata " 
often aids in the diagnosis, but an accurate opinion is sometimes 
a matter of considerable difficulty and is arrived at by a pro- 
cess of exclusion. Accomplished surgeons have been known to 
operate on such joints and only on opening the joint to discover 
the absence of organic disease. The result of such operations, 
fortunately, is that the patient usually recovers from her 



For clinical purpoBee we have to consider three varieties of 
reflexes : — 

(1) Superficial or skin reflexes, e.g. the plantar reflex. 

(2) Deep or tendon reflexes, e.g. the knee-jerk. 

(.3) Organic or visceral reflexes, e.g. vomiting, micturition, 

Of these three groups, the first two have to do with striated 
voluctary muscles. They have their reflex centres within the 
cerebro-spinal axis, and many of them can be inhibited by voluntary 
effort. The third group, that of the visceral reflexes, is concerned 
not with voluntary muscles alone, but also with involuntary non- 
striated muscles which are controlled by the sympathetic nervous 
system and are incapable of direct voluntary restraint— e.y. the 
muscular walls of the stomach, bladder, rectum, or uterus. Such 
visceral reflexes can be performed, more or less perfectly, inde- 
pendently of the central nervous system. Normally, visceral 
functions go on, for the moat part, unconsciously. But even , 
they may occasionally evoke consciousness, as when visceral pain 
occurs, or when striated voluntary muscles are required to 
supplement an act originally initiated by non-striated muscles, 
or when the reflex act causes stimulation of a cerebro-spinal 
sensory nerve. Thus, to take an example, the act of defajcation 
is practically unconscious and uncontrollable, so far as the move- 
ment of the large intestine is concerned. But when the lower end 
of the anal canal has its mucosa stimulated, the perineal muscles 
come into action, and the act then becomes a conscious one and is 
more or leas under control. 

Skin Reflexes. — These are movements obtained by slight stimu- 
lation of certain areas of skin or mucous membrane. The result 
is a movement, quick or slow, of the skin near the point of stimula- 



tion, but not exactly under it. In certain animals such as the 
horse, skin reflexes can be obtained by touching almost any part 
of the trunk. But in man the skin as a whole is less mobile, and 
it is usually only from certain special areas that skin reflexes can 
be elicited. If the stimulus be too strong, it may cause a reflex 
so violent as to involve almost all the voluntary muscles of the 
body. Or if the stimulus, even though slight, be a painful one, as 
for example a pin-prick, the result is a rapid " defensive " move- 
ment — e,g, sudden flexion of a limb or abrupt closure of the eye. 

The following table gives a hst of the chief skin reflexes which 
are of clinical importance, and the mode of testing each. All 
are more easily elicited in young people than in old ; in fact, 
if we wish to demonstrate the skin reflexes with certainty, we 
select a child for our subject. 


Palatal . . 
Scapular. . 
Epigastric . 

Abdominal . 


Gluteal . 
Plantar . 

Superficial Anal . 

Touching cornea. 

Touching posterior wall of pharynx. 

Touching soft palate. 

Stroking likin in inter-scapulnr region. 

Stroking downwards fruiu nipple. 

Stroking downward from costal 

Stroking inner and upper part of 
thigh. Or pressure over Hunter s 
canal, or over adductor tubercle. 

Stroking skin of butU>ck. 

Strokhig sole of foot. 

Pinching dorsum nf glans penis. 
Pricking skin of perineum. 

Orbicularis <x;u]i contracts, 
rharynx contmcts. 
Palate is elevated. 
Scapular muscles contract. 
Epigastrium dimples on side of 

AlKlorainal muscles contract on side 

of stimulus. 
Testicle is pulled up. 

Gluteal muscles contract. 

Tensor fasciie femoris contracts, 

hallux and other toes flex, ankle is , 

Bullxms urethra contracts. 
External anal sphincter contracts. 

Skomkntal ' 
Lkvel. ' 

C5 to Thl. 
Th7 to Th9. 

Til 11 to LI. 

II and L2. 

L4 and Ui. 
Ui to S2, 

S3 II nd S4. 
S5 and 

Absence of the abdominal reflex is not uncommon in acute 
abdominal conditions, notably in appendicitis and enteric fever. ^ In 
young adults whose abdominal walls are apparently normal and 
in whom there is no oedema or excessive obesity, absence of this 
reflex is strongly suggestive of disseminated sclerosis, as has been 
pointed out by Striimpell, E. Miiller,^ and others. 

Of all the superficial reflexes, the plantar reflex is the one 
which has the greatest practical importance. In order to test it, 
the patient should be lying down, his feet being comfortably 

^ Rolleston, Brain, 1906, p. 99. 

* Neurologischea CerUralblaU, 1905, p. 593. 



rm. The limb to be tested is now partially flexed at the hip and 
knee, and also rotated so aa to rest on its outer aide. Then with 
some hard object such as the end of a penholder, we gently stroke 
the sole of the foot from behind forwards, especially towards its 
inner side. Meanwhile we watch carefully for the first movement 
of the great toe. Normally this is a movement of plantar flexion 
(see Fig. 161). The movement of the other toea is of less im- 
portance. It is interesting also to note that, simultaneously with 
the toe movement {a " cortical " reflex) we have a brisk con- 
traction of the tensor fascia3 femoria (Brissaud's reflet), medullary 
in origin, which may occur even in cases where the toe« show no 
movement. This proves that the plantar reflex is not a pheno- 

menon confined to the foot but that it implicates the whole lower 
limb. It we employ a stimulus which is too strong, we may have, 
in addition, dorsiflexion of the ankle, and this may obscure the 
toe movement. Hence the importance of a gentle stimulus, 
graduated so as just to elicit the toe phenomenon and no more. 

This normal plantar reflex, flexor in type, only occurs when 
the reflex arc is intact, and when, in addition, the lower reflex 
arc is in comiection with the cerebral motor cortex by an un- 
injured pyramidal tract. In this sense it is a " cortical " reflex. 

If the pyramidal tract, conveying motor impulses downwards 
from the cortical " leg-centre," be interrupted in any part of its 
course by injury or disease, or if it be non-developed, as in 
infants who have not learned to walk, the type of plantar reflex 
is different and is known as BabinsH's phenomenon, or the extensor 
■plantar reflex, whose spinal path, traversing the lumbo-sacral 
, region, is no longer controlled by pyramidal impukes. In 



this sense it is a pure "spinal" reflex. In the Babinski phei 
menon, stimulation of the sole produces extension of the hallux 
instead of flexion (see Figs, 161 and 162). Moreover, this extensor 
movement of the great toe is slower than is the normal, brisk 
flexion. Sometimes, in addition to extension of the hallux, we 
observe a fan-like spreading out of the toes — " pht'nomene 
d'eventail." An extensor plantar reflex is practically always 
pathological (except in infants too young to walk), and if con- 
stantly present it indicates an organic lesion, and one which 
implicates the pyramidal tract.' It is therefore of tht 
value in the diagnosis between hysteria and organic disea 

Somewhat resembhog the Babinski reflex, but appa 
tinct from it, is Gordon's ^ paradoxical flexor reflex, which consists 
in an extension movement of the great toe or of all the toes when 
we press deeply, through the calf muscles, on to the deep flexor 
muscles beneath. To ehcit this reflex, the physician should place 
himself on the outer side of the patient's leg, the muscles of which 
must be completely relaxed. This is attained either by directing 
the patient to lie on his back or making him sit with his feet on a 
stool. The " paradoxical flexor reflex " is never present in health : 
it occurs only in organic, and especially in irritative, lesions 
of the pyramidal tract, It is sometimes associated with the 

' There is one eiceptioii to this rule. This is in the caw of a lower 
motor neurono lesion affecting the fleior miiscleB of the toes and sparing 
In such a (laae the only possibie movement would be ei- 
the other signs of lower neurone leaion, eBpecially tlie oiectriool 
prevent error. 
. Mtdicint, 1904. p. 071. 

tension . But 



Babinaki reflex, but may occur in cases where the Babinstn sign j 
is absent. 

Oppenheini's reflex is an extension movement of the hallux 
elicited in a sUghtly different way, viz., by firm stroking with some 
hard object (such as the handle of a percussion -hammer] just behind 
the postero- internal border of the tibia, from above downwards. It« 
significance is the same as that of the paradoxical fiexor tefiex. 

The cremasteric reflex ia very easy to ehcit in young children, by 
stroking the inner side ot the thigh. But in old men it is sluggish 
or apparently absent. Even in them, however, it can usually be. 
elicited by sudden firm pressure backwards against the sartoriua 
muscle in the region of Hunter's canal, or against the adductor 
tubercle of the femur ; this often succeeds when stroking the skin 
in the usual fashion is of no avail. The cremasteric reflex is fre- 
quently exaggerated on the aSected aide in cases of sciatic neuralgia. 

The bulbo-cavemosus reflex is of great diagnostic value in 
determining whether the lowest segments of the spinal cord are 
intact in a lesion about the level of the third sacral segment — 
where the ordinary reflexes of the lower limbs give us no help. 
To obtain the bulbo-cavemosus reflex, we place one finger behind 
the patient's scrotum, pressing upwards against the bulbous part 
of the urethra. With the other hand we pinch, or prick with 
a pin, the dorsum of the glans penis ; the bulbous urethra is at 
once felt to give a brisk twitch. Loss of this reflex indicates a 
lesion somewhere in its reflex are, either in the anterior cornua 
of the third and fourth sacral segments, or in the correaponding 
motor or sensory roots of the cauda equina. Loss of the bulbo- 
eavernoaus reflex is a fairly common sign in tabes, being due in. 
that case to a lesion of the afferent fibres of the reflex are. 

The superficial anal reflex can be easily obtained by pricking 
the skin of the perineum with a long " bonnet-pin," and watching 
whether the external aphincter contracts. This reflex ia sometimes 
lost in ancEsthesia of the perineum, or in lesions of the fifth sacral 
or of the coccygeal segment, or of their corresponding motor roots. 

Organic hemiplegia usually produces, at first at least, loss of 
the unilateral superficial reflexes all down the paralysed side, with 
one exception— viz, the plantar reflex, which persists, but from the 



first is changed into the extensor type. In hysterical heuiiplegiA,! 
on the other hand, even though cutaneous hemi-anEestheeia bal 
present, the unilateral akin reflexes on the paralysed aide aroJ 
UBUtiily preserved, with the exception of the plantej refleJC whu^l 
is often lost. An extensor plantar reflex never occurs in puio'l 
hysteria. In hysteria there may be absence not only of any toal 
movement on stimulation of the sole, but there ntay alao be loss g 
the reflex contraction of the tensor fascife femoria. This " com-l 
bined " absence of reflex movement both of the toes and of thl 
fascia lata of the thigh is always strongly suggestive of hyaU 

Vie. ir,3._Meth(Ml of eliuiiing j»w-jurk. 
Deep or Tendon Reflexes. — The following table gives a lisfcl 
of those deep reflexes which we commonly study when invesfi*^ 
gating cases of nervoua disease : — 

M«THOII or ELieiTlNO. RMDlt. 



filcupi .... 


Tri™p. .... 


T.pplng lo.« law, .«ppon=d in J.» ol,«^ 

baU.dpeD pnaltlon. 
Tapping liloepa If ndnn. i Biwpi cnntncta. 

naur baie of ajrinc. iXi.. contncl. 
Tapping upper part of ™il«.. Wrt.l M>d Dnser. «l.nd. 
Tappliig trlpepi Mndon. Trioepa contnwU. 
Tapping donum of vriit. Flnggn flai. 
Tapping patellar Wndcm. Vaaini Inlernns, dr.. contnct. 
Ttpplni Undo AchUllL Cair tuuicIa cnntrut. 


L3 1IK1L4. 



The knee-jerk may be taken as a type of these tendon reflexes. 
It has been a matter of dispute whether it is really a true reflex 
or not. Strictly speaking, the jerk occurs too soon after the tap 
for a nerve impulse to have time to travel up to the reflex centre 
in the cord and down again to the muscles. But bo long as the 
reflex arc is intact, there is a (constant " I'eflex tonus " in the vastus 

intevnua muscle wliich, when ttic tendon is struck, permits the 
jerk to occur. If this reflex tonus be lost from interruption of 
the reflex arc at any point, the jerk can no longer be obtained. 
Therefore, for practical purposes, the knee-jerk, though not a true 
reflex action itself, ia an index of the integrity of the reflex arc. 

To obtain the knee-jerk, we feel for the patellar tendon and 
strike it either with the edge of the hand or with some other fairly 
heavy object, such as a rubber percussion-hammer or a heavy 



paper-knife. The reault is a brisk contraction of the quadriceps. 
If we grasp the vastus internus with our other hand we can feel 
the jerk in cases where it is too feeble to move the knee- 
joint. The knee must be somewhat bent to put the quadriceps 
slightly on the stretch, and the muscles must be absolutely re- 
laxed. This latter point is of importance ; for sometimes it happens 

that a patient may have his muscles in a state of excesuve api 
so that we may fall to elicit the knee-jerk, and yet, if we buoC 
in relaxing the muscles by passive movements, the knee-jerk is 
not only present but found to be increased. The knee-jerk in such 
a case is not absent, but only " concealed " by the spasticity 
of the muscles. 

In testing the knee-jerk the patient may be sitting on a table 


f'With his legs dangling in the air, or better, on a. chair with the 
E'AoleB of the feet flat on the ground and the knees gently semi- 
Eflexed, or one knee may be creased over the other. A feeble jerk 
Emay be "reinforced" either by Jendrasaik's method (Fig. 164), 
r in which the patient hooks both handa together, pulling them one 
I against the other, and looksup towards the ceiling, thereby diverting 

othmi of diuiting ankle- jerk. 

hia attention and relaxing the leg muaclea, An even better 
method of reinforcement ia Laufenaucr's, in which we gra^p the 
patient's quadriceps whilst the patient aita with hia solea flat on 
the ground. The patient then grasps our upper arm with one 
hand, and auddeoly aqueezea when told to do ao ; meanwhile, 
down cornea the percussion -hammer (Fig. Itif)). The advantage 
of this method is that we can feel for ourselves whether the patient 
really is directing hia attention to the act of reinforcement. More- 



over, this method can be employed to reinforce feeble reflexes t 
the upper limbs, whereas Jeiidraasik'a method ia only available 
for reflexes of the lower limbs. Many other methods of reinforce- 
ment have also been suggested, e.g. by making the patient gaze 
at the ceiling and draw a long breath (Kronig '), or by making 
him read aloud from a newspaper or book as fast as possible 
(Rosen bach ') . 

Kiii. HH.— Supiimlof-jerk. 

Reinforcement will make a feeble jerk more evident ; but it I 
has no effect if the jerk be absent. 

The ankle-jerk has a diagnostic significance equal to that of 
the knee-jerk. To teat it, we make the patient kneel on a cbur 
with his feet projecting over the edge, and then tap the tendo I 
Achillis (Fig. 1(16) ; a brisk extension movement of the ankle ia ' 
the result. In tabes the ankie-jerk is often lost before the knee- I 
jerk. ' 

In the upper extremity we have various deep reflexes at our 1 
disposal. Of these, the guidtutior-jerk is ordinarily the niost aoc«s- 




aible. In testing it, we support the patient's hand in a aemi- 
aupinated posture, with the elbow loosely bent to a right angle. 
We tap with our hammer close above the styloid process of the 
radius (Fig. Ifj7). The supinator longus at once contracts and 
produces a flexion movement of the elbow. To elicit the triceps- 
jerk, the best way is not, as stated in some text-hooka, to allow 
the elbow to hang over the back of a chair, but rather to 
support the upper arm horizontally, with the elbow loosely flexed 
at a right angle. Then, feeling for the triceps tendon, we tap 
it with our hanuner, and the muscle at once contracts. 

Loss of Deep Reflexes. — Sometimes these reflexes cannot be 
elicited, even on reinforcement. This is always pathological, and 
generally indicates a lesion of the reflex arc. If thia lesion be in 
the afferent limb of the arc, there may also be anapsthesia of the 
corresponding nerve- or root-area. If it be in the anterior corn u, 
the efferent motor path, there will be muscular paralysis, 
with atrophy of the particular niuaclo. 

The following is a list of some of the chief conditions in which 
there is loss of the deep reflexes : — 

Ncarllla (Ak-ahol, mahctn, IHphtherIa, Lewi, Anenii:. ^ 

T.ilwniLB, C«i:he«U. *c > Jl-eriphcn 

Parlphenl Naric PBlitei I 

TiUh IXirMLIa 

Uoniinl Punljrili ol Inimia (Ulnlic type — 1 

™AW{u«; ;::::;: if""""" 

SobacatH Cnmhined DegeDermtlon ot FiMtirlor 

lateral Culunni^ltts (tags ot .... 
Anj tsul iHion In anj Hitter ot Conl . 
InbDtlle Pinljils (Acute ADlarktrl^illiiniyeUtli) . 
Fngmiive MuKiiUr Atroph]' (llhronlc Anb 


AniTotrophla Latanl Bclaroili 



L«,d,y.P.r.l,.i. {■'"^S.Vn^™.'" '"'' ^"^"' 

Myopathlei (Pieudohn»rtrophlc tnri Atmplik tjiH'S) . j ]||„,.ie iihII 

cephilDi mnd TuDioiiri of FDsterltir touo). 

Kmnlly Periodic Punlyili (darine uttKkiX 
I mmeil lately liter attack r,t Major Epilepay 
Daring Spinal AnBuilmla. 
Oompliitii traoivene laaluri ot Cord, 

From thia list we sec that, in addition to permanent orgamo 

lesions within the reflex arc itself, there are other conditions where 

I the deep reflexes are aboliahed- Tliua those reflexes are lost in 


the final stages of increased intra-cranial pressure, especially in 
hydrocephalus and in tumours of the posterior fossa. 

This is attributed by Raymond and others to a curious degeneration of 
the jK>sterior spinal roots, which sometimes occurs in such conditions, whereas 
van Gehuchten ^ ascribes it to loss of function of the rubro-spinal tracts, from 
pitissure on the mesencephalon. 

The knee-jerks are often lost during pneumonia. In the attacks 
of the rare disease known as family periodic paralysis (see p. 240), 
the deep reflexes in the affected limbs are temporarily abolished, 
owing to temporary paralysis of the muscle-fibres. The deep jerks 
are abolished for a few minutes just after an epileptic fit, during 
the stage of coma and flaccidity. Spinal anaesthesia temporarily 
abolishes all the deep and superficial reflexes in the lower limbs 
(see p. 400). We should also, remember that in complete 
trans-section of the spinal cord, all the deep reflexes below the 
level of the lesion are lost. If, however, the lesion be not com- 
plete, and there still survives some nervous tissue connecting the 
upper and lower portions, then the deep reflexes are exaggerated. 
In both instances the plantar reflex, if present, is extensor in type. 

Exaggeration of Deep Reflexes.— Sometimes the deep reflexes 
are exaggerated, so that the slightest tap on the tendon produces 
an unusually brisk contraction. This may be the result of various 
poisons — e.g. tetanus, or strychnine-poisoning — rendering the reflex 
centres unduly explosive ; or it may occur in simple neurasthenia. 
But organic lesions of the pyramidal tract are by far the com- 
monest causes of permanent exaggeration of the deep reflexes. In 
cases of organic disease, we look also for the presence of clonus. 
A clonus is a rhythmic series of muscular contractions, produced 
by sudden passive stretching of the tendon, the clonus continuing 
so long as the tension of the tendon is maintained. 

AnkU'chnus is the commonest clinical variety of clonus. To 
elicit it, the knee is passively flexed (the angle of flexion varying 
in different cases), and the ankle is suddenly dorsiflexed by upward 
pressure on the sole of the foot (Fig. 168). Ankle-clonus is due, 
as Weir-Mitchell has pointed out, to contraction, not of the 

* Lc Nevraxef 1907, vol. ix. p. 39. 



gastrocnemiuB but of the soleua muacle, since the posittoa of the 
knee which is best for eliciting ankle-clonus is one in which the 
gastrocnemius is relaxed. 

A spurious ankle-clonus is sometimea obtained in cases of hysteria. 
This can usiiatlv be diffffpriflRtw! from iipmiinc dfinnfi hv a char- 

acteristic feeling of voluntary contraction in the muatlea, especially 
at the commencement of the clonus, ditiiciilt to describe in words. 
Spurious clonus is generally poorly sustained and often irregular 
in rhythm. It is never asaooiated with an extensor plantar reflex. 

Knee-clonus or rectus -clonus is beat obtained by sudden down- 
ward traction on the patella, the knee being passively extended. 

In chronic organic affections of the pyramidal tract, practically 
every one of the deep jerks may become exaggerated into clonus. 


Thus in advanced disseminated sclerosis we may find in the same 
patient jaw-clonus, elbow-clonus, wrist-clonus, finger-clonus, knee- 
clonus, ankle-clonus, toe-clonus, &c. 

The presence of true clonus indicates that the reflex arc is 
hyper-excitable, owing to withdrawal of the regulating or restrain- 
ing influence normally exerted through the pyramidal tract. Ex- 
aggeration of the deep reflexes is therefore one of the cardinal signs 
of a chronic lesion of the upper or cortico-spinal motor neurone. 

It is unnecessary to give a Ust of the various organic diseases 
in which the deep reflexes are exaggerated. Suffice it to say that 
any chronic lesion of the pyramidal tract will produce exaggeration 
of the deep reflexes below the level of the lesion. Thus in 
paraplegia due to myeUtis, to lateral sclerosis, or to some other 
affection of the lateral columns, or in hemiplegia from organic 
brain disease, there is exaggeration of the deep reflexes in the 
paralysed limbs, owing to injury or disease of the pyramidal fibres. 

There is an important exception to this rule, to which we 
have already referred, namely in total trans-section of the spinal 
cord, as in some cases of fractured spine. Such total lesion 
produces a permanent flaccid paralysis of the lower limbs, with 
loss of the deep reflexes. But if the lesion be incomplete, we have 
the usual spastic type of paraplegia, with increased deep reflexes. 
In both instances, whether the lesion be total or partial, we have 
an extensor type of plantar reflex. 

We should also mention that in the early stages of 'peripheral 
neuritis the deep reflexes may be exaggerated. But this soon 
passes off and is succeeded by their diminution and loss. Again, 
in subacute cornbined degeneration of the lateral and posterior 
colunms of the cord, there is an early stage of spasticity with 
increased deep reflexes, and a terminal stage of flaccid paralysis 
with loss of reflexes. 

Sometimes in spastic paraplegia the muscular rigidity of the 
paralysed limbs is so excessive that it may be almost impossible 
to obtain the knee-jerks and other deep reflexes, which we should 
ordinarily in these cases expect to find exaggerated. This is 
because the muscles are already in a state of tonic spasm. But 



if we succeed in temporarily relaxing them, by passive cbanges 
of postme, we can Bometimes obtain tbe increased jerks and even 
the clonus. In most cases, the spasticity and tbe presence of 
an extensor plantar reflex will prevent errors in diagnosis. 

PttpiltaTjf LigSU Reflex. — ^This occupies & special category of its 
own. The reflex is elicited by exposing tbe pupil to light, after 
previous shading. Normally under such conditions the pupil 
contracts briskly, both when stimulated directly and when the 
pupi! of the opposite eye is exposed to light {consensual reflex). 
In some respects the pupil reflex to light, although occurring in a 
non-striated muscle, is analogous to a deep reflex, and it is useful 
to remember that in tabes this reflex disappears, as do the ordinary 
tendon- re flexes. But the subject of the various pupil-reflexes and 
their connections with the third nerve, with the ciliary ganglion, 
and with the cervical sympathetic is discussed elsewhere (see 
"Cranial Nerves," p. 1^0, and "Cervical Sympathetic," p. ."ilO), 

Organic Motor Reflexes. — These arc concerned with the 
sympathetic nervous system and with the contraction of non- 
atriated, involuntary muscles. The contraction of non-striated or 
smooth muscles is alow, unlike the brisk twitch of a reflex in a 
striated muscle. The following is a. list of organic reflexes which are 
of diagnostic interest. In some of these, such as tbe cilio-spinal 
or the scrotal, the reflex movement is executed entirely by non- 
atriated muscle. In others, such as tbe vesical, uterine, or rectal, 
the non-striated muscle is reinforced by voluntary striated muscles. 

MKTllon l>r KHOITIKU. 


Vgiical . . . 

SectaJ . . , 
Ocilllal . . . 

KcpcaUd •troklDE ot perliieun) or ap> 


D^tonalooin-lrrltaUoii dI tlp|»r pu-t 

From cenbrlini nr periphery. 

DlttcDilon of aniu by nngsr. 

Fnpil d)Ut«. 

Kectilm contracU. 

Ereolion of dorpon cavertiou. 

In all of them, with the exception of the cilio-spinal, the reflex 
movement can be accomplished, more or less perfectly, independ- 
ently of the central nervous s}^tem. 


In some text-books the statement is made that the reflex 
centres for the bladder, uterus, and rectum are situated within 
the cord. But within recent years clinical and pathological 
evidence has been brought forward, notably by L. R. Miiller,^ 
showing that the lowest reflex centres for the contraction 
of the bladder, and of the neighbouring hollow viscera 
possessing non-striated muscular walls, are situated extra- 
spinally, in the hypogastric and hsemorrhoidal plexuses of the 

The sympathetic vesical centre can be stimulated from the 
cerebro-spinal system. Micturition in the adult is a voluntary 
act, but only to this extent that it can be voluntarily initiated. 
This is accomplished by contracting the diaphragm and abdominal 
walls, producing a rise in the intra-vesical tension, which starts 
the reflex ; meanwhile the striated constrictor urethrae is 
voluntarily relaxed. But the non-striated bladder-wall itself, the 
so-called detrusor urinse, is not under control of the will. Once 
started, the bladder empties itself spontaneously, and we can stop 
the act only by forcibly innervating the constrictor urethree, 
usually a matter of considerable effort. But reflex micturition 
is often excited by irritation of the urethra, especially of its 
vesical end. Thus if a few drops of urine trickle into the 
prostatic urethra, an imperious reflex act of micturition results, 
which is difiBcult to prevent. Similar phenomena are produced by 
the irritation of a posterior urethritis. 

The fibres from the brain and spinal cord to the sympathetic 
vesical centre reach it through the lowest spinal roots, so that 
lesions of the spinal cord or cauda equina constantly cause 
bladder trouble. This generally takes the form of initial retention 
of urine, followed after several days by reflex incontinence ("in- 
continenza a getto " of Italian writers % in which the bladder con- 
tracts intermittently and expels the urine at intervals. Such reflex 
incontinence is generally associated with incomplete emptying, so 
that a certain amount of " residual urine " remains in the bladder. 

* Deutsche Zeitechrift f&r Nervenheilkunde, 1901, Band 21, s. 86. 

* Kebizzi, Riviata di Patologia Nervosa e MerUale, 1905, p. 80. 


In coses of coma or of the deep insensibility of fevers such as 
typhoid, we observe an initial retention of urine, followed by 
dlBtension, paralysis of the bladder-wall and overflow dribbling 
(" incontinenza per regurgito "). 

The sensory nerves from the bladder pass thiough the sym- 
pathetic by the rami comraunicantes, and along the posterior roots 
into the spinal cord. They serve to inform us of the distension 
of the bladder. There are also higher micturition centres, some in 
the spinal cord, others higher still in the brain, in the corpus 
striatum and optic thalamus ; others, highest of all, in the motor 
cortex, between the arm and leg centres, controlling the lower 
centres. When these higher centres are hyper-excitable, whether 
from disease or from emotion, we may have jyredfitancy of 
micturition, or even enuresis, a condition in which the brain and 
spinal cord on the slightest provocation send impulses which relax 
the compressor urethne. A similar condition exists in infanta 
who have not learned to control their subcortical micturition 

True dribbling of urine (" incontinenza vera "), as distinguished 
from intermittent contraction of the bladder, occurs most typically 
in cases of tabes and is mainly due to anaesthesia of the bladder, 
which being now insensitive to distension, is no longer stimulated 
to contract by the normal accumulation of urine. The tabetic 
patient with an anseathetic distended bladder expels his urine, not 
by contraction of the bladder but by pressure, with his abdominal' 
walls. This can readily be verified if we have to pass a catheter 
for the purpose of emptying a tabetic patient's bladder. True 
diibbhng also occurs in an over-distended bladder which, from 
obstruction in the prostate or urethra, has become flaccid, paralysed 
and atonic. 

The inierrtal anal reflex is tested by inserting a finger within 
the anus. Normally the finger is tightly grasped by the non- 
striated internal sphincter, This reflex is independent of the 
superficial anal reflex of spinal origin, to which we have already 
referred. When the internal anal reflex is lost, the : 
grasps the finger but remains open for several seconds, '' yawning," 


Iready ^J 

longer ^^M 
ning," ^H 


after the finger has been withdrawn. Such loss is most commonly 
due to anaesthesia of the anus, as in tabetic or other lesions of the 
Cauda equina. The result is incontinence of faeces. If there be a 
lesion within the spinal cord, above the spinal centre in the conus 
medullaris, there is intermittent rectal incontinence. But if the 
lesion be in the afEerent nerves from the rectum, the internal 
sphincter remains relaxed, and the faeces, if fluid, dribble away 
continuously when they enter the rectum, the patient being 
unconscious of the fact. 

To test the scrotal reflex, which is an excellent example of a 
purely sympathetic motor phenomenon, the patient stands bend- 
ing forwards with his legs wide spread and scrotum hanging free. 
The skin of the perineum is now stroked with some hard object 
five or six times in succession. After a few seconds an extremely 
slow, worm-like contraction appears in the non-striated dartos 
muscle, beginning near the perineal part of the scrotum and 
spreading forwards. This reflex can also be elicited by the applica- 
tion of cold to the perineum or scrotum. 



To moat of us the mention of the Cervical Sympathetic recalla 
memories of our early day« oa Htudenta of physiology, and mote 
particularly the memory of a classic experiment of Claude Bernaxd 
upon the rabbit. But it is perhaps not sufficiently realised that 
the cervical sympathetic is also of considerable uUnical importance. 
First of all, let us recall a few anatomical points. The sympa- 
thetic nervous system forma two gangliated cords, coursing like two 
strings of beads, one on each side, close in front of the vertebral 
column, and extending from the base of the slaill to the front 
of the coccyx. Above, these chains are connected with plexuses 
which enter the cranial cavity ; below, they converge and end 
in a loop on the coccyx. Each chain is made up of multipolar 
nerve-cells and nerve-fibres, all of them involuntary fibres des- 
tined mostly for organs which posBesa smooth muscle-fibres and 
for blood-vessels. In addition to its own longitudinal fibres, the 
sympathetic chain receives connecting- fibres from the central 
nervous system. These are called the rami communicantes — some 
of them white, some of them grey. They unite the sympathetic 
to the anterior primary divisions of the spinal nerves. The white 
rami, consisting of medullated fibres, pass from the spinal cord 
to the sympathetic ganglia; they are all efferent in function, 
and leave the cord through the anterior nerve-roots. A certain 
number of white rami, viz. those emerging along with the seventh, 
ninth, and tenth cranial nerves, and those emerging with the 
second and third sacral nerves, pass du-ectly to the viscera and 
blood-vessels, to end in small peripheral ganglia, without joining 
the sympathetic chain itself, To these two sets of splanchnic 
nerve-fibres, cranial and sacral, the name para-gympatketi 
has been given, to distinguish them from the ordinary sympatheti 

lanchnio ^J 
■ic fibre* ^H 
pathetic ^^^1 


nerves and ganglia. The grey rami, consisting of non-medullated 
fibres, originate in the sympathetic ganglia, and, like the others, 
join the spinal nerves. Some of them are afferent, going into 
the spinal cord, reaching it through the posterior nerve-roots ; 
others turn off with the peripheral nerves and supply to the skin 
involuntary efferent fibres, whose functions are vaso-motor, vaso- 
inhibitory, pilo-motor, secretory, &c. In addition, the sympathetic 
cords give branches, either directly or through the great pre- 
vertebral gangUa (the cardiac, solar, and hypogastric plexuses), 
to the various glands and viscera of the body, to the heart and 
blood-vessels, to the genital organs, and to the non-striped 
muscles of the body generally. 

In addition to the ordinary ganglia of the sympathetic chain, 
there are also minute micrO'SympcUhetic ganglia or hypospinal 
ganglia of Marinesco and Minea,^ which are so small that they 
can only be identified by microscopic examination of the spinal 
nerves immediately below the junction of the anterior and 
posterior nerve-roots. These microscopic ganglia are closely con- 
nected with the rami conmiunicantes. Their precise function is 
still obscure. 

Lastly, the cervical part of the sympathetic chain has very 
special " oculo-pupillary " fibres, which are clinically of consider- 
able importance. These supply the dilator pupillse, the non- 
striated part of the levator palpebrae superioris and the orbital 
muscle of Miiller — a small bundle of non-striated muscle which lies 
behind the globe of the eye and bridges across the spheno- 
maxillary fossa at the back of the orbit. The cervical sympathetic 
also suppUes secretory fibres to the submaxillary gland, and, 
like the sympathetic elsewhere, it supplies fibres to the cutaneous 
blood-vessels, also (through the hypoglossal nerve) to the vessels 
of the tongue, and, lastly, fibres to the sweat-glands of the head 
and neck. 

The pupil-dilating fibres have a peculiar course, which it is 
important to remember (see Fig. 169). Arising from the pupil- 
dilating centre in the medulla, they descend in the lateral column 

1 Neurologiaches Centralblatt, 1908, p. 14G. 



of the spinal cord to tbe cilio-spinal centre in the lower cervical 
region. They emerge from the cord through the anterior roots of 
the first and second thoracic segments, and enter the inferior 
cervical ganglion of the cervical sympathetic by white rami 
commutiiamlcs. They then ascend in the cervical sympathetic to 

of eurvical 

the Gasserian ganglion and pass thence to the orbit (along the 
ophthalmic division of the fifth cranial nerve), and vtd the long 

cihary nerves to the pupil. They do not traverse the ciliary 
ganglion (see Fig. 4ti, p. 11«). 

It is evident that ocular and other symptoms may be produced 
not only by lesions of the ascending fibres of the cervical sympa- 
thetic, but also by lesions within the cord, afEecting the fibres in 


their downward course from the medulla (this being remarkably 
frequent in syringobulbia and in unilateral lesions of the medulla), 
or by lesions of the first two thoracic nerves or of their anterior 
roots, or even by lesions of the ophthalmic division of the fifth 
cranial nerve, though this last is rare. 

The signs of paralysis of the cervical sjanpathetic are very char- 
acteristic. Fig. 170 shows a woman who was sent to hospital with 
the history that six years previously she had some tuberculous 
glands removed from the right side of her neck. When she 
recovered from the anaesthetic, she learned that the jugular vein 
had been injured during the operation. But other structures had 
also been injured, and amongst them was the cervical sympathetic 
(which Ues behind the carotid sheath), because afterwards she 
noticed that the right eyeUd drooped a little, that the right 
side of the face flushed less than the left, and that when she 
chewed, a small patch of excessive perspiration appeared below 
the right eye. We observe from the photograph that the right 
pupil is smaller than the left, from paralysis of the dilator 
pupillflB. Moreover, the affected pupil does not dilate when 
shaded, yet it contracts briskly to light and on convergence, 
since the third cranial nerve, which through the ciliary ganglion 
innervates the sphincter pupillae, is unaffected. Further, we 
notice that the upper lid droops, making the palpebral fissure 
narrower than on the healthy side. This is due to paralysis of 
the non-striated part of the levator palpebrse, which is inserted 
into the upper edge of the tarsal cartilage. The voluntary, 
striated fibres of the levator, inserted into the skin of the 
upper Ud and suppUed by the oculo- motor nerve, are unaffected, 
and the patient is therefore able to elevate the lid voluntarily 
to its full extent. This, therefore, is not a true ptosis, but a 
" pseudo-ptosis." 

We also notice that the right eye has sunk into the orbit, owing 
to paralysis of the non-striated muscle of Muller, which normally 
keeps the globe pressed forwards. This " enophthalmos " narrows 
the palpebral fissure still more. The difference in antero-posterior 
projection between the two eyes is seen best if we make the patient 



lie down, we then stand behind and look down at the forehead 
and ejebaila from above. 

On palpating the two globes, we find that the intra-ocular 
tension is diminished on the affected side. 

Such are the " oculo-pupillary " symptoms of cervical sympa- 
thetic paralysis. There are, however, one or two additional points. 
"When the cervical sympathetic is paralysed, it no longer responds 
to stimulation. There nre two clinical ways of stimulating it. One 

is by pinching or pricking the aide of the neck, when we produce a 
dilatation of the pupil on the same side ; this " cilio-apinal reflex " 
ifl abolished in cervical sympathetic palsy. Another method of 
stimulating the cervical sympathetic is to drop into the conjunctiva 
a few minims of a solution of cocaine. The result is that the 
pupil dilates, the upper lid retracts, and the eyeball is pushed 
slightly forwards. All these phenomena were absent in the 
patient just referred to. She also told us that when her face flushes, 
it does 80 only on the aHected side. Moreover, her face on the 




aiTected side no longer sweats except in one little patch below t 
orbit, where it sometimea sweats spontaneously when she chews. 
To verify this point we made her sweat profusely by means of 
pilocarpin, and found that the right side of the faoe remained dry, 
except in a small area below the inner canthua of the eye. This 
survival of a little oasis of sweating on the dry side might perhaps 
mean that a small twig of the sympathetic had escaped injury, 

Kiu. 171.— I'limljsis nf ihE l«Ct corvioalajrnpathetio from a tomonr I 
ttt the root uf the neck. 

or more probably that sweat fibres to that part of the face J 
supplied through a branch of the trigeminal nerve. 

So much for lesions of the sympathetic chain itaelf. But the 
oculo- pupillary and other fibres may also be damaged at some 
point between the spinal cord and the inferior cervical ganglion. 
Fig. IT 1 represents a boy of seventeen who had felt a tingling sensa- 
tion down his left arm for several months, A few weeks before 
he came under observation, he noticed that a swelling had 
appeared in the lower part of the neck on the same side. At a 
glance we see that the cervical sympathetic is affected. There 
are pseudo- ptosis, niyosis, and enophthatmos. The left check 


is a little fuller than the right. The cilio-spinal reflex was 
absent on the left side. On examining the root of the neck, 
we found that the left clavicle was bulgetl forwards at its inner 
end, the supra-clavicular fossa being filled up. Further, there 
was percussion-dulneas all over the apex of the left lung, with 
diminution of breath sounds and of vocal resonance. There was 
also a strip of diminished sensation to touch and pain along the 
inner aide of the left upper limb, reaching to the wrist and corre- 
sponding to the cutaneous areas of the first and second thoracic roots. 
Moreover, there was slight wasting of the hypothenar muscles of 

the left hand, supplied by the first thoracic root. The skin of 
the left hand was dry, whilst that of the right was moist, and the 
patient himself noticed that in hot weather only the right side of 
his face sweated. On comparing corresponding arteries of both sides 
we found that the pulse in the left upper limb was smaller than in 
the right. All this pointed to the presence of a soUd mass behind 
the left clavicle, compressing the subclavian artery, aSecting the 
first and second thoracic nerves, including not only their sensory and 
motor fibres but also the cervical sympathetic fibres. This diagnosis 
was confirmed by radiography, which showed very clearly {Fig. 172) 
a tumour at the apex of the left lung. This tumour grew rapidly> 



compressed the subclavian vein, producing cedenia of the 
upper linib, and within six months the patient died. 

Fig. 173 is that of a seaman on an Atlantic liner who ' 
thrown by a heavy sea againat an iron rail, rupturing the whid 
ot the brachial plexus on the right aide. He was unconscioas 
for a number of days, and during this period he was trephine*! 
over the left Rolandic area on the supposition that the paralyi 

Fjd. 173.— Iluplurp of l>rapUial plesus on riRht =Mc ToU.1 ni 
of right upper liiiili bfilnw bUnk line. 

of the arm was of cerebral origin. In addition to complete moj 
and sensory paralysis of the upper limb, nbvioiisly of lower motor 
neurone type, reaulting from the brachial plexus palsy, he showed 
very beautifully the oculo -pupillary signs of cer^ncal sympathetic 
paralysis on the right side— «nophthalmo8, myosis and pseudo- 
ptosis (see Fig, 174), In this patient, however, the pupil still 
dilated to cocaine, probably because aonie pupil -dilating fibre 



entering the cervical aympathetic from the second thoracic root, 
had escaped injury. 

Figs. 175 and 176 are those of a soldier who came under my 
observation during the South African war in 1901. He had been 
wounded in the neck by a Mauser bullet. At the time of hie 
injury he was IjHng on his face, firing at the enemy. The bullet 
entered his neck an inch and a half below the left mastoid proceaa, 
crossed the middle line in front of the vertebral column, and came 
out through the seventh right interspace in the posterior axillary 

line, lodging in his bandolier. He immediately felt a eenaation 
" like an electric shock " all over his body, but especially in the 
right upper extremity, which became at once totally paralysed. 
He had htemoptysis owing to the perforation of the lung, and 
for a few days some difficulty of swallowing, probably due to injury 
of the oesophagus. In about three weeks the htomoptysis gradually 
ceased, and the right upper limb recovered power, so that when 
I first saw him, two and a half months after the injury, he was 
able to move it freely at all joints. Ever after the accident he 



noticed that he did not sweat on the right side of the i 
iietk. nor in the right Upper limb. 

The photographs show that the patient has an area of alight 
analgesia (hounded by the thick black line) along the inner border 
of the right upper limb, corresponding to the areas supplied by 
the eighth cervical, first thoracic, and second thoracic nerve-roots. 
He also has slight weakness of the small muscles of the thumb. 

FigB. 175 and 17tl.— ParaljMs oC the ri^bt oerrioal Bjmp&Cbetic, from afl 
bullet wound of the lower ruots of the brachial plexus. The arekl 
of the right upper limb within tbe black line is anieathetio. Ths J 
crOBBea oD tbH trunk indioale the boundary o! an area of anidroBis. 

innervated by the first thoracic root. We also observe that the 
right cervical sympathetic is paralysed, ao that he has contraction 
of the pupil, enophthalmos, and pseudo-ptosis on that aide. 

But there is a point of special interest in this patient's photo- 
graphs. They demonstrate a point which, so far as I know, had 
not previously been mapped out in the human subject, viz., the 
extent of skin supplied with sweat-fibres by the cervical sj-rapa- 
thetic. In the tropical heat to which we were exposed, this 


patient sweated profuselj, except in an area on the right side 
of the head, neck, upper limb, and upper part of the trunk. That 
area remained dry, and the boundary between sweating and non- 
sweating akin was aharp and diatinct. In order to photograph 
it, the happy thought occurred to blow powdered charcoal on 
the skin. Thia stuck on the sweating side, and blew off on the dry 
side. We were then able to photograph the non-aweating area, to 
which the cervical sympathetic should have been distributed. As 

may be seen from the photc^apha (Figs. 175 to 177), the boundary 
of this area, marked by croaaea, runa down the middle line of the 
head and neck, and turns horizontally acroaa the chest at the 
level of the third rib in front and the spine of the scapula behind, 
including the whole of the upper limb. 

Before leaving the aubject of cervical sympathetic palsy, it 
should be mentioned that excision of the cervical sympathetic has 
beeu employed therapeutically in certain diseases. Thus in cases 
of glaucoma, ophthalmic surgeons have recommended this opera- 


tion to diminish the intra-ocular tension, and a certain amount of 
benefit has resulted. Bilateral excision of the cervical sympathetic 
has also been tried for the relief of epilepsy, in the hope of paralys- 
ing the cerebral vasomotor nerves and thereby rendering the 
brain hypersemic, especially in cases where fits were ushered in by 
blanching of the face. But the results recorded have not been 
sufl&ciently good to warrant us in recommending this procedure. 

Let us now consider briefly the reverse condition, viz., irrita- 
tion or stimulation of the cervical sympathetic. The signs are 
exactly the opposite of those produced by paralysis. We there- 
fore have dilatation of the pupil, exophthalmos or forward projection 
of the eyeball, widening of the palpebral aperture (Stellwag's sign), 
and delayed descent of the upper Ud when the patient looks 
downwards (von Graefe's sign). All these phenomena can be pro- 
duced, to a certain degree, by dropping into a healthy eye a 
solution of cocaine, which stimulates the cervical sympathetic. 

Fig. 178 is that of a man who had lymphadenomatous enlarge- 
ment of the lymphatic glands. During his stay in hospital, we 
noticed that quite rapidly, within a day or two, he developed on 
the right side exophthalmos, widening of the palpebral fissure, 
and some dilatation of the pupil. There was also in hospital at 
the same time a soldier who had similar signs in one eye due to 
an aneurism at the root of the neck, pressing on and irritat- 
ing the cervical sympathetic. If such pressure continues, the 
signs of stimulation may pass off and be replaced by those of 
paralysis. Our lymphadenomatous patient, however, died nine 
weeks after the appearance of stimulation phenomena, without 
any change in the direction of paralysis. 

Certain cases of apical phthisis are accompanied by inequality 
of the pupils, probably due to irritation of the cervical sympathetic 
by changes in the pleura. There is a good deal in favour of 
the view that many of the signs of exophthalmic goitre are the 
result of stimulation of the sympathetic, whether by excessive or 
perverted thyroid secretion. Figs. 179 and 180 are from a case of 
exophthalmic goitre where the symptoms were preponderatingly 
right-sided. The tachycardia of this disease is probably due to 


stimulation of cardio-accelerator fibres, which we know are 
derived from the sympathetic. The thyroid enlargement may 
perhaps be explained as a result of vasomotor paralysis of the 
cervical vessels, including those of the thyroid gland itself. 

But though afTections of the cervical sympathetic are the most 
readily recognised, we must not forget that the thoracic and 
abdominal portions of the sympathetic may also be diseased, 
although the symptoms thereby produced, being mainly visceral, 

less easy of diagnosis. Thus some cases of angina pectoris 
may be the result of irritation of the cardiac plemis, while the 
peculiar reflex vaso-conatriction of the pulmonary vessels, with its 
transient dilatation and irregularity of the right heart, met with 
in certain gastric and hepatic disorders, has been regarded as 
an affection of the thoracic part of the sympathetic. Affections 
of the abdominal sympathetic or of its great pre-vertebral ganglia 
produce still more striking cUnical phenomena. Thus the rare 
condition known as acute dilatation of the stomach, and many of 



the symptoms of acute peritonitis, such as the inteatinal paraljr 
sis, meteorism, amal! pulse, and general collapse, may be the 
result of acute paralysis of the solar plexus — the " abdominal 
brain " ; while irritation of the solar plexus is exemplified in 
cases of lead colic, with its pain, constipation, and increased 
arterial tension. The various \-iRceral " crises " of tabes — gastric. 


Exopbbhatmic goibi'B, the ocul&r iytDptoms being more marked 01 

side, Kig. IHO ebows von Giaefe'e sign in the right eye o 


intestinal, renal, &c. — may also be due to irritative changes in the 
various parts of the abdominal sympathetic. To the same cause 
also may be attributed the intestinal symptoms of exophthalimo 
goitre, consisting not in ordinary diarrhcea with loose motions, but 
rather in an abnormal frequency of defiecation. Muco- membranous 
colitis, with its characteristic paroxysms, has been ascribed bv 
Mathieu and others to some disorder of the solar plexus, though 
pathological evidence on the point is scanty. To solar or 




Bplanchnic disease may also, perhaps, be attributed such affections 
aa orthostatic albuminuria, diabetes insipidus, and certain forms 
of gtycoBuria. 

In a^ition to visceral disorders, disease of the abdominal 
sympathetic is also associated with certain pigmentary changes in 
the skin. Of these, the most striking examples are furnished by 
the cutaneous pigmentation which is occasionally present in 
exophthalmic goitre and, still more, by Addison's disease, with its 
characteristic bronzing of the skin, its asthenia and its paroxysmal 
diarrbcea. Addison's disease is probably the result of two factors 
—irritation of the abdominal sympathetic and inadequacy of supra- 
renal function, the proportional rule played by each of these 
varying in diSerent cases. 

Angio- Neuroses. — These comprise a group of diseases which 
appear to depend on disorders of the sympathetic fibres which 
regulate the blood-vessels. The paroxysmal dyspncea of asthma, 
with its slow and laboured breathing, is doubtless to be referred to 
a neurosis of the thoracic sympathetic, whether, as some hold, 
< the phenomena be the immediate result of a sudden vascular en- 
I gorgement of the bronchial mucous membrane, or whether produced, 
according to another view, by spasm of the non-striated bronchial 
muscles. In any case, the paroxysmal nature of the aflection, its 
apparent toxic origin in some cases, its connection in other cases 
with nasal or other reflex sources of irritation, its frequent asso- 
ciation with the gouty diathesis— all these facts indicate a 
' functional and not an organic lesion of the sympathetic. 

Most angio -neuroses, however, affect the blood-vessels of 
the more superficial parts of the body, such as those of the 
skin or of the muscles. Amongst the cutaneous angio -neuroses, 
perhaps the commonest is the syndrome known as Raynaud's 
I disease. The mildest degree of this is local ■pallor (" local syncope " 
^L or " dead finger "), where the affected parts, usually the fingers, 
^1 less frequently the toes, the odgea of the ears, or the tip of the 
^1 nose, suddenly become cold to the touch and of a waxy 
^B white colour. Together with this, the patient feels a tingling 
^H or other peculiar sensation (acro-pariesthesia). Actual blunting of 


sensation to touch may be present. One or both hands may be 
affected, sometimes identical fingers in both hands ; the thumb 
is less often affected than the other digits. The attacks last from 
a few minutes to several hours and are commonest in winter. 
They are often brought on by washing the hands in cold water, or 
by fine digital movements such as sewing or piano-playing. As the 
attack passes off, the patient feels a sensation of tingling or even 
of pain. A more severe variety is that of local asphyxia or cyanosis, 
in which the affected digits suddenly become discoloured, varjring in 
tint from a dusky blue or slate-colour to an intense purplish- 
black. Pressure on the discoloured area causes a white mark which 
persists for several seconds, before the lividity slowly reappears. 
The pain is usually more intense than in local syncope. As 
the attack passes off, the affected part often sweats freely. But 
the most severe variety of Rajmaud's disease is symmetrical 
gangrene^ which is usually preceded by local asphyxia and some- 
times by local syncope. As a rule, the gangrenous process is 
confined to a small part of the cyanosed area. In its mildest form 
the necrosis is limited to the epithelium, so that only desquamation 
results; more often a small blister forms, with blood-stained 
contents. This bursts, leaving an ulcer which subsequently 
cicatrises. The nails may be lost and subsequently reproduced. 
Or the necrosis may extend deep into the tissues, forming a dark 
slough. Whole phalanges may imdergo dry mununification and 
be cast off, leaving a conical stump. The bones as a rule escape 
necrosis. Pain is usually severe during the initial cyanosis. The 
sjrmptoms of Raynaud's disease are due to local spasm of the 
vessels, the sudden onset and disappearance of the symptoms 
being incompatible with any other hjrpothesis. The coexistent 
sensory symptoms are probably due to imperfect blood-supply. A 
paroxysm of local syncope or cyanosis can usually be relieved, 
as Gushing has pointed out, by applying a tight flat rubber 
tourniquet aroimd the Umb above, so as to occlude all the vessels, 
both arteries and veins, and leaving it on for several minutes. 
Then, when the tourniquet is taken off, there is a temporary vaso- 
motor paralysis, the whole limb flushes to the finger-tips, and a 


Case of ErjUuttDMU^^ in a man age<l 5:!. I'be coudiliou affected 
both lower limbs. 

The upper drawing shows the appearance of one foot daring a 
parozjam when Che lower limb la lupported in a horizontal position. 
The sole of tbe foot 1b at a bright pink coloiu, this coloar also extending 
on to the domm of the terminal phalanx of each too. 

The lowBi drawing shows the effeot of allowing one foot to Lang 
dependent for a few mJnntea. There is extreme cjonoeiB extending as 
high as ttM ankle. There fs alto eevere pain, which is partiallj relieved 
bj resuming the horizontal postnre of the limb. 



resembling Raynaud's disease. Fig. 181 represents three brotbi 
aged five, four, and three years respectively, in all of whom, one 
winter, areas of local necrosis appeared in the feet. The eldest 
child had necrosis of the skin of both heels, followed by similar 
areas on the dorsum of the right foot and on the fourth left toe. 
The second chihl had cyanosis and some necrosis of the dots«l 

surfaces of both feet, whilst the yomigest had severe necrosis"! 
the hallux, fourth and fifth toes on the right side, and n smaDer 
area of necrosis on the plantar surface of the left hallux. It 
is poaaible that the paroxysms of family periodic paralytis 
(see p. 240) may be the result of a recurrii^ vaso- motor 
spasm of the anterior spinal arteiy, which, as we have acbd, 
supphes the anterior comua of the spinal cord. 




Another paroxysmal disease of a ngio- neurotic origin is inter- 
mittent limp, whose symptoms we have already described (p. 238). 
where the arteries not of the akin but of the deep structures are 
in a state of temporary spasm. 

Acute angio-neuTolic asdetna is undoubtedly a vaso-nenrosia. It 
is characterised by the sudden appearance of areas of transient 
osdema in the loose cellular tissue of various parts of the face, 
trunk, or Umbs. After lasting a few hours or days, the swelling 
passes off spontaneously. It may also attack mucous mem- 
branes, for example, those of the respiratory or gastro-intestinal 
tract'. A gastric attack may cause urgent vomiting, an intes- 
tinal attack meteorism. colic, and bloody diarrhcea, and if the 
patient happens to have an attack in the larynx, death may 
result from asphyxia. In the sldn, the parts most often attacked 
are the lips, cheeks, and eyehda. The disease sometimes runs in 

In chronic hemiplegia it is not uncommon to &ad (edema of the 
hand or foot on the paralysed side. Permanent coldness and 
cyanosis are very common in the paralysed hmbs in cases of 
old anterior poliomyelitis. Even in warm weather the flaccid 
hmb remains cold and sometimes blue in the hand or foot, aa the 
case may be. Such cyanosis diSers from that of Raynaud's group 
in being permanent and not paroxysmal, 

Certain varieties of urticaria may be referable to affection of 
the nervous system, as in certain cases where the characteristic 
itching wheals appear on sudden emotional excitement. These 
patients appear to have a specially low coagulability of the 
blood due to deficiency of calcium salts in the liquor sanguinis. 
But urticaria is much more often toxic in origin. Dermoffmphism, 
on the other hand ('" factitious urticaria " or " urticaria scripta "), 
is a reflex cutaneous phenomenon. It is elicited by stroking 
the skin firmly with a smooth, hard object, such as the head of 
a pin or the fijiger-nail. If, for example, we draw a diagram 
or write on the patient's skin in this way, a red area appears 
within a few seconds. The skin then becomes elevated into 
a hard, white ridge, which can not only be felt hut seen, as if the 



pattern or writing had been embossed on the skin (see Fig. Ill 
p. suit). Thia laata for many minutes and passes oil graduallj. 
Unlike true urticaria, dermographism is unaccompanied by itching. 
The phenomenon is commonest in neuropathic people, but is not 
confined to them : it is particularly common in exophthalmic 
goitre/ and may sometimes be found in apparently healthy 

Lastly, we have to refer to certain abnormalities of sweating 
which are due to nervous disorders. We have already alluded to 
localised anidrosis or absence of sweat in certain cases of cervical 

t'lO. 1 82.— Area of lucaliswl 
fweotioK daring masti- 
cation of pilD^PIlt Ellll- 

usetl 39. The oonciition 

Fio. ISil-Area of localised J 
sweating during innstioa- 1 
tioD of pungent substances.,'! 
From a. man afced 36, inl 
whom thi! iTODdition ap-J 
poared at the agn of 2S. 

sympathetic palay. But sometimes we meet with -part 
localised hyperidrosis or excessive sweating. Figs, 182 and I8S 
show the areas of excessive sweating in two patients. In one the 
condition was congenital, and consisted in excessive sweating on 
the left side of the scalp and face, corresponding to the whole of 
the first division and part of the second division of the trigeniinal. 
In the other, the whole area of the trigeminal on the right side was 
affected and the condition appeared at the age of twenty-eight. 
In both these patients, who were otherwise healthy, the paroxysms 
of sweating occurred only on chewii^ highly-flavoured articles, 
such as onions or pickles. This condition Bugge3t« some hypei- 

' Drenuhfi'lfl, Bril. Med. Journal. XuvpitiIht IS. 19I)C, 


^■^citabilitj of the reSex sweating centre fur tht; fare, possibly 
* witliin the pons. Fig. 184 ia a photograph of an area of hyper- 
itlrosis on the left hand and wrist of a young woman of nineteen. 
Ill her, the paroxysms occurred three or four times a day, spon- 
taneously, chiefly about the time of the menstrual period or 
when she was excited. In this case the distribution suggested a 
segmental or root area, apparently about the eighth cervical and 


first thoracic segments, and counter-irritation over the lower part 
of the neck, front and back, near the exit of these roots, 
produced rapid amelioration of the condition. 

In certain chronic cases of hemiplegia, we not infrequently 
observe excessive sweating of the hand and foot on the paralysed 
side. This ia doubtless due to changes in the sweating centres in 
the central nervous system. 



The boundary between organic diseases and the so-called func- 
tional diseases or neuroses is entirely imaginary. The old defini- 
tion of a neurosis as a nervous disease devoid of anatomical 
changes is inadequate. Disease is inconceivable without some 
underlying physical basis. The lesion need not be visible micro- 
scopically ; it may be molecular or bio-chemical. In certain 
diseases, such as epilepsy and paralysis agitans, the essential 
underlying lesion is still undiscovered, yet we no longer class 
them as neuroses in the strict sense of the word. Therefore when 
we as physicians talk of neuroses, although we may have a fair 
general idea of what we mean, we find it difficult to express our 
definition in words. 

In " functional " nervous diseases the underlying physical 
changes are slight in degree and they are often capable of cure. 
In this respect they differ not only from ordinary organic diseases 
due to gross anatomical lesions, which almost always leave behind 
them some permanent damage, but also from such steadily pro- 
gressive and incurable affections as paralysis agitans. Neverthe- 
less we must recognise that the neuroses are real diseases, as real 
as small-pox or cancer. A sharp distinction must be drawn 
between a hysterical or a neurasthenic patient, and a person who 
is deliberately shamming or malingering. The imitation of other 
diseases — neuromimesis — ^which is often seen in hysteria is not a 
volimtary affair. The hjrsterical or neurasthenic patient usually 
has no knowledge of the disease which he or she may unconsciouslv 
simulate. The various paralyses and pains from which hysterics 
and neurasthenics suffer are as real to the patients as if they were 
due to gross organic disease. 

The three chief neuroses proper are neurasthenia, psychasthenia, 




and hysteria. Neurasthenia is an " exogenous " neurosis ; 
psychaathenia is essentially " endogenous " ; so also is hysteria, 
although outside factors may act as exciting or precipitating 
causes. Each of these neuroses has fairly distinctive character- 
istics of ita own, hut in practice they are often combined with 
each other and may also coexist with organic diseases. Thus a 
hj-sterical patient may suffer from neurasthenia, or a pBychaethenic 
patient from hysteria ; nor is there anything to prevent a neuras- 
thenic patient from having, say, an attack of cerebral hcemorrhage. 
Moreover, any gross organic disease may induce hysterical or neur- 
asthenic phenomena in addition to the signs of organic lesion. 
In fact certain cases of grave organic disease (especially disseminated 
sclerosis and some cerebral tumours), may at first produce symptoms 
which are indistinguishable from those of functional disease — 
which, in fact, are functional. In such cases the neurologist must 
be on his guard to detect the underlying organic affection, and to 
distinguish its symptoms from those of the superadded hysteria 
or neurasthenia. Functional symptoms, then, may coexist with 
gross organic disease. 

Let us briefly recall some of the characteristic symptomfl ot 
the chief neuroses — neurasthenia, psychasthenia, and hysteria — and 
note in what respects they differ, if at all, from analogous symptoms 
produced by gross organic diseases. 

Neurasthenia is not a primary disease. It is exogenous, the 
result of something else. The commonest cause is over-strain, 
.mental or physical. It may also be produced by excess in drugs 
Buch as alcohol, tobacco, ot cocaine ; or, again, by the toxins of 
various infective diseases such as influenza, enteric fever, &c. 
Or neurasthenia may result from organic diseases, whether these 
be of the nervous system (e.g. tabes, disseminated sclerosis) op of 
other systems (as in gout, rheumatism, cancer, and so on). Lastly, 
a particularly frequent cause is traumatism, especially in railway 
accidents which produce a common type of neurasthenia including 
the so-called " railway spine." Patients with a low power of 
resistance are, of course, specially liable to become neurasthenic 
from any accidental cause, but we must remember that even 


healthy individuals, without neuropathic taint, may be rendered 
neurasthenic as a result of over-strain or trauma. 

The symptoms of neurasthenia are chiefly subjective. The 
patient complains of undue fatigue and feebleness of attention, 
so that sustained mental efEort becomes impossible — so-called 
" brain fag." There is " irritable feebleness," with general depres- 
sion of the whole nervous system. The patient's memory, however, 
is unimpaired, and he relates his woes with great wealth of detail. 
He is full of aches and pains, but on physical examination there 
is little or nothing to be made out in the way of anaesthesia or 
motor paralysis. The knee-jerks in neurasthenia are sometimes 
abnormally brisk and accompanied by a sudden feeling of shock 
in the spine, making the patient start. True ankle-clonus, however, 
does not occur, and the plantar reflexes, if present, are of the normal 
flexor type. Most neurasthenics are poorly nourished, but not all 
of them. For purposes of treatment neurasthenic patients can 
be divided into two classes, viz., those in whom the arterial tension 
is above normal and those in whom it is abnormally low. The 
cases where there is increased arterial tension, according to Fleury, 
are generally toxic in origin and require special attention to the 
organs of excretion. In cases with subnormal arterial tension, 
on the other hand, we devote ourselves to augmenting the 
patient's nervous energy by anabolic treatment in the form of 
diet, massage, electrical and hydro-therapeutic measures. 

Psychasthenia is a much more serious affection, in which the 
mental phenomena overshadow the physical. Unlike neurasthenia, 
which is usually a disease of adult life resulting from some extraneous 
cause, psychasthenia is an endogenous disease, the culmination of 
an ingrained neuropathic heredity, and its earliest indications 
appear in adolescence or even in childhood. In short, the psych- 
rsthenic, like the poet, is bom, not made. Moreover, while neur- 
asthenia is an eminently curable affection, the psychasthenic patient 
remains psychasthenic all his life, though his symptoms may 
be alleviated. 

The outstanding symptoms of psychasthenia, as Janet has 
emphasised, are the psychasthenic "stigmata," the obsessions 





and the imperiouB acte, Tbe stigmata of peycha^thenia may 
be psychical or phyBical. The psychical stigmata of psych- 
asthenia are mental anergia and irresolution. The psychasthenic 
feels himself incapable of fixing his attention, whether for physical 
or mental effort ; he has a feeling of general hesitation and doubt, 
and has to lean for moral support on others possessing a stronger 
character than his own. Sometimes he has a feeling of double 
personahty, in which he feels as if be had two co-existing egos. 
The doublepersonalityofpsychasthenia differs from that of hysteria, 
in which the duality is an alternating one, unknown to the patient. 
The physical stigmata of psychaathenia are evidenced in the 
patient's actions. Kverything he does tends to be clumsy and i/auchc- ; 
his very gait may be ungiinly ; he is often a " liqueur " ; he is 
full of affectations and mannerisms. In addition he may have 
numerous neurasthenic symptoms, amongst which all sorts of 
cephalic sensations are 8j>ec.ially common, e.g. sensations of fulne.sB 
or emptiness in tbe head, of looseness or tightness, of creaking 
or sawing, and so on. Physical or mental over-exertion or excite- 
ment may even induce an epileptiform fit. Gastro -intestinal 
atony is common, with all its train of symptoms in the form 
of dyspepsia, constipation, &c. ; the circulatory and vaso-motor 
systems may be affected, e.g. by paroxysms of palpitation, attacks 
of blushing or pallor, excessive sweating or abnormal dryness of 
the skin ; the sexual functions are usually diminished, in male 
patients spermatorrhcea is particularly common, and, as in neur- 
asthenia, the general nutrition is usually below par. 

The second great characteristic of psychasthenia is the presence 
of obseaaions or dominant ideas of various sort£. These are 
almost always of a depressing type and may be of the most varied 
forms. A psychasthenic obsession comes on spontaneously in 
jiaroxysms and cannot be inhibited by any effort of the patient. 
When the obsession arrives, it occupies the patient's entire atten- 
tion, so that, for the time, he can think of nothing else. Although 
the obsession is often an idea which is repulsive to the patient, 
yet it is most insistent and t«nd8 to lecur again and again. The 
patient recognises it as being a morbid idea, yet he cannot 


throw it ofE. The different obsessions vary in their tendency 
to become translated into actions. Thus, though psychasthenics 
often have obsessions of suicide, they very rarely attempt suicide ; 
on the other hand obsessions to steal (kleptomania), to drink 
(dipsomania), and to perform sexual acts are more difficult to 
resist. A certain proportion of professional " tramps " are simply 
psychasthenic individuals obsessed by the impulse to wander 
from place to place, unable to settle down, even when offered 
the work for which they profess themselves to be looking. We 
should note that though the psychasthenic patient may have 
obsessions, he has no delusions or hallucinations ; his reasoning 
powers are unimpaired. He must therefore be clearly distinguished 
from the insane patient. 

The third characteristic feature of psychasthenia is the occur- 
rence of imperums acts (i,e. an irresistible tendency to perform 
some special act), and of paroxysmal imperious ideas. Imperious 
acts include the innumerable varieties of tics. As to the paroxysmal 
imperious ideas, these include such varieties as the mania for per- 
petually asking questions {folie de pourquoi), the mania of fussy 
tidiness the mania of counting things over and over, the mania of 
searching for objects, and so on. Manias of this sort, of course, 
interfere with normal mental processes, interrupting them to such 
an extent that the patient finishes by accomplishing practically 
nothing in the way of mental work. Imperious idea3 may also be 
of an emotional nature ; these include the innumerable forms of 
phohiay such as agoraphobia (fear of being in open spaces), claustro- 
phobia (fear of being inside buildings, especially public buildings), 
aichmophoba (fear of sharp objects), rupophobia (fear of dirt), 
toxicophobia (fear of being poisoned), ereuthophobia (fear of 
blushing), fear of death, fear of illness, fear of performing organic 
functions such as micturition or defsecation, imreasonable fear of 
certain animals or insects, and so on, ad infinitum. In most of these 
psychasthenic phobias there is, coexistent with the repulsion for the 
particular act or object, a strong attraction to that same object or 
act. This mixture of apprehension and attraction, as Rajnnond* 

» BuUetin Medicale, 1907, No. 30. 






has pointed out, is one of the causes of the mental agitation 
which accompanies a psycliastheiiic phobia. 

Ijastly, we come to the subject of Hysteria. Space does not 
permit us to discuss its various predisposing and exciting causes, 
such as sex, age, nervous heredity, physical and mental shock, or 
its frequency in certain peoples, notably tlie Latin races and the 

Hysterical states shade imperceptibly into normal mental 
states, there being no hard and fast line of demarcation. A 
certain susceptibility to suggestion and a certain emotional re- 
action exist, of course, in normal individuals in widely varying 
degrees. Such phenomena are especially marked in children. Tn 
tact, as Schnyder ' has said, we may speak of the " physiological 
hysteria " of childhood. But if an adult reverts to the childish 
susceptibility to suggestion and to infantile emotional reactions, 
we consider him or her pathological, hysterical in fact. 

For purposes of convenience we shall consider the symptomB 
in four groups — psychical, sensory, motor, and lastly, visceral and 
vascular. In each of these groups we may find excess, diminution, 
or perversion of the normal nervous processes. 

Psychical Symptoms. — These are invariably present in hysteria 
to a greater or less degree. The most outstanding feature is 
deficiency of inhibilion. The patient reacts too readily to stimuli or 
suggestions, whether originating in the outside world or within her 
own body. One of the most striking instances of this is found in 
the phenomena of hypnotic suggestion, whereby a pecuhar form 
of temporary hysteria — the hypnotic trance — ia artificially induced 
by suggestion, and can be made suddenly to disappear by the same 
means. This disappearance of symptoms during or after hypnosis 
is sometimes taken advantage of in the treatment of hysteria by 
hypnotic suggestion. But it is open to the objection that instead 
of strengthening the patient's feeble inhibition, it utilises that 
fault. Yet if the result be that the patient has a hysterical sup- 
pression of her hysterical sjinptoms (on the mathematical prin- 
ciple that — X — = + ) it ia, to some extent, a benefit. But 
' Journal dr NtanJajie, 190", p. 3:^1. 



results obtained by this plan are leaa likely to be permanent than 
when we strengthen the patient'a inhibition or self-control by 
positive measures. 

Deficient inhibition being the keynote of the hysterical " ■>^i'3t»J," 
we find, accordingly, that the patient is excessively emotional 
and changeable in disposition, often excitable and perhaps 
passionate. She giggles or cries on alight provocation, and one of 
the most familiar forma of hysterical " fit " consists merely in 

Figs. 1S5 oni] IHIi. — Case ot liyBti^rfoal pnraplegia of foiirreen ypara* 1 
duration. Showiug a cliarauUiristic hysterical poslme of the feel 
wben llie patient is passively Bujjportea. 

alternate loud laughter and crying. Her will-power is feeble, she 
is swayed by passing whims ; and this want of self-reliance leads 
to another very characteristic symptom — the craving for sympathy. 
If that sympathy be shown, as is so often the case, to an in- 
judicious extent by the patient's relatives and friends, her re- 
covery may be indefinitely delayed. Henc« it is generally of 
supreme importance to remove the hysterical patient com- 
pletely from her old surroundings, and to isolate her until thv 
vicious circle is broken. 


H Figs. 185 and 186 are photographs of a woman aged 37, who for 

f over fourteen years had lain on a bed of Hickness unable to move 

her lega, a case of hysterical paraplegia. But she was cherished 

by the sympathy of a devoted mother and of various benevolent 
lady- visitors, anxious to soothe her dying momenta. She was 
admitted to hospital, and as a result of six weeks of isolation 
and massage, she recovered the power of walking, as will be Heen 
from the other photograph (Fig. 187). This succeasful result 


was due quite as much to the isolation as to the other measures 
such as special diet, and massage. 

It is convenient to mention here, in connection with the 
psychical symptoms, the hysterical affections of speech. Some- 
times there is excessive volubility — a diarrhoea verborum. In 
other cases we find the reverse condition of hysterical mutism, 
where the patient is absolutely dumb. In less severe cases it 
is not uncommon to find merely loss of voice, or hysterical 
aphonia — ^where the patient can only utter her tale of woe 
in a whisper, breathing it softly into the ear of a sympathetic 
listener. Hj^terical aphonia has characteristic laryngoscopic 
appearances, in the form of adductor paralysis of the cords, 
with which we are familiar. 

Patients with mutism or aphonia sometimes suddenly recover 
their voice when the dominant obsession is loosened, e.g. by 
administration of chloroform (by the physician), or of an excess 
of alcohol (by the patient), or by some sudden shock, physical 
or mental. Intra-laryngeal faradism cures immediately many 
cases of hysterical aphonia. 

Articidation in hysterical and psychasthenic patients may be 
affected in all sorts of curious fashions. I have seen several 
patients who drew a breath between each separate syllable, 
e.g, " hos — ^pi — ^tal." Some psychasthenic " tiqueurs *' interpolate 
curious barking, grunting, or snorting noises amongst their 
words. One lady was afficted in this way to such an extent 
that new neighbours who settled in an adjoining house thought 
the noise was made by a sick dog, and made a humane suggestion 
that the animal should be put out of its pain. And yet this 
lady could recite long dramatic passages of poetry and prose, 
though in ordinary conversation, or even when not talking, her 
bark made her society a mixed pleasure. 

Stammering in its different varieties is not uncommon in 
hysterical patients. Unlike ordinary stammering which comes on 
in childhood, hysterical stanmiering may develop suddenly in 
adult life. Thus in a hospital nurse aged '^3, who stood up 
sharply and knocked her head against a mantel-shelf, severe 


hysterical hemiplegia came on next day, and stammering some 
six weeks later, lasting for several months. 

Sensory SjrmptomB.— These are of greater diagnostic import- 
ance than is commonly realised. Pain of aome sort occurs in nearly 
every case of uouraBthenia and in many ciises of hysteria, Unhke 
ordinary pains, which are generally caused by some peripheral 
irritation, hysterical and neurasthenic pains are entirely central 
in origin — psychalgia — and should really be classed as halluci- 
nations. But in every case we must be careful to see and to 
examine the painful spot, and to exclude peripheral irritation, 
before labelling any pain as hysterical or neurasthenic. 

Hysterical pains may be referred to any part of the body ; but 
they are especially common in certain situations. For example 
hysterical headache is often of the " clavus " type, which is a 
boring pain localised to one small spot on the skull. Occipital 
headache ia particularly common, so is hemicrania. Pains in the 
spine may simulate those of organic disease. Pain in the breaat 
— mastodynia— or in the jointa may lead to difficulties in diagnosis. 
It is only by careful local and general examination, revealing the 
presence of other hysterical stigmata and the absence of signs 
of structural disease, that we can avoid errors. Cases have been 
known in which amputations have been performed for hysterical 
joint-pains. Some time ago I saw a young lady who had already 
had one toe removed by a surgeon, but the pain recurred in 
another toe, and the case was undoubtedly hysterical. 

Closely related to these pains are the areas of hyaleriail hyper- 
iTsllie^t, and especially of hyperalgesia or excessive tenderness. 
Universal hyitereesthesia is rare. We also meet with cases of hemi- 
hypera«theaia. More usually this excessive tenderness is circum- 
scribed in small areas — little islands of skin or subjacent tissues 
of the head, trunk, or limbs. Sometimes the tenderness is 
cutaneous and elicited by gentle stroking of the skin ; sometimes 
it is subcutaneous, and only elicited on deeper pressm^, 

Such tender points are chiefly situated in the vertebral, infra- 
mammary, epigastric, and inguinal regions, and except when 
mesial, are more frequently left-sided {except in left-handed people. 


in whom they are more commonly right-sided). Tender points are 
less common on the head, and rarest on the limbs. Graves ^ has 
directed attention to the frequent presence, in hysterics of either 
sex, of hyperalgesia to pin-pricks together with tactile anaesthesia, 
confined to the nipples anl their areolae. 

Of all the tender spots, that in the left inguinal region is per- 
haps the commonest. From some supposed connection with the 
ovary, it has been called " ovarian " tenderness, but the symptom 
is as frequent in male hysterics as in females, so that the term 
is a misnomer. Moreover, in this connection, Steinhausen' 
examined 500 healthy soldiers — males, not Amazons — ^and found 
that in no less than 88 per cent, brisk pressure in the inguinal 
region on either side produced a reaction of some sort, the pheno- 
mena being either sensory (unpleasant tickling or pain), motor 
(hardening of abdominal muscles, various reflex and protective 
movements), psychical, or vasomotor and sympathetic (dilatation 
of pupils). And yet there was not a single ovary amongst them. 

These tender points may be associated not merely with pain, 
but with so much disturbance as to be actually hysterogenic. This 
does not mean that they induce hysteria — ^the hysteria is already 
present. It means that pressure on such a spot induces a hysterical 
fit or paroxysm. The best-known hysterogenic area is in the left 
inguinal region, but such areas may be anywhere. I know of one 
patient who had a hysterogenic spot in one axilla and who wore 
a sort of truss over it, to prevent accidental pressure. 

Sometimes deeper pressure on the hysterogenic spot or else- 
where may arrest a hysterical fit when in progress. Areas, pressure 
on which causes cessation of the paroxysms, are called hystero- 
frenic. The inguinal region is the best known of these. Strong 
faradism over the inguinal region will stop most hysterical fits ; 
so also will a hypodermic injection of apomorphine with its 
resultant vomiting. 

Hysterical hj^ersesthesia may also affect the special senses, so 
that there may be hyper-sensitiveness of smell, vision, hearing, 

* 'Journal of Nervous and Mental Diseases, Oct obor 1905. 

* Steinhausen, Ueber die physiolofjische Orundlage der hysterischen OvarU. 
Deutsche Zeitsch. /. Nervenheilk.f xix. p. 369. 



This is less common than loss or diminutioii of special 
sensea, to which we shall refer later. I had for some time under 
ray care a patient who could not tolerate bright light, especially 
if the room had a blue wall-paper. He preferred to stay in a 
darkened chamber ; or if the blinda were up, he shaded his eyes 
with hia hand. After some woeka of tre-atmeiit, he completely 
lost this photophobia. 

In rare cases an actual enlargement of the visual field has 
been observed, generally in one eye only. Thus, in a soldier with 
hysterical wry-neck and antesthesia of one side of the body, the 
visual field on the non-ana38thetic aide, when measured with the 
perimeter, was much larger than in a normal individual. 

Bysterical anwsthesia is extremely common, and is of the greatest 
diagnostic value. A degree of anasthesia exists, I am convinced, 
in the overwhelming majority of hysterical cases, except those 
occurring in childhood. Some time ago I looked through my notes 
of ti3 consecutive cases and found that anaesthesia was present in 
50 and absent only in 12. The remaining case of the series had 
unilateral hyperrosthesia. 

Hysterical anEesthesia is usually unnoticed by the patient her- 
self, and only discovered on examination by the physician.' Some- 
times, however, the patient complains of actual nmnbness, and 
this is chiefly in cases where the affected limb has motor paralysis 
as well, so that her attention is called to it. 

Janet showed an ingenious method of demonstrating that 
in some cases of hysterical anEesthesia, sensory impulses really 
reach the brain-centres, though the patient does not consciously 
perceive them. Taking a case of complete hemi-anteathesia he 
makes the patient shut her eyes, and tells her to say '* Yea " 
each time she feels a touch or prick, and to say " No " when she 
does not feel it. In certain cases the patient not only says " Yes " 
every time she is touched on the normal side, but also says " No " 
every time she is touched upon the ansesthetic side. This is 
pathognomonic of hysteria. 

' Babinaki comideTH that hysterioftl tuiffiithoBJa ia mainly the rpsult of 
Buggest.ion by the examining phyBlcian. With this view I cannot agree. 
Many patients who are highly suaoeptible to etiggeation have no anndtheaia. 


Cutaneous anaesthesia in hysteria may be complete or partial 
in degree, or it may be dissociated. Diminution or loss of painful 
sensations is even commoner than tactile anaesthesia. Many of 
the mediaeval witches were simply hysterics. Their hysterical 
analgesia was usually demonstrated by sticking pins into them, 
and if an analgesic area was discovered, they were promptly thrown 
into the nearest pond or stream. If they sank and were drowned, 
their innocence was established ; but if they floated, it was 
additional evidence of guilt. 

Whatever be its degree of intensity, hysterical anaesthesia 
never maps out an individual nerve-area such as that of the radial, 
median, ulnar, or external pophteal. Its commonest distribution 
is a hemi-ancesthesia (27 out of 50 cases) which is mostly left-sided, 
except in left-handed patients. It is a remarkable fact that a 
hysterical patient never suffers any physical disability owing to 
the existence of anaesthesia, no matter how profound. Unlike a 
patient with organic anaesthesia, the hysteric never cuts or bums 
herself unconsciously in an anaesthetic area. 

Hysterical hemi-anaesthesia, including the accessible mucous 
membranes of the eye, nose, mouth, pharynx, vagina, and rectum, 
is usually accurately bounded by the middle line ; but not always. 
It may either extend farther over and encroach on the non-anaes- 
thetic side, or it may leave certain areas with normal sensation, 
even on its own side, especially the head and the genitals, as may 
be seen from the charts (Figs. 188 and 189). 

Bilateral universal anaesthesia is rare (see Fig. 75, p. 187). 
We generally find, somewhere or other, one or more islands of 
normal sensation, or even of hyper-sensitiveness. Pharyngeal 
anaesthesia is one of the commonest hysterical stigmata. It is 
not necessarily accompanied by loss of the pharyngeal reflex. 

In many cases the anaesthesia, though unilateral, is more marked 
on the face or Umbs than on the trunk. It may affect special 
levels of a Umb (knee, elbow, or shoulder), or it may stop abruptly 
at some horizontal line (shoe, sock, stocking, mitten, glove, sleeve). 
This " segmental " ancesthesia sometimes occurs in association with 
hemi-anaesthesia (10 out of 50 cases) or by itself (12 out of 50) on 
one or both sides (Figs. 190 to 192). 




(The mode of onset and disappearance of hysterical anfPBtheaia 
IB interesting. Sometimes the anKstheaia comes on gradually, and 
the patient is unconscious of the defect. In other cases it occurs 
suddenly, especially after a hysterical fit, and the patient is then 
more likely to notice her " numhncsa." 

We seldom have the chance of watching the onset of hysterical 

anEDstbesia, but we may often study its mode of disappearance, 
and Figs. 189 to 192 show charts of several cases of hysterical 
anrosthesia in various stages of recovery. Unlike organic antes- 
thcsia, which, if it recovers, fades gradually all over the recovering 
area, hysterical hemi-anBBsthesia may suddenly fade to segmental 
(Fig. 1^0), and segmental ansasthesia recedes by jumps from a 
higher to a lower level, bounded usually by an " amputation bno " 


drawn transversely across the limb. Sometimes it relapses temp 
rarily to its old level before resuming its progress towards recovei 
(Figs. 190 and 191). More rarely it clears up first at the peripher 
Atusaheaia of Special Senaes. — Most caaea of hysterical ame 
thesis also have diminution or loss of the special aenaea — smel 

vision, taste, and hearing — generally unilateral and on the sam 
side as the cutaneous anaesthesia, rarely on the opposite aid< 
This combination of unilateral affection of special senses and c 
cutaneous sensation is pathognomonic of hysteria, and does no 
occur in organic disease. 

The affection of vision in hysteria is not a hemianopia such a 
we often get in organic hemiplegia. It is a concentric contractio 
of the whole visual field, as will be seen from the accompanyin 
perimetric charts (Fig. 193). It is more marked in one ej 



than in the other—" crossed amblyopia " — the smaller field being 
on the hemi-aujesthetic side, usually the left. 

The colour-fields are also contracted, but in a different order 
to that which occurs in organic optic atrophy. In hysteria the 
blue field diininishes first and the red last of all, whereas in 
organic atrophy the red field is usually first affected. 

■gi^d ji), 


Sometimes, when charting the visual field of a hysterical patient, 
we notice that the field becomes progressively smaller and smaller, 
as we continue our examination, so that our perimetric outline 
has a helicoid or spiral shape (Fig. 194). This form of perimetric 
tracing does not occur in organic disease. 

Sometimes we have hysterical blindness or apparent amaurosis 
in one eye, and yet by means of prisms we may produce a 
diplopia, which in organic cases would be impossible. In very 



tare cases complete bilateral hysterical blitidn«ss 

Space does not permit us to discuss the other pecaliaiitiet 
hysterical eye-affections and of hysterical loss of amel), taste, 1 

hearing, but we may mention, in pasfling, that complete 1 
loss of taste, as Hughtings Jackson pointed out, is practici 
always hysterical. 

Hysterical ParasOiesui, or Perversion of Sensation. — In gt 
cases of hysteria a touch on one limb or one side of the bo^ 
felt by the patient at the corresponding spot on the opposite sii! 



aliocJmria (Obeiafceiner), In another variety, of which I have seen 
an example, a touch on the radial border of the limb waa felt on 
the ulnar, and wee verad. Haphaigesia (Pitres) ia the term used 
when intense pain is caused by touching the patient with certain 
substances, such as metals, which normally should only cause a 
tactile sensation. 

Panestheaia may also afiect the special senses, as for example 

le of bjBteria. 

m ' 

to Fia. 1!*4.— Hsliooirl ooatraotlon ol viBoal Selds i 

^■in monocu/ar diplopia or polyopia, which is always hysterical. 

" A/ttTop«wi, where everything looks very minute, and jnocropsMt, where 
surrounding objects aeeni gigantic, are both frequently hysterical. 
Motor Phenomena. — These may be subdivided into irritative 
and paralytic. Amongst the trritaiive phenomena, the most 
striking are the so-called hysterical fits or paroxysms. Hysterical 
fits vary enormously in type and in severity, from a simple emo- 
tional outburst of uncontrollable laughing or crying, accompanied 
perhaps by the hysterical " globus " or " ball in the throat," to the 
moat prolonged, dramatic and violent muscular movementa, together 

One variety of hysterical fit is sometimes mistaken for epilepsy, 
and there ia all the greater liability to make this mistake since the 
fit is generally over before we reach the patient, and we are 



dependent for our information upon the accounts, more or less 
accurate, of imskilled witnesses. But if the physician is lucky 
enough to be present during a fit, there is seldom any difficulty 
in diagnosis. Thus, for example, the patient never hurts herself 
in falling ; there is no stertorous breathing ; her face is not livid, 
nor does she bite her tongue as in epilepsy ; she may, however, bite 
her lips or snap at the fingers of the bystanders. She never 
empties the bladder or rectum during the fit ; her eyes are gene- 
rally tightly closed, and if the physician tries to open them, the 
patient actively resists. A hysterical fit is not followed by coma 
and hardly ever by vomiting. 

But we must remember that sometimes we have hysterical fits 
which are post-epileptic — i,e, which immediately succeed an attack 
of true epilepsy. The antecedent epileptic fit in such cases is 
usually of the " petit-mal " tj^e, consisting perhaps in a mere 
transient pallor of the face, with momentary loss of consciousness, 
and then passing directly into a hysterical fit. Therefore, in every 
case it is important to inquire very carefully as to the precise mode 
of onset, lest we overlook a case of combined epilepsy and hysteria. 

Charcot's "grrarwfe hystSrie,^^ with its initial period simulating 
epilepsy and its subsequent phases of contortions, kicking, and 
struggling (clownism), passionate attitudes (opisthotonos, cruci- 
fixion attitude, &c.), and delirium, often with hallucinations of 
animals, is less common in this country than in France, but once 
seen, it is a magnificent performance and can never be forgotten. 
It is totally unlike any kind of epileptic or organic fit, and its 
diagnosis is easy. It may last from a quarter of an hour to several 
hours at a time. This " status hystericus " is commoner than the 
"status epilepticus," but the patient has no subsequent stupor 
such as that which succeeds a severe epileptic fit. 

Amongst other varieties of fits, to which we can only briefly 
refer, we may mention catalepsy, in which the patient suddenly 
becomes speechless, motionless, and stiff. Sometimes she is 
conscious all through the fit, at other times she is in a dreamy 
mental state. Meanwhile, if the limbs be passively moved into 
any posture, however fantastic, they remain fixed there like a 

doll's limba. In one case of niino the patient, a woman of 28, 
could be lifted np during the attack by the head and heels and 
laid across two chairs like a log. 

Hysterical (ratict may came on spontaneously, or may succeed 
a hysterical paroxysm. It is a condition in which the patient 
ajipeare as if in a deep sleep ; but the muscles are seldom com- 
pletely relaxed, and we may observe slight tremors of the eyelids. 
In more severe cases, the heart and respiration may become so 
feeble and slow that the condition simulates death. Hysterical 
trance may last hours, days, or weeks ; and several cases havo 
been authenticated where such a patient lias been buned alive, 
either deliberately, as in the case of some Indian fakirs, or by 
accident in this country. Novelists know this, and when the 
heroine is thus buried, she is exhumed in the last chapter by the 
villain for the sake of a magnificent diamond ring on her finger ; 
whilst her finger is being cut, to get the ring off, the patient awakes. 

We c«n only mention other varieties, such as somnambulism 
and double cotuciomnf^s, this latter, when in extreme degree, 
being a condition in which the patient's character altt'mates 
between normal and abnormal, the two individualities being 
mutually unconscious of each other, but each one, as its turn 
conies, takes up the tliread where it left off last. 

minor degree of double consciousness can be demon- 
strat^'d. by a simple exiKTimcnt, in many raises of hysteria where 
tlu-re luipjM'ns Ut be hj-stcrical Mnn«th«-9tia o( the upper limb. 
If in such a case wti screen the antmthctic limb from the patient'a 
view, she docs not feel pin-pricks or touches on the limb, nor does 
the recognise familiar objects when placed in the hand. But if a 
pencil be placed in the " screened " hand. It Is grasped in a position 
suitable tor writing, and if we now trace a letter or a word on the 
back of the aii8«thetic hanil (the patient's attention meanwhile 

I being divert^M by another observer) this letter or word is re[)ro- 
duced in writing, entirely unknown to the [tatient's coiuiciousneMi. 
Analogous sub-conscioun phenomena can be demonstrated in many 
apjwrently normal ]ieo|ile by me^na of a small wheeled platform 
or " planchette " carrying a pencil. 







We also meet with a hysterical type of amiulcUory auiomaiism 
where the patient (moce often a man than a woman) has attacks 
in which, without adequate motive, he has a sudden and irresistible 
impulse to wander from home. He makes a long journey, some- 
times undergoing great hardships en route. Finally, days, weeks, 
or even months afterwards, he suddenly wakes up in some strange 
town or country, entirely unaware of how he got there. For 
example, I have known of a boy who disappeared from school in 
this way, of a young officer who deserted from his regiment, and 
of a business man who left his wife and family, all these cases 
without any adequate cause. These cases are closely related to 
the somnambulistic stage of the hypnotic trance, and if such a 
patient be hypnotised he becomes able to give a complete account 
of his wanderings from the moment of his disappearance to the 
time when he woke up and "found himself." The diagnosis 
between hysterical and post-epileptic ambulatory automatism, to 
which we have already referred (p. 64), is not always easy. We 
should carefully inquire for evidences of epilepsy, major or minor, 
we should look for the presence of hysterical stigmata (though 
even in hysterical cases stigmata may be absent), whilst the recon- 
struction of the " lost " period of time when in the hypnotic trance 
is highly suggestive of its hysterical origin. 

Various localised motor disturbances also occur in hysteria and 
psychasthenia. Such, for example, is the large group of "tics" and 
"habit spasms" which we have akeady studied (p. 84). A true tic is 
essentially and primarily a psycho-motor act, either an emotional 
expression or a movement which has become a habit. Of these tics, 
the commonest are grimaces, jerkings of the head, trunk, or hmbs, 
and tremors of various parts, rapid or slow. Thus, for example, a 
lady's maid, aged 46, had tonic spasm of the orbicularis oculi on 
both sides (blepharospasm), and could open her eyes only by 
opening the mouth as well. Another girl, set. 19, had a clonic or 
jerking paroxysmal blepharospasm, associated with " humping up " 
of one foot. Another girl of 19 had rapid " twiddUng " movements 
of the left thumb and fingers, with pronation-supination movements 
of the forearm and a pseudo-clonus of the left ankle. Another 





girl aged 20, who previously had suffered long from recurrent 

vulval abscesBSS, had attacks of rapid antero-poBterior movementB 
of the pelvis. Another patient had rapid violent flexion-extension 
movements of the left elbow whenever a thunderstorm oceurred, 
the hand meanwhile dangling loosely at the wrist. Such casea of 
localised motor disturbances might be multiplied almost ad infinitum. 
Hygtmcal Paralysis may be either flaccid or spastic in type, 
and may affect any of the voluntary muscles ; but. unlike paralysis 


due to organic lesions, it never attacks a single muscle nor the 
muscles supplied by a single nerve, nor are the electrical reactions 
of degeneration ever present. A further point about hysterical 
paralysis is that though it may roughly resemble the posture of 
an organic paralysis, it never does so with accuracy ; there is 
always some point of difference to be detected. The reason for 

I this we have already discussed (p. 25tf). 

^L Let us study one example each of hysterical monoplegia, of 

^^ paraplegia, and of hemiplegia. 

Fig, Itl5 is that of a nurae, aged 32, with hysterical moDoplcgU 
of the right arm of eight montha' duration, in whom there ww 
extreme muscular wasting and claw-hand. The paralysis came on 
after a strain of the shoulder in lifting a heavy patient, and 
somewhat resembled a lesion of the brachial plexus. But we 
observed that the trapezius was paralysed, and that the vhoU 

scapula was displaced downwards — unlike an organic brat 
plexus case, in which the arm would be displaced downwards^ 
the shoulder-joint. Moreover, the electrical reactions were normal 
in the wasted muscles, and there was a " glove " of anesthesia, 
unlike the "root" anEesthesia of an organic case. The patient 
was treated for several weeks by battery and massage, without 
effect at first, but the result proved our diagnosis to be cortecL, 
for at a religious meeting she was suddenly cured. 




Figs. 185 and 186 are from a case of hysterical flaccid paraplegia 
of fourteen years' duration in a woman of 37, which at firet sight 
might be mistaken for a cord-leaion with muscular atrophy and 
amesthesia. But the antcatheaia was of the "stocking" type, 
the electrical reactions were normal, the sphincters were unaffected, 
and there were no bed-sores ; and the result of six weeks' isolation 
and maasage waa to restore the power of walking (Fig. 187), 

In some cases of hemiplegia the posture is sufficient to diagnose 
hysteria. For example, in the patient shown in Figs. IIC and 117 
(p. 257), instead of the ordinary posture of an organic case, with the 
upper extremity flexed and pronated, the lower extremity flexed at 
the hip, extended at the knee and ankle, and shghtly inverted, there 
was a curious posture of the hand and foot imhke that of organic 
disease. Moreover, her face entirely escaped, in spite of the severe 
paralysis of the arm and leg; and she had hemi -anaesthesia and 
loss of special senses down one side, a combination which never 
occurs in organic hemiplegia. 

The face and tongue are rarelj' affected in hysterical hemi- 
plegia. But in certain cases we may find instead of weakness, 
spasm of the face and tongue on the affected side, when the patient 
shows the teeth or protrudes the tongue. This hysterical glosso- 
himl hemispasm is rare, but Figs. 196 and 119 {p. 2.58) are good 
examples of the condition. 

We may also refer to " Lasi'gue's symptom " {Nothnagel's 
"Seelen]iihmung")in which a patient with an anasthetic limb cannot 
move it when the eyes are closed, but is able to move it when she 
opens hor cyea and looks at it. Another feature worthy of mention 
is hysterical pseudo-ptosis. In organic ptosis due to lesion of the 
third cranial nerve, there is always a compensatory over-action of 
the frontalis muscle. But in hysterical pseudo-ptosis this is absent, 
and the condition ia really due, not to paralysis of the levator 
palpebriE. but to spasra of the orbicularis oculi (see Fig, 52, p. 126). 

Before leaving the motor phenomena of hysteria, it may be 
well to refer to the gaits of hysterical and psychasthenic patients, 
which are sometimes most peculiar. 

Aslasin-iihasia is a liysterical condition in wliich, although the 



pBtii>nt can move his legs normaUy when lying or sitting, he 
collapses at once when he tries to stand or walk. Children are 
more often affected than adults. A boy, aged 12, had this syruptom 
for a long time, but was cured by an application o£ the faradir 
wire-brush to his apine. One patient, a doctor aged 55, used to 
flourish hia left leg in the air and bring it down with a stamp Uk<^ 
that of a unilateral locomotor ataxia. The phcnomeiion, an 
ambulatory tic, waa 30 dramatic that he had to carry a 8tick to 

FifJ. 107.— lIvKteriual 

beat oft the crowds of little boys who studied his gait i 
streets. Another patient was a worthy married lady who every 
now and then, when walking, sat down suddenly on the ground, 
rolled backwards and spread out her lower limbs like the letter V. 
Perhaps the commonest hysterical gait is a dragging g^t, in 
which the patient trails the limb helplessly along, often scraping 
the imier border, or even the dorsum of the foot, on the ground 
(see Fig. 126, p. '2GG), unlike an organic hemiplegia in whicli. , 
the outer side of the sole is dragged. 



THE NEtmOSE^ 365 

Some authorities state tbat muscular atrophy does not occur 
in a hj'sterical limb. But this is not accurate, for in certain 
rare cases, one of which is shown in Fig, 195, we may meet with 
profound atrophy. But this atrophy is due to disuse and is not 
associated with the electrical reactions of degeneration. 

Contractures of the most pronounced type may be met with 
in hysterical paralysis. But here, again, they always differ in 
some respect from those of organic cases. Fig. 197 is the photo- 
graph of a soldier, aged '62, whose horse rolled on him at the Tugela, 
and who afterwards developed a stiff left arm, flexed at the elbow 
and wriat, and with the thumb and index finger held stiffly parallel. 

A study of the reflexes is of great diagnostic importance in 
every case of hysteria. The deep reflexes may be normal or 
exaggerated, but in pure hysteria they are never lost, although 
sometimes they may be " concealed " by the presence of mus- 
cular spasm. True ankle-clonus does not occur, but a pseudo- 
ankle-clonuB is often met with. In a girl of 19, the subject 
of thread-worms and pruritus ani, this pseudo -ankle-clonus used 
to come on spontaneously when sitting or standing at ease. One 
can often distinguish it from a true organic clonus by the peculiar 
upward start of the foot before it sets oft on its first downward 
push. Further, paeudo-clonus is, as a rule, poorly sustained. 

The superficial reflexes are often diminished especially on the 
antesthetic side. The plantar reflex in hysteria, if present, is 
always of the normal flexor type, never of the extensor or Babinaki 
type. A persistent extensor plantar reflex only occurs in cases 
of disease of the pyramidal tracts, and in infants who have not 
learned to walk and in whom the pyramidal tracts are not yet 

The pupil -reflex to light is never lost in pure hysteria, 
though in rare cases it may be "concealed" by the presence of 
pupillary spasm. I remember one case of fixed dilated pupils 
in a hysterical woman, but this was due to the taking of 
belladonna by the patient. 

As to the bladder and rectum, although we may have frequency 
of micturition in hysteria, we never have trae incontinence. Re- 


tention of urine, on the other hand, is a fairly common sympto 
It once broke out as an acute epidemic in a school for young lad 
and continued until the doctor judiciously handed over the du 
of catherisation to a female nurse of mature years. The sympt< 
at once subsided in a gratifying manner. 

Visceral and Vasomotor Phenomena. — It is important 
remember that hysteria affects the sympathetic nervous systi 
as well as the cerebro-spinal. Let us refer very briefly to soi 
of the visceral and vascular phenomena. 

We may meet with abnormal slowness of the heart, or we m 
observe abnormal rapidity with palpitation, chiefly paroxysn 
constituting a variety of pseudo-angina, especially in hysteric 
or neurasthenic yoimg mothers who have been lactating too loi 
These cases are easily distinguished from true angina by t 
absence of signs of organic cardio-vascular disease. 

In the digestive system we meet with curious hysterical phei 
mena. A^rophagy, or swallowing of air, is achieved chiefly 
gulping movements of the pharynx. I remember a Uttle scho 
boy who could swallow air and distend his abdomen till 1 
waistcoat could not be buttoned. We are all famiUar wi 
hysterical dysphagia or spasm of the oesophagus, with its sudd 
intermissions and the difficulty experienced equally with liqui 
and with solids, in which nevertheless a large stomach-tube can 
easily passed. The hysterical " globus " or " ball in the throal 
which the patient tries to swallow, is an emotional phenoniem 
often met with at the onset of a hysterical paroxysm. Hysteric 
vomiting has always to be excluded in gastric disorders of youi 
women. It is often associated with anorexia nervosa, where t 
patient will take hardly any food. " Fasting giris," of whom i 
now and then read in the daily press, are generally examples 
this kind of hysteria. They may become extraordinarily emaciate 
but even they do take a little food now and then. 

Rhythmic movements of the stomach or intestine accompani 
by curious rumbling noises are sometimes met with. The conmiom 
variety is the intestinal, and at dinner-parties one sometimes hea 
these noises in neTVOu^yo\m^^^TN^\vV\aa\da^aitiu^at table. Mu 



lesa frequently we hear violent gastric borborygmi. One young 
girl whom I saw had constant, noisy to-and-fro gurgling in the 
upper part of the abdomen, like a steam-pump, and on palpating 
the abdomen the stomach could be felt rhythmically contracting 
and relaxing, blowing and sucking air backwards and forwards 
through the pylorus. This phenomenon was so startling to 
strangers that the unfortunate girl had to retire to her own room, 
if friends came to call on the family. Somewhat similar abdominal 
noises in another hysterical patient, a lad of 19, were apparently 
produced by spasmodic contractions of the diaphragm, for they 
ceased when he drew a deep breath and held it. 

The French patient who earned an honest Uving at a Parisian 
music hall by making musical noises with his anus was probably 
another example of visceral hysteria. 

We must also bear in miud tlie pseudo-pregnanciea which now 
and then occur, in which spurious enlargement of the abdomen 
sometimes goeg on to a spurious labour, Then " parturiunt montes, 
naacitur ridiculus mus "^all that is produced being, at the most, 
a small uterine cast. Phantom abdominal tumours can best be 
differentiated from genuine ovarian or uterine enlargements by 
giving an anesthetic, when the abdomen at once collapses. 

It is sometimes more difficult to diagnose pseudo- appendicitis. 
Thus one patient whom I saw, aged 33, had had her abdomen 
opened twice in different London hospitals for supposed appendicitis, 
the symptoms being those of recurrent pain and tenderness in the 
right iliac fossa, with constipation and vomiting. But .she had 
also right-sided herai-antEtsthesia, with loss of special senses all down 
that aide. We were thus led to suspect the hysterical nature of 
the abdominal symptoms, and accordingly her next attack was 
cured by sal volatile, without laparotomy, and she has had none 

Hysterical diarrhira sometimes occurs, as in the case of a pubhc 
fapeaker who was often attacked' in this awkward way just when 
l^s turn arrived to address the audience. 

Spontaneous hferaorrhages are very rare in hysteria, and no 
lorrhage should ever be diagnosed as hysterical uui«£& «Si ■ji^'w 


causes can be excluded. But a certain number of cases of pseudo- 
h8Dmopt}rsis and pseudo-haDmatemesis occur. In one girl whom I 
watched, the phenomenon seemed to be produced by suddng of 
the gums ; in another it was apparently the result of pharyngeal 
suction. In both cases, physicians of wide experience who sair 
the case in consultation failed to discover any organic cause in the 
chest or abdomen. 

Sometimes a limb affected by hysterical paralysis and ansesthesia 
may show abnormal vasomotor spasm, so that if pricked or cut it 
bleeds less freely than normal. 

Secretory phenomena also occur, though rarely, as for example 
in blood-stained tears or blood-stained sweat, which may be 
unilateral. Polyuria often occurs after a hysterical fit, whereas 
hysterical anuria or suppression of urine is extremely unconunon. 

Certain skin affections occur in hysteria. Cutaneous haemor- 
rhages are rare, if we exclude cases of voluntary traumatdsm. Bed- 
sores do not occur. The gangrenous patches described as hysterical 
gangrene are always self-inflicted, by means of caustics or other 
methods (see Fig. 126, p. 266). Hysterical blue oedema sometimes 
occurs, especially in contractured limbs ; it usually affects the skin 
over a joint and produces a degree of cyanosis and swelling, but 
this swelling does not pit on pressure. Hysterical oedema may Ust 
for weeks or months. It generally disappears suddenly. Thus b 
a case recorded by Raymond, it suddenly cleared up when the 
patient had the glad stimulus of an unexpected legacy. Dermo- 
graphism is commoner in hysterics than in normal people. Fig 
198 is an excellent example in a girl with hysterical tremor of tk 
legs, in whom, when the skin was stroked with the finger-nail, s 
white raised wheal appeared and remained for an hour or more. 
This " factitious urticaria," or *' urticaria scripta," unlike ordinary 
urticaria, does not itch. 

Hysterical cough is very common; it is usually loud and 
hacking, going on all day and ceasing during sleep. It is not 
accompanied by expectoration, and is commonest in young 
hysterics. We may have other peculiar modifications of respira- 
tion. Thus in a girl of 24 who had hysterical fits, expiration 


was a curious grunting noise of a bigeminal type — two grunts 
between each inspiration. We also meet with paroxysmal rapid 
breathing, sneezing, hiccup, and yawning. One girl aged 10, the 
subject of hysterical hemi-ana'stheaia, yawned persistently for three 
weelfs during her waking hours. She then stopped and had an 
attack of hysterical mutism lasting for two months. 

Fio, 108.— Casu of derraogropbiHio in a. hysterical young 

When hysteria occurs in childhood it is often mono-sympto- 

latic and the ordinary hysterical stigmata are frequently absent. 
■iris are nmch more frequently affected than boys, even before 
le age of puberty. Perhaps the commonest symptoms of hysteria 
1 childhood are astasia-abasia and hysterical aphonia. The various 
)rms of habit-spasm are common in young psychasthenics. 


The diagnosis between hysteria and organic disease is soou 
times easy; in other cases it is a matter of extreme di£Eiciilt] 
In doubtful cases special attention should be paid not only to tl 
psychical symptoms but to the special senses, to the condition < 
the optic discs, to the type of anffisthesia which may be preses 
to the posture of the Umbs in cases with motor paral3rsis, and t 
the condition of the reflexes, especially the plantar reflex and tli 
bladder functions. Further, we should never forget that hysteii 
and organic disease may coexist in the same case. 



i not necessary to enter into a full discussion of the various 
(hyaiological phenomena produced by electrical stimulation of 
iifferent tissues, still less to discuss the nature of electricity itself 
' the rationale of its effects, It will suffice here to recall a 
Bw of the more practical points in the physiology of electrical 

Clinically, electrical stimulation is of value chiefly in the 
izamination of muscles and of motor nerves. Electrical examina- 
ion of sensory functions is of but little practical importance, 
xcept perhaps when mapping out areas of loss of taste, where 
mild galvanic current is an excellent gustatory stimulus. 

For diagnostic ])urposeB the three m.oat important forms of 
lectricity are the jaradic, interrupted, or induced current, the 
olvanic or continuous current, and the vihraTit electricity, which 
I the result of discharging a powerful induced current through 
: Crookes' vacuum-tube, producing the well-known X-rays. The 
pplication of this latter — so-called skiagraphy, though of great 
ractical importance, does not specially concern the neurologist, 
ffe have to consider more particularly the faradic and the galvanic 

To produce the galTanic current, we employ a galvanic battery 
preferably a dry-cell battery, which can be carried about without 
pilling) and this battery must have sufficient electro-motive force 
2 to overcome the resistance of the skin, which is a bad 
Dnductor, and to stimulate the muscles and nerves underneath. In' 
ities where there is an electric hght system run by the continuous 

rent, we can utilise this current to charge an accumulator which 
KVi be carried about, or we may use the current direct from. ^A.& 


main, provided we are careful to reduce the voltage sufficiently. 
This is accompUshed by means of shunts, resistances, or rheostats. 

Faradic, or induced electricity, is obtained by induction. In 
a faradic machine there are two coils of wire, concentrically placed 
— ^the primary coil within the secondary. When a galvanic 
current passes along the primary coil, there is produced, at the 
moment of closure and again at the moment of opening of the 
primary current, an instantaneous faradic shock in the secondary 
coil, no shock occurring during the period of flow of the primary 
current, so long as its strength remains constant. Within the 
primary coil there is usually a bimdle of soft iron wire, which 
becomes converted into a magnet when the galvanic stream flows 
round the primary coil. Now a magnet pushed within a coil pro- 
duces an instantaneous faradic or induced shock in that coil ; so that 
as the soft iron is alternately magnetised and then de-magnetised 
by the primary coil, we have the effect of the magnet superadded 
to that of the primary coil. We can vary the strength of the 
faradic shocks in the secondary coil in several ways, by pulling 
the iron bundle in or out, or by sUding a cylindrical brass shield 
between the primary and secondary coils (the effect on the 
secondary coil being greatest when no shield is interposed), or 
lastly, by having the secondary coil on a sUding sledge, so that we 
can pull the two coils apart. This last is the best and most deli- 
cate way of varying the intensity of the faradic shocks in the 
secondary coil. 

We apply the electrical current to muscles and nerves by means 
of metal electrodes of various sizes, some flat and disc-like, others 
with rounded bulbous ends. The metal surface of the electrode 
should be covered with chamois-leather. The electrode is 
screwed on to a holder, which must have a contact-key whereby 
we can interrupt the current at will. The chamois-leather should 
be soaked before use, and the skin should also be well moistened, 
in warm water to which a little salt has been added, to render it a 
better conductor. The salt, however, spoils the leather, which 
must in consequence be frequently renewed. 

We should have a galvanometer in the circuit of the galvanic 


Hii 1 lit! 


current, so as to measure the strength of current which 
trates the tissues. There should also be a commutator or sliding 
switch, whereby we can reverse the direction of the current. 
The galvanic battery should be fitted with a collector whereby 
we can switch in the different cells, one by one, gradually in- 
creasing the strength of the current. 

In testing the electrical reactions of muscles, one electr 

FiQ. 200.— Motor Points of Abdominal Wall. (Ecb.J 

should be placed on the spot we desire to stimulate, whilst t 
other is placed on some far-distant " indifferent " spot, where t 
muscular contractions that may occur will not interfere with tlu 
part we are observing. Thus the indifferent pole may be pla< 
on the back of the neck, or on the front of the abdomen, or t 
patient may sit upon it, or he may hold it in the opposite hai 
We then fix our attention on the other pole which we are watch! 
To stimulate isolated nerves or muscles, cither the electrode shoi 
be a small one, or we may employ the edge of a disc electrode. 


The patient must be placed in n good llgbt, so that we can 
Q the slightest movement of the muscle we are examining. Some- 

Fia. an.— Motor Points of Upper Limb. (Brb.) 

times by placing our finger on the tendon of the muscle, we can 
(eel a contraction too faint to be visible. The patient should be 
made to relax all the muscles of the region which is under 
examination. Before applying the electrodes to tb& ^q^<«e&-, 


It. ■bduotor dirld ml 

M. fluor digit. m\ 

U. oppoixuia digit mi 

Flu. 2(li.-M(.lor PuinlB of Upi«r Limli. (Erb.) 



we should make it an invariable rule to test the strength of the 
current on our own skin, to avoid startling him by too violent a 

Electro-Diagnosia.— We should commence with faradic shocka. 
Ordinarily these are produced in rapid auccesaion by a vibrating 
Neef's hammer, "making" and "breaking" the circuit of the 

Thifii Muwlej 


primary coil. If these are too painful to be borne, we may often 
r overcome the difficulty by loosening the spring of the Neefa 
\ hammer and making and breaking the primary current by moving 
the spring with our finger. This produces an isolated faradic 
shock, each time we press the spring into contact with or remove it 
from the screw. Such single shocks are often tolerated by a patient 
who cannot bear the ordinary series of shocks in rapid succession. 
In children, however, it is sometiniea impossible to ^^ \}&» i^i)!a.i«& 



to submit even to single shocks, and it may be necessary in them 
to give a general anaasthetic, in order to make an accurate electro- 

Whenever possible, we should compare the reaction of the 
suspected muscles with that of other muscles which are healthy, 

M. titua. antlo. 

H. extens. digit oomm. 

H p«ronaeas hrvrh 

M. txtenior hillacis 

■d. Interoisel donAlts { 

Penmeal nerve 

M. gt8fxocn«iB. (outer head) 
M. peronaeos longvs 

M. soleus 

M. flexor ballacii long. 

M extens. di^nt. comm. 

M. abductor digfti mifl. 

Fig. 204.— Motor Points of Leg. (Erb.) 

preferably the corresponding muscles of the opposite limb. Of 
course, when the disease is bilaterally symmetrical, this is im- 
possible. An electrical examination, to be complete, would have 
to include observations on every accessible muscle and motor nerve 
in the body; this, however, is practically unattainable, and we 
usually content ourselves with selecting a group of muscles in the 
affected area and testing each muscle carefully, both with faradic 



shocks and with the continuous current, commencing with the 

Faradic Reactions. — ^Faradism stimulates a muscle most 
efficiently, not by direct action on the muscle-fibres but through 

Sciatic nerve 

M. biceps fem. (long head) 

M. biceps fem. (short head) 

Pfrwneal neroe 
M. gastrocneni. (outer head) 

M. WfAvoM 

M. flexor hallaoifl loogof 

j M. glvtMQt m&xiDiii 

M addvetoi; magnns 
M. lemitondinosat 

M. lemimeinbrmnotaf 

Posterior tilnal nerve 

M. gaftroenem. (inner head) 

IL ioleai 

M. flaxor difitor. eomm. 

Posterior tibial nerve 

Fig. 205.— Motor Points at back of Thigh and Leg. (Erb. ) 

the motor nerve. To stimulate an individual muscle by faradism 
we seek for the place where the nerve enters the muscle. 
This is usually a well-defined spot known as the " motor point " 
of the particular muscle. Faradism applied at such a " motor 
point " provokes a maximal contraction in that indiv\d»a.V \ss»as^^* 


The positions of the chief " motor points '* are indicated in Erb's 
well-known diagrams (Figs. 199 to 205). A faradic shock of a 
given strength produces a much greater effect when applied at 
such a " motor point " than when applied dirertly over an in- 
different bundle of muscle-fibres. 

Besides stimulating individual muscles, we can stimidate whok 
groups by applying our electrode over a nerve-trunk, such as tiie 
ulnar or musculo-spiral. 

In testing faradic reactions we commence with feeble shocks and 
gradually increase their strength until we just get a contraction 
of the muscle. We then compare this contraction with that pro- 
duced by the same strength of shocks applied to a healthy muscle, 
preferably the same muscle of the opposite limb, if available. 

Oalvanic Reactions. — ^The galvanic current stimulates a mot^r 
nerve-fibre at the moment of closure, and again at the moment 
of opening of the current, but not during the period of flow, so 
long as the strength of the current remains constant. In the case 
of muscle-fibres, galvanism stimulates them at closure and again 
at opening, and even throughout the whole period of flow, pro- 
vided the current be strong enough. Even when a nerve b 
degenerated, directly applied galvanism is stiU able to produce 
contractions in the muscle-fibres. 

The " polar reactions " of a muscle to galvanism are of great 
clinical importance. Normally, in a healthy muscle, when we 
stimulate it with a galvanic current, not too strong, we get a 
brisk twitch at closure, then during the period of flow the muscle 
remains relaxed until the current is suddenly opened, when we mav 
get another twitch at opening. The contraction at closure is 
greater if we stimulate with the kathode (negative pole) than if 
we employ the anode (positive pole). This is expressed by the 
formula KCC > ACC (kathodal-closure-contraction greater than 
anodal-closure-contraction). To verify this clinically on a heahhv 
muscle, we gradually increase the strength of our current bv 
means of the collector. Meanwhile, we make an occasional double 
movement of the commutator, whereby the testing pole i^ 
suddenly changed from kathode to anode and back again. Pre- 



Bentlj, as the current is increased in strength we iind that at 
■one position of this double movement we get a brisk twitch of 
tte muscle, whilst in the reverse position we get none. The 
first twitch in a healthy mustile always appears at the kathode. 
Then if the current be stiU further increased, a twitch appears 
at both phases of the commutator, but the kathodal contraction 
remains the greater. As a matter of convenience it is best to 
employ a current just strong enough to give KCC', whilst aa yet 
there is no ACC. Meanwhile we notice on the galvanometer the 
number of milliamperes of current which were required to produce 
the earliest twitch at closure. 

If the strength of the galvanic current be still further increased 
we obtain a twitch at opening, the anodal contraction being pro- 
duced first and the kathodal opening contraction last of all. The 
order of appearance of these difierent contractions in a healthy 
muscle, as the current progressively increases in strength, is there- 
fore as follows : KCC > ACC > AOC > KOC, and is indicated in 
the following amplication of the same facts : — 

1. Weak current 

. KCC 

2. Medium current 

. KCC 


3, Moilei'at*ly strong curren 

t . KCC 



i. Very strong tiirrent 

. KCC 



Of these phenomena, we usually concern ourselves, for practical 
purposes, only with the first two, that is, with the contractions on 
closure, observing whether the kathodal closing contraction is greater 
than the anodal closing contraction, as it ought to be in health. 

To recapitulate, in a norma! nerve-muscle organ wc obtain a 
good contraction on faradic stimulation, while to galvanism there 

1 brisk twitch on closure, KCC being greater than ACC'. 

Abnormalities in Electrical Reactions. — Sometimes the ex- 
citability of the nerve-muscle organ b increased, both to faradism 
and to galvanism. This condition of hj^jcrexcitability is met with 
moat typically in tetany, where both nerve and muscle are too 
easily thrown into contraction. Somewhat similar is the so-called 
" neurotonic " reaction, described by Marina in certain cases of 
hysteria, and by Bemak in patients with progressive muscular 



atrophy. This consists not only in excessive excitability botii 
to faradism and galvanism, but also in a tendency for the muflde 
to remain in a state of tetanus for some time after the stimulus 
has ceased. The phenomenon is not provoked by stimulation of 
the muscle itself, but only by excitation of the nerve. 

We sometimes meet with simple diminution of excitability, botJi 
to faradism and to galvanism, but without alteration of polar 
reactions — ^that is to say, KCC remains greater than ACC. Suck 
diminution of electrical excitability is met with in simple arthritic 
muscular atrophy, in the atrophy of disuse and also in the various 
myopathies, whether pseudo-hypertrophic or atrophic in type. 

Temporary loss of faradic excitabihty occurs in myasthenii 
gravis, though not in every case. When present, the myasthenic 
reaction consists in the fact that after a certain number of faradic 
shocks, the muscle gradually reacts less and less, until at last 
it shows no contraction to the strongest faradic shocks. We wait 
a few minutes and then test again, when we find that the faradic 
excitabihty has reappeared, but can again be exhausted in i 
similar fashion. The galvanic reactions of the affected muscles 
remain unchanged throughout the disease. A myasthenic reaction 
can also be produced experimentally, e.g. in the frog^s muscles, by 
poisoning with yohimbine.^ This suggests that the phenomenon 
is toxic in origin. 

During the paroxysms of the rare disease known as famHf 
periodic paralysis, the paralysed muscles are, for the time, totally 
inexcitable either by faradism or by galvanism. In the intervals 
between the attacks of paralysis, the muscles react normally. 

The myotonic reaction is met with only in Thomsen's disease 
(myotonia congenita). It consists in the fact that on • faradic 
stimulation the muscular contraction persists for some time after 
the stimulus has ceased, as if the muscle, once contracted, cannot 
relax. Moreover, in this disease galvanic stimulation of the 
muscle produces curious wave-like contractions, and KCC is equal 
to instead of greater than ACC. 

Reactions of Degeneration.— By far the most important modi- 

* Guni), J{ev, of Neurol, and PaychicU., 1908, p. 160. 



fication ot electrical reactions is the condition known aa the 
" reactions of degeneration," or coUoquially as R.D. This condition 
ia present when the nerve-muscle organ has undergone degenera- 
tion, from disease or destruction of the spino- muscular motor 
neurone. As a result of such a lesion, the motor nerve-fibre dis- 
integrates within a few days and loses its power of conducting 
impulses. The corresponding muacle-fibre undergoes important 
changes ; it loses its fibrillar or anisotropic element, the element 
which contracts with a brisk twitch and can be stimulated 
with a faradic shock ; whilst it retains only its sarcoplasm, a less 
excitable element, which contracts slowly and can still be stimu- 
lated by galvanism, 

In a typical case the phenomena are aa follows : — to faraditm 
there ia no response, since the nerve has degenerated ; to galvanism 
the muscle-fibres still respond — in fact after a time they become 
liyperexcitable, contracting to a weaker current than in health. 
But their polar reactions are altered. The anodal contraction on 
closure is now equal to, or greater than the kathodal (ACC > KCC). 
Moreover, what is equally characteristic, the response of the 
muscle is no longer a brisk twitch ; it is a slow, sluggish, almost 
vermiform movement. If a nerve be divided, the reactions of 
degeneration do not appear at once. It is only after some ten 
days or so that they develop. Once established, the reactions 
of degeneration persist, unless the nerve regenerates and re- 
establishes a connection between the muscle and the motor nucleus. 
In the process of recovery, voluntary motor power reappears before 
faradic excitability returns. In many cases recovery does not take 
place and the nerve-muscle organ remains permanently degene- 
rated, as. for example, where the motor nucleus in the cord or 
medulla is destroyed, or where a nerve-trunk is completely divided 
and its ends have not been reunited. 

In certain cases we meet with partial or incomplete reactions of 
degeneration. These consist in a sluggish contraction to galvanism, 
ACC being greater than KCC, but the reaction to faradism is not 
lost, but only diminished. This condition indicates a less severe 
injury of the nerve-fibres than if typical R.D. be present. 


Sometimes we have mixed reactions, where some fibres of a 
muscle retain their normal reactions whilst adjacent fibres have 
reactions of degeneration. This is best exemplified by cases of 
progressive muscular atrophy where degenerated muscle-fibres are 
interspersed amongst the healthy. 

To sum up, then, the presence of B.D. always indicates a lesion 
somewhere in the lower or spino-musciJar motor neurone. We 
should be careful to wait ten days or a fortnight from the onset 
of the paralysis, before giving this verdict, inasmuch as we have 
seen that it takes some time for degeneration to become estab- 
lished. B.D. occur in lesions of peripheral motor nerves, also in 
gross nuclear diseases such as acute anterior poliomyelitis, haemor- 
rhage, or thrombosis in the anterior cornua or motor nuclei. Mixed 
reactions, on the other hand, are found in progressive muscular 
atrophy and in bulbar palsy, where the nerve-cells of the motor nuclei 
are picked out one by one, leaving adjacent nerve-cells unaffected. 

Electro-Prognosis. — In many paralyses due to organic lesions 
of peripheral motor nerves (of which the conmionest instance is 
that of a neuritis of the facial nerve), it is of importance to be able 
to estimate not only the degree of degeneration which has occurred, 
but also the prospects of recovery. To make an accurate prognosis 
we must wait at least ten days, and preferably a fortnight, before 
making our investigation, so as to allow time for degenerative 
changes to have occurred. Electrical examination at any earlier 
date is practically valueless for purposes of prognosis. If, after a 
fortnight's motor palsy — say, in a case of Bell's paralysis — ^we get 
typical R.D., the degeneration of the nerve is severe and recovery 
will not commence for three months at least, possibly not for a year, 
and the patient may even remain permanently paralysed. And 
at the best, if recovery does occur, it will probably be imperfect 
and associated with some contracture. If partial R.D. be 
present, the prognosis is less grave and recovery may be expected 
within six or eight weeks. If the reactions be normal, or if there 
is simply a diminution to faradism and galvanism, but without 
polar changes, recovery may be looked for in from three to six 
weeks, or even sooner. 



HE cerebro -spinal fluid is secreted by tlie epeiidyma coveiing 
le choroid plexuses. It receives various products of metaboliam 
: the nerve-centres, and may participate in lesions of these 
mtres or of their meninges ; hence the clinical importance of its 

In the adult, the spinal cord terminates at the level of the lower 
irt of the first lumbar vertebra. Below that level the arachnoidal 
ic extends as a hollow cavity as low down as the second sacral 
jrtebra (see Fig. 1^06). There is thus a considerable extent of 
rachnoidal cavity devoid of spina! cord, occupied simply by the 
iota of the Cauda equina and by the cerebro-apinal fluid which 
ithea them. From this region we can withdraw cerebro -spinal 
lid without risk of injury to the spinal cord. In order to do 
I, we enter the cerebro-spinal cistern from behind, somewhere 
itween the laminee of the second lumbar and the second sacral 

The two widest inter-lanunal spaces are the one between the 
bird and fourth, and the other between the fourth and fifth 
umbar lamina. Of these we usually select the space between the 
Burth and fifth laminse, because, as a rule, it is slightly the larger. 
!hese two inter-laminal spaces are very easily found as follows : we 
[raw a horizontal line across the patient's back, at the level of the 
ighest margin of the ihac crests. This hne intersects the vertebral 
oluimi at the tip of the fourth lumbar spine. We make our 
luncture immediately below this spine (Fig. 207). 

It is convenient to use an all-glass syringe which is readily 
terilisable on which to mount our needle, which should be of 
uriy large calibre. The needle itself is made of platinum 
nd iridium, which is less liable to snap and can also b>^ W^\Wk 



without rusting, unlike a steel needle. It must be long en> 
to reach into the arachnoidal sac, and yet short eDOO^ to t 
short within the sac without penetrating to the dura on the 
side. For this purpose the most aniteble len^h of needle is al 
8 centimetres, or just over three inches. 

¥111. ■:()(■..— (Aflur Itiiyniotiil.) Diagmm ot lower end of vertebral 
culmiiii ni»l it« n'lnliuiiB to tLc spin&l coni uid cauila eiiuina. 
1 'J'hi- Joiiblc-Bbn<le<1 purtion of the cord la the ckidiu temiinalis 

with which the filiiiu Icrminole is coDtinuona. 

As to the patient's posture during the opentiou of "Inn 
puncture," he may be l^-ing on a bed or couch, in the left lat 
position, with the knees and shoulders approximated. But 1 
better, if possible, to have him sitting on a low seat, 8too{ 
well forwards, with his knees separated, his arms Kanging lo 
and his hands touching the ground. In this way the lamine 
separated to t\ie\t iAi»oa\, «x^tA. (jea ¥114, 207), 

We carefully ateriliBe the skin at the site of puncture and render 
it anteflthetic by means of a spray of ethyl chloride. The operator 
places his left index finger on the fourth lumbar spine as a guide, 
and with his right hand pushes in the needle, about half an uich 
below and half an inch to the right of this spot (so as to avoid the 
dense interspinous ligament), directing the point of the needle 
horizontally forwards and a little inwards. The ligamentum 
flubflavum. deep in, between the laniiuEe, is somewhat resistant. 



into tesl-luW. 

ind the nee^dle is felt to be checked here. But we push firmly 
m, if no bone is struck, and suddenly the needle penetrates the 
igament and dura-arachnoid and is now in the arachnoidal sac 
Bee Fig. 208). If we strike on a lamina instead of the ligament, 
we withdraw slightly and try a point above or below- 

Soraetimes during the operation the patient feels a sudden, 
sharp pain shooting down his right thigh and leg. This simply 
eans that our needle has touched one of the roots of the cauda 
:uina en route, and is of no other significance. 
We now detach the syringe and allow the cerebro-apinal fluid 
escape through the needle, collecting from 3 to 5 e.c. in a 
erilised test-tube. It is better not to ^m'^VQ^ &\isAiia\L\i^ 'i^'t , 


syringe, imleSB some difficulty be experienced in getting the flti 
to run. The pressure of the fluid as it escapes may be measure 
if desired, by means of a rubber tube with a manometer attack 
Normally the fluid trickles out slowly, drop by drop. The fii 
few drops should be discaided, since they may be mixed with bio 
from our needle-wound of the superjacent tissues. 

Occasionally it happens that even when we have saccessfii 
penetrated within the ligamentum subflavum, no fluid will flo 
This is usually due to blocking of the needle by a small ^ 
of blood-clot or shred of muscle or connective-tissue, during t 

CoiuniCJi lUxu: Arier^LAS- 

procesa of puncture. Or it may be due to one of the cam 
equina roots floating against the end of the needle. Such co 
ditions are easily rectified by passing a sterilised atilette along t: 
needle, to clear it. Sometimes it happens that the needle pieic 
the ligamentum subflavum but pushes the spinal tbeca in front 
it, so that, even though the stilette shows the needle to be free fro 
obstruction, no fluid comes. In such cases it is beat to withdrs 
the needle and puncture at the next space above. 

Sometimes the intrathecal pressure is increased, so that the fin 
escapes in a jet, instead of drop by drop. This occurs chieflv 
intra-cranial tumours and in the various forms of mcninrit 
although even in t\ieaei TOTi^xKHwa m\ vaaY^Ased pressure of flu 


1 the lumbar region is by no means constant, for sometimes in 
meningitis there is occlusion of tlie foramen of Magendie, or of 
the foramina of Key and Retzius, cutting off the intra -ventricular 
om the spinal pond. 

The fluid may be accidentally mixed with blood from the 
Wounding of an arachnoidal vein during the puncture ; this is 
1 accident which cannot be foreseen. In moat cases such bleed- 
ing clears up after a few seconds, the fluid becoming progressively 
clearer and clearer. But admixture of blood also occurs in cases of 
pre-existent subarachnoid haemorrhage, cerebral or spinal, as in frac- 
ture of the skull, intra-ventricular haemorrhage, or in trauma of the 
Bpinal cord. We can sometimes distinguish between hsemorrhage 
due to the local puncture and hsemorrhage which results from 
a previous intra-thecal lesion. We do this by centrifuging the 
fluid. In local hseraorrhage due to puncture, the blood corpuscles 
iail to the foot of the centrifuge-tube, leaving the superjacent 
fluid clear and limpid, whereas in a pre-existing cerebral or spinal 
hiemorrhage the fluid (which during its flow is equally tinged 
from start to finish, and generally less deeply tinged than in local 
lEDmorrhage), remains of a yellow colour even after centrifuging. 

The withdrawal of a small quantity of cerebro -spinal fluid in 
most cases causes the patient no discomfort. But in a small pro- 
portion of cases he may complain of severe headache, appearing 
an hour or two later, and lasting perhaps for several days. This 
I usually in patients who have been walking about as usual aft-er 
the puncture, and headache can generally be prevented by re- 
commending the patient to rest for a day or so, or at least to 
avoid physical exertion. 

Normal cerebro-spinal fluid is absolutely colourless, like water. 
It has a specific gravity of 1006 to 1008. It is alkaline, contains 
t trace of serum-globulin and of albumose, and also a substance 
which reduces Fehling's solution and forms glucosazone crj-stals. 
Jlicroscopic&Uy it contains a few large, flat, endothelial plates, 
and perhaps an occasional lymphocyte. It cflntains no organisms. 

The Diagnostic Sigiuflcance of Cerebro-spinal Fluid.— For 
diagnostic purposps, the fluid may be examined in various ways. 


(1) Physical Characters. — ^Instead of being clear and li 
like water, the fluid may be opalescent, turbid, cloudy, or 
purulent, as in some cases of meningitis. In severe jaundi 
has been observed to be yellow and clear, whilst in cases of f 
hsemorrhage either into the brain or cord, as we have menti< 
it may be blood-stained. In haemorrhages of older date, 8 
week or more, the fluid may be of a clear yellow colour. 

In cases of sudden hemiplegia, we are sometimes in d 
whether the lesion is haemorrhage or thrombosis. The diag 
between these two conditions may be very diflScult. But 
treatment of the two is diametrically opposite. In a cai 
thrombosis we stimulate, whereas in cerebral haemorrhage w( 
to lower the intra-cranial blood-pressure and diminish the : 
of the heart. If in a doubtful case we perform lumbar pun( 
and obtain blood-stained fluid, or fluid which has a yellow 1 
even after centrifuging, the diagnosis may be much simpli 
I have performed lumbar puncture in a comatose patient moril 
from cerebral thrombosis and obtained normal clear fluid, 
traumatic cases it is of great value in indicating the presenc 
intra-cranial haemorrhage. Cathcart of Edinburgh * recorde 
case in which, after a head injury, examination of the cere 
spinal fluid helped to settle the diagnosis of intra-cranial hfei 
rhage. He trephined, tied the ruptured artery, and saved 
patient's life. But in compound fracture of the skull Iudd 
puncture may yield nothing, if the fluid happens to be escai 
by other channels, viz., through the lacerated membranes. 

The freezing-point of the cerebro-spinal fluid has been stud 
by various observers : — so-called cryoscopic eocamtnation, Wi 
Sicard, Ravaut,*^ and others have recorded a lowering of 
freezing-point in certain diseases such as meningitis, tubeicsi 
or otherwise. But, on the whole, cryoscopy has not been of ns 
practical value. 

(2) Chemical Characters. — These are of some value. Thus, 
example, a marked excess of albumin is found in acute meniuf 

^ Scot, Med. and Surg. Journ., Edinburgh, 1902, p. I45. 
* Compt. rcTid. Soc. de B\ol., Y«n&, A^vi^uat 20, 1900. 



and in general paralysis of the inHane. In pure tabes there is do 
albumiii. Lf fibrin is found, this also is pathological. 
Gtiillain and Paraut ' recorded some interesting obeetvations od 
the cerebro-Bpioal fluid in cases of general {laralysis of the insane. 
When normal eerebro-spinal fluid is boiled, the globulin coagulat4?s 
and the fluid becomes slightly opalescent. But i( the globulin be 
precipitated by adding an equal quantity of a saturated solution 
of magnesium sulphate, the fluid filtered, an<l the clear liltrat« 
again boiled, it should remain clear. In general paral)-sis of the 
insane, however, the second boiling yielded an albuminous pre- 
cipitate in every case out of a series of sixteen general paralytics 
examined by these observers. 

In acute meningitis, whether tuberculous or septic, sugar is 
almost always absent. In chronic meningitis, in tabes, and in 
general paralysis of the insane, it is often diminished. 

Another chemical point, which my colleague. Dr. Hebb, in- 
vestigated in a number of my cases at the Westminster Hospital, 
is as to the presence of cholin in the cerebro-spinal fluid. Nor- 
mally cholin is not detectable in any appreciable quantity. But 
in organic degenerative diseases of the nervous syst«oi, cholin may 
be demonstrat«d in the blood and cerebro-spinal fluid, and can be 
crystallised out as a combined platinum salt, according to the 
method of Halliburton and Rosenheim.'' Thus, for example, Hebb 
obtained cholin-platinum crj-stals from the cerebro-spinal fluid in 
cases of cerebral hsemorrhage, syringomyelia, disseminated sclerosis, 
&c. This test may occasionally be of value in the diagnosis between 
hysteria and gross organic disease. But it is too complicated for 
ordinary clinical work. 

(3) BaderitAigical Characters. — These are chiefly of value in 
cases of memogitis. to determine the particular organism causing 
the diseaae. Thus, for example, in epidemic cerebro-spinal 
meningitis the meningo-coccus {diplomcau itUra-txHularin) is found ; 
in tuberculous meningitis, the tubercle bacillus ; and in other 
varietlea of meoingitiB we may find staphylococci, streptococci, 

• Bm. NturtO.. Pwu, April 30, IMS. 

• BriL Mtd. Joum.. 1907. p. 1043. 



pneumococci, and so on. We should remember that failme to 
discover tubercle bacilli does not necessarily exclude tuberculous 
meningitis, though their presence would confirm such a diagnosis. 

To demonstrate the bacilli in tuberculous meningitis it is convenient to 
allow the fluid to stand for 12 to 24 hours, by which time a fine coagoloBi 
has usually formed. This is removed by a needle, spread on a slide, fixed asd 
stained in the usual manner. 

In doubtful cases inoculation experiments on guinea-pig9 are of 
value. In Landry's paralysis various organisms (tetracocci and 
others) have occasionally been isolated from the cerebro-spiiud 
fluid and blood. 

(4) Microscopic Characters. — Clinically, microscopic investiga- 
tion has proved by far the most valuable mode of examination 
of the cerebro-spinal fluid. A good method is to centrifuge a 
given quantity of the fluid, say 5 c.c. for five minutes, thereby 
collecting into a small deposit all the cellular elements which may 
be present. We then carefully decant off all the superjacent fluid, 
turn the empty tube upside down and scrape the bottom with 
a fine capillary pipette. In this way we collect the sediment, 
which is transferred to a slide, fixed by heat, stained by methyl 
blue or by Jenner's stain, mounted in Canada balsam and examined 
with the microscope. 

Specimens prepared as above described afford a permanent 
record of the variety and intensity of the cellular contents present. 
To obtain absolute accuracy of counting we employ Fuchs and 
Rosenthal's ^ counting-chamber, a modification of the Zeiss blood- 
counting chamber. In using this, a small quantity (10 cubic mm.) 
of cerebro-spinal fluid is mixed by means of a special pipette with 
1 cubic mm. of a staining fluid containing methyl violet and 
acetic acid. A drop of the mixture is placed on the counting 
stage, and the cells are counted. The results so obtained corre- 
spond with those found in centrifuged deposits, but are more 
accurate. But the preparation so obtained is not a permanent 
one, and I am, therefore, now in the habit of employing both the 
centrifuge and the counting chamber — the one to yield a permanent 

• Wiener mediziniache Pre sue. 1J)04, p. 2084. 



specimeD, the other to ensure accurate coimtiEg of the cellular 
.contents in the fluid. 

In rare cases we inay find parasites. Thus, for example, 
Castellani and Bruce ^ found the trypanosonie of sleeping-sickness 
not only in the blood of such patients hut also in the eerebro- 
•pinal fluid. In fact, it is easier to identify the tryimnoaorae in 
the cerebro-spinal fluid than in the blood, where it is likely to be 
obscured by blood corpuscles. In a few cases of malignant growths 
of the spinal cord or of its meninges, tumour-cells have been found 
in the fiuid. But this is inconstant, though tuniour-ceUs, if present, 
would have a high positive diagnostic value. 

By far the most valuable point to be determined microscopically 
B the presence or otherwise of leucocytes, observing not only their 
number but their type. This is the so-called cyto-diagnosis. 

Normal cerebro-spinal fluid contains no polymorpho-nuclear 
leucocytes and only an occasional small mono-nucleated lymphocyte, 
with now and then a few endothelial plates. Examination of the 
centrifuged deposit with a magnification of 400 diameters, accord- 
ing to the technique described, should show an average of not more 
than two or three lymphocytes to the field, or from I to 2 per 
ibic mm. Sometimes we find no cells of any sort. But in 
certain organic diseases of the central nervous system or its mem- 
branes, there may be a large eJtcess of leucocytes — polymorphs 
Br monomorphs. Briefly stated, in cases of acute microbic in- 
fection of the brain and meninges, especially the suppurative 
Varieties,- we find a polynuclear leucocytosis, where the leucocytes 
ftre mostly polymorphs, with some large monomorphs as well, 
ffhen recovery begins in acute infective meningitis, the poly- 
auclear leucocji«s in the cerebto-apinal fluid diminish in numbers 
md become replaced by lymphocytes. These latter in turn dis- 
appear as convalescence becomes complete. 

I Brit. Mtd. Jaum., November 21. 1903. 

' But it is the ucuteneHS uf tho inflammatory procesB, not its microbic 

in, which appears tu be tlie chief [ni'tor in producing polynuclear leueo- 

leis. Thus I have experimentally produced abundant polynuclear leuoo- 

) monkeys by injetling sterile aolt solution or a, sterile emulsion of 

iloured partieles into the spinal theca. 


If a brain abscess be present without implication of the 
superjacent meninges, as sometimes occurs, the cerebro-spinal fluid 
shows no excess of leucocytes. Examination of the fluid is there- 
fore a valuable means of distinguishing between meningitis and 
brain abscess. In both conditions a blood-count shows a great 
excess of polymorphs in the blood : these may number from 
10,000 to 25,000 or more (instead of from 8000 to 10,000 per cubic 
millimetre as in health), the leucocytosis of the blood being higher, 
as a rule, in meningitis than in brain abscess. 

But in subacute and chronic affections of the meninges, whether 
tuberculous, syphilitic, or otherwise, also in certain chronic de- 
generative diseases of the central nervous S}r8tem, we usually find 
a lymphocytosis, i.e. an excess of small monomorphs, sometimes 
accompanied by a small proportion of large monomorphs. In 
cases of acutely advancing tuberculous meningitis I have also 
found a considerable proportion of polymorphs (30 per cent, and 
upwards) amongst the monomorphs. There is often a marked 
lymphocytosis during an attack of herpes zoster and for a number 
of days afterwards. In functional nervous diseases the fluid is 

In several cases of lymphatic leukaemia, and in a case of 
chloroma at the Westminster Hospital, Hebb has also observed 
marked lymphocytosis of the cerebro-spinal fluid. 

Let us study some illustrative cases. One case was an example 
of epidemic cerebro-spinal meningitis in a patient who was comatose 
and apparently moribund. The cerebro-spinal fluid was under 
excessive pressure, of turbid appearance, and the centrifuged 
deposit showed microscopically an average of 87'3 polymorphs to 
the field. Within many of the leucocytes the meningo-coccus was 
readily distinguished. The withdrawal of about an ounce of fiuid 
caused marked improvement in the symptoms and the patient 
made a good recovery. Another case was that of an officer who 
had chronic otitis media on the left side. He rapidly developed 
mental dulness and slight aphasic symptoms, with some fever. In 
his case the fluid was turbid, and showed no fewer than 371 poly- 
morphs to the field. Operation was at once undertaken and an 



inflamed area nf brain tisHue was exposed in the teni]>()ral lobe. No 
abscess waa (oiuid. The symptonis rapidly Bubsided and the 
patient niadc a complete recovery. 

As an instance where the cerebro-spinal fluid was normal may 
be mentioned the case of a child, in whom, as is so often thu 
case, a deep-seated pneumonia was ushered in by head symp- 
toms simulating meningitis — so-calletl "meningism." There was 
marked headache, some head- retraction, and squint. Moreover, 
an elder child in the same family had previously died from menin- 
gitis, and the parents were therefore in considerable anxiety as to 
the possibility of a second case. The cerebro-spinal fluid, however, 
showed no excess of cells, and Kemig"s sign was absent. Meningitis 
was therefore less likely than a functional meningism, and an 
encouraging prognosis was given, which proved correct. 

With regard to the cases of lymphocytosis, the most striking 
results are those observed in general paralysis of the insane and 
in tabes dorsalis. The lymphocytosis in these two affections 
(which are essentially the same dise^iso etio logically, and which 
clinically are not infrequently combined in the same patient) is 
more marked than in any other form of organic nervous disease. 
Thus in a rectnt series of twelve cases of general paralysis examined 
by me. the average number of lymphocytes was l-tl per cubic mm., 
the lowest count in any one case being VH), and the highest 295, 
In a series of fift«en tabetics, the lowest count was 14, the highmt 
477'1, and the average number per cubic mm. for the whole series 
was 125*4. This closely approximates to the average for general 

A point of importance notictHl in casra of tabes and general 
paralysis is that not only is lymphocytoais present in practically 
every case, but it is often extremely marked when the other 
symptoms of the disease are very slight. Thus, for example, one 
patient had lightning- pains, analgesia of the t«Ddo Achillis, but no 
ataxia, no abnormality of the pupils, and brisk knee- and ankle- 
jerks. Yet his cerebro-spinal fluid showed 150 lymphocytes [ler cubic 
millimetre, and he was undoubtedly an early case of tabes. The 
same applies to general paralyats. One patient vitfa 2396 lympho- 


cytes per cubic mm. was an early case, with practically no menU! 
symptoms, simply a slight loss of memory and a history of two 
attacks of unconsciousness followed by transient aphasia aod 
weakness of the right hand — " congestive attacks." 

We therefore possess in the cytological examination of tbe 
cerebro-spinal fluid a valuable means of recognising tabes and 
general paralysis in their earliest stages. If no excess of lymphocytes 
is present, these two diseases can usually be excluded.^ Another 
point of interest is that during the pyrexial attacks of genenl 
paralysis, there is a temporary poljoiuclear leucocytosis not only 
of the blood but of the cerebro-spinal fluid. Thus in a case o! 
my own there were 118 poljrmorphs and 25 monomorphs per cubk 
mm. Pappenheim ^ has also recorded similar cases. 

A further point of interest is that the lymphocytosis in tabes 
and general paralysis is uninfluenced by the most energetic anti- 
specific treatment. In several of my cases, the fluid was examinsl 
at intervals of a month, the patient meantime having W 
daily hypodermic administrations of mercury; yet the lyrnplw- 
cytosis remained unchanged in its intensity. This is in marked 
contrast to what occurs in active syphiUtic lesions. Thus, k 
example, in a case of gumma of the spinal cord, the lymphocytes, 
which numbered 52 6 on admission, were reduced after this 
weeks' treatment to 16*1, and the patient, who was totally pan- 
plegic and anaesthetic in the lower Umbs on admission, "f^ 
discharged in a couple of months able to walk, without anflesthestt. 
and with the sphincters under control. 

Another point of importance is that syphilis by itself, unl«»| 
there be an active syphilitic lesion of the central nervous systeit 
produces little or no excess of lymphocytes in the cerebro-spiitil 
fluid. Thus in my series of twelve cases, in the five seconcUiJ 
cases the average number of lymphocytes was 2-7 that *' 

^ ThiH rule, however, is not without exceptions, for I have seen a ca^i* 
tabes, with ntaxia, Argyll-Robertson pupils, and absent knee- and ankle-jerb' 
in which the cerebro-spinal fluid contained only 3*3 lymphocytes per roit' 
Erb [Deutsche Zcitsch. /. Nervcnheilkutule, 1007, s. 438) has also recoil 
similar cases. 

* Moiuitschri ft fur P«\jcK\atTit \uv{ Neiiroloqie, 1907, s. 536. 



^e six tertiary cases was 0-9, the twelfth case being one of 

man who had a syphilitic chancre twenty-six years before. 

! tertiary cases with active syphilitic lesions, such as gum- 
latous ulcers, rupia, and so on, had more cells than the others, 
Rit even in them the number was less than the average of the 
Kondary cases. 

We thus see that the presence of a lai^e lymphocytosis in a 
patient who has had syphilis, is of grave significance and indicates 
serious organic disease, either a sj'phihtic lesion of the central 
nervous system, or, if very marked, tabes or general paralysis. 
In such cases we should carefully examine for other signs of organic 
disease, especially for Argyll -Robertson pupils, early optic atrophy, 
alterations in the reflexes, and sensory changes. Even if no 
other sign of organic disease be present, the presence of lympho- 
cytosis of the cerebro-spinal fluid is an indication for the most 
energetic anti-specific treatment, in the hope, perhaps, of preventing 
subsequent developments. 

The presence of lymphocytosis in tuberculous meningitis is 
readily understood, also that which occurs in tuberculous tumours 
on the surface of the brain It is more difficult at present to 
account for the occasional excess of lymphocytes in cerebral 
neoplasms. Thus one case of glioma of the centrum ovale had no 
fewer than 75 lymphocytes to the field, a count which led one 
to expect a tuberculous mass, there being no possibility of syphilis. 
Yet the autopsy showed a glioma which had in no way 
approached the meninges, and where a hemorrhage into the 
substance of the tumour ultimately caused death by bursting 
into the lateral ventricle. 

Therapeutic Applications of Lumbar Pnnctiire.— Lumbar 
puncture was originally introduced by Quincke for the purpose 
of relieving intra-cranial pressure in tuberculous meningitis. This 
it does for the time, though it is more often palliative than curative. 
In one case of mine the patient, a young man, comatose and 
apparently moribund, regained consciousness for a day, after the 
withdrawal of 22 c.c. of cerebro -spinal fluid. The fluid was allowed 
to flow until the increased intra-tbecal pressure i«ll ^ ^orwiii^. 



The importance of this procedure, not only from sentimcnu! 
reasons but possibly on medico-legal grounds, is obvious. 6m 
sometimes lumbar puncture has undoubtedly proved curative, evfi 
in tuberculous meningitis. Thus in cases recorded by Freyhan,^ 
Henkel,^ Barth,^ and others, tubercle bacilli were demonstrated 
in the cerebro-spinal fluid and yet the patients ultimately recovered, 
after repeated punctureff. 

In other forms of meningitis associated livith a polynuclea: 
leucocytosis (apart from infective cases secondary to bone disease), 
especially in epidemic cerebro-spinal meningitis, good results havr 
been obtained by the injection of antiseptic substances, after with- 
drawal of a corresponding quantity of cerebro-spinal fliuid. For 
this purpose, a 1 per cent, solution of lysol has been found usefuL 
10 cubic centimetres being introduced at each sitting. 

In intra-cranial pressure due to other causes, as, for exampk. 
in inoperable or inaccessible cerebral timiours, lumbar punctured 
sometimes of distinct benefit as a palliative measure, by diminifthiif 
urgent pressure and thereby relieving headache, vertigo, and other 
symptoms. Hitherto to relieve intra-cranial pressure and ti- 
diminish optic neuritis it has been the custom to trephine tfe 
skull as a palliative measure. But lumbar puncture is quickfl. 
simpler, and less dangerous than a major cranial operation. I per- 
formed it in three cases of intra-cranial timiour where the symptoffls 
pointed to deep-seated cerebellar disease. In all of them A 
headache and vertigo were greatly relieved for several weeks ate 
the puncture, and an opportunity was afforded of studying tk 
patient's focal symptoms with a view to subsequent removal of tbf 
growth. In intra-cranial growths we must be careful not v 
withdraw too large a quantity of cerebro-spinal fliuid, lest suddttl 
diminution of pressure cause a haemorrhage into the tumour Ij 
result, by the way, which sometimes occurs after a palliati^ 
trephining). In a case recorded by Masing * this actually occomd: 
but in his case the fluid was allowed to run for a quarter of an hof | 

' Deutsche medizinische Wochenschrift, 1904, No. 36. 

* Munchener mediziniache Wochenschrift^ 1900, s. 133. 
> Ibid., 1902, No. 21. 

* Neurol. Cenlralbl., \^^\, v ^'^^'^^ 


IHi<i no less than 10 c.c. were withdrawn. I have liad under my 
observation several cases of persistent tinnitus and giddiness, of 
tn&iiy months' duration, in which a single lumbar puncture with 
the removal of less than 10 c.c. of fluid permanently relieved the 
londition. We must, of course, be careful to eliminate all the 
►rdinary causes of tinnitus and giddiness, aural or otherwise, before 
Bsorting to this treatment. In fracturea of the base of the skull, 
mma may be relieved in a remarkably short time by the with- 
Irawai of cerebro-spinal fluid. I saw such a patient after a 

irriage accident, iu whom lumbar puncture was followed by 
apid improvement. The procedure may, if necessary, be repeated 
everal times on successive days. 

Uriemic coma and convulsions, and cases of puerperal eclampsia, 

e often relieved in a striking manner by lumbar puncture, and in 
everal instances life has undoubtedly been saved by this means. 
?or example, McVail ' records two cases of acute nephritis in which, 
Lotwithstanding energetic treatment by purgatives, hot-air baths 
md pilocarpi!! to induce free perspiration, coma and convulsions 
lupervened. Lumbar puncture was performed, 20 to 2y c.c. of 
«rebro-8pinal fluid were withdrawn, and within three or four 
lours the coma passed off, the convulsions ceased, and both patients 
dtimately made a complete recovery. Cases like these raise the 
juestion as to whether the headache, coma, and convulsions in 
lephiitis are really caused entirely by " ursemic poisoning " of the 

■ain-centrea, or whether they may not be largely due to a sudden 
Dcrease of intra-cranial pressure — part of the general asdema. 

Again, in cases of tetanus, we know that the tetanus poison 
las a selective action on the motor nerve-cells of the spinal cord 
ind brain. Therefore, in addition to removing the tetanus 
lacilli at the site of inoculation, by excision of the original wound, 
endeavour to neutralise the toxin by means of antitoxin. 
Phis is sometimes administered hypodermically ; but it is mure 

Eficacious, as Roux and others have shown, if injected into 

he cranial cavity through a small trephine opening, and some 

emarkable recoveries have followed this method of treatment. 

' Bril. Mtd. Joum., 1B03, vol. ii. 


But the procedure is not free from danger. In one case at least,^ 
a patient died of cerebral abscess at the site of the trephine- 
opening eight weeks afterwards, long after all symptoms of tetanus 
had disappeared. It is simpler and better to administer the anti- 
toxin (with perhaps the addition of stovaine and morphine) by 
means of a lumbar puncture needle. Strychnine poisoning is also 
successfully treated by intra-thecal administration of eucaine. It 
may be necessary to give a general ansBsthetic to relax the 
opisthotonos, before performing the spinal puncture. 

Injection of anaesthetic drugs by lumbar puncture — so-called 
spinal anasthesia — ^is useful when we desire to perform operations 
on the lower limbs or trunk without rendering the patient's brain 
imconscious. Various substances have been successfully employed 
as spinal anaesthetics, amongst which may be mentioned cocaine, 
stovaine, and novocaine.^ It is desirable, if possible, to have a 
solution which is isotonic with the blood-serum, i.e. having the 
same osmotic tension. 

For spinal anaesthesia we generally select the second lumbar 
interspace and perform our puncture in the mesial line, so that 
the roots of both sides may be equally affected. Before injecting 
the anaesthetising solution, we withdraw a quantity of cerebro- 
spinal fluid, from 10 to 15 c.c, considerably exceeding in amoimt 
the fluid to be introduced. 

Spinal anaesthesia is essentially a root anaesthesia, due to 
paralysis of the posterior roots. On injecting a solution of stovaine 
and suprarenin, the earliest objective signs are disappearance of 
the knee-jerks (usually within one minute), then of the ankle-jerks 

1 Gibbs, Brit, Med, Joum., July 1, 1899. 

• The following are examples of ansesthetising solutions ; — 

1. Stovaine, 5 per cent. ; glucose, 5 per cent, in water. Sp. gr. = 1023. 
Do8e = l c.c. (Barker, Brit. Med. Joum., 1908, p. 248.) 

2. Stovaine, 4 per cent. ; sod. chloride, 0*11 per cent. ; suprarenin 
borate, 0*01 per cent, in water. Sp. gr. = 1005. Dosesl c.c (Bier, 
quot^'d by Barker, Brit, Med, Joum., 1907, p. 666.) 

3. Stovaine, 1*5 per cent. ; cocaine, 0*5 percent, in water. Dose = 4 c.c. 
(Chaput, La Preaae MSdicale, 1907, p. 763.) 

4. Novocaine, 2 per cent. ; suprarenin borate, 0*009 per cent. ; NaCl. 
0*9 per cent. Sp. gr. = 1014. Do8e = 5 c.c. (Braun, I^etUachc tnerf. 
Wochenachrifi, 1^05» a. U^il .^ 



p(within two or three minutes), the Buporficial reflexes remaining as 
unchanged. Concurrently with the abolition of the deep 
[leflexea there occurs slight analgesia of the perineum and genitals, 
without loss of tactile sensibility. The analgesia gradually deepens 
land spreads over the lower limbs, and after four or five minutes 
■the plantar and cremasteric reflexes disappear. Temperature- 
Kflense becomes lost. Tactile and pressure-sense disappear much 
■later and may be preserved throughout. Sense of position is last 
land least aflected. The dartos or scrotal reflex is unaffected. 
■ Motor paralysis, due to affection of the anterior roots, supervenes 
ist of all, in five or six minutes, beginning in the feet and soon 
■effecting the whole musculature of the lower limbs. The deep 
' structures also become analgesic, except the testicle and spermatic 
cord, which are difficult to render analgesic, since their nerve- 
supply is derived from the firat lumbar roots which are rarely 
reached by the solution if the patient lies horizontally after the 
injection. If it is desired to reach these higher roots by a heavy 
anEBfithetising fluid, it is advisable to elevate the pelvis higher 
than the thorax, to permit the flmd to gravitate towards the 
thoracic region. In this way the ansesthesia may extend as high 
as the nipples, or even to the upper limbs. If the injection be 
ma<le with the patient lying on his side, the heavy anaistlietising 
solution gravitates to the dependent aide and therefore exercises 
its effects chiefly, and it may be entirely, on the roots of that 
side. Thus, for example, by laying a patient on his left aide and 
injecting in that posture Barker^ was able to amputate the left 
leg paiiileasly, without producing sensory or motor impairment of 
the right lower limb. 

After lasting for 45 to 90 minutes, the paralytic phenomena 
begin to pass ofl. First motor jmwer returns, then the analgesia 
fades away, and last of all, the reflexes, superficial and deep, 
reappear. In spinal amesthesta by cocaine the phenomena are 
slightly different. Analgesia sets in without affection of reflexes 
or of motor power ; tactile sense and temperature -sense are also 
only slightly affected. 

' Bril. Mvl. Jouni.. 1908, p. 246. 




Spinal ansesthesia is contra-indicated in severe scoliosis, because 
of the difficulty in accurately penetrating the theca. It is also 
better avoided in young children and in meet cases of hysteria. 
Even apart from such cases, it should, I believe, be reserved for 
very special conditions, as, for example, acute abdominal cases, 
conditions of shock, and severe cardiac or pulmonary diseases 
where a general anaesthetic is particularly dangerous. From the 
patient's point of view, complete unconsciousness is generally 
preferable to the mental strain of remaining conscious whilst as 
operation is being performed on his analgesic legs or trunk. 

Of the morbid phenomena which sometimes follow spinal 
anaesthesia, the most frequent is headache ; this is often of great 
severity and may last for days ; it is probably due to the altered 
intra-cranial pressure produced by the addition of the anflesthetising 
solution, and may generally be relieved by a simple lumbar puncture, 
withdrawing from 10 to 20 c.c. of fluid. In three-fourths of cases 
of spinal anaesthesia, according to Schwarz,^ there is a slight transient 
albuminuria, lasting for a week or more. Another sequela, forta- 
nately an uncommon one, is ocular palsy, chiefly of one external 
rectus but sometimes of some other ocular muscle ; such pakj 
may last for days or weeks, but ultimately clears up. 

* ZeiUchrift fur Chirurgie, 1907, a. 651. 



" Ths iiinoc«Dt slecip, 
Sleep thot kaita up tha ravelled sleavo of care, 
Tlie death of each day's life, sore labour'^ bath. 
Balm oC hurt miDde, grout naturo'a xef^ond (bourse, 
Chief DouriBher in life's fOB*l." 

:, Jlfoodcfft. 

Hoar of UB spend about one-third of our life asleep. Neverthe- 
a the physiology of sleep is not yet completely understood. Let 
} recall the chief phenomena of ordinary healthy sleep. Firstly, 
here is diminution and then loss of conscious recognition of ordi- 
lary stimuli, such aa would ordinarily attract our attention, 
whether these stimuli be derived from the outer world or from 
lithin the sleeper's own organism. There is also, as consciousness 
I becoming blunted, a characteristic and indescribable sense of 
!ll-being. Voluntary movements become languid and ultimately 
we, and the mosclcs of the limbs relax. Meanwhile there 
tevelops double ptosis or drooping of the eyelids ; the respiratory 
Dovements become slower and deeper, the pulse is slowed, the 
intaneous vessels dilate to a slight extent and the general tempera- 
are of the body falls, whilst many processes of metabolism, such 
B those of digestion and of certain secretions, are retarded. 

Various explanations have been oSered to account for all these 

ihenomena. But at the outAet we should recognise that the 

)ce8S is a complex one, implicating many other organs besides 

> brain. An animal from which the cerebral hemispheres have 

len removed still showa regular alternations of sleep and waking. 

As regards the condition of the brain during natural sleep, it 

1 generally admitted that it ia amomic. If we observe a patient 

an animal that has been trephined, we see that during sleep 

! volume of the brain is diminished ; it sinks in and becomes 



pale, i.e. the cortical vessels are contracted. This vaso-coc- 
striction is not confined to the superficial vessels alone ; it implicates 
the whole cerebral circulation, for if we succeed in examining the 
patient's retinal vessels with an ophthalmoscope without wakening 
him, we find that they present a similar vaso-constriction. Cerebral 
anaemia, then, is one important factor in natural sleep. After a 
heavy meal we are all familiar with the difficulty of doing mental 
work and the tendency to fall asleep. This is doubtless explained 
to some extent by the occurrence of temporary abdominal hyper- 
a3mia together with compensatory cerebral anaemia. 

Let us next consider the condition of the nerve-cells during 
sleep. The activity of some of them, certainly of the cortical 
cells, is temporarily diminished. Some writers have suggested 
that this is due to a retraction of the dendrites, by a sort of amoeboid 
movement whereby nerve-cells previously in contact become, as it 
were, temporarily insulated. But the evidence in support of this 
theory is far from convincing. In fact, modem histological obser- 
vation goes to show that nerve-cells are not merely in contact 
but that neuro-fibrillae are continuous from cell to cell throughout 
the nervous system. 

Other writers ascribe the phenomena of sleep to poisoning 
of the nerve-cells by accumulation of COg, or to intoxication bv 
other waste -products of metabolism acting as narcotics. Be this 
as it may, we must bear in mind, as Clapar^de ^ has urged, that 
neither CO2 poisoning nor intoxication is a necessary antecedent 
to sleep. On the contrary, we usually sleep for the purpose of 
avoiding auto-intoxication and of preventing exhaustion not 
because auto-intoxication or exhaustion has supervened. Healthy 


sleep is not necessarily a poisoning of certain nerve-centres by 
toxic by-products. Moreover there is a regular periodicity wherebv 
a healthy person, whether fatigued or not, has a recurrent appe- 
tite for sleep. Sleep has a constructive, anabolic, invigorat- 
ing effect on the whole body. Part of this effect is doubtless 
due to physical rest, part perhaps to interruption in the pro- 
duction of toxins arising from muscular contraction, and part to 




the absence of stimuli which during waking hours excite nervous 

Some writers have assigned special importance to a particular 
legion of the brain in connection with the function of sleep, and 
eepecially to the Hoor of the third ventricle and the Sylvian aque- 
duct. In support of this they point out the familiar ptosis and 
the tendency to divergent strabismus, both of which might be 
explained as due to paresis of the ocuSar nuclei. They also recall 
the well-established fact that tumours in this region of the brain 
ate specially likely to have as an early symptom persistent drowsi- 
ness. But some of these phenomena can also be explained as due to 
cerebral anremia, the tumour at the base mechanically compressing 
and narrowing the arteries which form the circle of Willis. This 
has been demonstrated in several instaucee, notably in a case of 
tumour of the hypophysis recorded by Franceschi.' I myself had 
under my care a similar case in a young woman, aged twenty-six, 
with a large cystic growth of the pituitary body and floor of the 
third ventricle, in whom the chief symptoms were paroxysms of 
ioverpowering sleep. She ultimately passed into a atuporose con- 
dition and died. No paralytic phenomena occurred during life, 
nor was there any optic neuritis. Another case was that of a 
^ung man of thirty-four who had intense drowsiness, paroxysmal 
beadaches, and total loss of sexual power. He also had blindness 
if the right eye and temporal heniianopia of the left, with slight 
»llor of the right optic disc, signs pathognomonic of a lesion of 
lie optic chiasma. All these phenomena were due to a tumour of 
the pituitary body. His drowsiness was so intense that he tell 
asleep if he sat down and only with difficulty could he be roused 
for examination. 

Another factor in the production of natural sleep is the absence 
of violent external stimuli such as loud sounds or dazzling light ; 
therefore silence and darkness, by withdrawal of stimuli, conduce 
to sleep. The pleasing monotony of gently reiterated stimuli often 
has a similar soothing effect which is quite sui generis and 
is closely analogous to the condition of hypnosis. It cannot be 
' Rivigla di palologia ncrvom* c mentale, 1904. p. ■Ifi?. 


ascribed to cerebral ansemia, to exliaustion, nor to any tosc 

We recognise different degrees of normal sleep, according to 
the strength of stimulus necessary to rouse the sleeper to a con- 
sciousness of his surroundings. The lightest is that of mere 
drowsiness, a stage in which the sleeper, though not directum 
his conscious attention to surrounding objects, can still be easilj 
wakened by moderate stimuli such as ordinary conversation, ligbt 
touches, &c. A deeper stage is sleep with dreams, where the 
sleeper is unconscious of his surroundings but yet his psychical 
centres, uncontrolled and deprived of the faculty of .comparison 
with his environment, produce a series of fantastic mental pictum. 
Under the influence of dreams a sleeper may, if his cortical moto 
centres are still active whilst the psycho-sensory centres are un- 
inhibited, perform motor actions, as in the well-known stage of 
sleep with sonmambulism. But sonmambuUsm is rare in health, 
because ordinarily the cortical motor centres are dulled simul- 
taneously with the sensory. Still more profound is the stage of 
deep dreamless sleep. This variety merges into what unto 
pathological conditions we call stupor and ultimately coma. 
The chief distinguishing point between deep sleep and coma is 
that a sleeping person can be roused whereas a comatose patient 

Disorders of Sleep.— We sometimes meet with pathologkil 
drowsiness. Perhaps the most common instance is that of an 
anaemic young woman. Here the drowsiness may be partly toxic 
due to absorption of poisons, whether from a loaded . intestine, 
from decaying teeth, or from other sources, but the main elemeni 
in causation is probably vascular. In such a case the heart is devoid 
of energy, and the vessels throughout the body are flabby and 
deficient in tone. Therefore in the erect attitude the vessels of the 
brain are badly filled, and if the patient sits down during the daj 
she feels drowsy. But when she lies down at night, the brain iwf 
becomes hyperscmic from want of vascular tone, and the result b 
that she lies awake. This combination of diurnal drowsiness vitk 
nocturnal wakefuhiess is highly characteristic. In treating the 




condition, besides attacking the aiuemia, we often administer 
digitalis, sini^, besides being a cardiac tonic, it haa also a well- 
larlced vaso-constrictor action. li digitalis be combined with 
on and with bromide of potassium, the condition generally 
apidly iniprovea. ' 

Drowsiness also occurs in other conditions. Myxcedematous 
patients are habitually sleepy and stupid, probably from toxtemia. 
also are many idiots and cretins. After a severe fit of epilepsy 
is common for the patient to fall into a deep post-epileptic sleep, 
largely due, no doubt, to toxic products produced by the nervous 
md muscular systems during the fit. Certain tumours of the brain, 
especially in the region of the floor of the third ventricle, as we 
liave already seen (p. 405), are aaaociated with early and persistent 
drowsiness ; so also are some cases of punctured wounds in the 
same region.^ Elsewhere in the brain, tumours may also produce 
drowsiness at a late stage of the disease, probably from increased 
intra -cranial pressure, though in these cases the condition more 
iarly approaches coma and ultimately merges into it. The 
irowsiness produced by the combination of exhaustion with 
extreme cold, as in people who are in danger of being frozen to 
death, is probably largely due to deficient circulation, and unless 
rigorous measures be taken to stimulate the heart and the general 
eirculation, sleep passes on to coma and death. The hibernation- 
Bleep of certain animals is largely due to winter-cold, for if such 
animals be kept in a warm atmosphere throughout the winter, 
they do not sleep more than in summer time. The delightful 
Irowsiness produced by gazing into a red fire on a winter afternoon 
I something entirely different. It is probably a mild variety of 
hypnotic sleep, the continuous red glow acting through the optic 
neT\'e8 by a summation of stimuli. It is not a. question of the 
•e heat of the fire, for unless the blaze be seen, drowsiness is 
likely to supervene. A similar summation of stimuli probably 
explains the well-known chuich drowsiness. The soothing mono- 
lony of the sermon, combined with the sitting posture of the 
iBt«ner (who thus has the additional excuse of a degree of cerebral 
' Knegg. Lancet, 19(17. p, 1477, 


ansemia) and lastly the common habit of closing the eyes to avoid 
visual distractions, all these combine to make church-drowsines 
a popular disorder. I do not refer, of course , to wild "revival" 
meetings, nor to militant political or sensational sermons, where 
the conditions both of preacher and of audience are entirelT 

But there are other pathological varieties of sleep to which we 
must refer. There is the drowsiness of impending urctnm a 
diabetic cavia, both toxic in origin. There is also that remarkable 
tropical disease, sleeping'Sickness, endemic in certain parts d 
Africa, and associated with the presence of trypanosomes in tk 
blood, glands, and cerebro-spinal fluid. The drowsiness in thk 
malady is doubtless due to some toxin produced by the parasites. 
In the later stages of the disease a peri- vascular ceUular infiltnl 
tion is found around the cerebral vessels, a variety of chrook 
meningo-encephalitis. Narcolepsy is another condition where tk 
patient has sudden paroxysms of sleep, in the midst of whaters 
occupation he may be pursuing at the moment. These cases m 
hysterical. I remember one such patient who used to fall asleep 
when playing the piano or during a game of cards (especially if fe 
held a losing hand). He had numerous other hysterical stigmau. 
and the diagnosis presented no serious diflBiculty. The A^ysft^n 
trance is another condition, analogous in some respects to ordin^y 
sleep, but time does not allow us to discuss it here. Suffice it 5 
say that the phenomena of hypnosis can be induced by repeat«:| 
monotonous stimuli, visual, auditory or otherwise, aided by si 
tion. The patient is thereby made to fall into a sleepy conditi( 
varying in intensity from mere drowsiness to dreams (the incid( 
of which are controlled by suggestion), to somnambulism, or ?| 
deep dreamless slumber lasting perhaps for many hours. There a?| 
also the well-known phenomena of spontayieaus somnainbulism, dn 
to the remaining awake, as it were, of the cortical motor cent 
when the higher sensory and psychical centres have lost 
power of inhibition. Such a patient gets up and acts his 
Nightmares are horrifying dreams which produce so much di 
that they sometimes waken the patient up. They are genenH 



toxic in origin. Their commonest cauae is gastro-intestinal fermen- 
tation, certain articles of diet (proverbially a lobster supper), being 
Ipecially liable to produce bad dreams. In children nightmares 
often recur again and again with the peculiarity that the terrifying 
talluci nation is the same on each occasion. Here again gastro- 
ntestinal fermentation is often a factor. Still more frequently do 
we find that the child has adenoids, which int«rfere with respiration 
and produce a degree of C'O^ poisoning. Removal of adenoids and 
attention to the bowels cure most cases of night-terrors in children. 
Patients with tropical abscess of the liver, curiously enough, are 
particularly liable to horrible dreams, so much so that they may be 
afraid to fall asleep. Here again the condition is doubtless toxic. 
Jlightmare is also a frequent symptom in patents with aortic 
regurgitation. Tn them the condition is not toxic but vascular in 
Origin, due to irregularity in the blood-supply and to pulsation in 
the cortical capillaries. 

Lastly let us consider the subject of BleapleasneBs or insomnia. 
iJaaea of insonmia may be divided into two great classes, the 
atrinsic and the intrinsic. 

Extrinsic insomnia includes those cases where the sleeplessness 
IB secondary to some outside cause, not directly arising in the 
perebrum or its blood-vessels. For example, physical pain of any 
Bort, cough, vomiting, frequent micturition, diarrhcea, pruritus, 
ind so on, may keep a patient awake. In all such cases we must 
!at the primary symptom ; when it is relieved, sleep will follow 
laturaily. This group also includes emotional insomnia, which 
B more often the result of grief than of joy, and more commonly 
associated with fear or apprehension for the future than with 
ir sorrow for the past. When pleasurable emotion does 
jmnia, it is generally due to anticipation of some happiness 
n the immediate future. A man does not usually lie awake because 
lome one b going to leave him a fortune twenty years hence, but 
he may spend a sleepless night on the eve of his wedding. The 
uitment of emotional insomnia, apart from assuaging the patient's 
jrrow (a matter which is often beyond the physician's sphere), 
1 best accomplished by giving some cerebral sedative, such s.b 


a mixture of chloral and potassium bromide. The insomnia o 
extreme joy seldom calls for treatment, but if the patient become: 
too excited, here again a cerebral sedative may be given. 

We are much of tener consulted with regard to the other idnii 
of insomnia, which we may call intrinsic insomnia. This is 
commonly due to vascular, toxic, or nervous faults, or to com- 
binations of all three. 

As to vascular causes, the brain may be hyperseniie, rendering 
sleep impossible. Hypersemic insomnia may be either of the higi- 
tension or of the low-tension type. In high-tension insonmia the 
patient may be the subject of general arterio-sclerosis or of leoal 
disease, and the hyper-tension is readily demonstrated by tk 
Riva-Rocci sphygmo-manometer. In such cases the patien: 
complains of a difficulty in falling ofE to sleep. The best remedy, 
as Broadbent^ urged, is to give a mercurial aperient such a? 
blue pill or calomel, say two or three times a week. This oftt»3 
brings down the tension in a remarkable way and induces sleep. 
Of course we also lay down careful regulations as to diet, 4c. 
in these cases. Hypersemic insonmia from low tension occurs b 
anaemic and neurasthenic patients, as already explained, and i* 
characterised by the fact that when the patient sits erect in ^ 
chair he becomes drowsy, whereas when he lies down in bee 
the brain becomes over-filled with blood and the patient canno: 
get to sleep. In such cases the best remedy is a combination <i 
a cardio-vascular tonic like digitalis with a moderate dose 'i 
bromide of potassium. Hypersemic insomnia, whether of h^h- 
tension or of low-tension type, is often associated with cold feet 
If the feet can be made warm, the cerebral hyperaemia tends t-^ 
become alleviated. A cup of hot milk or hot soup, by producini' 
abdominal hyperaemia, often relieves hyperaemic insomnia. 

Insomnia is one of the most distressing symptoms of chrom 
heart-failure. Just when dropping off to sleep the patient suddeni^ 
starts awake with a feeling of suffocation, gasping for breatl 
This is probably due to deficient circulation in the medui^ 
oblongata. We treat the condition by cardiac tonics togetki 

1 Practitioner, July li)06. 


(ritli one of the noii-depreasant pure hypnotics, or even by morphia, 

lUtiously administered and combined with atropine. 
Next we have toxic insomnia, which b one ot the commonest 
varieties met with in practice. Many cases are associated with 
gastric or intestinal fermentation, and especially with dilatation 
of the stomach. The symptoms are characteristic. The patient 
a Is asleep, but, after an hour or two, varying according to the 
legree of gastric dilatation, he wakes up, perhaps after a horrible 
dream, with palpitation, profuse sweating or gastric uneasiness. 
He may have a sinking feeling with craving for food, and if he 
Bats a biscidt or some other simple food, the stomach contents 
ftre temporarily diluted and he feels relieved for the time. Tlua 
may mislead him into thinking that his sleeplessness is due to 
(exhaustion from want of food, which is far from the fact. During 

i waking hours he is often very depressed, hypochondriac, and 
almost melancholic. When we have a clinical history ot this 

jrt, we should carefully examine the abdomen. If we find the 
physical signs of dilated stomach, we treat the patient accordingly, 
putting him on a dry dietary, free from starchy foods or green 
tables, and attending carefully to the bowels. We meanwhile 
administer gastro -intestinal antiseptics such as carbolic acid, 
oreaeote, ft naphthol, or sulpho-carbolate of soda. To give hypnotics 

I such cases, without correcting the gastric condition, is worse 

lan useless. 
Amongst the toxic forma of insomnia we must not omit to 
tefer to the sleeplessness produced by chronic excess in alcohol, 
Culminating sometimes in delirium tremens, also the insomnia of 
acute fevers. Both in fever and in delirium tremens, sleep can 
often be induced by a cold pack or cold sponging. Insomnia may 
yesult sometimes from excessive tobacco smoking, which produces 
Sts effect partly by it« action on the nerve-cells, partly by its 
influence on the circulation. Strong tea or coffee may also act 

a a similar fashion, keeping a patient awake. 

Lastly, there ia primary or " neroom " imomnia, due to over- 
Eattgue, especially from mental over-work. We see many instances 
amongst busy professional or bueineBS men. But in most cases 


there are several factors involved, not only the toxins of exham 
but those of hasty and ill-digested meals, together with a 
cession of powerful mental stimuli, and the persistent cen 
hjrpersemia of the brain-worker. 

In every case of primary insomnia, besides correcting any gsj 
intestinal, or vascular fault that may be present, we should i 
it a golden rule to send the patient away for a complete holi 
These are also the cases for the employment of the pure hypno 
which have a direct sedative action on the psycho-sensory coi 
The name of these drugs is legion, and I do not propose to die 
them exhaustively. Amongst the most reliable is paraldeh 
Its somewhat nauseous taste is no drawback, since it prev 
the patient from acquiring a habit for the drug. Of the o 
hjrpnotics I need only mention a few, such as chloral hyd] 
sulphonal, and veronal. We should never allow a patient < 
blanche to take a hjrpnotic drug on his own initiative. ! 
drugging with hjrpnotics is highly dangerous. A hypnotic sh 
never be taken without the express authority of the physif 
Nor should any one, even though he be a medical man, presc 
hypnotics for himself ; he should call in a professional colleagu 

Drugs like hyoscine and morphia are our last resort in obsti 
insomnia. In severe cases of excited mania or melancholia gr. 
of hyoscine, hypodermically, or gr. J of morphine with gr. x^ 
atropine, soothe the patient in a remarkable way. Persie 
insomnia in cases of insanity is of serious omen. Most ali< 
physicians insist on having charts kept of the amount of i 
obtained by each insane patient, since severe insomnia recui 
regularly for a month in cases of insanity renders the progi 
as to recovery very unfavourable. 



OK clinical purposes we Include under this heading not only the 
leoplasma proper (glioma, sarcoma, endothelioma, fibroma, carci- 

loina, iStc), but also gummatous and tuberculous growths, para- 
ntic cysts, and even aneurisms and abscesses. All of these may be 
togarded as slowly -growing foreign bodies which, sooner or later, 

Bcording to their situation within the cranial cavity, produce 
^nical phenomena rendering their diagnosis possible. Most 
nimours produce their effects by displacement, distortion, and 
»mpression of the nerve-elements. Only in a few instances 
{e.g. in carcinoma, melanotic sarcoma) are the nerve elements 
rectly destroyed by the tumour cells. Two classes of signs and 
bymptoms result ; firstly, general symptoms of increased intra- 

ranial pressure, independent of the position of the tumour, and 
secondly, foail symptoms, which vary according to the particular 
b of the brain implicated by the growth. General symptoms 
enable us to say that there is a tumour somewhere within the 
■kuU ; in order to locate the growth precisely, we must search 
for localising symptoms which are usually, though not necessarily, 
later in onset. If localising symptoms are absent, focal diagnosis 

lay be impossible. 
General Symptoms. — The cardinal phenomena of intra- 

ranial tumour are three in number, viz. headache, optic neuritis, 

nd vomiting, To these may be added others, such as mental 

ihanges, generalised convlilsions, giddiness, slowing of the pulse, &c. 
The triad syndrome of headache, optic neuritis, and vomiting should 
always suggest the possible presence of an intra-cranial growth. 
But before diagnosing cerebral tumour from these three signs 
Uone, we must be careful to exclude three other conditions, any 

[ which may produce the triad syndrome. These conditiouB *«>(, 


kidney disease, severe ansBmia, and lead-poisoning, all of tkm 
easy of recognition if we bear the point in mind. 

Headache is the most constant symptom of intra-cranial tumour; 
it generally appears at some time or other, sooner or later. Its 
severity is sometimes intense. Usually it is a constant dull pain 
with paroxysms of agonising intensity. The pain may be diffuse 
or localised, but if localised its position does not necessarily co^^ 
spond with the situation of the tumour, except in tumours at or 
near the surface of the brain, where the pain may sometimes be 
directly over the growth and accompanied by local tenderness 
on percussion or pressure, or even by a local alteration of percussion- 
note. But too much stress should not be laid on the existen« 
of localised pain, imless accompanied by other focal signs. Thus, 
for example, cerebellar tumours often produce frontal headack 
and in one case of my own ^ a right-sided cerebellar growth was 
accompanied by pain limited to the left frontal region. The 
headache of intra-cranial tumour is intensified by excitement, by 
exertion, or by any temporary cerebral hypersemia. 

Oftic neuritis or " choked disc," detected with the ophthalmo- 
scope, should be looked for in every case of suspected intra-cranial 
tumour. But it should be borne in mind that while the presence 
of optic neuritis is one of the strongest evidences of intra-cranial 
mischief, no weight should be laid on its absence if other signs 
point to intra-cranial growth. Optic neuritis from brain tumour 
is relatively more frequent in hypermetropic than in myopic eyes/ 
Another point of importance is that intense optic neuritis mav 
coexist with perfect vision. But in time, optic neuritis generally 
progresses to optic atrophy, with its accompanjring blindness. 
Many patients with intra-cranial tumour have early transient 
blindness, sometimes momentary, sometimes lasting for a few 
hours or days at a time, in one or both eyes. Trephining the 
skull and opening of the dura mater relieve optic nemitis even 
though the growth be not removed ; they also give considerabfe 
relief to the headache. The optic neuritis of brain tumours, thougl 

^ Edin. Hoap. Reports, 1895. An almost identical case has been reoordeii 
by Sachs {Medical Record, Doceniber 22, 190(5). 
» Gunn. Brtt. Med. Joura., X^^l , \>. \\*lvs. 



generally affecting both eyes, may be unequal on the two sides, 
or it may even be monocular. On the whole, the greater intensity 
tends to be on the same side as the tumour, especially in frontal 
and cerebellar tumours, though this rule is not invariable. In 
^cerebellar tumours optic neuritis is Bpecially early in onset. 

VomUing is a less constant phenomenon than headache and 
optic neuritis, except in tumours of the posterior fossa, in which, 
irom the very outset, it is rarely absent. " Cerebral " vomiting 
differs from the ordinary vomiting of abdominal disorders. It 
usually occurs independently of food, and is unassociated with 
other gastro- intestinal symptoms, Moreover, it is often unprecoded 
by nausea and thus has a curious " projectile " character. A 

ige of posture of the head is sometimes enough to induce an 
attack of cerebral vomiting. 

Amongst the other ' general ' symptoms we must mention 
progressive mental dulness. This is apparently to a large e3ct«nt 
the result of the persistent headache. The patient becomes 
apathetic, dull, and slow in answering questions ; he loses interest 

lis ordinary affairs. Sometimes he becomes overwhelmingly 
drowsy and finally comatose. In the later stages the sphincters 
are imcontrolled. Mental changes are particularly early of onset 
in tumours of the pre-frontal region, altogether independently of 
■the intensity of the headache. 

Generalised epHeptilorm contmUions (as distinguished from 
Jacksonian attacks) may be produced by tumours in almost any 
lart of the brain, not necessarily in the immediate neighbourhood 
if the motor areas. Such convulsions probably result mainly 
from increased intra-cranial pressure and, as a rule, occur com- 
jaratively late in the disease. But they may also, though less 
mmmonly, appear as the initial symptom of an intra-cranial 
growth. In such cases epilepsy is sometimes diagnosed, and 
iimtil further phenomena (such as optic neuritis or focal signs) 
develop, the error is unavoidable. More usually general con- 
vulsions are a late phenomenon, and there are antecedent physical 
signs to guide us. 

Aliacks of giddiness are often corapkined of in brain tumour. 


Sometimes these are merely indescribable feelings of confouon 
in other cases there is a true vertigo or feeling of uncertainty i 
equilibration. Vertigo is specially early and severe in tumours c 
the cerebellum, cerebellar peduncles, and corpora quadrigemini! 
and in them it is often associated with the motor phenomenon c 
a reeling or staggering gait. 

Slowing of the puhe, permanent or transient, is a valnaU 
corroborative sign of intra-cranial abscess. It may also occnr a 
one of the general symptoms of tumour, especially in the neigl 
bourhood of the medulla oblongata. In other cases, again, i 
may meet with tachycardia. Therefore the pulse-rate of itsd 
is not of high diagnostic significance, compared with the othc 
signs already mentioned. Slowness of breathing and a Chevw 
Stokes type of respiration may occur, but mostly in the lat« 
stages of the disease. Paroxysms of yawning or of hiccough ma 
also be produced by intra-cranial growths, especially those of tl 
posterior fossa. 

Localising symptoms are sometimes absent, and a tumoc 
may only be revealed by post-mortem examination. Thi 
experience is commoner with temporal tumours than with th« 
occurring elsewhere. In most cases, however, focal sympton 
develop, which enable us to determine the position of the growt 
with greater or less precision. In a few cases radiography ma 
reveal an abnormal shadow in the position of the tumour. I 
superficial tumours local percussion of the skull may occasionaD 
yield an altered note. But in some cases we can only form a 
approximate idea as to the site of the disease. For example, if 
patient with headache, vomiting, and optic neuritis develops 
gradually increasing left hemiplegia, all that we are justified i 
diagnosing is a growth somewhere in the right cerebral hem 
sphere, probably in the neighbourhood of the motor tract. Unl« 
additional signs appear, it may be impossible to say more sine 
such hemiplegia may be produced not only by tumours direct! 
implicating the pyramidal tract, but also by frontal, temporal, < 
even occipital tumours compressing the motor path. Again tl 
occurrence of cranial nerve palsies is always suggestive of a lesio 


ftt the base of the brain ; but this rule is not invariable. For 
example, isolated ocular palay of one external rectus has little or 
no localising value, since the sixth nerve may be paralysed (whether 
from traction or from increased intra -cranial pressure) by a growth 
anywhere within the skull. Further, we may have "falae localising 
signs " ' from compression or distortion by growths in distant 
parts of the brain. Thus, for example, a tumour of the frontal 
lobe may at a later stage produce signs of contra -lateral cerebellar 
taae, or a cerebellar growth may afterwards be associated with 
Jacksonian fits of one limb, suggestive of a lesion of the motor 
Brea, but really due to distension of the lateral ventricle of the 
corresponding side, and so on. Or again, localising symptoms 
oay be masked or concealed, as in some occipital tumours in which, 
E the optic neuritis goes on to atrophy and blindness, the hemi' 
>nopia becomes lost which might have led to a correct diagnosis. 
Localising signs, to be of value, should generally be early. Ab' 
Sence of local signs suggests that the tumour is above the tentorium 
bince sub-tentorial growths almost always produce localising signs 
■ly in their courae. 

Bearing the above points in mind, let us now consider the chief 
localising symptoms of tumours in the various regions of the brain. 
Tumours of the Motor Cortex. — The motor area, as we have 
Iready seen, comprises the pre-central convolution and the ad- 
icent end of the second frontal g3^u8, together with part of the 
Sortex on the mesial surface of the hemisphere. Tumoure of the 
region are the easiest of all to recognise clinically. In them, 
In addition to the general signs of intra-cramai tumour, we usually 
ibserve two classes of phenomena, irritative and paralytic. 

The irritative group consists of Jacksonian fits, commencing in 
he contra-lateral face, tongue, arm, or leg, as the case may be, 
ccording to the part of the motor cortex which happens to be 
chiefly implicated. In a Jacksonian fit the convulsion, generally 
consisting of tonic spasm followed by clonic jerks, may be strictly 
localised to a small group of muscles, or it may spread from them 
to other muscle-groups, but always in a regular order (as shown 
in Fig. 3, p. 5). Less commonly the whole of the muscles of 
' Collier, Brain, \yOA, p. WO. 


the contra-lateral face, arm, and leg are thrown into convulsion 
simultaneously. During Jacksonian convulsions, unlike ordinary 
epilepsy, the patient usually retains consciousness all the time, 
and can study his own fit. But if the convulsion spreads across 
the middle line and becomes bilateral, consciousness becomes lost 
at or before the moment of crossing. 

The paralytic phenomena in tumours of the motor region consist 
in weakness of the convulsed muscles during the inter-paroxysmal 
periods (see Figs. 25 and 26, p. 67). Such weakness is most 
marked immediately after a convulsion. There is also temporary 
atopognosis in the afEected limb and loss of the sense of position. 

According as the growth is primarily cortical or sub-cortical, 
convulsions precede muscular weakness or vice versd. A cortical 
tumour, for example one growing from the meninges, is irritative 
from the first ; a sub-cortical growth is usually indicated by an 
initial monoplegia, followed later by Jacksonian convulsions. 
Moreover, the precise starting-point of the convulsions in a sub- 
cortical growth is less constantly localised to the same muscle- 
group ; thus, for example, a sub-cortical tumour immediately 
under the arm-area may produce Jacksonian fits, conmiencing 
sometimes in the thumb, at other times in the elbow. The extent 
of a Jacksonian fit also varies with the extent of the tumour. A 
small superficial tumour will produce a highly localised fit followed 
by monoplegia of the afEected part, whereas a tumour of the same 
size, situated deeper beneath the cortex, will produce an initial 
monoplegia, convulsions being weeks or months later in onset. 
The deeper the growth, the less tendency is there to localised con- 
vulsions. Tumours of the pre-central or motor area, if extending 
backwards across the Rolandic fissure to the post-central convolu- 
tion, are usually associated with a distinct sensory aura in the 
Affected limb at the beginning of the motor convulsion, together 
with a degree of anaesthesia, monoplegic or hemiplegic in distribu- 
tion. The differences between cortical and sub-cortical types of 
anaesthesia have already been discussed (p. 189). 

Tumours of the Frontal Region.— For clinical purposes this 
region of the brain-cortex, anterior to the motor area proper, may 
be subdivided into two parts : (1) A pre-frontal or higher psychical 



area, devoid of motor centres. This area, when electrically 
stimulated, produces no convulsion. (2) A post-frontal area, con- 
tinuous posteriorly with the pre-central convolution and including 
the cortical centre for conjugate deviation of the head and eyes 
"towards the opposite side. On the left side it contains, in addi- 
tion, the cortical motor centres for spoken words. 
, Pre-frontal tamours. besides having the general signs of 
■cerebral tumour, tend to exhibit mental symptoms specially early, 
•"Bonsisting in duluesa, failure of memory, tendency to childish 
liilarity, deficiency of attention, and neglect of the sphincters. 
These mental symptoms are equally likely in tumours of the 
jight side and of the left,' Fost-&ontal tumours have, in 
addition, local Jacksonian fit«, especially attacks beginning with, 
■<a consisting entirely in, deviation of the head and eyes to the 
, contra -lateral side; also, in left-sided tumours, fits commencing 
"with sudden attacks of motor aphasia (though the absence of 
aphasia does not necessarily exclude a diagnosis of left-aided post- 
frontal growth). General epileptiform convulsions, and even 
attacks of j>etit mal, are not uncommon in frontal tumours, in- 
■ eluding pre-frontal cases. Tumours beginning on the under or 
■orbital surface of the frontal lobe may also be associated with 
■early and persistent anosmia on the homo-lateral side, from im- 
^plication of the olfactory bulb and tract. Difficulty in moving 
'the head and eyes to the contra -lateral side would point to a sub- 
> cortical mid-frontal growth. Frontal tumours, whether pre- or 
post-frontal, are sometimes associated with a fine vibratory 
tremor of the homo-lateral arm, and less markedly of the leg, on 
holding the hmbs outstretchet.!,- and with loss, or speedy exhaus- 
tion, of the contra -lateral superficial reflexes, especially the ab- 
dominal and epigastric. If the grovrth be sufficiently extensive 
to press backwards on the pyramidal tract, there may be an increase 
in the contra -lateral deep reflexes, with an extensor plantar reflex 
in the contra -lateral foot, and even a degree of motor hemi-paresis. 
Optic neuritis, generally late in onset, tends to be more intense on 
the side of the tumour, whilst local tenderness and alteration of 
' Boevor. LettTOmian Lectures, 190T. 


percussion-note are relatively common. Some cases of fn 
tumour are associated with a reeling gait, like that of cereb 
disease ; whether this is due to backward displacement of 
brain, producing compression of the cerebellum, or to the ti 
mission of abnormal impulses along the crossed fronto-cereb 
path, is at present difficult of decision. 

Tumours of the Temporal Lobe are the most difficult o 
to localise, especially right-sided tumours. This is because 1 
symptoms are produced chiefly by pressure on adjacent p 
and only to a lesser extent by true focal lesions. There are, 1 
ever, two focal symptoms which are of diagnostic value. Fir 
tumours at the tip of the lobe, in the region of the uncinate g] 
are often associated with sudden attacks commencing witl 
olfactory or gustatory sensation, the smell being usually an 
pleasant one. This aura is followed by a curious *'*' dreamy stc 
lasting several seconds, during which everything seems to 
patient to be unreal or " far away." These " uncinate fits " 
occasionally accompanied by smacking movements of the 
Secondly, tumours of Heschl's convolution (on the Sylvian sui 
of the lobe) and of the adjacent first temporal gyrus, if on the 
side, may produce word-deafness. But many temporal turn 
are totally devoid of focal symptoms, and only produce sympi 
of pressure on neighbouring parts. Thus pressure on the int< 
capsule may cause a slight hemiplegia, with its accompanying 
ordered reflexes. Or tumours of the antero-intemal aspect oi 
lobe may implicate the optic tract, or may extend to the cms cei 
or to the corpora quadrigemina, producing corresponding sympt 

Tumours of the Post-central Convolution. — ^Here the 
symptoms of a cortical growth consist of attacks commei 
with a sensory aura either of tingling or of pain in the opposite 
arm, or leg, according to the position of the irritative lesion 
the growth extends across the fissure of Rolando to the pre-ce; 
or motor convolution (or even in many cases where the pre-ce; 
convolution is not actually invaded but only compressed), the 
in addition, a motor spasm of the corresponding part. Bot 
cortical and in sub-cortical tumours of the post-central con 
tion there is \]fiwa\\7 ^.tiseaXXi^^Nsv., \£karcLQ^^'s^^ ^^ ^^^^s^s^sii^c^ 



of cortical or capaiJar type as the case may be (see p. 189). 
Ast^reognosis in the contra -lateral hand has also been recorded, 
IB in a case of my own.' 

Tumours of the Supra-marginal and Angular OouTolutions. 
—General Hvmptoms are usually lat« in onset. The chief focal 
■ymptoniB are due to afiection of the visual paths. In left-aided 
!B, implicating the angular gyrus, word-blindness may occur ; 
1 irritative lesions this is transitory, in destructive or aub-cortical 
lesions it is permanent. A superficial tumour limited to the angular 
gyrus may produce " crossed amblyopia " (see p. 34), Thus a 
lesion of the right angular gyrus produces concentric contraction 
of the visual field of the left eye (see Fig. 43, p. 113). Such cases 
ire uncommon, but have been occasionally recorded.* More 
iBiially the growth dips in so as to affect the underlj-ing optic 
mdiattons, and then hemianopia results in the contra -lateral half 
of both visual fields. He mi -anaesthesia and hemi -analgesia may 
be present in addition, when the posterior end of the internal 
capsule is affected : motor hemiplegia is uncommon. 

Tnmours of the Postero-parietal Lobule are sometimes said 
to be characterised by astereognosia in the contra -la t«ral hand. In 
juch cases the patient cannot recognise the form and qualities of 
»mmon objects placed in his hand if his eyes are closed, whereas 
rith the healthy homo-hteral hand he recognises them at once. 
But stereognoiis is a complex intellectual function, a judgment 
ttased on many sensory fact^ra, and astereognosis has also been 
observed in other conditions, as in disease of the post-central gyrus, 
of the optic thalamus, of the posterior spinal nerves and of the 
peripheral sensory nerves. 

Tumours of the Occipital Region.— This area of the brain is 
Bsociated with the half-vision centre. The cortical half-vision 
sentre is situated mainly on the mesial aspect of the occipital lobe, 
partly above and partly below the calcarine fissure. The lower 
quadrant of the half-field is represented above the fissure, i.e., in 
le cuneate lobule, the upper quadrant is below the fissure, i.e. 
I the lingual gyrus. Tumours of this region, therefore, produce 

' JCev. of Neurol, and Pin/chialry, 1908, p. 370. 
» B«evor, Lancet, 1907, p. Tift. 


as their most constant symptom half-blindness or hemiano{ 
which may be complete or incomplete (quadrantic), according 
the whole of the cortical centre is afEected or only part above 
below the calcarine fissure. Wernicke's hemiopic pupillary phe 
menon (see p. 121) is absent in hemianopia from occipital lesio 
Tumours on the surface produce irritative phenomena, whilst th 
extending deeper, into the optic radiations, produce paral} 
symptoms. The irritative phenomena consist of crude subject 
visual hallucinations, such as luminous sparks or flashes of light, 
the contra-lateral halves of the visual fields of both eyes, or id tl 
part of the half -field corresponding to the area of cortex afiect 
Such luminous sensations are usually followed by hemianopia 
the same area of the visual field, a hemianopia which may becc 
permanent. Tumours of the cuneate and lingual gyri may s 
press downwards on the cerebellum, in which case cerebe 
phenomena are superadded. 

Let us now pass to the consideration of tumours deep wit 
the substance of the brain. These are more difficult to loca 
than in the case of cortical growths. 

To distinguish between growths in the Corona Badiata and tt 
in the Internal Capsule is often difficult, especially when the turn 
is a large one. All that it may be possible to state is that 
tumour is somewhere in one cerebral hemisphere. But with 
extensive growths, producing less complete hemiplegia, the dej 
of paralysis of different limbs is of diagnostic value. Thus 
closer a lesion is situated to the cortex, the greater is the tende 
towards a monoplegia. Also if there be a hemiplegia whicl 
complete in the lower limb but incomplete in the upper, am 
we find that the hand is more afEected than the shoulder, 
would point to a capsular lesion rather than a sub-cortical < 
since in the cortex the shoulder centre is the one nearest to t 
for the lower limb (see Figs. 3 and 7). 

Tumours of the Central Ganglia.— In this region growths i 
develop without producing enough focal symptoms to rer 
localisation possiole. From the close proximity of the o 
thalamus and corpus striatum to the motor, sensory, and vi 
paths in the mt^Tii«u\ c^^xaXa, «. ^o^Vj ^^^^g:s»3svNj^ V^\sa^-^ 



iiemiplegia may occur, accompanied by hemianopia and a 
■ee of henii-anfesthesia. But if these phenomena be present, 
on the right side, and nothing more, beyond the general signs 
pf intra-cranial tumour, all that we can diagnose is a grovrth some- 
where within the left cerebral hemisphere, and probably in its 
posterior two-thirds. But sometimes we can be more precise. 
For example, Nothnagel long ago showed that the optic thalamus 
ia a lower reflex centre for the emotional movements of laughing 
and crying, and cases of thalimic lesion have been demonstrated 
where voluntary movements of the face were preserved whibt 
emotional movements were impaired or lost on the contra -lateral 
side of the face. Further, a small lesion in the lower and posterior 
part of the thalamus may cause (probably from affection of the 
adjacent nibro-spinal path) spontaneous slow rhythmic move- 
ments of the contra-lateral limbs, athetoid or choreiform, increased 
on voluntary exertion. The plantar reflex in these cases remains 
flexor in type, provided the internal capsule be not involved. 
Again, the optic thalamus, as we have already seen, is an important 
station in the general sensory path, and therefore sensory symptoms 
are sometimes prominent, especially subjective sensations of pain, 
heat, and cold, in the contra -lateral side of the body, together with 
a degree of hemi-aniesthesia. Many cases of thalamic tumour, how- 
ever, run their course without any sensory impairment whatever. 
Tumours of the Corpus Oallosum have no focal symptoms 
which can be regarded as pathognomonic. Tumours in the anterior 
part of this great commissure generally produce early mental 
symptoms, to which may be superadded imilat*ral or bilateral 
hemi-paresis or convulsions (cranial -nerve jialsies, as a rule, bemg 
absent). But these symptoms may be the result of extension into 
neighbouring parts, so that to diagnose a callosal growth is always 
hazardous. Moreover it is rare for a tumour to be limited to the 
corpus callosum without extension into one or both hemispheres. 
Attention has recently been drawn to the occurrence of apraxia 
(inability to perform certain movements when there is no actual 
paralysis of the limb) in callosal tumours. ' 

Tumours of the Corpora Quadrigemina (and of the Pineal 

' B. A. K. Wilson, Brain, ITOft, ¥. VSA. 


Body which lies in close apposition) are localised with compantivt 
ease by the presence of characteristic ocular phenomena. Thoe 
consist in a paraljrtic affection of the third nerve nuclei, more (8 
less sjomnetrically on the two sides. The commonest sign is a com- 
bination of bilateral ptosis with weakness of upward and downviid 
movements of the eyes and feebleness of convergence. Tb 
pupillary reflex may be sluggish or absent. Less constantly, ii 
unilateral quadrigeminal disease, a degree of deafness has beei 
noted in the ear of the opposite side, the sub-cortical auditcH] 
centre being located in the posterior corpus quadrigeminom. I 
the superior cerebellar pedmicle, which is in close proximitj, b 
also implicated, we have a corresponding cerebellar ataxia an 
reeling gait, while if the adjacent external geniculate body or opti 
radiations be involved, there is hemianopia. 

Tumours of the Tegmental Region of the Oxiis or Fa 

produce characteristic focal symptoms from implication of the rnki 
spinal tract (Monakow's bundle) which starts from the red nuckn 
runs down in the pons, crosses the middle line and traverses i\ 
antero-lateral column on the opposite side of the spinal oon 
Lesions in the crural or pontine part of this tract produce a slo 
rhythmic tremor of the contra-lateral hand and foot, somewb 
like that of paralysis agitans, increased by voluntary exertion ( 
excitement and ceasing during sleep. If the lesion be in the w 
nucleus itself, which is transfixed by the fibres of the third nervi 
we have, in addition, third-nerve palsy of the homolateral sic 
with tremor of the contra-lateral arm and leg — a conditic 
known as '* Benedikt's sjmdrome." If the growth implicat 
the sensory tract of the fillet, there may be hemi-ansesthesia i 
the contra-lateral side of the body, but this is less common wil 
tumours than with sudden vascular lesions such as haemorrhage, 4 
A Tumour of the Crusta or Ventral Region of the On 
Cerebri is easy of recognition, from the characteristic alternate pa 
alysis which is produced, consisting in third nerve palsy, general 
incomplete, on the homolateral side, with hemiplegia of the conti 
lateral face, arm, and leg — *' Weber's syndrome " (see Fig. ^ 
p. 205). As the tumour increases in size, it tends to cross i 
middle Une and *\uip\\cia.\yft \\vfc oy^q^vXr. \>dL\t<^t^^t^^ ^s^^^'*^^ 


Pituitary TnmotirB produce diagnostic symptomfi in two 
.entirely different ways. Firstly, they may influence the growth of 
the bones throughout the body, causing acromegaly or gigantism, as 
tiie case may be (see p. 275). But skeletal changes are not constant. 
They seem to occur chiefly in cases of adenomatous growth, ac- 
wmpanied by Iiyper-activity of the gland, and not in purely 
destructive lesions as in the sarcomata. Secondly, and more 
Bonstantly, there are focal symptoms produced by presBure on 
kdjacent parts, notably on the optic chiasma. Bi-temporal 
Kmianopia, with a hemiopic pupil -reaction, results. This may 
afterwards progress to total blindness of one eye with temporal 
heniianopia of the other (see p. 115'. Curiously enough, in 
pituitary tumours primary optic atrophy is commoner than optic 
heuritis. A growth in the pituitary gland may also press back- 
IPards on the third nerves, causing ocular palsies, or it may extend 
upwards towards the floor of the third ventricle, in which case we 
lometimes note persistent somnolence. Occasionally an adult 
male patient with a pituitary tumour develops a remarkable 
tendency to approximate to a female type : the mammary glands 
Hilarge, the testicles diminish in size, the abdomen becomes rounded 
ike a woman's, and the pubic hair becomes restricted in area — 
''pituitary eunuchism,"' accompanied by loss of virility. The 
diagnosis of pituitary tumour can occasionally be confirmed by 
radiography, which may show deepening of the sella turcica. 

TtiinoQrs of the Cerebellum and Cerebellar Peduncles.— The 
ftnatomical connections of the cerebellum are all-important and 
ibould be carefully borne in mind (see pp. 18 to 2;i). Of all intra- 
iranial tumours, those of the cerebellum are the most frequent, 
[ntra -cerebellar growths are usually tuberculous or glioraatous, 
irhereas extra -cerebellar growths, commonly situated in the ponto- 
(erebellar angle of the posterior fossa, if arising from the ventral 
lurface of the cerebellum, are generally gliomata, anl if arising 
rom the sheaths of cranial nerves (especially the auditory nerve) 

r are most commonly fibro-myxomata. 

Vertigo, a reehng gait uninfluenced by closure of the eyes, 
tystagmus, and early optic neuritis are the outstanding symptoms 


commoD to growths anywhere in the cerebeUum, bat a cloBer stik 
usually enables us to localise the lesion more exactly. 

Tumours of the lateral lobe, whether intra- or extn-cei 
bellar, produce symptoms in the homolateral arm and leg ; tk 
consist in paresis and diminished muscular tonus, with flacd 
flail-like muscles, together with ataxia on voluntary movemei 
more evident in the arm than in the leg. In the upper limb y 
sometimes observe slowness of diadocokinesia, a term applied 1 
Babinsld^ to rapid alternate pronation-supination movements 
the forearm. In lateral-lobe tumours, this is performed sloi 
and awkwardly {dys-diadocokinesia) on the homolateral side. Wi 
this the homolateral limbs are often unnaturally steady wh 
held actively extended in the air ; this is best seen in the Ion 
limb. If the patient tries to stand on one leg, he does so I^ 
securely on the affected side. He lurches or reels as he wall 
sometimes towards the side of the lesion, sometimes away from 
This lurching appears to be due largely to weakness of the spii 
muscles. There is often weakness of conjugate movement of t 
eyes towards the side of the lesion, together with horiion 
nystagmus, which is coarser on looking towards the homolat^ 
side. The patient has a subjective vertigo in which surroundi 
objects appear to rotate towards the contra -lateral side. 1 
condition of the reflexes is inconstant ; they may be diminish 
normal, or exaggerated in the homolateral limbs. In some eai 
there is a characteristic posture of the head (see Fig. 128, p. 269) t 
ear being tilted towards the contra-lateral shoulder, and the h 
slightly turned towards the homolateral side. 

According as the growth is extra- or intra-cerebellar, ceru 
additional phenomena can be recognised. Extra- cerebellar growi 
most frequently arise at the ponto-cerebellar angle from i 
sheath of the auditory nerve and are consequently associated w 
nerve-deafness, more or less complete, on the affected side, usua 
accompanied by tinnitus. To these is frequently added pan 
of the facial nerve, a sign of great value when present. L 
commonly we may have affection of other cranial nerves, such 
the sixth or fifth, on the same side. In intra-cerebellar tumoi 
on the other hand, deafness in not an essential symptom. 1 

^ Revw* Neurology qae,\SiV^'},,^.\'^V^, - 


|itant)ir reflexes in pure intra-cerebellar growths are unaltered, 
whereas in extra -cerebellar cases, from pressure on the pyramidal 
tracts, there may be exaggeration of deep reflexes on one or both 
Bides, together with an extensor type of plantar reflex, but this is 
far from constant. In some intra -cerebellar cases the subjective 
sense of rotation felt by the patient is the same in its direction as 
that of the apparent rotation of outside objects, viz.. towards the 
contra -lateral side. In extra -cerebellar cases this is sometimes re- 
versed, and the patient has a subjective sensation of rotation 
towards the homo-lateral side.^ Some cases of tumour of the lateral 
lobe or of the middle cerebellar peduncle are associatad with spon 
taneouB ''forced rotatory movements" around the long axis of the 
body, analogous to those produced by experimental stimulation 
(flee p. 22). Thus in one case of my own, where there was a large 
Batconia of the right lateral lobe, the patient rolled round per- 
sistently to the right side and occasionally fell over the right edge 
of his bed. Unfortimately the direction of rotation is not so con- 
stant as to be of absolute diagnostic value in determining the side 
of the lesion ; but when the phenomenon occiu'S, it is a valuable 
corroborative sign, indicating an affection of one middle peduncle. 

Tumours of the Vermis or middle lobe have the general 
Bymptoms of cerebellar growth — vertigo, reeling, nystagmus^ 
without unilateral preponderance of ataxia on either side, until 
■the growth extendi into one or other lateral lobe. There is also 
ft tendency to fall forwards or backwards, according as the growth 
is situated in the anterior or posterior part of the vermis. 

In a few cases, both in middle lobe and in lateral lobe tumours, 
we may observe " cerebdhr fits " of a tonic type (se-e p. 72). 

It should be noted that ataxia is not necessarily present in all 
cases of cerebellar disease. Sometimes its absence is due to com- 
pensation by other parts of the brain, and some cases are in- 
stances of lesions limited to the white matter at a distance from 
the cortical or central nuclei and their main connecting paths. 
Ataxia is moat constantly present in lesions implicating the 
posterior part of the vermis. 

This alleged difterenL>e belween intra- and estra-cerebellar I 
rda BHbjwtive aenw ot rotation is doubted by Oppenheim and by Qthet 


Tumours of the Pons. — In this region focal symptoms usual) 
appear early, but general symptoms, especially optic neuiiti 
tend to be late in onset. The most characteristic sign of a mi 
lateral pontine lesion is an "" alternate " paralysis of the fiftl 
sixth, or seventh cranial nerve or nucleus on the homolater 
side, together with hemiplegia of the contra-lateral arm and V 
and an extensor plantar response, or, if the growth be situated i 
the dorsal region of the pons, there may be hemi-ansesthesia of tl 
contra-lateral side of the body. According as the growth 
primarily intra-pontine or extra-pontine in origin, the afiecdc 
of cranial nerves will be primarily nuclear or infra-nuclear in tj] 
and the grouping of the symptoms will be slightly different. ^ 
have already studied the differences between a nuclear and i 
infra-nuclear affection of the sixth and seventh nerves (see pp. It 
and 142). Tumours of the auditory nerve are relatively commo 
and often bilateral ; they ultimately produce signs of eztra-oei 
bellar growth, as we have seen (p. 426). 

The clinical picture of alternate paralysis is often masked 1 
the fact that pontine tumours rarely remain confined to one sid 
but tend to spread bilaterally. In such cases we depend for oi 
diagnosis on the existence of nuclear or infra-nuclear paraljrsis i 
the fifth, sixth, and seventh nerves, together with signs of ii 
plication of the motor or sensory tracts or of the cerebellar peduncle 

Tumours of the Medulla Oblongata. — In this region the chi 
diagnostic feature is paralysis, unilateral or bilateral, of the lowei 
cranial nerves, from the ninth to the twelfth, producing disorden < 
articulation, deglutition, «ic., together with signs of interruptic 
of the afferent or efferent tracts coursing through the medulla. 

Tumours of the Fourth Ventricle may arise either from tl 
ependyma, or from the choroid plexus, or they may be parasit 
cysts caused by cysticerci. In such ventricular growths foe 
symptoms may be absent. If, however, the lesion extends im 
the dorsal part of the pons or medulla, or into the cerebellui 
corresponding symptoms develop. Glycosuria is relatively coi 
mon. We have already referred to the peculiar form of vertij 
which occurs in cases of free cysticercus in the ventricle (p. 150). 

Pathological TiiagnwSs^ o1 '\xto^-^^TX!^ ^x5shwX5m^^_^ ^ 



given c&Be it nmy be impoBsible to diagnose with certainty the nature 
of the growth, since the symptoms depend not on the structure 
but on the anatomical position of the tumour. But if there is a 
history of ayphilis, a gumma may be suspected, and in most cases 
the patient should be given the benefit of energetic a nti- syphilitic 
b«atment for a time. It must not be forgotten, however, that 
even gummata sometimes resist medicinal treatment, and it may 

necessary to remove a cerebral syphiloma by operation. 
Syphilitic lesions of the central nervous system are associated 
rith an excess of lymphocytes in the cerebro-spinal fluid ; a normal 
fluid would, therefore, be against a diagnosis of syphiloma. But 

ixcess of lymphocytes occurs in other tumours not only in 
tuberculous, but even in true neoplasms. A sudden apoplecti- 
form aggravation of the symptoms is suggestive either of glioma 
or of aneurism, gliomata from their loose texture and high 
vascularity being particularly liable to spontaneous htemorrhageB. 
Aneurisms sometimes, and arterio -venous aneurisms more often, 
may be accompanied by pulsating bruits ; these nmy not only be 
perceptible by the patient but can sometimes be auscultated by 
the physician. Cerebral abscesaea are mostly secondary to local 
infection, especially from the middle ear" or other accessory air- 
sinuses (frontal, ethmoidal, or sphenoidal), or they may follow 
compound fractures of the skull ; less commonly we find metastatic 
.abscesses without local infection in the head. Tuberculous 
growths are specially common in the pons and cerebellum, and 
the existence of tuberculous disease of the lungs, abdominal viscera, 
or elsewhere, would tend to suggest a similar cause for the intra- 
cranial miachief, particularly if the patient be a child or young 
sdult. Calmette's ophthalmo-reaction (by dropping a solution of 
tuberculin on to the conjunctiva), is sometimes of value in such 
cases. Symptoms of cerebral tumour supervening in a patient 
who has already had a malignant tumour elsewhere in the body 
■ suggest that the cerebral mischief is metastatic in nature. In 
such cases a curative operation is out of the question, since it is 

KrobaUe that other tumours will be present, besides the one which 
as been diagnosed. 


Abadie's 8ign of tabes, 193 
Abdomen — 

motor points of wall (Erb's 
diagram), 374 
Abdominal reflex — signiflcance of 

absence, 300 
Abdominal sympathetic, disease of — 

pigmentary changes, cutaneous, 

visceral disorders, 329 
Abductor palsy of larynx, 156 
Abscesses of brain. 4^9 — 

aphasia from, 92 

cerebro-spinal fluid in, 394 

fits due to cortical. 68 

headache due to, 164 
Absinthe-poisoning, coma and con- 
vulsions from, 65 
" Acetone '* breath, 58 
Achilles-jerk, 308 
Achromatopsia, 114 
Acromegaly, 114. 274, 275, 425 
Aero paraesthesia, 331 
Active muscle-sensation, 179 
Acute yellow atrophy, coma of, 59 
Addison's disease. 331 • 
Adductor paralysis of larynx, 157 
Adiposis dolorosa (Dercum's disectse), 

Aerophagy, 366 
Afferent impulses, 2, 11 e^ seq. ; path 

of. 13 : diagrams, 12, 15 
Ageusia. 134 
Agoraphobia, 342 
Agraphia, 91, 97. 98 
Aichmophobia, 342 
Akinesia algera, 178 
Albinism, nystagmus in. 124 
Albumin, excess in cerebro-spinal 

fluid, 390 
Albuminuria, orthostatic, 331 
Albuminuric retinitis, diagnostic sig- 
nificance, 65 
Alcoholism — 

amblyopia of. 114 

articulation in, 104 

ataxia. 250 

coma and convulsions. 56, 65 

factor in nervous disease. ^ 47 
ct seq. 

gait in, 268 

insomnia in. 411 

Alcoholism (continued)' — 

men and women, effects in, 47 
neuritis from, 48 ; multiple 

neuritis from, 194, 220 
peuralysis, 145 
Quinquaud*8 sign, 78 
toxic vertigo, 150 
tremor, 78 
Alexia, 96 et seq. 
Allocheiria, 182, 185, 366-7 
Alopecia, 288 

Alternate paralysis, 198, 204-5, 428 
Amaurosis, hysterical, 355 
Amaurotic family idiocy, 116 
Amblyopia, crossed, 34 (diagram), 114 
in hysteria, 114, 354-5; of 
tumours, 421 
Amblyopia, tobacco. 111, 114, 116 
Ambulatory automatism, 360 
Amyotonia congenita, 262 
Amyotrophic lateral sclerose, 74, 103, 

208, 212, 309 
Anaemia — 

cerebral, causing vertigo, 149 ; 

and sleep, 405 
headache of, 165-6 
mydriasis in, 119 
optic neuritis in, 116 
primary thrombosis of sinuses 

in, 55 
tinnitus in, 147 
Anaesthesia — 

auto-exploration of sensibility, 

crossed, 14 

cutaneous, 32, 180 et aeq. 
dissociated, 185, 191-2 
hemi-ansesthesia. See thcU title 
hysterical, 113-4, 188. 349-367 
mode of disappesurance, 353 ; 
diagrams of cases, 351-5 ; 
of special senses, 354-6 
mapping of cu'eas, 181-2 
para-ansesthesia, 190 
in peripheral neuritis, 177 
spinal, mode of inducing, 400 et 
aeq. ; contra-indicat^, 402 ; 
after-effects, 402 
of spinal lesions, 190 

incomplete, 190-1 
tabetic. 192 
tactile, 185 




Anffisthesia {continued) — 
thermo-, 185, 191 

in tuberciila dolorosci, 177 
univerBal, of hysteria, 188 ; 

(fig.), 187 
Anaesthetics, delayed poisoning bv, 
spinal, examples of solutions, 
400 noU 
Anal reflex — 

internal, 313, 315 
superficial, 300, 303 
Analgesia, 185, 193 

in tabes, 183, 193 
Anarthria, articulative, 91, 99 
Aneurisms, intra-cranial, 147, 429 
pulsating sounds in, 147, 429 
Angina pectoris, 171, 329 
Angio-neuroses, 47, 331 et seq. 
Angio-spastic hemiplegia, 239 
Anidrosis, localised, 327 (fig.), 336 
Ankle-clonus, 201, 265, 310 ; spurious, 

201, 311, 365 
Ankle-jerk, 304. 308 
Anorexia nervosa, 274, 366 
Anosmia, 45, 68, 110, 136: in brain 

tumours, 419 
Anterior comua, cells of, 2, 3, 24, 
lesions, 74, 211 
deep refiexes, loss of, 309 
motor palsy in, 209 
motor tract throuch, 2, 11, 

posture in muscular paralysis 
from, 252 
Anterior nerve roots. See Spinal 

Nerves — Roots 
Anterior progressive muscular atro- 
phy, 213 
Anterior polio- myelitis (infantile 
paralysis) — 
acute, 209 
chronic, 211 

loss of deep refiexes in, 309 
Anterior transverse gyrus of Heschl, 

36, 90 
Antrum of Highmore, empyema of, 

Anuria, hysterical, 368 
Aortitis, reflected pains in, 171 
Aphasia, 89 et seq. 

auditory, 91, 94, 99, 420 

causation, 99 

cortical centres involved in 

(diagrams), 90. 92,91 
dysarthria distinct from, 101 
functional, or temporary, 93 
lachrj'mosis in, 47 
motor, 91, 97, 99, 419 
sensory. 90-91, 94-7, 98-9 
scheme for investigation of, 93 
total, 99 
visual. See (hat title 

Aphemia, 91 

Aphonia, hysterical, 108, 346, 

Apoplexy, dietgnosis of, 52, 390 
Appendicitis, pseudo-, 367 
Apraxia, in callosal tumour, 423 
Arcu^hnoidal sck;, 385 
Argyll-Robertson pupil, 118, 120 
Arsenical poisoning — 

cutaneous affections, 286 

multiple neuritis due to, 220 
.\rteries — 

cerebellar, 40 

cerebral, 30 et aeq, ; diagrams, 
37, 38, 39 

of spinal cord, 40 
Arthropathies, 292 et aeq. 
Articulation, disorders of, 101-9 

alcoholic, 104 

ataxic* 104 

deaf-mutes, 108 

functional cortical disturbance, 

general paralysis of insane, 105 

fiysterical, 10-^, 346 

idioglossia, 109 

infra-nuclear and nuclear affec- 
tions of, 102 

lalling and lisping, 109 

paralytic, 102 et aeq. 

supra-nuclear affections of, 104 

tests for, 101 

tics of, 108 
Articulation distinguished from 

speech, 101 
Asphyxial convulsions, 69 
Astasia-abai^a, 266, 363, 369 
Astereognosis, 184 ; of brain tumour, 

Asthenic bulbar paralysis, 235 
Asthma, dyspnoea of, 331 
Astigmatism, headache of, 1 05 
Ataxia. See Inco-ordination 
Athetosis, 45, 81, 251; double, 105; 

figures of ceu^e, 82 
Atopognosis, 182 

Atrophy, muscular, 197, 224 et seq., 
381 ; Werdnig-Hoffmann tvpo, 
213; in hysteria, 234 
Auditives and visuals, 92 et aeq. 
Auditory aphcusia, 91, 94-5, 99 

of brain tumour, 420 

cortical and sub-cortical, 94-5 
Auditory centre, 35, 90 it atq., 

Auditory gyrus (Flechsig), 36, 90 
Auditory nerve, affections of, 146 
Auditory path, 35-6 
Auditory word centre, 90 et aeq. ; 

diagrams, 90, 92, 96 
Auriculo-ventricular muscle- bundle 
of His, 69, 70 



Automatism, 3 

hysterical ambulatory, 360 
post-epileptic, 64 

Babinski's combined flexion of hip 
and trunk, 200; extensor plantar 
reflex, 301 
Babinsld and Nageotte, imilateral 

bulbar syndrome of, 249 
Bed-sores, 46, 222, 281 ; non-occur- 
rence in hysteria, 368 
Beirs paralvsis, 139, 219, 384 
Benedikt's syndrome, 80, 205. 424 
Beri-beri, multiple neuritis from, 

Biceps muscle, 31 

atrophy from cuiterior comual 

lesion (flg.), 253 
myokymia in, 74 
reflex, 304 
Biemacki's sign in tabetic ansesthesia, 

Bi-temporal hemianopia, 115 
Bladder — 

disorders due to lesions of cord 

or Cauda equina, 314 
dribbling from, 315 
in hysteria, 365 
innervation, 314-5 
reflex centre for contraction, 
Blanching of hair, 137, 288 
Blepharospasm, 87, 360 
Blindness, hysterical, 355 

in amaurotic family idiocy, 116 
Blood-pressure, in coma, 51 

intra-cranial, 390 
Blood-vessels — 

angio-noiu*oses affecting, 331 
cervical - sympathetic fi bres to , 3 1 7 
Blue cedema, hysterical, 368 
Bones — 

atrophic changes in paralysis, 

brittlpness in disease, 291 
convulsions due to injury of, 69 
trophic changes in, 289 et seq. 
Borborygmi, 366-7 
Bracliial neuralgia, 173 
Brachial paraplegia, 198 
Brachial plexus, paralysis of, 324 
Brain — 

abscess. See that title 
arterial supply, 3»>-41 
concussion, headache after, 166 
lesions — 

diplegia in, 206 
haemorrhage from, 54 
rhythmic tremor in, 80 
motor areas, localisation of, 4 
in sleep, 403 et seq. 
tumours. See under T\rrcvo\M^, 

venous suppVy, 4\-^ 

Breathing — 

in cerebral hsemorrhage 

in diabetic coma, 58 

in hysterical trance, 59 

** Breites Bein," Heilbronnei 

Bri8saud*8 reflex, 301 

Broca, cortical centre of. 39 

Brown-S^uard paralysis, 
184-5, 190. 206,* 208 
diagram of symptoms, 1 
Bulbar pcOsy (jBrloeso-labial-l 
paralysis), 103 
articulation in, 103 
lachrymoais in, 47 
mixed reactions of degc 

in, 384 
pseudo-, 105, 206 
tongue tremors of, 74 
Bulbar phenomena in Menx 
ease, 151 

Bulbo-cavemoeus reflex, 300 

Caisson disease, 175 
Calccurine fissure, 33: lesions 

Calmette*8 ophthalmo-reactic 
Carcinoma, 413 ; coma of, 58 
Caries — 

headache due to, 164 
neurcdgia due to, 169 
spinal, 176 
Carpo-metcu;arpal reflex. 304 
Case-taking, method, 44-50 
Cataract, cortical, 112 
Catalepsy, 63, 368 
Catheterisation, rigor foUowin 
Cauda equina — 

lesions of, 22 1 et meg. 
anal anaesthesia from, 
bladder trouble in, 314 
bulbo-cavemosus reflex 

of, 303 
gait in, 269-270 
motor paralyses dv 
relations with vertebral 

(diagram), 386 
roots of, 385-6 
Caudate nucleus (diagrams). 7 
Cavernous Sinus, thromboi 

Central scotomata, 113 

for colours in tobacco ami 
HI, 114 
Cerebellum — 

anatomy, 18-23 
arterial supply, 40 

ascending tracts in eon] 

with, 26 
ataxia. 240- 250 
^ciww^etions of (diasram) 



Cerebellum {continued] — 

equilibration, co-ordinating 
' centre for, 148 

» functions, 21-3 

> indirect action on spinal cord, 

I 22-3 

I intoxication of, 104, 2c 

lesions of — 

ataxia due to, 244, 246-250 
attitude in (fig.), 269 
dysdiadocokinesia, 426 
fits due to, 72. 427 
gait in, 268 
motor effects, 22 
nystagmus in, 124 
skew deviation of eves from, 

vertigo in, 148, 150 
peduncles of, 19-21, 148 
tumours of, 150, 167, 268, 414-t, 
Cerebellar tract, direct, 17, 21 
Cerebral abscesses, 56, 68, 92, 164, 

394, 429 
Cerebral anaemia, 149 
and sleep. 404-5 
Cerebral arteries, thrombosis of, 55 
Cerebral ataxia, 250 
Cerebral circulation, 36 et seq. ; 

arterial. 36 ; venous, 41 
Cerebral compression, traumatic, 54 
Cerebral cortex, histology, 5-6 
Cerebral hfeniorrhage — 
aphasia from, 92 
artery of (diagram), 37 
blood- pressure, 390 
cerebro-spinal fluid in, 389-391 
in children, 53 
, coma of. 154 

diagnosis of, 49, 54, 390 
in general paralvsis of insane, 54 
headache preceding, 165 
M^ni^re*8 disease distinguished 

from, 152 
spontaneous, 52-4 
trophic changes in nails in, 289, 

fig. 287, and Plate I. 
vertigo from, 149-50 
Cerebral hy perse mia, 149 
Cerebral localisation, 4 et seq. 
Cerebral membranes, innervation, 162 
Cerebral meningitis, coma due to, 

Cerebral sensory tracts (diagram), 

Cerebral sinuses, thrombosis of, 41-3 
Cerebral tumours. S:e Tumours, 

Cerebral veins, 41 ef seq. 
Cerebro-spinal fluid, 385-402 
cryoscopy. 390 
cyto-diagnosis, 393 
diagnostic significance, 48, 66, 

Cerebro spinal fluid {continued) — 
examination of, 389 et seq. 
Ivmphocytosis of, 66, 1.0, 241, 
" 281 note, 393 
parasites in, 393 
pathological conditions — 

bacteriological characters, 

cellular changes, 176-7 
chemical characters, 390 
microscopic characters, 392 
physical characters, 390 
puncturing for, 385-9 
therapeutic applications of, 397- 

tumour-cells in, 393 
Cervical region of cord. See Spinal 

Cord, Cervical Region 
Cervical sympathetic — 

course and distribution, 117, 132, 

159, 317-19 
in diagnosis, 47 
excision of, 328 
lesions, 319 
oculo-pupillary fibres, course of 

(diagram), 319 
paralysis of — 

from tumour, 322 
from brachial plexus rup- 
ture, 324 
symptoms of, 320-2 
stimulation of, clinical, 321, 328 
sweat-fibres supplied by, 326 
Cervical plexus, 26, 135; diagram 

of, 27 
Charcot's ** grande hysteric,'* 358 
** migraine ophtalmopl^gique,'* 

tabetic joint, 292 
Charcot and Marie's progressive 

neuritic amyotrophy, 213 
Chemosis, 42 

Chloral poisoning, tremor in, 78 
Chloroma, cerebro-spinal fluid in, 394 
Cholin in cerebro-spinal fluid, 391 
Chorda tvmpani, 133, 138, 142, 145 
Chorea, 45, 80-81 

articulative defects in, 107 
ataxia in, 250 
gait in, 271 
Huntington's, 81 
hyoscene, 81 
rheumatic, 81 
sores in, 281-2 
tic, distinct from, 85 
Choroiditis, 45. 116 
Chvostek'e sign of titany, 71 
Cigarette smoking, toxic efl'ects of, 78 
Ciliary ganglion, 117-119, 129; de- 
generation (diagram), 118 
Ciliary muscle, innervation (diagram), 

Ciliary nerves, 119 



Cilio-spinal reflex, 47, 313, 321, 323 

Circumflex nerve, 26-7 

Circum vallate papiUse, 133, 135 

" Claudication intermittente," 238-9 

Claustrophobia, 342 

Clavuft hv8tericu8, 167, 347 

Clonus, 310-12 

pseudo-clonus, 310, 365 
Cocaine — 

injection by lumbar puncture, 

ocular phenomena produced by, 
119, 324, 328 
CoccygodvTiia, 173 
Cochlear fibres, auditory nerve, 35, 146 
Colitis, muco- membranous, 330 
Colour blindness, 112 
Colour vision, tests for, 112; in 

hysteria. 355 
Coma, 51-9 

of alcoholic intoxication, 56 

bladder trouble in. 315 

carcinomatosum, 58 

from cerebral haemorrhage, 54 

from cerebral meningitis, 55 

diabetic. 58 

diagnosis and causation, 51 

malarial, 58 

opium poisoning, 56 

of pontme haemorrhage, 55 

post-epileptic. 57 

and sleep. 406 

in sunstroke, 58 

in thrombosis of central sinuses, 


toxaMnic. 52 
Combined degeneration of spinal 

cord, 312 
Congenital ptosis. 130 
Conjugate deviation, 9, 128; centre 

fo", 410 
Conjunctiva — 

anaesthesia, in fifth nerve par- 
alysis, 135 

nerve-supplv, 132-3 

reflex, 140, 300 
Consanguinity of parents, 45 
Consonants, articulation of, 104, 

Constipation — 

occipital headache of. 166 

toxic vertigo from. 150-1 
Constrictor urethra?, 314 
Contractures, hysterical, 305 
Conus medullaris. 222 
Convulsions — 

generalised epileptiform, 415 

infantile, 68 

strychnine, 70 
Coprolalia, 85 
Corona radiata, 6 
Corpora dentata, 18 
Corpus quadrigeminimi, 20, 33, 424 
Corpus striatum syndrome, 276-7 

Cortex — 

arterial supply, 36 
lesions — 

ansesthesiA due to, 

fits, 60. %6et8tq. 
motor palsy from. 2(1 
motor, inco-orcUnation ii 
venous supply, 41 
Cortical centres — 

auditory, 35. 90 et seq., i 
half- vision, 29, 33. 97. 11 
of hunger and thirst, 36 
motor. 4—6 ; diagrams, 
olfactory, 33, 110 
sensory, 3 

of speech, 90-91 : diagn 
92 ; mal-development, 
of taste, 34 
of vision, 33, 99 
of writing. 91 
Cortical cells in sleep, 404 
Cortical localisation (diagram 
Cortico-spinal motor neurone. 
See Motor Paredyses — ^Uppt 
rone Type 
Cough, hysterical, 368 
Craft palsies and cramps, 239 
Cranicd bones, headache fron 

tions of, 164 
Cranial nerves — 

Abducens (Sixth), 117:w 

of. 43, 127. 417 
Auditory (Eighth). 14 
cochlear division. 35 
vestibular, 146 
Facial. 138-146 — 

motor root. 138 t 
sensory root. 35, I 
lesions at different 

secretory and taste 
coiu^e of (diagrar 
132, 139 (diagram 

Glossopharyngeal (Xint] 
133. 153 

course of taste-fibre 
gram). 132-3. 145 
Hypoglossal (Twelfth), i: 

paralysis. 159 ; uni 
102 ; figures, 160- 
Nervus mtermedius of W 
35. 145 

Oculo-motorius (Third) 

distribution. 117 
paralysis of, 4*> 
1 25-6, 204-5 ; figxn 

Olfactory (First), 110-11 
Optic (Second), lH 
Patheticus (Fourth), li: 
alysis, of. 42, 126-7 



Cranial nerves (continued) — 

Recurrent laryngeal, unilateral 

paralysis of, 103 
Short ciliarv nerves, 119 
Spinal £M?ce88ory (Eleventh), 1 57 ; 
paralysis (diagrams), 157-9; 
and hypoglossal, 101 
Trigeminal (Fifth), 131-7, 
diagram, 132 

cutaneous supply to head (dia- 
gram), 131 
distribution. 131-3 
incidence of rodent ulcers 

over. 282-3 
lingual branch of, 133-4 
ophthalmic division, lesion 

of, 320 
pains in region of, lfi8-9 
paralysis of, 134, 135 
sensory root of, 14, 35 
sweat areas corresponding 

with area of, 330 
taste fibres, course of (dia- 
gram), 132 
Vagus or Fneumogastrio (Tenth), 
distribution. 153 
paralysis, 154-7 
Vidian nerve. 132 
Cremasteric reflex, 300, 303 
Crime, in post -epileptic automatism. 

Crossed amblyopia, 3."), 114; dia- 
gram <. 34, 113; of hvst^'ria. 
1 1 4, 355 
amesthfHjiia, 14 
hemi -anesthesia (diagram), 10, 

paralysis, 9-10, 40, 198. 428 
Crus cerebri — 

lesions of, 9, 424 

motor palsv due to (lig.). 

tegmental region. 80 
Cuneate lobule, visual half-centres 

in, lesions. 110 
Cutanciius an-rsthc^ia in hvsteria, 350 
Cutaneous pigmentarv changers in 

disea^ie, 284-0, 331 
Cutaneous sensibility, 12, 13, 180 et 

loss of. 193 
rt*covery, 219 
CyanosiH in ervthn>melalffiM, 333; 
chronic hemiplegia. 335 ; Ray- 
naud's dis<»ase. 332-3 
Cysticerus in Fourth Ventricle, diag- 
'nosis. 150, 428 

Dartos reflex. 310. 401 

T>eaf-mut€»»«. l<>8-!» 

Deafnort-*. 142. 140-7. 152-3. 424 ; due 

to drugs. 148 
Decubitus, acute. 281 
Deep sensibility. 1 1 

Defaecation. 299 

Degeneration, Wallerian, 24 tt aeq. 

ascending, 26 

descending, 24 
Deiters* nucleus, \S ct aeq. 
Delirium, 45 
Delirium tremens, 48, 78 
Deltoid, atrophy of (diagram),213, 216 

myokymia in, 74 

paralysis from cuiterior comual 
lesion (flg.), 253 
Dementia, bed-sores in, 281 
Dercum*s disease (Adiposis dolorosa), 

Dermatomes, 30 

Dermographism (diagram), 120, 335- 
6 ; in hysteria, 308; (diagram), 369 
Diabetes — 

breath in, 58 

coma of, 58 

insipidus, 331 

multiple neuritis due to, 221 

optic neuritis in. 110 

perforating ulcers in, 278 

tic douloureux, bilateral, in, 168 
Diadocokinesia, 420 
Diaphragm, myoclonus of, 75 
Diarrhoea, hysterical, 307 ; paroxys- 
mal, of A<ldison*s disease. 331 
Dilator pupillfe. 118. 132, 318 
Diphtheria, neuritis after, 121, 221 
Diplegia. 81, 198. 200, 265; definition, 

Diplococcus intra-cellularis, 391 
Diplopia, 127 

false image, position of. 122, 127 

gait in, 208 

mcmocular (hysterical). 357 

ocular vertigo with, 151 

tests for, 122-3 
Dipsomania, 342. See also Alcoholism 
Disseminated sclerosis — 

al>sence of alxlominal reflex, 300 

ataxia in, 240. 251 

cholin in cerebro-spinal fluid in, 

clonus in. 312 

emotional state in, 47 

ervthromelalgia a s\inptom of, 

motor paraplegia due to, 208 

nvsta<;nuis m. 124 

optic atrophy in, 110, 121 

stacfato speech in, 106 

transient paralysis in, 242 

vertig«» in, 150 
Disuse, atrophy from, 233, 365 
Double consciousness, 341, 359 
Drop-foot and drop-uTist in peri- 
pheral neuritis, 194. 220 
Drowsiness. 45, 406-9 

hvpnotic, 407-8 

pathological, 406, 408 

toxic, 408 



Dumbness — 

of deaf-mutes, 108 

of imbeciles, 108 
Dysaethesiae, 162 
Dysarthria {see also Articulation — 

defects), 101, 104-5, 245 
Dysbasia angio-sclerotica, 238 
Dysdiadocokinesia, 426 
Dysphagia, hysterical, 366 
Dystrophy, muscular. See Myopathy 

Ear disorders — 

gait in. 148, 151, 268 

herpes of external auditory canal, 

138, 145, 280 
otitis media. See that title 
vertigo from, 146, 151 
Echolalia, 85 
Ectopia pupillae. 119-120 
Electricity — 

abnormal reactions, 381-2 
clinical application, modes of, 

faradic reactions, 379 
galvanic batteries, 371 ; reac- 
tions, 380-1 
reactions of degeneration, 382-4 
Electro-diagnosis, 377 

prognosis, 384 
Elephantiasis nervorum. 280 
Embolism, 36, 39, 41, 92 
Endolymph. 149. 152 
Eaophthalmos. 47. 320. 322, 326 
Enteric fever, absence of abdominal 
reflex in. 300: ** coma-vigil " of, 
59 ; headache of. 165 
Enuresis. 315 
E ;>icritic cutaneous sensibility, 12 : 

loss of, 193 ; recovery, 219 
Epigastric reflex, 300 
Epilepsy. 60-72 

bilateral excision of cervical 

sympathetic for. 328 
chronic, posture and gait in, 272 
distinguished from hysteria, 6 1 -4, 
<»(), 357 ; and from Meniere's 
disease, 152 
infantile, 68 
Jacksonian. 60. 66. et seq., 189, 

417 €/ scq. 
major, or *' grand mal," 60, 64 
masked or larval, 64 
minor or "petit mal," 60, 63-4, 

post -epileptic automatism, 64 : 

coma, 57 
premonitory symptoms. 61 
sudden falling, 241 
"true," 6^ 
Epileptiform fits. 60, 70. 72 
in alcoholics, 65 
aphasia following. 93 
in cerebellar disease, 72 
cerebral, classification of, 60 

Epileptifoxin fits {ctitUinu^d] 
deep reflexes, abolitioE 
in f^eneral paralysis of 
heaclache following. U 
in intra-cranial tumoii 
Jacksonian, 06. 181^.4! 
myoclonus allietl with, 
in psychasthenia. 66 
sensory, 67 
toxic, tto 
vertigo, the aura of, li 

Epistaxis, 41, 1G5 

Equilibration — 

afferent fibres for, 17 
centre for. 21, 148 
impulses, 21 
nerve of, 146 


juvenile atrophic myoj 
motor points (diagram 
tetany, sigm. of. 71 

Ereuthophobia, 342 

Er>'thromelalg:ia, 47. 177, 3 

Eulenberg's disease (Pars 
congenita), 237 

Eunuchism, pituitary, 425 

Eustachian tube, obstruct ic 
vertigo, 148 

Exophthalmic goitre — 
alopecia in, 288 
cramp in. 24 1 
cutaneous pigmentatio 
dermographism in, 33i: 
von Greiefe's sign of. 3 
intestinal symptoms, 3 
stimulation of syr 
symptoms due to, 3*2 
tremor in, 77 

Exophthalmos. 47, 328 

External ociilar muscles. 
tion, 117: paralysis. 121, 

External popliteal nerve — 
gait in paralysis, 270 
posture in paralysis. 2< 

ifixtemal pterygoid muscle- 
congenital ptosis, 131 ; 
of. 135 

Eyebrow in Third nerve par 
hystericfld ptosis, 125 

Eye muscles, innervation, 
alysis of, 121, 127-130 

Facial hemi-atrophv. pr 

137, 289-290 ^ 

Facial hemi spasm, 87. 144 
Facial motor points (Erb'*^ 

Facial muscles. 46 ; innerva 

138 et aeq. 
Facial palsy, 1 39- 1 45 

articulative difficulty in 
auditory nerve riiseas< 

pan>nng, 147 
contracting socondary 



Facial palsy (ontinued) — 

lesion of Sixth nucleus, associated 
with, 130 
Facio - Rcapulo - humeral myopathy. 

103. 225. 229, 230 
Fapces, incontinence of, 316 
Fallopian aciueduct, 133, 138: lesions. 

Family periodic paralysis, 240, 310, 

334,* 382 
Fatigue — 

temporary ataxia of, 250 
tremor of muscular. 77 
Fevers, bladder trouble in, 315 
Fibrillary movements. 45, 74 
Field of Vision, tests. 112-114. .35l-r» 
Fillet, 35 ; degeneration, 26 ; superior 

decussation of, 16 
Fissures — 

calcarine, 33: lesions, 116, 421-2 
parieto-occipital. 38 : diagram, 8 
Kolandic. 4 6. 14. 17 
Sylvian, 4, 8. 36, .H-y, SH) 
Fits, 60-72 

cerebellar, 72 
cerebral. 60 
claasi Beat ion. 60 
cortical lesions and, 6(V-68 
epileptiform. See that title 
hysterical. See under Hysteria 
.lacksonian. •S'**' that tide 
scheme of investigation. 61 
in Rub-cortical tumours, (i6, 415 
*•/ tftg. 
Flaccid paralysis, 25. 202, 36l-;i: 

figs.. 344 
Foramen — 

of Key and Ret/.ius. 38ft 
of Magendie. 38ft 
Format in rt^tiiMilaris, lesions of, 14 
Fonnication. 46 

Fractur€»s, depressed, fits due to. 68 
Fragilitrt** ossium. 2ft 1-2 
FriednMchV ataxia. 83. 24<W8 
articulation in. 104 
diH»p refiexes, loss in, 246, 30ft 
tinit in. 268 
Mane's ataxia conifmrtHl with. 

nystaemus in, 124 
s|x"»ntan»*ous m«»vt»ments in, 83 
tal)ert. diAtinguisheil from, 248 
Functional and Orgrtnic disease, 
boundary line l>etwet»n. 48 note, 
338 et jt/f/. 
Fundu»«, patholot;i«'al condition** t)f, ' 

Oait, 26;i 272 
ataxic. 267 

<»erelH>llar. 24ft. 268-ft 
in chorea. 271 

in cysticercus of Fourth Ventricle, 

Gait {continued) — 

of chronic epilepsy, 272 

in deformities, 272 

high-stepping, 26ft 

hysterical, 266, 363-4 

of paralysis agitans, 270 

side , 266 

spastic, 264 

testins, mode of, 263 
Galvanic batteries, 371 et 9tq. 
Ganglia. See Ciliary, Gasserian, 

Geniculate, &c. 
Gangrene — 

family, 333-4 

hysterical, 368 ; fig., 266 

symmetrical of Raynaud^s dis- 
' ease. 282, 332 
Gasserian ganglion (diagram), 118, 
lift, 131, 133, 137. 31ft: inflamma- 
tion (diagram), 280 
Gastric headache, 16,5 

hysterical phenomena, 366-7 

pains. 171-3 

symptoms of vagus parah'sis, 154 
General paralysis of insane — 

Argyll-Robertson phenomenon 
iti. 118, 120 

articulation of, 105 

ccn»bral ImMuorrhage in, 54 

cen>bro -spinal fluid in. 241. 3ft 1, 

deep reflexes, loss in. 30ft 

epileptiform fits in, 65 et aeq. 

hemiplesia in. 23ft, 240-1 

pupils in, 118, 120 

tremors, spontaneous in, 84, 10,5 
Geniculate ganglion, 133, 138 et 9eq., 

inflammation of, 13>«, 145, 280 
Genital reflex. 313 
(Jenu rtM'urvatum. 261 : fig.. 25ft 
Giddiness, 127, 142. 164, 3ftft, 413, 
41.V«i; hysterical, 151. See altio 
undtr Vertigo 
Gigantism, 275, 425 
(Jlauconui, 152. 327-8 
Globus hvsteritus. 63. TO. 357. 366 
Glosso-labial hemi-spasm. 2tM). 363 
Glossy Hkin. 46. 277 
(;iut«»al n*flex. 300 
(;iycomiria. \M), 331. 428 
Gi»rdon'H paradoxical flexor reflex. 302 
(lowers* tract. 14: diagram. 15 
"Grande hysteric"' of Charcot. i\X 

(irasset and GausiM»rs test, 200 
CSumma, intra-(Tanial — 

fits from, 67 

headache due ti>, 164, 167 

neuralffia due to. 16ft 

syphilitic. 16ft, 42ft 
Gustatory path, 35, 133: diagram, 132 
Gyrus, angular — 

arterial supply, 39 




G>TU8, angular {continued) — 
cortical lesion, 114, 421 
visual word centre, 35, 91 
(diagram), 96-7 

Gyrus, uncinate. See that title 

Habit spasms, 84, 87, 360, 369 
Haemoglobinuria, paroyxsmal, 333 
Haemorrhage — 

cerebral. See Cerebral Hapmor- 

fits due to, 68 
hysterical, 367-8 
pontine, 55 
retinal, 45, 117 
subarachnoid, 389 
Hair — 

blanching of, 137, 288 
falling of, 45 

in progressive facial atrophy, 137 
trophic changes. 287-8 
Half- vision centres. 33, 97, 116, 421 
Hallucinations — 
auditory, 147 
olfactory, 1 10 
pain, hysterical hallucinations of, 

visual, 67. 422 
Haphalgesia, 357 
Headaches, 163 rt aeq. 
angio-neurotic, 167 
of gross intra-cranial disease, 

164, 414 
hvsterical. 167. 347 
local (extra- and intra-cranial). 

in Meniere's disease. 152 
migraine, 167 
neurasthenic. 16() 
post-epileptic. 166 
reflex, 165 
sunstroke, 16(i 
toxic, 165 

unilateral, \()ii et seq. 
Head-rolling, 80 
Hemeralopia, 111 
Hemi-achromatopsia, 97 
Hemi-anjesthesia — 

definition, 185, 188 

hvsterical, segmental tvpe, 188, 

* 274. 350-3 
organic, 188 

capsular or thalamic, 9, 80. 

163, 189 
cortical and sub-cortical, 

189, 418 
crossed, 190 

lesions causing, 14(diagram), 
16, 189, 423 et arq. 
Hemianopia — 

definitions and cause, 114 
diagrams. 34, 113 
lesions producing, 9, 33-5, 114. 
417. 421-2 

Hentiianopia {continued) — 
quadraxitic, 33-4 
sub-cortical word-blindn« 

ciated with. 97 
varieties of. 114-7 
Wernicke's pupillary reai 
121, 422 
Hemi-atrophy, facial. 137, 2$ 
Hemicrania. hysterical, 347 
Hemi-hyp>era?8th€»<sia, hj^steric 

thalamic, 185 
Hemi-hj'pertrophy, facial, (fi^ 

90 ; universal, fig. 276-7. 
Hemiopic piipillarv reactioi 

nicke's. 121, 422* 
Hem i- paraplegia, 46 
Hemiplegia (organic) — 
alternate, 198 
angio-spastic. 238-9 
aphasia in, 93 
articulation after, 105 
ataxia associated with. 2 
athetosis followinxj, 81 : 
bilateral, 105, 198 
bed-sores in, 281 
bone changes in, 290-1 
capsular lesion causing. S 
chronic, 29.i, 335, 337 
crossed, 198 
definition and forms of. 
dolorosa, 163 
gait in, 264-7 
of general paralysis. 240 
Grasset and Gaussel's sigi 
headache preceding. 165 
hysterical (functional). 1 
257-260. 26,5-6 
anosmia in. 1 10 
reflexes, loss in. 302 
infantile. 291 ; figs.. 256 
joint affections in ehroni< 
lesions causing, diasma 

80, 390. 416 
muscular wasting in. 233 
pandiculation in, 82-3 
posture in, 255-7. 363. 3 
reflexes, loss in, 303 
transient, 239 
tumour of, 416 r/ seq. 
visual fields in cases of (di 
356 ^ 

Hereditarv ataxia, Friedreich 

Marie's* 249 
Herpes, facial, 138, 14,1, 280- 
Herpes zoster, 163. 170, 1S6. : 
Heschl's gyrus, 36, 90; tiun 


Hiccough, of intra-cranial disc 
Hippus, 120 

Holmgren's tests for colour vis 
Homo-lateral pyramidal tract 
Huntington's chorea, 8 1 
Hydrophobia, 70 ; hysterical 
Hvoscine chorea, 81 



Hyperacousis, 142 

Hyf>er8emia, cerebral, 147, 149, 164, 

Hyperapsthesia, 184-7 

hysterical, areas of, 178, 186, 347 
mapping out areeis, 181 
Hyperalgesia, 187, 347 
Hyperidrosis, localised, 336 
Hypermetropia, 165 
Hyper- pyrexia, 63, 55, 166 
Hyper-trichosis, 287 
Hypertrophy of muscle, 197 
Hypnotic suggestion, 59, 343-4 
Hypnotic trance, 59, 343, 359 
Hypo-apsthesia, 185 
Hypoglossal nerve. See Cranial 

Hypoglossal nucleus, 138, 160 
Hypo spinal ganglia, 318 
Hypotonia of muscles, 245 
choreic, 81 

tabetic (diagrams of cases), 260-2 
Hysteria, 338-370 

affections of speech in, 346 
age and sex, effect in, 61, 369 
allocheiria in, 182 
alternating personality, 341, 359 
ambulatory automatism, 360 
anaesthesia. See under Anaes- 
ankle-clonus, spiurious, 201, 311, 

articulation in, 108, 346 
ataxia in, 251 
bio -chemical changes underlying, 

49 note 
Charcot's ** grande hysteric," 63, 

in children, 343, 369 
concentric contraction of visual 

field, 114, 354 
contractures, 258 et eeq. 
crossed amblyopia, 35, 114 
cough in, 368 
dermographism in, 368 
double consciousness in, 241, 359 
fits in — 

catalepsy, 63, 358 
classification, 60 
distinguished from epileptic 

fits, 61-5, 357-8 
post-epileptic, 64, 358 
gait m, 265-6, 363-4 
glosso-labial hemispasm. 260 
hemiplegia, distinguished from 

organic, 199-201, 257-260 
hydrophobia, simulated, 70 
hyperaesthetic areas, 178, 186, 

inhibition deficient in, 343 
joint pains in, 297-8 
major, 60. 63, 358 
minor, 60, 63 
motor phenomena in, 357 

Hysteria (continued) — 

musculeur wasting in, 234 
neurotonic reaction in, 381-2 
organic disease, distinguished 

from, 49 note, 338-9, 370 
pains of, 178 
paralysis. See that title 
plantar reflex in diagnosis of, 

302, 304 
postures in, 257-260 
psychical symptoms, 343 
ptosis, 126-7 

reflexes in, 63, 303-4, 365 
respiratory modifications, 368 
sensory S5rmptoms, 347 
skin affections, 368 
spasms in, 88 
trance of, 59, 359 
transient paralyses in, 242 
vasomotor phenomena in, 366 
visceral phenomena in, 366 

Hysterof renic and hysterogenic areas, 
186, 348 

Idiocy, amaurotic family, 116 
Idioglossia, 109 
Imperious acts, 342 
Inco-ordination (ataxia), 243-251 

articulative. 101-109 

cerebellar, 249, 427 

due to fatigue, 250 

hysterical, 251 

from lesions oi rubro-spinul 
tract, 251 

in new-bom child, 243 

post-febrile, 250 

pre- and post-hemiplegic, 250 

sensory origin of, 244 

tests for, 243 

toxic, 250 
Infantile convulsions, 68-9 
Infantile spinal paralysis (acute an- 
terior poliomvelitis), 209-212, 

lesions causing, 209 et aeq. 

loss of deep reflexes in, 309 

trophic changes of bones in, 291 
Inguinal region, hysterical tender 

spots in, 347-8 
Inner ear, afferent impulses from 

semicircular canals, 148 
Insomnia, 409-412 

alcoholic, 411 

drugs, use of, 409, 412 

extrinsic, 409 

and insanity, 412 

intrinsic, 410 

primary or nervous, 411 

vascular causes of, 410 
Intermittent limp, 175, 177, 238, 

Internal capsule — 

anatomy, 6-8 ; diagram, *^ 

auditor V fibres of, 36 



Internal capsule {continw^d) — 
lesion, 9, 128. 188-9, 204 
motor fibres, 6 
sensory fibres, 8-9 
tactile fibres, 14 
visual fibres, 9, 33 
Internal ocular muscles, lesions, 129 
** Interosseal attitude," 270 ; dia- 
grams, 271-2 
Intervertebral gans;lion (ganglion cell 
of posterior root), 25-6, 279-280 
Intra-cerebellar tumour, rotatory 
movements with, 427. Sze also 
Intra- cranial diseases and growths, 
52 et aeq., 66, 149. 162, 164, 166, 
41 3-429. See also Tumours 
Intra-cranial hsemorrhage, 52-5 
Intra-cranial pressiu'e, 51), 66, 164, 
309-310. 390, 407 
lumbar puncture in relief of, 
Involuntary movements, 73-88 
myokymia, 74 
reflex spasms, 87 
ricjors, 73 
in tabes, 83 
tremors, 77-81 
Ischaemic paralysis, 223 

Jacksonian fits. 66-8, 189, 417 et 

Jaw reflex. 304 

*' Jaw-winkinj?," 131 

Jendrasi^ik's reinforcement of knee- 
jerk. 305-8 

Joints — 

hysterical pains in. 297, 347 
trophic changes in, 292-7 

Joint-sense, 170, 245; tests for, 1«2 

Keratitis, bacillus of. 136 
neuro- paralytic. 136 

Kernig'a sign of cerebro-apinal men- 
ingitis, 56. 281. 395 

Kidney, floating, 172. See nlao 
Renal Diseeuso 

Kiniesthetic sense, 3. 179, 245 ; test 
for, 183 

Kleptomania, 342 

Knee-clonus, 311 

Knee-jerk. 304-8 

Korsakow's psychosis, 47 

L.iBiALS and labio-dentals. articula- 
tion of. 102 
Labvrinth. disease of. 146-8. 151 

cerebellar gait in, 249 

vertigo of, 151-3 
Lachrymal secretion, paralvsis, 135 
Lactation, t«tanv during, 72 
Lalling, 100 

Landouzv-D ^jdrine tvpe of mvo- 
pathy,* 103, 225, 229, 230 

Landry's paralvais, 209, 2: 

Larynjtosmus stridulus, 68, 7 
Larynx — 

ataxy of, 104 
innervation, 1 53 ei ttq. 
myoclonu.««. 75 
paralysis, 154—7: recurre 
unilateral. 154 
Las^gue*8 symptom. 363 
Latercd lobes of cerebellum, 1 
Laufenauer*8 method of rei 

knee-jerk, 307 
Lead poisonin^r — 
convulsions, 65 
optic neuritis in. 116 
palsy in. 194. 221 : abs 
sensory changes in, 19 
tremor of. 78 
visceral symptoms, 3.30 
Lenticular zone, lesions^ of. 9S 
Lenticulo-striate artery, 38 ; d 

Leprosy arthropathies of 
neuritis of. 278 ; maoulo-ani 
type, 284 
Leucocvtosis of cerebro-spini 
393-97 ; polynuclear. 393 f 
Leucoderma, 284 
Leuk.'emia, 54 ; cerebro-spin 

in, 394 
Levator palpebral superioris 
vation, 117, 319 (diagram). 
125, 130, 140. 320 
Light reflex. Sec under Refl< 
Limp, intermittent, 1 '5. 177,: 
Lingual consonants, articula 

Lips, paralysis of, 160 
Lisping. 109 
Lock-jaw. 70 
Locomotor ataxia, 244. 5 

Lordosis (with figs.), 225-7, 2 
Lumbago, 173, 223 
Lumbar puncture. Sec C 
spinal fluid— Puncturing foi 
Lumbo-abdominal neuralgia. 
Lmnbo-sacral cord — 

disease s\Tnptoma in, 176 

muscular localisation in(di 
Lumbo-sacral plexus and bi 

(diagram). 28 
Lymphocytosis of cerebri 
fluid, 66, 170. 211. 281 note, 
diagnostic significance, 

Macropsia. 357 
Malarial coma. 58 
Mammary neuralgia, 171, 347 
Marie's hereditary cerebellar 



Masked epilepsy, 64 
Mastodynia, 171, 347 
Mockers ganglion, 132, 133 
Medulla — 

auditory fibres in, 35 

lesions of, 10, 189, 205, 248-9, 

M^niere*8 disease, implicated in. 

pupil-dilating centre in, 318 
respiratory centre in, 4 
sensory fibres, course of, 14 ; 
diagram. 7 
Memory, 45, 47 ; postepileptic loss 

of, «4 
Meniere's disease (labyrinthine ver- 
tigo), 151-3 
Meninges — 
cerebral — 

convulsions from haemor- 
rhage in. (Ut 
pain, sensitiveness to, U>2 
spinal, diseases of, 17(^7. 281 
root pains of, 109, 170 
Meningism, 395 
Meningitis — 

basal, 55-6 (fig.), 145, 170 
cerebro-spinal fluid in. 56, 389- 

395, 397 
fits due to, 69 
fluid pressure in, 388-9 
headache in. 164, 167 
lumbar puncturt* for. 397-8 
septic cert»bro-spinal, 281, 360. 

391, 394 
spinal, root pains in, 176 
syphilitic bawd. 145. 169-170 
tulH»rculouH, 397 
Menstrual periods, hcadacht*s during. 

Mental functions, examination of 

higher. 45-7 
Meralk'ia panestliotica, 175 
Mercury poisoning, trem<»r of. 78 
Metameres and root distribution of 

H«»nsory and motor fibres, ."^0 
Metoorisiu. 330. 335 
Meynert's fil'-n'K, 117 
Micr»»-sympathetic ganglia. 318 
Microi>Mia. 357 
Micturitiim. 314 : tHMitr»»« ft»r. 314-5 : 

in hysteria. 365 
Middle ear — 

diM*ase of. 143. 146, 151 
innervation. 132-3 
Mi);raine, 167-S; ophtalmoplcgiMue. 

l.-^O. 16H 
Millard-Cublcr rtvndroiue. 10. 205 
Min»»n*' nyHtaK^^l^<. 124 
Mole«. hairy. 287 
MoliuM<'um tibroHum, 286 
Monakow's bun<ne (rubro-spinal). 

lesions in. 129. 251. 310. 424 
Mi>nocular diplopia, 357 

Monoplegia, 9-11. 46. 198; definition, 

1^8; hysterical, 361 H stq, 
Morvan's disease. 192, 279 
Motor aphasia, 91, 97, 99, 419 
Motor areas, localisation of, 4-6 
Motor centres in cerebellar cortex, 

Motor cortex, 6. 17 note ; lesions, 9 
Motor functions, investigation of, 

46, 195 (/ stq. 
Motor nerves — 

fibrillary tremors in paralysis, 

regeneration of fibres, 220 
Motor neurones, upper and lower, 24, 

Motor paralyses, 195 et ncq, 
functional or organic, 199 
lower neurone type. 209-234; 
distinguished from upper 
neurone type, 201-3 
from anterior comual and 
nerve- rt»ot lesions, 209 tt 
from Cauda e(|uina lesions, 

Landry's paralysis, 209, 221, 

level of lesion, diagnosis of, 

from multiple peripheral 

lesions. 215-6. 220-1 
nuis<*les, afTections within, 

postures in. 252 
plantar reflex in, 202. 302 

stMisory phenomena in, 209 
rt»current and transient, 235- 

up|»er neurone type. 202-8; 
distinguished fn>m lower 
neunme tvpt*. 201-3 
»»ilateral. 206 
exaggeration of deep reflexes 

in, 312 
le\'el of liMtion. diagnosis of, 

203 rt «rq, 
p»>sturt*s in. 255 
unilateral, 203-6 
M<itor points, 371^380 : diagrams. 

Miiller. non-striated muscle of. 

paralysis. 320 
Muwles — 

atrophy i»f — 

(>au«ation. 24 rt tirq.^ 209, 

224 rt tirq., 273 
fibrillary tremors in, 74 
in hemiplefiic arthritis, 297 
in hvHteria, 36.5 
idiopathic. Set Myopathy 
atrophy of — 

p«'roneal t>*pe. Tooth's, 213 



Muscles (continued) — 
atrophy of — 

progressive (chronic anterior 
poliomyelitis), 74, 212, 
309. 384 
varieties of, 213, 233-4 
dystrophy of. See Myopathy 
electrical reactions, 377 et acq. ; 

tests for, 374 
fatigue-paralysis, in niyewthenia 

gravis, 103-4 
hypotonia, 81, 245, 249, 200-2 
motor palsies from affections 

within, 223 
motor points, Erb's diagrams, 

non-striated involuntary, re- 
flexes of, 299, 313 
paralysis and paresis, definition. 

sensibility to pressure, 183 
striated voluntarv, reflexes of, 

testing, in motor paralysis, 1P5-7 
Muscle-spindle, a trophic centre, 25 
Muscular cramp, 241 
Muscular analgesia in tabes, 183 
Muscular localisation in cervical en- 
largement, 31 
in limibo-sacral cord. 31 
" Muscular sense,'* 179 ; definition, 

Musculo-spiral nerve, paralysis of, 

26-7, 254 
Mutism, hysterical, 108, 346, 369 
Myalgia, 170, 173 

Myastheniagravis, 103-4, 1 25, 235, 382 
Myasthenic reaction, 382 
Myatonia congenita, 262 
Mydriasis, 119 

Myelitis, 50, 208, 281, (fig.) 282 
Myoclonus, 74-7 ; diagram, 75 ; 

nystagmus, 77, 124 
Myoclonus epilepticus (Unverricht's), 

(fig.) 75, 76 
Myoidema, 197 
Myokymia, 74 
Myopathy — 

atrophic t>T5e, 24, 209, 224 et seq. 

See Muscle, Atrophy of 
diagrams of cases, 225-233, 270 
atrophy of nuclear origin distin- 
guished from, 224-5 
Erb's juvenile type, 230 
facio-scapulo-humeral type, 103, 

gait and posture in. 269-270 
pseudo-hvpertrophic type, 225, 
Myosis, 119. 322 
Myositis, 127, 183, 223 
Myotomes, 30 

Myotonia congenita (Thomsen's dis- 
ease), 237, 382 

Myotonic reaction, 382 
Myxoedema, 407 

Nails, trophic changes, 289 

Nfievi, cutaneous, 284 

Narcolepsy, 59, 408 

Nausea. See under Vomiting 

Neck, motor points (Erb's diagram), 

Nepliritis, lumbar puncture for, 399 ; 
optic neuritis in, 116; ui8?nuc fits 
of, 65 
Nerve areas, trophic changes in skin 

and hair over, 279-281 
** Nerve deafness," 146 
Nerve fibres — 

afferent, influence on tissue nutri- 
tion, 273 

motor, 6-9 ; diagram, 7, 24 
et seq. 

sensory, 8, 25 et seq. 
Nerve plexus. See Plexuses 
Nerve roots. See Spinal Nerves 
Nerves. See under Cranial, Motor, 
Peripheral, Spinal, also names of 
partrculur nerves 
Neuralgia — 

blanching of hair in, 288 

brachial, 173 

coccygodynia, 173 

hyperapsthesia in, 186-7 

mammary, 171, 347 

meralgia paraesthetica, 175 

poRt-herpetic, 280 

sciatic, 174, 303 

'* tender points,' 169, 174 

trigeminal. 169 
Neurasthenia, 338 et seq. 

causes and diagnosis, 33t»-340 

deep reflexes exaggerated in. 

distinguished from hysteria, 338 

headaches associated with. 166 

mydriasis in, 119 

toxic. 339-340 

traumatic, 171 
Neuritis — 

alcoholic, 47, 187 ; diagram of 
case. 220 

arsenical, 286, 289 

brachial, diagram of case, 278 

diabetic, perforating ulcers in, 
278 I 

lead. 221 

leprous, 278 

loss of deep reflexes in, 309 

multiple or peripheral, 47. 177, 
183, 186-7, 194, 269, 289, 312 

optic. S-'fi that titlf 

post-diphtheritic, 102, 121, 145 

retro-bulbar, 116 

sciatic, 176 
Neuro-fibromata, 177, 286 
Neuromimesis, 338 



Neurones — 

cerebello-dentate, 26 

cortico-bulbar, 102, 104 

dentato-thalamic, 26 

lower motor (spino-muscular), 
24 ; lesions, 200. See Motor 
Paralysis, Lower Neurone type 

sensory lesions of, 25 

spino-cerebellar, 26 

thalamo-cortical, 26 

upper motor (cortico-spinal), 24 ; 
lesions of, 23, 203. See Motor 
Paralysis, Upper Neurone type 
Neuroses, 338-370 
Nicotine poisoning, tremors of, 78 
Nightmares. 408 
Nuclear ophthalmoplegia, 129 
Nuclei — 

ambiguus, 153 

auditorv, 36, 147 

bulbar/l02, 104 

caudate, 6, 38 

cerebellar, 18, 22 

cerebral motor, 21 

cuneate, 13, 16 

Deiters', 18-22 

dentate, 20 

Edinger-Westphal, 118 

glosso-pharyngeal, 133, 145 

gracile, 13, 16 

hypoglossal, 138, 160 

lenticular, 6 : lesions, 105 

medullary, 13, 102 

ocular, 18, 22, 80, 117 

red, diagram. 20 ; lesions, 80, 
129, 205. 251, 424 

Sixth cranial nerve, 10, 130 
Nyctalopia, 111 
Nystagmoid jerks, 124, 152 
Nystagmus, 46, 79, 123 et aeq. 

aural or vestibular, 126 

facial, 83 

miner's, 124 

myoclonus, 77, 124 

reflex (optic, vestibular), 128 

rhythmic, 124 

undulatory, 124 

Obsessions of psychasthenia, 341 
Occupation neuroses, 86, 239-240, 

Ocular heaxiaches, 165 
Ocular muscles — 

innervation, 117 
paralysis, 121, 127-130 
Ocular paralysis. See under Paralysis 
Ocular symptoms in Raynaud's 

disease, 333 
Ocular verligo, 151 
Oculo-papillary fibres of cervical 

sympathetic, 318 ; paralysis of, 

3 1 9-320 ; diagTam. 3 1 9 
Oculo-motor (Third) nerve. See 

under Cran^'al Nerves 

CEdema, acute angio-neurotic, 335 
in cavernous thromboses, 42 
blue hysterical, 368 
(Esophagus, hysterical spasm of, 366 
Olfactory nerves, 32, 110 

path, 32 
Olivary body, 14, 21 
Ophthalmoplegia, 117-8 

nuclear (internal, external, 
total), 129; tiemor in, 129 
Ophthalmoscopic examination, 45, 

116, 164 
Opium poisoning, coma of, 56 
Oppenheim's reflex, 303 
Optic atrophy, 114, 116, 119, 120 
Optic chi£isma — 

course of visual' fibres in, 33 ; 

diagrams, 34, 115 
lesions at or behind, 115-7, 121, 
Optic nerve, 33, 111 
Optic neuritis, 116; ot intra-cronial 
tumour, 414-5, 419 
in diagnosis of coma, 56 
headaches with, diagnosis, 164 
lumbar puncture to relieve, 3C8 
Optic radiation, 33, 188 
Optic thalamus — 

lesions of, 80, ie3, 189, 204, 

micturition centres in. 315 
reflex centre of emotion, 423 
sensory fibres of, 14, 17, 423 
visual fibres in, 33 
Orbicularis oculi(p€dpebrarum), homo- 
logous with brancnial arch of fish, 
131 : innervation, 130 
Orbital muscle of Miiller, 318 ; 

diagram, 319 
Orthostatic albuminuria, 331 
Otic geuiglion, 138; diagram, 132 
Otitis media, 146-7 

cerebro-spinal fluid in diagnosis, 

vertigo from, 151 
Ovarian diisease, headache from, 166 
" Ovarian tenderness," 348 


course of fibres subserAing, 11-17 

diagnosis of cause, 162 

headache. 163-8 

hysterical, 178, 347 

in limbs, 173 ; bilateral, 176 

loss of sense of, 18, 138 et aeq., 

reflected, 171 
root, 176 

paroxysmal spontaneous, 177 
tests for sense of, 180 et acq. 
in trigeminal nerve region, 1 68-9 
in trunk. 169-170 
Palate, soft — 

hemi -atrophy, 137 



Palate, sofc (continued) — 

innervation, 133, 142, 153 
paralysis, bilateral, 102 ; uni- 
lateral. 154, 161 
reflex movement, 300 
Palpebral aperture, widening of, 140, 

Palsies. See Paralysis 
Panatrophy, local, 287 
Pandiculation, 82 
Partesthesia, 46, 187, 190 
definition of term, 184 
hysterical, 356 
mapping out areas of, 181 
Paradoxical pupillary reaction, 121 ; 

flexor reflex, 302 
Paragrapliia. 97 
Paralysis Agitans — 

articulative difficulties in, 106 
bilateral, 107 

dinp:rams of cases, 79. 271-2 
Parkinsonian mask. 107, 270 
posture and pait of. 270-1 
rigidity in, 78 
tremor, 78 
Paralvsis — 

alcoholic, 145, 194. 220-1 
alternate or crossed, 198, 204-5, 

atrophic changes in, 290-1 
Brown-S6quard, 11. 17, 184-5, 

190-1. 206, 208 
bulbar. 6^ -e that title 
of cervical sympathetic, 320 et 

cranial n<*rve3. 1 10 et seq. 
facial. 102-3. 130. 139-145. 20."); 

bilateral, 145 (diajiram) 
faniilv periodic. 240, 310, 334, 382 
Fifth* nerve. 135-6 
glosso-labio-laryngeal. .S'c Bul- 
bar Palsv 
glosao-pharvnsjeal. 153 
hvpujilossrti, 102, l:{7, 159-161 
hysterical. 234. 242, 257-'?60, 
3()l-5 ; diagrams, 2(i5, 344-5. 
352-5. 301-2. 364 
infantil«. 32. 211-3 (diagrams), 

29i>-l (flu.) 
isch:iMiii( , 223 
Landry's, 209, 221. 309 
larvngcal. orcranic and functional 

(diae:ra?iis), 155-7 
Motor. Ser Motor Paralvses 
motor and sensorv combined. 

207. 215, 312 
musculo-spiral (diagram), 254-5 
mvasthcnia gravis. Sep that title 
ocular, from lesions of individual 
nerves. 121, Vl'y H seq 
beniirn, 127 
infra-nuclear. 128 
nuclear lesions, 1 27- 1 30 
supra nuclear, 128 

Paralvsis {coniinuefl) — 

palatal, 89, 102-3, 142. 
peripheral motor nerv 
electro- prognosis of, 
post-diphtheritic, 89, I 
m tumours. 418 et stq. 
Paramyoclonus multiplex 
reich's), 75-7 ; diagram. 
Paramyotonia congenita (Ei 

disease). 237 
Paraphasia. 95 
Paraplegia — 

bed-sores in, 281 
brachial and eruraJ, 19! 
chronic, trophic change 

definition, 198 
gait. 264-5, 267 
hysterical. 257. 265; 

266, 344-5 (figs.), 32 

spastic. 49, 201. 207. 2 

Paraplegia dolorosa, 176 

Para-sympathetic fibres. 31 

Parathyroids, tetany from 

tion of, 72 
Parkinsonian mask, 107, 27 
Parosmia, 45, 110 
Pathological diagnosis, 44-5 
Penis, analgesia of. in tabes 
Perforating ulcers, 46, 278 
Pericarditis, reflected pain i 
Perimeter, xiso of. 112, 354 
Periostitis of skull. 164 
Peripheral irritation, i*efle3 

sions from, 68 
Peripheral nerves — 

cutaneous areas (diagra 
lesions — 

anaesthesia. 193 
ataxia. 245 
motor paralvsis. 19J 
210, 309/384 
lesions of mixed, 209, 2 
Peripheral neuritis. Sec 

Pernicious malaria and comt 
Peritonitis. 183. 330 
Peroneal muscular atropliv, 
Personalitv, alternating, 341 
*' Petit-mal," 60, 63-4," 241 
Petrous gangUon (diagram). 
Pharyngeal reflex. 300 
PharxTix — 

anjesthesia, 46 
innervation, 1 53 ; pa~ab 
Phobiae. 342 
Pill-rolling tremor, 271 
Pit uitarv disease. 114—5 "^7^ 
and hemianopia, 114 
" Planchette." sub-consciout 

inena of, 359 
Plantar reflex. 2, 17, 53 
207, 300 



Plantar reflex (coniinuea ) — 

Babinski's phenomenon, 301-3 
in hysteria, 303-4, 3b6 
Pleurodynia, 170 
Plexiform neuroma, 286 
Plexuses — 

brachial, division of posterior 

roots, 246 
cervical, 26, 135 ; diagram, 131 
cervico-brachial and branches 

(diagram), 27 
hypogastric and hjemorrhoidal, 

lumbo-sacral (diagram), 28 
solar, disorders associated with, 
Pneumonia, loss of deep reflexes in, 

"Polar reactions " of muscle, 3B0etseq. 
Polio-encephalitis, superior, 69 
Polio-myelitis, acute. See Infantile 
Spinal Paralysis : muscles, progres- 
sive atrophy of 
Polio mvelitis, chronic anterior, 74, 

212. 309 
Poly-fiesthesia, 186 
Polyopia, monocular, 367 
Polyuria, hysterical, 368 
Pons — 

arterial supply, 36 
facial nerve, origin in, 138 
haemorrhage, 53, 55, 56, 119 
lesions, 10, 49, 80, 142, 190, 192, 

nuclei, 102, 129 
sensory fibres, course in, 14 ; 

diagrams, 15, 16 
tumours of, 428 
Ponto-cerebellar angle, lesions of, 192 
" Port-wine stains,'^ 284 
Post-diphtheritic paralysis, 102, 145 
Posterior cerebral artery, 36 
Posterior columns of cord, lesions, 13 
etaeq.. 184, 245, 246, 267. 309, 312 
Posterior fossa, tumours of, 164, 310 
Posterior nerve roots. See Spinal 

Nerves, Roots 
Postures, 252-263 

cerebellar, 268-9 
erect and at rest, 252 
in functional disease, 257-260 
in organic disease, 252, 260 
Pot belly, 227, 270 
Pregnancy — 

pseudo-, 367 
tetany in, 72 
Press lure — 

blood, in coma, 51 
intra-cranial, 56, 66, 1 64, 309-3 1 0, 
390, 407 ; lumbar puncture in 
relief of, 397 
intra- thecal, 388 
labyiinthine, 153 
Pressure-pain, 11 

Pressure-sense, 181, 183 

Progressive muscular atrophy, 74, 

212. 213, 309 
Progressive neuritic amyotrophy 

(Charcot and Marie), 213 
Proptosis, 42, 47 
Protopathic cutaneous sensibility, 12 ; 

loss of, 193 ; recovery, 219 
Pseudo-angina, 171, 366 
Pseudo-appendicitis, 367 
Pseudo-bulbar paralysis, 105, 206 
Pseudo-hapmatemesis, 368 
Pseudo-haemoptysis, 368 
Pseudo-memories, 47 
Pseudo-pregnancy, 367 
Pseudo-ptosis, 47, 320. 322, 326; 

hysterical, 126 (diagram), 363 
Psychalgia, 347 
Psychasthenia, 66, 340 ei eeq. 
imperious acts in, 342 
obsessions in, 34 1 
phobiffi of, 342 
stigmata, 340-1 
Psychic epilepsy, 64 
Ptosis, 125, 363 
bilateral, -^24 
congenital. 130 
hysterical, 125, 363 
pseudo. See above^ Pseudo-ptosis 
Puerperal eclampsia, 65, 399 
Pupillary reflex. See under Reflex, light 
Pupillary unrest, 120 
Pupils — 

Argyll-Robertson phenomena in, 

118, 120 
contraction — 

in affections of cervical 

sympathetic, 320 
in opium poisoning, 56 
in pontine hemorrhage, 55 
dilating fibres, course of (dia- 
gram), 118, 132, 318 
dilatation of, 53, 57. 119, 126. 

328 ; psychical, 121 
examination of, 46, 119 
irregularity in shape, 53 ; diag- 
nostic significance, 119-20, 328 
light reflex. See under Reflexes 
motor innervation, 117-8 
painful stimulation of neck, 

reaction to, 121 
paradoxical reaction, 121 
psychical dilatation, 121 
reaction to accommodation, 121 
size, variations in, 119 
Pyramidal tract — 

course, 11, 24 ; diagram, 7 
lesions of, 9 et aeq. 
gait in, 264-5 
motor paralvses due to, 80, 

reflexes affected by, 301-2 
and note, 310, 312 ; in 
hvsteria, 3C5 



QuixQL'AUD^s sign of clironic alco- 
holism, 78 
Quadrantic hemianopia, 334 

Rabies. 70 

Rami commimicantes, 317, 319 

Raynaud's disease, 47, 49 note, 177, 

282, 331-3 
Raactions of degeneration, 25, 197, 

202, 382-4 
von Recklinghausen's disease, 286 ; 

(%.). 285 
Recti muscles of eye, 117, 121-131; 

diagram?, 122-3 
Recurrent and transient motor para- 
lyses, 235-242 
Recurrent-laryngeal palsy, 153-7 
Recurrent utterances, 100 
Red nucleus, connections (diagram), 
lesions. 80, 129, 251. 424 
Reeling or titubating gait, 249, 208 
Reflected pains of visceral disease, 

Reflex arc, 2, 25, 120, 301 
Reflex convulsions, (>8 
Reflex spasms, 87 
Reflexes — 

abdominal, 300 
anal — 

internal, 313. 315 
superficial, 300. 303 
Babinski's extensor nlantar re- 
flex, 31) I 3 
Rrissaud's, 30 1 
bulbo-crtvernosus. 300, 303 
cihc-spimil, 47, 313. 321, 323 
conjunctival, 140, 300 
cortiortl and spinal. 301-2 
consf'ious and unconscious. 2 
cremA<*tp ic, .100, 303 
darto?, 3H). 401 

d??p or tendon. 40, 209, 304-313 
in ataxic conditions. 245 
epileptiform fits. ()3 
exa^jixerated. 17, 103, 310 
Jacksonian fits, increased 

bv. (M 
loss\)f. 303-4, .309-10 
deep or tendon — 

in upper and lower neurone 
motor paralyse.^, 25. 202 
epica^^tric. 300 
jrenital, 313 
gluteal, 300 

in hvsteria. 51), ri3, 303-4, 305 
jaw.' 304 
light. 2. 120. 313 

in hvsteria, 59. 03. 305 
loss of, 117. 120. 121 
path of. 119: diaijram, 118 
muscle, involuntarv, 313 
Oppenheim ft, 'AO^ 
optic . Sec V.\g\\t te^e-s. 

Reflexes {corUin*Aed) — 
palatal, 300 
paradoxical fleror, 302 
pliar>Tigeal. 300 
plantar. Sje that titU 
pupillarv% See Light reBei 
rectal. 3'l3 
scapular, 300 
scapulo-humeral. 304 
scrotal, 313. 316 
sexual. 4, 313 
superficial (or skin), 46, 5; 

« i s.q. 
uterine, 313 
vomiting, 4 
Renal disease — 

cerebral hseniorrhage in, oi 
floating kidney, 172 
nephritis, 65, *116, 399 
unemic convulsions of, 65 
arterio-sclerosis of chronic 
tip:o in, 149 
Restiforin body, 21, 35 
Retina, 33, 120 
Retinitis pisrmentosa, congenita 
Retinal oedema, diagnostic s 

cance, 54 
Retro-bulbar neuritis, 116 
Retro-quadrigeminal heiuian< 

light reflex in, 121 
Rheumatic myo.sitis of extenui 

lar muscles, 127 
Rickets, convulsions and tetar 

to. 68, 7 1 
Rigors, 73 

Rinne's test for hearing, 1 46 
Rolando, fissure of, 4-6, 14. 1" 
Romberg's sign in tabes, 244- 
Root-areas. diafirpam of, 32 
Root-lesions, 26', 184, 209-223 
Root pains. 169-170, 176 
Rosenbach's sign of hemiplegii 
Rotatory movements in intn 

bellar growths. 427 
Round-worms, convulsions due 
Rubro-spinal tract, 80, 129, 
loss of function, 310, 423, 42 
Rupophobia, 342 

Sacral pain, 173 
Sacral plexus, 26 
Sacral segments, lesions, 303 
Saliva, irregularity in flow of. 
Saltatory spasm. 88 
Scapular reflex. 300 
Scapulo-humeral reflex, 304 
Sciatic nerve, paralysis' of rfitr 
Sciatica, 174 ^ ^' 

Scissor gait, 265 
Scleroderma, 283 
Sclerotomes, 30 
Sclerosis — 



Sclerosis (continued) — 

disseminated. See Disseminated 
Sclerosis • 

multiplex dolorosa, 170 

postero-lateral, 268 

primary lateral, 208 
Scotomat a, central. 113, 117 ; of mi- 
graine, 167; for red and green in 
tobacco amblyopia. Ill 
Scrotal reflex. 313, 316 
** Seelenlamimg,*' Nothnagel's, 363 
Segmentation of spinal cord (dia- 
grams), 26-32 
Semicircular canals, 148; disease of, 

Senile tremor. 78 
Sensation — 

clinical investigation of, 179-1 8 i 

return aft^r mixed nerve para- 
lysis. 219 
Sensory fits, 67-8 
Sensory paths, 11-18 
Serratun magnus, paralysis of ( fig. ), 2 1 9 
Sewer-gas poisoning, 276 
Sexual reflex, 4, 313 
Shivering. See Rigor 
Shoemakers' t€»tanv, 72 
Side-gait (*' Flankengang "), 266 
Skew deviation of ov<»8, 128 

hvsterical a^ections, 368 


pigmentary changes. 284-6, 331 

trophic changes. 277-289 
Sleep, tlisordcrs of. 403 ct seq. 

patliological. 40r»-9 

phyniology of. 403-6 
Sleeping »icknc88, 4(>h 

paniMJtiMji in cert»bro-spinal flui<l. 
Smell, disorders of, 4r», 68, 110-111, 
13.'>-6: hysterical, 348-9. 3.'>4-6; 
tests for sense of. 110 
Somnamf)uliHm. 3r)9. 406. 4(»8 
Spasms, habit. 84 

hysterical, 88, 360-1. 369 

reflex. 87 

saltatorv. 88 

See also Tics 
Spasmus nutan'*. 79 
Sp«wti<ity. 2.">. 202 
SpM'ial K*»nst»j*. paths of, 32-6 
Sp<H»ch — 

articulation distinguiHluHl from, 

autlitory origin of, 91 
cortical ccntrt*s for. 1H>-1 
disortlers, in diagnosing nervoun 

<lis*^ase. 4.V8 
hysterical affections, 34<V-7 
loHH of — 

aphasia. See that title 
arti<*ulation. <lefects. .SVf 

causes. claHsification of. 89 

Speech, loss of {continued) — 

\ocal and consonantal ele- 
ments in, 101 
Sphincter ani ; extemus, 31, 300, 

303; intemus, 313. 315-6 
Spina bifida occulta. 278, 287 
Spinal accessory nerve, 153 
Spinal anaesthesia. 400 et »eq. 
contra-indications. 402 
after-effects of, 402 
Spinal cord — 

arterial supply, diagram, 40 
cervical region — 

lesions in. 119. 170. 198, 206 
muscular localisation in, 31 
Clarke's colunm, 17 
coccygeal segment. 173, 303 
endogenous tracts, 17 
grey matter, focal legion of, 309 
lateral column. 13, 14 
degeneration. 312 
lesions of — 

anaesthesia in. 190-2 
bladder trouble due to. 314 
complete and incomplete, 

190. 20<W7 
hemi-section of. 11, 17, 184. 

189 190. 206 
paraplegia duo to. 207 
posterior roots and columns 

of. 11-18. 245-6 
in pyramidal tract. See 

Pvramidal Tract 
rtH'tal incontinenc»efrom.314 
root pains due to, 176 
trans 8e<"tionH, complete, 190, 

207, 309. 310, 312 
unilateral. 206 
lumbo-sacral region. See Luml)0- 

sacral cord 
malignant growths in, 393 
micturition centres in, 314-.'> 
poHterior cohunns. *S' e that title 
rclaticms with vertebral column 

(diatrram). 386 
root irritation from diseases of, 

segments (diag*am\ 26- 32 
sensorv paths (diagrnms). 10. 1 1- 

17. 15 
sub-ttcute c<^mbine<l degenera- 
tion. 312 
tracts in. 10 */ geq. 
tumours. intra- and extra- 
medullary. 170, 207; cerebro- 
spinal fluid in. 393 
\asM.niotor centres, diseases of, 
Spinal nerves — 

anterior nxits. 2. 24. 26 ; lesions 

of, 26-32. 209-1M2 
lesions, mixed motor and sensory 
paralysis due to. 207. 215, 312 
motor paralysis due to. 24 f ^ $ q. 



Spinal nerves (continued) — 
posterior roots — 

cutaneous areas (diagram), 

distribution, 25-32 
inflammation of ganglia, 

17tt, 279-281 
irritation, 169-170, 176, 

lesions of, 25 et aeq., 245, 

sensory path through, 13 
Spino-muscular motor neurone les 
ions. See Motor Paralyses, Lower 
Neurone Type 
Spino-thalamic tract, 14 
Splanchnic disease, 330-1 
Squint, 46, 122 et aeq. 
Stammering, 107 ; hysterical. 346 
Stellwag's sign of exopthalmic goitre, 

Stereognostic perception, 184, 421 
Stemo-mastoid muscle (figs.), 85, 

Stokes- Adams' svTidrome, 69 
Stomach — 

dilatation of, 72, 154, 329 
hysterical rumbling in, 366-7 
reflected pains of, 171 
Strychnine poisoning, 70, 310, 400 
Stupor, 51 

Subacute combined degeneration of 
spinal cord, 312 ! 

Sub-corti(*al cerebral tumours, 68 | 

Sunstroke and alcoholics, b>^ ; and 

coma, 58, 106 
Supinator jerk, 308 

reflex. 304 
Sweating — I 

almonnalities, due to nerve dis- 
order. 47, 326-7. 336-7 
centre, 336 
cervical svmpathetic connected I 

with, 318, 321-2, 32G-7 
of hysteria, 368 

in Mf^niere disease, 151 I 

Sylvian Hssure. fl, 3(). 38. 00 | 

Symmetrical gangrene, 332 
Sympathetic nervous system — , 

anatomical course and distribu- 
tion, 1. 317 et aeq. ! 
lesions of. 319 et aeq. 
thoracico-abdominal, diseases of, 

visceral reflexes controlled bv. 
209, 313-5 
Svncope distinguished from " petit 

*mal," 64 | 

Syphilis — 

cerebro-spinal fluid in diagnosis 

of lesions, 396-7 
epilepsy secondary to, 66 
irregularitv of pupils in. 65, ' 
119 ^ I 

Sv-philis {continuei) — 
meningitis of, 169 
palatal perforation fro 
Third nerve palsy fi 
Syringo-bulbia, 191 
SjTingomyelia — 

artliropathy (diagrams 

292- 6 
eerebro-spinal fluid, 39 
dissociated anaesthesia 

(diagram), 208 
exaggerated deep refle: 
fibrillary tremors, 74 
loss of deep reflexes, 3( 
oeiilar symptoms, 119 
pain from, 102 
perforating ulcers. 278 
spontaneous fractures, 
thermo- anaesthesia and 
(diagrams) 191. 1^2. 
trophic changes in jo 

Tabe5 — 

anaesthesia of, 192-4. ' 

gram, 193 
ankle- jerks, 308 
anosmia. 110 

Argyll-Robertson phei 

118, 120 
arthropathy, diagrams 

ataxia, 244-8 

bulbo-cavemosus reflex 

eerebro-spinal fluid in 

of, 396-7 
crises. 172. 330 
delayed sensation. 182 
gait. 267-H 
girdle pains, 1(>9 
hair, loss of, 288 (fig.), : 
hyperapsthetic areas, li 

gram, 193 
hypotonic, 260-2 (figs.) 
involuntary movementj: 

joint and kinapsthetic 

loss of, 183 
laryngeal, 104 
lightning pains, 170, 1ft 
hght reflex, loss of, 118. 
muscular and tendino 

gesia. 183, 193 
mvosis, 119 

optic atrophy, priniarv. 
perforating ulcers, 278 
piipils, irregulnritv of, I 
reflexes. 118-120,* 303. : 
spontaneous fractures. ; 
sudden falling, 241 
trophic changes, 278 et i 
\-ibration sense, loss of. 



Tactile senae, 11 ef seq, ; loss of, 18, 

Talipes equino- varus, 213 
Taste, cortical centre for, 35 

course of fibres serving, 35, 
133, 145, 153 ; diagrams, 132, 
disorders of, 134-5, 145, 153; 

hysterical, 348, 354, 350 
in Fifth nerve palsy, 133 
tests for sense of, 134 
Tear secretion, paralysis of, 135 
Teeth, traumatic changes in, 130 
Tegmental lesions, 80 
Temperature sense, fibres serving, 
13-17 : diagrams, 15 
tests for, 179 et seq. 
Temporal lobe, disease of, 67, 420 
Tetanus, 70, 310, 399 
Tetany, 70-2, 241 
and cataract, 72 
endemic, of shoemakers, 72 
from extirpation of parathvroids, 

Trou8Aeau*s sign of, 7 1 
Thalamic syndrome, 185 
Thigh, motor points (Erh*8 diagrams), 

377, 379 
Thomsen^s disease (Myotonia con- 
genita), 237, 382 
Thoracic nerves, lesions producing 

ocular symptoms, 320 
Thrombosis, biltitorul, of corpus stria- 
tmn syndrome, 270-7 
cerebral.' 39, 41-3. 55. 92. 95, 
149-50. 105. 3iK) 
of cavemouri sinus. 42 
spinal. 41, 49 
Tics, 84-0. 108 : distinguished from 

chorea, 85 ; hysterical, 325 
Tic douloureux, 87, 108 
Tinnitus, 140. 147, 152. 104 

lumbar puncture to relieve, 399 
Tobacc4) amblyopia. 111, 114, 110 
Tongue — 

ataxy of, 104 
biting, in epilepsy, 02 
hcmi-atrophy. 137. 101 
innervation. 133. 153. 159. 318 
paralysis, 102, 159-100 
taste fibres to, 133, 142, 153 
Torticollis, idiopathic spasmodic, 85 : 
labyrinthine, 80 ; neuralfric. 80 ; 
pn^fessional, 80 
Touch. See Tactile Sense 
Toxicophobia. 342 
Trance, h.vsterical. 59, 359 
Traumatic cerebral compression, 54 
Tremor. 77 

Quinqiiaud*s sign in alcoholism, 

toxic. 78 ; in tumours of frontal 
lobe, 80 

Triceps jerk, 304, 309 
Trichiniasis, 223 
Tricho-anassthesia, 180 
Trigeminal nerve. See Cranial Nerves 
Trigeminal neuralgia, 108-9 
Tropho-neuroses, 273-298 
Trypemosome ojf sleeping sickness, 

Tubercles of choroid, 117 
Tubercula dolorosa, 177 
Tuberculin, Calmette*s ophthalmo- 
reaction, 429 
Tuberculous meningitiB, 48, llOt 104, 

Tumours — 

abdominal phantom, 307 
diagnosis, 50, 413 ; differential, 

207, 428-9 
intra-cranial, 00, 110, 150, 104, 
100-7, 405-7, 413-429 
diagnosis, 20, 413, 428-9 
and drowsiness, 407 
epileptic fits from. 00 
headache of,' 104, 100-7, 

hemianopia from, 114 
optic neurititi, 110, 414 
s^^nptoms indicative of 

localisation in : 
Central Ganglia, 422 
Cerebellum. 147, 150, 107. 
250, 208, 272; extra-, 
intra - cerebellar, 425 ; 
lateral lobe, 420 ; middle 
lobe, 427 ; fits due to, 08 
Corona radiata, 422 
(Corpora quadrigemina, 423 
Corpus callosnm, 423 
Crusts of Cnis Cerebri. 424 
Fourth Ventricle, 428 
Frontal Region. 4 1 8-20 ; 
anoKmia in, 419; tremor 
of, 80 
Internal Ca}>sule, 422 
Medulla oblongata. 428 
Mid- brain, ophthalmoplegia 

from. 117 
Motor Cortex. 417 

irritative phenomena. 

paralvtic phenomena. 
0(*cipitnl Region. 421 
Pineal Bodv. 423 
Pituitary-. 115, 276, 405. 425 
Pons, 428 
Post-central Convolution, 

Postero-parietal Lobule, 

Supra-marginal and Angular 

Convolutions, 421 
Temporal Lobe, 420 




Tumours, intra-cranial (continued) 

Tegmental Region of Cms or 

Pons, 424 
Vermis, 427 
lumbar puncture for inoperable* 

of mid-brain, 117 
pelvic, 176 

of spinal cord, 207-8 ; differ- 
ential diagnosis, 207; menin- 
geal. 170, 176. 176 
Tuning-fork, tests for hecuing, 146 
Typhus fever. ** coma- vigil" of, 69 

Ulcers — 

perforating, 46, 278 

rodent, 282 
Ulnar paralysis, 217 
Uncinate gyrus, lesions of — 

fits due to, 67-8 

olfactory centre, 33 ; disorders, 

tumours of, 420 
Unilateral nasal hemianopia, 116 
Unverricht*s family myoclonus, 76 ; 

diagram, 76 
Uraemia — 

coma of, 57-8, 408 

convulsions. 65, 69 

Jacksonian fits in, 68 
Urine — 

in alcoholic poisoning, 66-7 

diabetic, 68 

dribbling, 316 

hysterical incontinence and re- 
tention, 366-6 ; suppression, 

reflex incontinence, 314 

retention, 316 

in luwmic come^ 57 
Urticaria scripta. 336-6, 368 ; dia- 
grams. 126. 369 
Uterine disease, headache from, 

Uterine reflex. 313 

Vaso- CONSTRICTION in sleep, 403-4 
Vascular causes of insomnia, 410 
Vaso-motor neuroses. 331-6, 366-70 
Vermis. 18. 22, 427 
Vertebral arteries, 36, 40 
Vertebral column, 47 ; diagram, 386 
Vertigo — 

ataxia in, 249, 268 

causes. 148-63 

pathologiced, 149-61 
Vesical reflex, 313 
Vestibular nerve — 

lesions, 128. 146 

testA lot vntfegiiVjj, \^\ 
Vestibvdo-spitvaV traet, \^, IX 

Vibration aense, 11, 18, 179, 
Vibrant electricity, 371 
Vidian nerve, 132 
Visceral disease, reflected 

Visceral phenomena of hyst 
Vision — 

fibres of, path, 33,35; 

field of, 33, 45 

concentric contract 

hysterical, 354r-5; 

mecisurement, 112- 
hy8teric€a blindness. 35J 
colour-vision, 354-J 
hypenestheaia. 348^ 
Visual acuity, tests for. 111 
Visual aphasia, 96-7, 99 ; d 
90, 91 
centres for, 33, 99 ; con 

sub-cortical, 96 
definition, 96 
lesions producing (diagr 

Visual cortex, 33-5, 421 
Visual hallucinations, 67, 42! 
Visual word-centre, 90 et seq. 
Visuals and auditives, 92 
Vocal word centre, 91, 419 
V. Volkmeuin's ischcemic d 

223 ^ 

Vomiting. 4, 69, 142, 146, 1 

151, 154, 164, 167; cerebr 

hysterical, 366 

Wallebiak, degeneration, 2^ 
ascending, 26 
descending, 24 
Weber*8 law, 183 
Weber's syndrome, 9-10, 20c 
Weber*s test for he£uing, 146 
Werner's " memoria technic 
„/^^,"^^?^(^ia^am), 123 
Wernicke s henuopic ounill 

action. 121, 422 ^ ^ 

Wernicke's zone, disintegratic 
Werdnig-HofTm€ttui type of 

sive muscular atrophy, 2U 
Whitlows, painless, 192, 279* 
Willis, circle of, 37 
Witches, 350 
Word-centre — 

auditory, 90; diagram. 

visual, 90-91 

vocal, 91, 419 
Word -blindness. See Visual 
^c^^^esa. Sec Auditory 




Wrisberg, nervus intermedius of, 138» 

Wrist reflex, 304 
Writers' cramp, 239, 250 
Writing, motor centre for, 91 

X-RAYS in neurology, 371 
tumour, 416 

Yawmino, automatic extensor move- 
ments in, 82 
in intra-cranial disease, 416 
Yohimbine poisoning, 382 

Z ACHARiAS, instance of motor aphasia, 


PriaUd bj BAUAsmiB, HAVsaji ^ Ci\ 
■dlBlMnfli 6* Londoo 

The Diagnosis of Nervous Disej 


Opinions of the Press on the First 'Edition 


The author has wisely avoided all abstruse details of purel) 
retical interest, and does not discuss treatment except incidental! 
and there, the whole aina of the book being directed to diagn 
purpose it admirably fulfils. The information on a subject wfc 
continually receiving fresh additions has been carefully brought 
date, and will be found thoroughly comprehensive, ever>' me 
clinical investigation receiving due attention. 


The lectures on organic paralysis of the upper and lower xa 
types respectively contain a large amount of information which \ 
found instructive to the student and useful for reference by the 
titioner. The same remark equally applies to the remaining pc 
in the book. The whole work is well written, and we can coi 
recommend it to our readers. 


This book cannot fail to be of great use to medical men. 
written by one who has made a special study of the subject, an 
has had a large experience. Dealing with the diagnosis, and nc 
the pathology or treatment, of diseases of the nervous systein 
written in a clear and interesting style, and it is fully illustratec 
by reproductions from photographs of typical cases, and also by 
often ingenious diagrams. 


Dr. Purves Stewart, in his volume, "The Diagnosis of N 
Diseases," has approached his subject in an original and simple ra 
and has produced a book on entirely new lines, one essentially i 
practitioner, which will be very welcome. 


Taking the work in its entirety, we have no hesitation in sayii 
it is one of the most practical, suggestive, and interesting publi< 
on a difficult subject which has been published in recent years. 


It is with considerable pleasure that we welcome the appe 
of this volume. Such a book has long been wanted, and the i 
writer has judiciously supplied the demand. 

41 AND 43 Maddox Street, Bond Street, W. 




To avoid fine, this book should be returned on 
or before the date last stamped below. 

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