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ON THE DIAGNOSIS OF DISEASES
OF THE BRAIN, SPINAL CORD, AND NERVES.
ON THE DIAGNOSIS OF
DISEASES OF THE BRAIN,
SPINAL COKD, AND NF.RVES.
BY
C. W. SUCKLING, M.U. (Lond.), M.R.C.P.,
professor of materia medica and theral'elftics at the
queen's college ;
PHVSICIAN TO THE QLEEn's HOSPITAL ;
EXTRA-ACTING PHYSICIAN TO THE CHILDREN'S HOSPITAL ;
PHVSICIAN TO THE WORKHOUSE INFIRMARY;
AND
CONSULTING PHYSICIAN TO THE ORTHOPAiDIC HOSPITAL,
BIRMINGHAM.
WITH ILLUSTRATIONS.
H. K. LEWIS, 136 GOWER STREET.
1887. -
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PRINTED AT THE HERALD FRESS, BIRMINGHAM,
BY WRIGHT, DAIN, PEYTON, AND CO,
PAr;E.
I— 20
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PRINTED AT THE HERALD PRESS, BIRMINtJHAM,
BY WRIGHT, DAIN, PEYTON, AND CO,
6^1
PREFACE.
By the courtesy of the Council of Queen's College
I have recently been privileged to deliver a Course of
Post-graduate Lectures at that Institution on the
" Diagnosis of Diseases op^ the Nervous
System." Many gentlemen who attended my
lectures have expressed a hope that I would
publish them. From conversations with numerous
professional friends I am led to believe that busy
practitioners still feel the want of a small and plainly
written work on the subject. This little volume, then,
is chiefly intended for them and for students. I hope,
too, that it may serve as an introduction to the more
valuable and standard works of Ross, Cowers,
Bramwell, Buzzard, and others. I must express the
great obligation under which I lie to my friend
Mr. Jordan Lloyd, for his kindness in reading over
and correcting the proof sheets.
1 08 Newhall Strket,
Birmingham.
February 1887.
KV
4
CONTENTS
PAGE.
Chapter I. — MEDICAL ANATOMY OF THE
BRAIN I— 20
The cerebral arteries. — The cerebral veins and
sinuses. — The cerebral convolutions. — The motor
and sensory tracts in the brain. — Descending and
ascending degeneration. — Relation of cerebral
fissures and convolutions to the scalp.
Chapter II.— THE CRANIAL NERVES. . . . 21—52
The olfactory nerve. — The optic nerve. —
Hemianopia. — Optic neuritis. — Optic atrophy. —
Asthenopia. — Pupil symptoms. — Ophthalmoplegia.
— Third nerve. — Fifth nerve. — Sixth nerve. — Facial
nerve. — Pneumogastric and hypoglossal.
Chapter III.— SYMPTOxMS OF BRAIN DISEASE. . 53-92
Hemiplegia. — Monoplegia. — Rigidity. — Athetosis. —
Spastic hemiplegia of infancy. — Functional and
organic paralysis. — Vomiting. — Temperature. —
Respiration. — Coma. — Headache. — Vertigo. —
Delirium. — Apoplectiform attacks. — Tremor. —
Cramp. — Contracture. — Aphasia.
II. CONTENTS.
PAGE.
Chapter IV. — THE DIAGNOSIS OF THE
SITUATION OF THE LESION IN DISEASES
OF THE BRAIN 93—108
Prgefrontal area. — The cortex. — Jacksonian epilepsy.
— Angular gyrus. — Corpus striatum. — Optic
thalamus. — Pons. — Medulla. — Cerebellum. — Crus
cerebri. — Alternate hemiplegia.
Chapter V.— THE NATURE OF THE LESION IN
BRAIN DISEASE 109—127
Diseases of the brain : Organic diseases. —
Meningitis. — Pachymeningitis. — Encephalitis. —
Tumour, — Aneurism. — Softening. — Cerebral
hemiplegia. — Chronic degenerative diseases. —
Functional affections of the brain. — Hysteria. —
Hypochondriasis. — Neurasthenia. — Chorea. —
Epilepsy. — Hystero-epilepsy.
Chapter VI.— THE USE OF ELECTRICITY IN
DIAGNOSIS 13S— 147
Electrical reactions in health. — Electrical reactions
in disease.
Chapter VII.— TROPHIC DISORDERS. . . 148-155
Raynaud's disease. — Perforating ulcer of the
foot. — Case of progressive unilateral facial atrophy.
Chapter VIII. — DISEASES OF THE SPINAL
CORD , . . . 156 — 174
The anatomy and physiology of the spinal cord. —
The reflex actions.
. CONTENTS. iil.
PAGE.
Chapter IX. — DISEASES OF THE SPINAL
CORD {Continued.) 175 — 193
Functional affections of the spinal cord. — Classifi-
cation of diseases of the spinal cord. — Spinal
irritation. — Hysterical paralysis. — Paralysis depend-
ing upon idea. — Reflex paraplegia. — Malarial
paraplegia. —Anaemic paraplegia.
Chapter X. — DISP:aSES OF THE SPINAL
CORD {Continued.) 194 — 252
Organic affections of the spinal cord. — Polio-myelitis
anterior acuta. — Subacute inflammation of the
anterior cornua. — Progressive muscular atrophy. —
Pseudo-hypertrophic paralysis. — Primary lateral
sclerosis. — Amyotrophic lateral sclerosis. — Loco-
motor ataxia, or tabes dorsalis. — Combined disease
of the postero-external and lateral spinal tracts. —
Friedreich's Disease. — Acute myelitis. — Acute
Hemi-lateral myelitis. — Acute acending paralysis :
Landry's paralysis. — Multiple sclerosis. — Extra-
medullary lesions. — Acute spinal meningitis. —
Pachymeningitis. — Spinal haemorrhage. — Spinal
tumours.
Chapter XL— DISEASES OF THE PERIPHERAL
NERVES 253—284
Peripheral neuritis. — Alcoholic paralysis. — Diph-
theritic paralysis. — Neuralgia. — Case of plantar
neuralgia. — Injuries of peripheral nerves. — Case
of division of the median nerve.
ILLUSTRATIONS
Plate I. — Normal Fundus of Eye.
Plate II. — Optic Neuritis. — White Disc Atrophy. — Grey Disc
Atrophy,
Fig. I. — (Charcot.) — Diagram of the distribution of the arteries at
the base of the cerebrum, p. 2.
Fig. 2. — Outer surface of the right cerebral hemisphere, p. 10.
Fig. 3. — Inner surface of the right cerebral hemisphere, p. 11.
Fig. 4. — (Flechsig.) — Horizontal section of the cerebrum through the
internal capsule, p. 13.
Fig. 5. — Diagram to show the relation of the cerebral fissures and
convolutions to the scalp (Reid), p. 18.
Fig. 6. — Diagram of the decussation of the optic tracts, p. 23.
Fig. 7. — Diagram of the relation of the field of vision, retina, and
optic tract on each side (Gowers), p. 25.
Fig. 8. — Fields of vision : Bitemporal hemianopia ; left hemianopia ;
right hemianopia, p. 26.
Fig. 9. — Diagram showing the fields of ct)lour vision in a normal
eye (Gowers), p. 35.
Fig. 10. — View of the floor of the fourth ventricle (Erb), p. 49.
Fig. II. — Spastic hemiplegia of infancy, p. 59.
Fig. 12. — Diagrammatic scheme of aphasia, p. 86.
Fig. 13. — Diagram of probable course of fibres from motor speech-
centre (Gowers), p. 87.
Fig. 14. — Diagram illustrating reaction of degeneration, with rapid
recovery (Erb), p. 145.
Fig. 15. — Diagram illustrating reaction of degeneration, with slow
recovery (Erb), p. 145.
Fig. 16. —Diagram illustrating reaction of degeneration where recovery
does not occur (Erb), p. 145.
Fig. 17. — Ilemiatrophia facialis, p. 153.
Fig. 18. — Diagrammatic representation of transverse section of the
spinal cord, p. 157.
Fig. 19. — Spinal cord (Flechsig) : Cervical, dorsal, lumbar, p. 159.
Fig. 20. — The leg type of progressive muscular atrophy, p. 205.
Fig. 21. — Acute multiple neuritis due to diphtheria, p. 267.
Figs. 22, 23, 24, 25. — Distribution of anaesthesia after section of the
median nerve.
CHAPTER I.
THE CEREBRAL CIRCULATION.
*
For much of our knowledge of the blood-supply
of the different portions of the encephalon we are
indebted to Charcot and Duret.
TJie Cei'ebral Arteries.
The brain is supplied by four large arteries, the
two internal carotid and the two vertebral arteries,
which together form an anastomosis at the base of
the cerebrum called the circle of Willis.
The branches of these arteries form two
systems : —
I. The cortical system, comprising the nutrient
arteries to the cortex and underlying
white matter and
II. The central or ganglionic system, comprising
the arteries which supply the basal ganglia.
The cerebral arteries are terminal ; that is, each
branch supplies its own area and does not anasto-
mose freely with neighbouring vessels.
The cortical arteries ramify in the pia mater,
and are distributed to the grey matter of the
convolutions and subjacent white matter. Tkof
2 THE CEREBRAL CIRCULATION.
vary in the extent of their inter-communication in
different individuals, but this inter-communication
is never a free one.
Fig, I.—
Diagram of the Distribution of the Arteries at the Base
OF THE Cerebrum.
C, (he internal carotid artery. C.A., anterior cerebral arttiy.
S., the middle cerebral or Sylvian artery. V., the vertebral artery.
B., the basilar artery, C.P., the (Kisteriot cerebral artery, i, a,
3, 4, the central or perforating arteries.
Their branches are divisible into two sets — the
long or medullary branches, which pass a considerable
distance into the white matter, and the short or
THE CEREBRAL CIRCULATION. 3
cortical arteries proper, which supply the grey matter
of the convolutions.
It is essential to know the distribution of the
cerebral arteries in order to understand the effects
of their rupture or obstruction. The anterior cere-
bral artery runs forwards over the corpus callosum
along the longitudinal fissure ; besides giving ofiF the
"anterior median group" of ganglionic vessels it gives
ofiF four cortical branches : — The first to the orbital
convolutions, the second and third to the marginal
and adjacent convolutions, the fourth to the quadrate
lobe and corpus callosum. The middle cerebral or
Sylvian artery is the largest and most important. It
gives ofiF five cortical branches. The first, or inferior
frontal branch, supplies the third frontal convolution.
The second, or ascending frontal, supplies the posterior
part of the middle frontal and the chief portion of
the ascending frontal convolution. The third, or
ascending parietal artery; supplies part of the
ascending frontal convolution, and nearly the whole of
the ascending parietal convolution, together with the
superior parietal lobule. The fourth supplies the
inferior parietal lobule ; and the fifth the superior
temporo-sphenoidal convolution. Thus the middle
cerebral artery supplies the convolutions especially
connected with aphasia of all varieties, both motor
and sensory, as well as the great motor centres of
Ferrier. Obstruction of the middle cerebral artery
at its origin by a thrombus or an embolon causes
necrosis of those portions of the central ^^xv^vsw -sceA
4 THE CEREBRAL CIRCULATION.
internal capsule supplied by it. The cortex may or
may not be affected, according to the extent of the
anastomosis between the cortical arteries, and in
fact it frequently escapes altogether. The posterior
cerebral artery supplies the under surface of the
occipital lobe, the lower portion of the temporo-
sphenoidal lobe, and the sensory portion of the
internal capsule.
The central or ganglionic system of arteries are
small branches given off from the trunks of the
main vessels. They form six groups : — an anterior
and posterior median, right and left antero-lateral
and right and left postero-lateral, and are all terminal
arteries.
The vessels derived from the middle cerebral,
the antero-lateral group, are of the most importance.
They pierce the anterior perforated space and ascend
to supply the corpus striatum, the internal capsule,
and a portion of the optic thalamus. The largest of
these branches is the lentiailo-striate artery (called
by Charcot the artery of cerebral hsemorrhage). It
ascends along the outer surface of the lenticular
nucleus, crosses the internal capsule, and then
passes forwards into the caudate nucleus.
'\ These arteries are prone to rupture, arising as
/ they do directly from a large vessel, and thereby
/ being subjected to high pressure. Hence cerebral
haemorrhage is most frequent in this situation.
The anterior median group of vessels derived
from the anterior cerebral and anterior communi-
THE CEREBRAL CIRCULATION. 5
eating arteries supply the caudate nucleus. They
are important in that haemorrhage from them may
rupture into the ventricles and rapidly cause death.
The postero-lateral group of vessels supplies
the hinder part of the optic thalamus. Haemorrhage
from them usually damages the posterior portion of
the internal capsule and often extends into the crus.
The posterior median vessels supply the inner
surfaces of the optic thalami. Haemorrhage from
these vessels finds its way into the ventricular
cavity.
It is necessary to bear in mind the following
facts as to the distribution of the cerebral arteries : —
The middle cerebral artery supplies the motor
region of the brain, both central and cortical, also
the cortical auditory centre and visual centre, and
all the cortical area concerned in speech.
The anterior cerebral artery supplies only a
small part of the motor region, viz., part of the leg
centre (paracentral lobule) and the centre for the
trunk muscles.
The posterior cerebral artery supplies the sensory
portion of the internal capsule.
The region of the ganglia is especially subject
to haemorrhage. The cortical region especially to
softening from obstruction of the vessels.
Obstruction of the artery to the superior temporo-
sphenoidal convolution on the left side causes word
deafness ; the patient being unable to understand what
is said to him, but not being deaf to soutvd.
6 THE CEREBRAL CIRCULATION.
Obstruction of the artery to the left third frontal
convolution will cause motor aphasia simply.
Obstruction of the basilar artery at its lower end
causes paralysis of all four extremities and of both
sides of the face. It causes also severe respiratory
trouble, dyspnoea, cyanosis, and death from asphyxia,
the respiratory centre in the medulla being deprived of
blood. It is generally attended with profound coma.
Obstruction of the tipper end of the basilar artery
is much less dangerous, respiration not being arrested.
The superior cerebellar artery crosses and sup-
plies the crus cerebri and the third nerve. Occlusion
of this branch causes paralysis of the third nerve on
the side of the lesion and hemiplegia on the opposite
side. I have met with a case in which this artery
was probably obstructed.
A gentleman, aged 55, who had suffered severely
from headache and vertigo, was seized with left hemi-
plegia and paralysis of the right third nerve, with
anaesthesia of the right side of the face, the paralysis
developing gradually in the course of a few hours
without coma. In a week all the paralytic symptoms
had passed off, and neuralgic pains were experienced
in all three divisions of the fifth nerve. These
pains finally ceased. There is little doubt that in
this case there was thrombosis of the right superior
cerebellar and upper portion of the basilar artery,
the branch to the fifth nerve being also occluded.
Obstruction of both vertebral arteries would
produce the same results as thrombosis of the basilar.
THE CEREBRAL CIRCULATION. 7
Obstruction of one vertebral artery produces
hemiplegic symptoms.
In atheroma and syphilitic disease of the cerebral
arteries, headache, vertigo, and numbness are usually
present and precede hemiplegia.
The Cerebral Veins and Sinuses,
The arrangement of the cerebral veins and
sinuses, while it tends to render the cerebral circula-
tion equable, yet greatly favours the occurrence of
local coagulation or thrombosis. The veins of the
surface of the cerebrum pass from behind forwards
to open into the superior longitudinal sinus, the
direction of the blood stream in the veins being
opposed to that in the sinus. The sinuses, moreover,
are rigid tubes unable to collapse, and traversed by
fibrous bands (chordoe Willisii), which also favour
thrombosis. The cerebral veins do not anastomose
freely with one another, hence thrombosis of them
is a serious accident, occasioning grave damage to
the cortex of the brain. The sinuses, on the other
hand, have a free intercommunication. Thrombosis
may occur either in the sinuses or in the veins.
Dr. Gowers believes that thrombosis of the
cerebral veins apart from thrombosis of the sinuses is
of frequent occurrence, and that this is probably the
lesion in those cases where young children are attacked
with hemiplegia, some form of mobile spasm and
frequently also partial epilepsy occurring in the
affected extremities.
8 THE CEREBRAL CIRCULATION.
Hemiplegia following the specific fevers is
probably . due to thrombosis of the cerebral veins in
the motor area of the cortex.
Thrombosis of the cerebral veins and sinuses,
like thrombosis elsewhere, is due either —
I. To alterations in the blood, rendering it more
prone to coagulate, or
II. To inflammation of the walls of the vessels.
Marasmus, prolonged diarrhoea, the specific
fevers, and carcinoma belong to the first group.
Thrombosis from these causes usually occurs in the
superior longitudinal sinus.
Disease of the adjacent bones, a blow on the
head, or erysipelas and other inflammatory affections
of the face and scalp belong to the second group.
In thrombosis of a sinus there is occasionally
swelling of the veins outside the skull in communi-
cation with it. The occurrence of epistaxis in
thrombosis of the superior longitudinal sinus is
explained by the existence of a vein passing from
the nose to this sinus through the foramen ccecum.
fThe vein from the mastoid cells passes into the
lateral sinus, and this sinus also communicates with
\ the veins of the scalp behind the ear through the
•' mastoid foramen. The occurrence of thrombosis of
this sinus in necrosis of the temporal bone or in
suppuration of the mastoid cells is thus explained.
Obstruction of the cavernous sinus does not affect
the veins of the retina, for the ophthalmic vein.
THE CEREBRAL CIRCULATION. 9
although it empties into this sinus, has a free
anastomosis with the facial vein.
The veins of Galen as they pass over the corpora f
quadrigemina and middle lobe of the cerebellum are /
readily compressed by tumours in this situation, C.
dropsy of the ventricles resulting.
THE CEREBRAL CONVOLUTIONS.
Tlu Motor and Sensory Tracts in tlie Brain.
It is unnecessary to describe here the convo-
lutions of the brain fully, but a knowledge of their
topographical anatomy is essential for the proper
Fig. a.
Outer Surface of thb Right Cerebral Hemisphere.
A.F., ascending frontnl convolution. A.P., ascending parietal
convolution. S.T.S., supeiioi temporo-sphenoidal convolution. P.C.,
pli coutbe. 0., ocdpilal lobe.
diagnosis and localisation of cerebral lesions. We
owe the greater part of our knowledge of the
functions of the cerebral convolutions to Ferrier,
THE CEREBRAL CONVOLUTIONS. II
Hitzig, and Munk. The motor centres are situated
in the convolutions bounding the fissure of Rolando,
the so-called central convolutions, the ascending
frontal and ascending parietal convolutions.
The tentorial surface of these convolutions is
called the paracentral lobule.
Schafer and Horsley have recently discovered
that in monkeys the centres for the trunk muscles are
situated in the paracentral lobule and precuneus or
quadrate lobule.
Inner Surface of the Right Cerebral Hemisphere.
M., the marginal convolution. P. marks the situation of the
paracential lobule (the inner surfaces of the ascending frontal and
ascending parietal convolutions!. Q., the quadrate lobe- U., the
uncinate gyrus. CO., the convolution of the corpus callosum.
The leg is represented in the upper third of
the central convolutions and superior parietal lobule.
The arm in the middle third. The face, Ups, and
tongue, in order from above downwards, in the
lower third.
12 THE CEREBRAL CONVOLUTIONS.
i
The lower extremities of the central convolu-
tions together with the posterior extremity of the
third frontal constitute the operculum, which, besides
containing the centres for the face, lips, and tongue,
on the left side also is concerned with voluntary-
speech.
Dr. Beevor and Professor Horsley have recently
proved by experimental investigation that in the
cortical centre for the upper extremity, as determined
by Ferrier, stimulation of the upper portion causes
movements commencing in the shoulder; stimulation
of the lowest portion movements commencing in the
thumb ; and stimulation of intermediate portions
movements commencing in the wrist.
Stimulation of these areas excites convulsion in
the limb represented ; destruction causes paralysis.
The motor regions, however, are not exclusively
motor; destruction of them causes loss of muscular
sense in the limbs represented by the area destroyed ;
moreover, in cortical disease of these regions an aura
is constantly present.
The order of the motor centres from above
downwards is trunk, leg, arm, face, lips, tongue.
From these areas the motor fibres converge to
the internal capsule^ a band of white matter placed
between the caudate nucleus of the corpus striatum
and the optic thalamus on the inner side, and the
lenticular nucleus of the corpus striatum on the
outer side.
THE CEREBRAl
It consists of an anterior and posterior half
it on each other at an angle, the concavity bein^
■(directed outwards.
14 THE CEREBRAL CONVOLUTIONS.
The function of the anterior half is unknown,
beyond that it contains fibres from the cerebellum.
The bend is called the knee or genu, and it contains
fibres from the tongue, lips, and face. The anterior
two-thirds of the posterior half contain motor fibres
from the motor centres around the fissure of
Rolando.
The order here from before backwards is tongue,
lips, face, arm, leg, trunk.
The posterior third of the posterior half of the
capsule is sensory. Destruction of it causes loss of
sensation of the opposite side of the body with
hemianopia, and loss also of the special senses on
the opposite side.
The motor tract can be traced continuously
from the motor convolutions to the muscles.
Thus, from the convolutions the fibres pass to
the internal capsule, then to the crus cerebri forming
the superficial portion or crust. Here 'the fibres lie
in order from within outwards, tongue, lips, face,
arm, leg, trunk. Thence they pass through the
pons to the medulla, decussating there between the
anterior pyramids to a variable degree, usually about
97 per cent, of the fibres passing down the opposite
side of the cord forming the crossed pyramidal tract
of the lateral column, and about 3 or 4 per cent,
down the same side of the cord forming the direct
pyramidal tract of the anterior column. (The
pyramidal tracts of the cord are so called because
they are continuous with the anterior pyramids of
THE CEREBRAL CONVOLUTIONS. IS
the medulla.) From these tracts the fibres pass to
the motor cells in the anterior cornua and thence
into the motor nerve roots.
The motor tract is not interrupted by the nuclei
of the corpus striatum. Disease of these nuclei
alone does not cause hemiplegia except by pressure
upon or involvement of the internal capsule.
In passing through the internal capsule the
fibres from each limb centre keep together in bundles,
so that it is possible to get a monoplegia produced
by a small lesion in the capsule. Such a case is
recorded in "Brain," Vol. VIII., p. 72>, by Dr. Hughes
Bennett.
The fibres from the tongue and face centres
leave the motor tract in the pons and cross to the
nuclei, from which the hypoglossal and facial nerves
proceed.
Our knowledge of the sensory tract is much less
certain and complete than that of the motor tract.
Brown-Sequard taught that sensation is chiefly con-
ducted in the grey matter, but there is evidence to
show that the posterior median columns of the cord
and a portion of the lateral columns in front of the
crossed pyramidal tract are concerned with the
upward transmission of sensory impressions,
Between the posterior roots of the spinal nerves
and the internal capsule we are unable to localise
accurately the sensory tract.
We know that the fibres cross to the opposite
side soon after entering the cord, and that the tract
l6 THE CEREBRAL CONVOLUTIONS.
then passes up on the opposite side through the
medulla, pons, crus, and posterior third of the
posterior half of the internal capsule to the cere-
bral convolutions.
As to the exact termination of the sensory
tract in the convolutions our knowledge is very
imperfect There is evidence pointing to the con-
volutions on the outer surface of the cerebrum about
its centre, being those concerned in sensation ; but
Ferrier, from his experiments on monkeys, finds
that the convolutions of the internal temporo-
sphenoidal region, the hippocampal, and other gyri
are the centres for touch, taste, and smell.
The superior temporo-sphenoidal convolution
is the centre for hearing.
The occipital lobe and possibly the pli courbe
or angular gyrus (Ferrier) are the centres for sight.
The centres for sight and hearing are bilaterally
associated, and the centres on both sides must be
destroyed to cause blindness or deafness.
The sensory tract in the cord and brain being
much less defined than the motor, we find that hemi-
anaesthesia is much less common than hemiplegia.
Still it does occur, not from cortical mischief, but
from damage to the internal capsule. I recently
had a case in the Queen's Hospital of haemorrhage
into the internal capsule, in which there was complete
hemiplegia and hemianaesthesia with hemianopia.
The muscular sense in this case was also com-
pletely abolished on the paralysed side, the patient
THE CEREBRAL CONVOLUTIONS. 1 7
six months after the attack being quite unable to
recognise the position of his limbs, or to perceive even
heavy weights. But the hemianaesthesia in these
cases is usually much less complete and persistent
than the hemiplegia as it usually results from pressure,
and is an indirect symptom. Since the lenticulo-
striate artery passes through the anterior portion of
the internal capsule the clot resulting from its rupture
will compress from before backwards the fibres from
the face, lips, tongue, arm, leg, and trunk centres,
and lastly the sensory tract. Hence we can readily
understand why sensation is rarely affected, and if
affected, why it is so quickly recovered.
In the cord, also, the diffusion of the sensory
tract explains the fact that sensation usually first
recovers in a myelitis.
Descending and ascending degeneration of the
motor and sensory tracts respectively : —
Waller many years ago showed that nerve
fibres severed from their nerve cells, experiment-
ally or pathologically, undergo degeneration in one
direction — that of functional conduction. The
portion left connected with the centre remaining
unaffected that dissevered degenerating; every
nerve fibre depending for its nutrition upon a
nerve cell.
This discovery has been of the greatest service
to the anatomist and physiologist in the eluci-
dation of the structure and functions of the brain
and cord.
i8
THE CEREBRAL CONVOLUTIONS.
Thus, after haemorrhage in the centrum ovale or
in the motor region of the internal capsule, des-
cending degeneration of the motor tract occurs; and
sclerosis of the crossed and direct pyramidal tracts
y^
a*
D
^"^^^
^/is:--^
({
)
SyMjis.
B tTans /.e
X
(j^/
'
Vjbase line i
KV
^^s
r""
hase line
Fig. 5.
Diagram to show the relation of the Cerebral Fissures
AND Convolutions to the Scalp. (Rkid.)
A, glabella. B, external occipital protuberance, e.a.p.^ external
angular process of frontal bone. B C, transverse fissure. A B, longi-
tudinal fissure. Sy.^s., Sylvian fissure. Sy. a.Jis.^ ascending limb
of fissure of Sylvius. Sy, h. Jis.^ horizontal limb of fissure of
Sylvius. D E, perpendicular line from depression in front of external
iiuditory meatus to middle line of top of head. F G, perpendicular
line from posterior end of base of mastoid process to middle line of
top of head. F H, fissure of Rolando, p, o.fis.^ parieto-occipital
fissure. + , most prominent part of parietal eminence.
THE CEREBRAL CONVOLUTIONS. 1 9
is found in the cord, the trophic cells for the
motor fibres being situated in the central convolutions.
This descending degeneration explains the late
rigidity and exaggeration of reflexes observed in
hemiplegia. If a transverse myelitis occurs, four
tracts of degeneration are found descending the cord,
the two crossed and the two direct pyramidal tracts,
accounting for the rigidity and exaggeration of deep
reflexes seen in these cases.
The Wallerian maxim applies also to the sensory
tracts. In transverse lesions of the cord ascending
degeneration is found in the postero-median columns,
in a portion of the lateral tracts and also in the
direct cerebellar, tracts, the trophic cells for the
sensory fibres being situated in the ganglia on the
posterior roots of the nerves.
The relation of tlie cerebral fissures , and convo-
lutions to tlu scalp is of the highest importance in all
operations on the brain.
Dr. R. W. Reid has recently published a practical
method of ascertaining the relation of the primary
fissures to the surface of the scalp {vide " Lancet,"
September 27th, 1884).
The fissure of Sylvius, To find this draw a line
from a point one and a quarter inches behind the
external angular process of the frontal bone to a
point three-quarters of an inch below the most
prominent part of the parietal eminence. Measuring
from before backwards the first three-quarters of an
inch of the line represents the main fissure and the
20 THE CEREBRAL CONVOLUTIONS.
rest of the line represents the horizontal limb. The
ascending limb starts from the posterior end of the
line indicating the main fissure and runs vertically
upward for about an inch.
The fissure of Rolando, This, and with it of
course the situation of the ascending frontal and
ascending parietal convolutions, is found in the
following way : — First mark out on the surface of the
scalp the longitudinal fissure (a line from the glabella
to the external occipital protuberance) and the hori-
zontal line of the fissure of Sylvius. Then from the
base line, which runs through the lowest part of the
infra-orbital margin and the middle of the external
auditory meatus, draw two perpendicular lines to
meet the line for the longitudinal fissure, one from
the depression in front of the external auditory
meatus, and the other from the posterior border of
the mastoid process ; a four-sided figure is thus
described on the surface of the head, bounded
above and below by the lines for the longitudinal
fissure and horizontal line of the fissure of Sylvius
respectively, and in front and behind by the two
perpendicular lines. A diagonal line drawn from
the posterior superior angle to the anterior inferior
angle of this space is over the fissure of Rolando.
CHAPTER II.
THE CRANIAL NERVES.
^
The cranial nerves in several instances have known
connections with the cortex of the brain.
T/ie olfactory nerves commencing in the olfac-
torial cells of the Schneiderian membrane pass to
the olfactory bulb, thence to the roots and onward to
the cortex of the brain. The centre for smell is not
definitely known in man, but in monkeys it is
localised by Ferrier in the hippocampal gyrus.
In testing the sense of smell, substances having
pungent odours should not be employed, to avoid
irritation of the nasal branch of the fifth nerve.
Hyperaesthesia of the olfactory nerves may
occur in hysteria, and illusions or hallucinations of
smell are common in the insane.
An olfactory aura may be present in epilepsy,
and is caused by irritation of a portion of the
cortex.
Anosmia, diminution or abolition of the sense
of smell, is present in ozoena, and is occasionally
present in locomotor ataxia.
Unilateral loss of smell has been observed in
hysterical and organic hemianaesthesia.
/
22 THE CRANIAL NERVES.
Anosmia of the left nasal cavity is sometimes
associated with right hemiplegia from embolism of
the left middle cerebral artery. The aphasia is
usually of the sensory variety and due to softening
of the angular and superior temporo-sphenoidal
convolutions. The anosmia is probably due not to
cortical softening, but to softening of the external
root of the olfactory bulb which is supplied by the
middle cerebral artery. Congenital loss of smell is
caused by arrest of development of the olfactory
tracts.
The Optic Nerve,
The fibres of the optic nerve partially decussate
in the optic commissure, and thence can be traced
through the white substance to the cortex of the
occipital lobe. There is no second decussation at
the corpora quadrigemina.
Destruction of one optic trac causes a loss
of vision in the opposite hal of each field —
liemianopia,
A similar hemianopia results from disease of the
cortex of the occipital lobe. Permanent and com-
plete blindness only ensues when the occipital lobes
and angular gyri (?) are destroyed on both sides.
Ferrier has shown that lesion of the angular
gyrus in monkeys causes temporary amblyopia of the
opposite eye ; hence he suggests that in the angular
gyrus there exists a visual centre representing the
whole of the opposite field. This crossed amblyopia
is accompanied with a slight restriction of the field
THE CRANIAL NERVES.
23
of the other eye, and is temporary ; the temporary
nature of the amblyopia being explained by the
substitutionary action of the angular gyrus of the
opposite side. But it is by no means generally
accepted that the angular gyrus is the centre for
sight in man.
Fio, 6.
Diagram of the Decussation of the Optic Tracts.
C. marks the semi -decussation in the chiusma. OP. TR., the
optic tracts. B.C., the basal ganglia, C.Q., the corpora quadri-
gemina, O.C., the occipital convolutions.
Lesions of the centre of the anterior surface of
the optic commissure cause bi-temporal hemianopia
(blindness in the outer half of each field), the decus-
sating fibres being damaged.
24 THE CRANIAL NERVES.
j Meningitis at the base of the brain, chronic
I hydrocephalus causing distension of the third
\ ventricle, or a cerebral tumour might cause bi-tem-
! poral hemianopia.
Nasal hemianopia, blindness in the inner half of
each field, is rare ; it might be caused by a lesion of
the outer fibres of the chiasma on each side.
Disease, then, anywhere in the optic tract beyond
the commissure right into the occipital lobe causes
hemianopia towards the opposite side.
When corresponding halves of the retinae are
affected the resulting hemianopia is called homony-
mous ; when the inner or outer halves of both retinae
are affected it is called heteronymous.
Hemianopia must be carefully looked for in
cerebral diseases, as it is frequently unnoticed by the
patient.
Persistent hemianopia is almost always due to
i organic disease, and very rarely hysterical ; but tran-
I sient hemianopia may be due to organic disease, as,
/ for instance, in haemorrhage in the region of the
internal capsule, when the hemianopia, if present,
soon passes off, and is probably caused by compres-
sion of the optic tract.
A man with left hemiplegia informed me that at
I the time of the attack and shortly after he was blind
I with the left eye ; his was clearly a case of haemor-
; rhage, and he had blindness of the left half of each
field of vision ; that is, he saw nothing on his left
side, and he accordingly thought his left eye was blind.
THE CRANIAL NERVES.
25
RF....
Fig. 7.
Diagram of the Relation of the Field of Vision, Retina,
AND Optic Tract on each side. (Gowers.)
R.F. L.F., right and left fields — the asterisk is at the fixing point.
R.R. L.R., right and left retina — the asterisk is at the macula lutea.
r,h, Lh,^ right half and left half of each retina, receiving rays from
the opposite half of the field. R.N. L.N., right and left optic nerves.
Ch,t chiasma. R.T. L.T., right and left optic tracts; below the
halves of the fields from which impressions pass by each optic tract
are superimposed.
I
THE CRANIAL NERVES.
Tumour or softening of the occipital lobe may
cause hemianopia towards the opposite side.
Hemianopia is frequently present during an
attack of migraine.
Impaired vision in one eye maj- be due to a lesion
at either end of the visual tract, in the optic nerve or
I in the cortical centre.
THE CRANIAL NERVES. 27
If cortical or central, the pupil reflex to light is
not affected, while disease of the nerve diminishes or
abolishes this reflex.
In disease of the nerve, too, changes may be
found in the disc with the ophthalmoscope.
Amblyopia of one eye with restriction of the
field of vision and slight affection of the other eye
may be caused by extensive disease of the cortex of
the opposite hemisphere, but it is chiefly met with in
hysterical hemi-anaesthesia.
Case of Amblyopia due to Cortical Disease.
The following interesting case was sent to me
on the loth of February by an old pupil, who diag-
nosed cerebral tumour, and thought the case would
be of interest to me.
The patient is a boy aged 2. Several months
ago he began to vomit ; this continued for several
weeks, the vomiting not seeming to distress him and
occurring independently of food. At the same time
the child frequently put his hand to the left side of
the head as if in pain there. Three months ago he
was attacked with convulsions, the spasm beginning
in the right hand, then attacking the right side of the
face and right leg, consciousness being lost late in the
fit, and not being lost in every attack. The con-
vulsions continued to occur daily for three or four
weeks, when the right arm and leg and right side of
the face were found to be paralysed. The leg and
face have since recovered, but the arm has reraa.i^e.d
/
/
28 THE CRANIAL NERVES.
the same. Lately the mother noticed that the child
could not see, and this greatly alarmed her. Vision is
not quite lost, for he runs about, though often running
against obstacles. The child cannot be made to wink
by passing the hand rapidly over the eyes, and
cannot recognise any object presented to him.
There is a marked family history of phthisis on
the mother's side, but no history of syphilis or cancer.
The child is drowsy sometimes, at other times very
irritable. Upon examination of the eyes no change
in either fundus could be discovered, and there was
no opacity of the cornea or lens. Mr. Priestley
Smith kindly examined the eyes for me, and he
agreed with me that there was nothing abnormal to
be detected. The right hand is paralysed, the thumb
being adducted into the palm and the fingers flexed
over it ; there is considerable rigidity, the bicipital
reflex being exaggerated. The right leg seems a
little weak, but the patient can walk well. The
mother thinks the boy sees a little with the
left eye.
As to the diagnosis. — The attacks of partial or
Jacksonian epilepsy beginning in the right hand, and
being followed at last by paralysis of the hand, indi-
cate a lesion in Ferrier's motor region of the cortex.
These seizures might result either from softening or
tumour. The absence of optic neuritis prevents our
diagnosing tumour with certainty ; still the marked
family history of phthisis, and the absence of any
evident cause of softening, make the diagnosis of
THE CRANIAL NERVES. 29
cortical tumour almost certain. The amblyopia is
evidently cortical too, for there is no change in either
fundus, and the pupil responds well to light.
We may conjecture that the growth occupying
the middle portion of the ascending frontal and of
the ascending parietal convolutions (the centre for
the hand and fingers), has extended backwards,
invading the angular gyrus, and perhaps also the
outer surface of the occipital lobe. Destruction of
the angular gyrus on one side has been shown to
cause amblyopia of the opposite eye, and partial
blindness of the eye on the same side (in animals).
The amblyopia is, however, said to be transitory.
Destruction of the outer surface of the occipital lobe
causes permanent hemianopia. It is of course impos-
sible to map out the field of vision in an irritable
restless child, but it is interesting that the mother
thinks that the child sees a little with the left eye.
The boy understands what is said to him and
presents no other symptoms.
By central scotoma is meant blindness in the
central portion of the field of vision.
It is usually due to (i) tobacco, (2) possibly to
alcohol, and usually recovers with removal of the
cause, there being no abnormal ophthalmoscopic
appearances. It may, however, be due to (3) lesions
near the macula lutea, as in syphilitic retinitis and
the retinitis of Bright's disease. By means of the
ophthalmoscope these lesions may readily be
detected.
30 THE CRANIAL NERVES.
Peripheral contraction of the- field of vision com-
monly results from atrophy of the optic nerve, either
primary or following optic neuritis ; it may also be
due to chronic glaucoma or to retinal neurasthenia.
Subjective disturbances of sight in the form of
colours or lights occur in epilepsy and migraine.
In migraine a spectrum of fixed or moving lines
of a bright colour, the lines presenting a vandyked
appearance, is commonly present. Sometimes a
hemianopia, at other times a central scotoma or
amblyopia.
Muscce volitantes — the spectrum of black objects
before the eyes, fixed or moving, are frequently
seen in functional disorders of the liver and in
hypermetropic individuals.
Dimness of vision or amblyopia may be present
in uraemia, hysteria, diabetes, epilepsy, diphtheria,
and in all debilitating diseases, without retinal change.
Optic Neuritis,
Optic neuritis or papillitis is recognised by
swelling and increased vascularity of the disc, with
tortuosity of the vessels, and obscuration of its edge,
partial or complete in extent. It is important to
remember that vision may be unimpaired even with
a considerable amount of neuritis present. Photo-
phobia and pain in the eye are very rarely present.
Restriction of the visual field, diminution in
acuity of vision, and defect of colour vision, are
usually present in extensive papillitis.
THE CRANIAL NERVES. 3 1
The causes of optic neuritis are numerous : —
I. -^Tumour of the brain being by far the most
common, and with tumour we may include aneurism,
hydatid, and abscess as causes.
We cannot localise or estimate the size of the
tumour by the optic neuritis.
A large growth may be present without optic
neuritis.
Tumours of the cerebellum are most constantly,
of all tumours of the brain, attended with optic
neuritis.
Generally all conditions which increase the intra-
cranial pressure cause optic neuritis ; but in nearly
all cases neuritis of the optic nerve is found, and the
papillitis is due to descending inflammation.
2. — The next most, frequent cause is menin-
gitis at the base of the brain.
3. — Anaemia, amenorrhoea, and chlorosis are
recognised causes and must be borne in mind, or the
presence of optic neuritis in girls might cause you to
wrongly diagnose the presence of organic brain
mischief
4. — Chronic Bright's disease. Occasionally it
is impossible from the appearance of the fundus
to diagnose between tumour cerebri and Bright's
disease. . .
5. — Lead poisoning. At the present time I
have in the workhouse infirmary a man completely
blind from atrophy of both optic nerves, who was
under Mr. Priestley Smith ten years ago . for
^
32 THE CRANIAL NERVES.
neuritis from lead poisoning, the man at that time
being a painter, and suffering from other symptoms
of plumbism.
6. — Syphilis.
7. — Exposure to cold.
Optic neuritis occasionally occurs in the specific
fevers, acute myelitis, and also in cerebral haemorrhage.
In all these cases the neuritis is as a rule double;
unilateral optic neuritis would suggest mischief in
the orbit.
It is important to remember that hypermetropia
predisposes to the occurrence of optic neuritis.
Optic Atrophy.
Optic atrophy may be primary or it may be
secondary. In the latter case following optic neuritis,
choroiditis, or occlusion of the vessels of the optic
nerve.
There is no diminution in the size of the disc as
this depends on the size of the sclerotic opening ;
but the disc is excavated, the retina) vessels dimi-
nished in size, and the margin of the disc extremely
well defined. The disc, moreover, is very pale, often
of pearly whiteness, and at the same time vision
is much impaired.
In primary atrophy the loss of sight is gradual
and insidious, and progresses pari passu with the
visible atrophy.
In secondary atrophy the loss of sight occurs
first, and the atrophy is observed subsequently.
[■
o
OQ
Grey dU.l At
(Aftar ■?.u&^')
THE CRANIAL NERVES. 33
Primary atrophy occurs in the following con-
ditions : —
I. — It may exist by itself, and without known
cause ; that is, it may be idiopathic.
2. — It is occasionally hereditary.
3. — It is common in locomotor ataxia, of which
it may be the first symptom, and may exist for
years without other symptoms ; moreover, in this
disease it is often of the grey variety.
4. — It may occur in other chronic degenerative
diseases of the nervous system, e.g. —
General paralytic dementia.
Multiple sclerosis, and also in
Lateral sclerosis.
5. — It may be caused by syphilis, or
6. — By diabetes.
7. — Pressure on the optic nerves or on the optic
commissure at the base of the brain may cause
optic atrophy without neuritis ; hence the frequency
of blindness in children suffering from chronic hydro-
cephalus, the pressure being caused by the distended
third ventricle.
8. — Unilateral optic atrophy occurring on the
side of the headache is occasionally met with in
migraine.
Hceinorrhage into the retina occurs in heart
disease, especially in mitral regurgitation; in chronic
Bright's disease, and after suppression of menstruation.
In gout, pernicious anaemia, leucocytha^mia, and
scurvy, whenever, in fact, the corpuscular richness of
34 THE CRANIAL NERVES.
the blood is below 50 pc, haemorrhage into the retina
is likely to occur. It also occurs in ulcerative
endocarditis, and this fact might help us to diagnose
this disease from simple endocarditis.
Diplopia often occurs in diseases of the cranial
nerves and brain. It is usually binocular and a result
of squint, due to recent paralysis of some of the
ocular muscles. It may be uniocular in rare cases,
such as early cataract.
The various movements of the eyes must be
carefully tested in all cases.
Hemeralopia means that defect where vision is
better in a dim than in a bright light. It is observed
in commencing cataract
Nyctalopia where vision is good in a bright light,
but unduly defective in a dim light. It occurs in
retinitis pigmentosa and in exhaustion of the retina.
There is, however, great confusion as to the proper
meaning of the terms hemeralopia and nyctalopia.
Asthenopia may be accommodative, muscular, or
neurasthenic. Accommodative asthenopia is often
present in hypermetropic individuals, and in them
often appears suddenly during or after any illness.
The symptoms, which are caused by enfeeblement
of the ciliary muscle, are a sense of pressure in the
eyes and headache after reading or sewing, or when
near objects are looked at for any length of time
the objects soon becoming indistinct.
Musailar asthenopia^ or insufficiency of the
internal recti muscles, is common in myopic
THE CRANIAL NERVES. 35
individuals. The subjects of this form of asthe-
nopia complain that after reading, &c,, for a time,
they find objects spreading and becoming indistinct,
and often doubled ; they also usually complain of
headache.
Neurasthenic asthenopia, or retinal antestliesia, is
occasionally observed in children over-worked at
school and underfed, in chlorotic and anEcmic persons,
and in all conditions in which the nervous system is
debilitated. The field of vision is contracted, and
acuity of vision diminished, but these symptoms are
fluctuating. Objects looked at too long may disap-
pear from view.
Colour vision is always affected in atrophy of
the optic nerves.
Fig. 9.
diackam showing the fields of coixjur vision in a normal
Eye on a Dull Day. (Gowers.)
The aslerisk indicates the iixing puint, the black dot the position
of the blind spot.
36 THE CRANIAL NERVES.
In health the various colours are not equally
perceived in different areas of the field of vision.
Blue is be3t seen at the periphery ; then comes
yellow, red, and green from without inward.
Colour blindness is frequently congenital, but it
may be present in locomotor ataxia and other
organic lesions, or it may be due to functional causes,
such as tobacco, alcoholism, hysteria, and migraine.
The pupil symptoms are of great importance in
cerebral disease.
The third nerve supplies the circular muscular
fibres or sphincter of the pupil ; the cervical sympa-
thetic conveys impressions to the dilating muscular
fibres from the cervical region of the cord. (It is
denied by some that there is any dilatator muscle.)
Contraction of the pupil is brought about reflexly,
the third nerve having no tonic action.
The sympathetic nerve exerts a tonic dilating
influence upon the iris.
Myosis, Persistent contraction of the pupil
occurs —
I. — In hypermetropia. In watchmakers and
engravers, who habitually strain the muscles of
accommodation.
2. — In paralysis of the cervical sympathetic
nerve or destructive lesions of the cilio-spinal centre.
3. — In cerebral irritation.
4. — In photophobia.
5. — In haemorrhage into the pons.
6. — After certain poisons, as calabar bean applied
locally, opium internally.
THE CRANIAL NERVES. 37
7. — In certain movements of the eye, e.g,^ con-
vergence and accommodation for near objects.
Myosis is common in locomotor ataxia, from
disease probably in the cervical region of the cord.
In destructive lesions of the brachial plexus con-
traction of the pupil on the side of the injury occurs.
The dilating fibres of the cervical sympathetic
nerve pass from the cilio-spinal centre in the cervical
region of the cord by the anterior roots of the first
dorsal nerve. Ferrier has shown that the intrinsic
muscles of the hand are supplied by this nerve, and
a small pupil unable to dilate when shaded has been
observed in the early stages of progressive muscular
atrophy.
Mydriasis. Persistent dilatation of the pupil is
observed —
I. — In optic nerve atrophy, except when due
to locomotor ataxia.
2. — In paralysis of the third nerve.
3. — In glaucoma.
4. — In cerebral compression.
5. — In shock and conditions of low tone, from
sexual excess or other cause.
6. — From the action of drugs, e.g.^ atropia,
cocain, &c.
Atropia acting on the third nerve.
Cocain on the sympathetic.
Argyll-Robertson pupil — this is that condition
described by Dr. Argyll-Robertson, where the pupil
responds to accommodation, but does not respond to
38 THE CRANIAL NERVES.
light. This condition is very commonly present in
locomotor ataxia.
The break in the pupil reflex for light is probably
situated near the floor of the aqueduct of Sylvius, for
the Argyll-Robertson symptom is often present when
sight is unaffected, showing that the lesion is not in the
optic nerve, and when accommodation is normal
showing that the third nerve is unaffected.
Loss of the pupil reflex for light may exist
either with or without myosis, the latter being a
spinal, the former a cerebral symptom.
This condition of the pupil is not limited to
locomotor ataxia ; it may be met with in general
paralysis of the insane and in multiple sclerosis.
We can readily produce reflex dilatation of the
pupils by pinching the skin and in many other ways,
but reflex contraction only by exposing the eye to
a bright light.
The size of the pupils after death is no reliable
indication of their size during life.
Inequality of the piipils is observed most fre-
quently in general paralysis of the insane, less
frequently in multiple sclerosis and locomotor ataxia.
The pupils may be unequal or irregular from
old iritis due to syphilis, and a pigmentary deposit
about the circumference of the pupil is important
evidence of syphilitic infection.
Clonic spasm of tlie iris I have observed in
multiple sclerosis, in cerebellar tumour, and also in
locomotor ataxia.
THE CRANIAL NERVES. 39
TJie conjugate movetnents of the eyes may be
lost in certain directions. In cerebral hemiplegia
from cerebral haemorrhage, conjugate deviation of
the eyes from the paralysed to the sound side is
observed, the head being also rotated to the non-
paralysed side. These deviations are, however, usually
transitory. This shows that these movements arc
governed by the opposite side of the brain usually^
but that they are also represented by the hemisphere
on the same side. In epilepsy, spasmodic conjugate
deviation to the convulsed side is observed.
Loss of the movements of the eyeballs either
upwards, downwards, or to either side may be present
in disease, the lesion being situated either in the
corpora quadrigemina or in the cerebellum.
In coma the eyeballs will be found to have lost
their parallelism — that is, they are divergent.
Loss of the conjugate movements of the eye-
balls downwards is usually accompanied with loss
of the power of convergence and accommodation.
Paralysis of the internal muscles of the eye — namely,
of the sphincter and dilatator pupillae and the ciliary
muscle, may exist without the external muscles being
affected. This affection, named by Hutchinson oph-
thalmoplegia interna (the pupils neither responding to t
light or accommodation), may be caused by syphilis i
or diphtheria, and is occasionally met with in loco-
motor ataxia and multiple sclerosis.
Paralysis of the motor nerves of the eyeballs
should at once cause you to look for locomotor
\
f
\
40 THE CRANIAL NERVES.
ataxia, syphilis, diphtheria, or some lesion at the
base of the brain.
Bilateral progressive paralysis of the external
muscles of the eyeballs was named by Hutchinson
ophthalmoplegia externa. It often occurs in the
course of chronic degenerative nervous diseases, such
as locomotor ataxia or multiple sclerosis, but it may
be due to syphilis or cold. Last year a case was sent
to me by Dr. Wood White, which resulted probably
from exposure, and which was quickly cured by
large doses of iodide of potassium.
Case of Ophthalmoplegia Externa,
J. B., a man, aged 6^^ a japan worker, was
admitted on November 17th, 1885, with almost
complete paralysis of the muscles supplied by the
right third nerve, and the left third and sixth nerves.
He could tell nothing of his family history of
importance. He himself had always been healthy,
and had never suffered from rheumatism, gout, or
syphilis. About five weeks before his admission he
was much exposed to cold weather, after which he
had conjunctivitis of the left eye and dropping of the
left eyelid ; the right eyelid also gradually dropped a
few days later, but not to such an extent as the left.
Dr. White sent the following report: — "Vision in
each eye = f . As the lenses were slightly hazy, this
was considered normal. Both fundi quite healthy.
Slight tortuosity of veins alone was noticed. Fields
of vision normal." When admitted, there was nearly
complete ptosis on the left side, and partial ptosis
THE CRANIAL NERVES. 4 1
on the right. The right eye could be moved out-
wards, and downwards and outwards to the normal
extent, but the upward, inward, and downward
movements were much restricted. The pupil was
in a medium degree of dilatation, and responded
normally to light and accommodation. The left
eye was much restricted in its movements, in a 1
directions except downwards and outwards. The
pupil on this side was a little larger than the right,
but responded normally. The muscles supplied by
the third nerve on the right, and by the third and
sixth nerves on the left, were affected. The plantar
reflexes were absent ; the knee-jerk on both sides
was normal. He complained of double vision; and
occasionally of slight vertigo, which caused him to
stagger in his walk ; and of frontal headache. The
memory was defective. There was no albumen in the
urine, no fever, and no change in either fundus oculi.
The patient was treated with iodide of potassium
in increasing doses, with counter-irritation over both
temples. He improved daily, and was discharged
on December 7th, greatly improved, having no diffi-
culty in keeping the eyelids open, and the movements
of the eyeballs being almost normal. At the time
of his discharge he was taking thirty-six grains of
iodide of potassium thrice daily.
As to the diagnosis in this case : — The symmetry
of the paralysis, the third nerve being affected on
both sides ; and the non-implication of the internal
muscles of the eye, the iris responding normally
42 THE CRANIAL NERVES.
with preservation of the conjunctival reflex ; indicated
a central lesion. Mr. Hutchinson reported seven-
teen cases of " ophthalmoplegia externa/' or " sym-
metrical immobility of the eyes with ptosis," in the
" Medico-Chirurgical Transactions" (Vol. LXIL,
1879). Incompleteness in the degree of paralysis
was a marked feature. Inherited or acquired syphilis
was present in ten out of his seventeen cases,
rheumatism in a few ; ten of the patients were
males, some quite old men. Usually the onset
was gradual, but occasionally rapid. The recovery
was not complete in any one case. Ox\q post-mortem
examination was made, and a degeneration of the
nuclei of origin of the motor nerves to the eye,
similar to that met with in the spinal cord in pro-
gressive muscular atrophy, was found. Dr. White
pointed out, and I agreed with him, that the rapid
onset, after exposure to cold, indicated in this case
an inflammatory rather than a degenerative lesion.
This was proved by his speedy improvement under
iodide of potassium in large doses, and counter-irrita-
tion. Mr. Hutchinson advises iodide of potassium in
large doses, and one patient of his took an ounce and
a half in twenty-four hours with good results.
January 14th. — The patient had now completely
recovered, the movements of both eyes being normal.
He had taken half-drachm doses of the iodide thrice
daily since he left the hospital.
Case of loss oftJie co?ijugate moveme?it of the eyeballs
downwards^ of convergence^ and of accommodation, —
THE CRANIAL NERVES. 43
M. O., a woman, aged 38, was sent to me in
March last, complaining of giddiness. She said that
she was taken ill after her last confinement twelve
months previously, her illness coming on gradually.
When standing she suffered from vertigo, which
made her stagger, and frequently fall. The vertigo
disappeared when the eyes were closed, and when she
was lying down. She had had two miscarriages, two
children died young, four were alive and well. No
definite history of syphilis could be obtained. Her
sight was not defective, but when reading the letters
became blurred. The conjugate movement of the
eyeballs downwards, the power of convergence, and
of accommodation were lost. In monocular vision
also these movements were lost. The movement of
the eyeballs to either side was unaffected, and she
could look up, but when doing so had great difficulty
in bringing the eyeballs down again, and had no
power at all of rotating the eyeballs downwards.
There was nothing abnormal in either fundus, the
pupils were of normal size, and responded normally
to light and accommodation. The intellect was
unaffected, the only psychical change being inability
to bear the least noise. There was a slight general
increase in the tendon reflexes, with slight ankle
clonus, the increase being greater on the left side. In
walking she held her neck and body stiffly, and seemed
afraid of stepping out, evidently on account of vertigo.
There was no nystagmus, no tremor, and no altera-
tion of speech.
44 THE CRANIAL NERVES.
Loss of the movement of the eyeballs down-
wards is nearly always accompanied with loss of
convergence and accommodation, the three defects
having been often observed associated, and in the
absence, too, of all other symptoms. The centre
governing these movements probably resides in the
cerebellum, and I think there is little doubt that the
above patient has cerebellar disease, but as to its
nature there is not sufficient evidence to justify a
positive opinion. I am inclined to consider it a
sclerosis.
Nystagmus or clonic spasm of the muscles of
the eyeballs, causing oscillation, is always bilateral.
Its causes may be local or central.
Congenital defects, cataract, corneal opacity,
and retinitis pigmentosa are some of the local causes.
Nystagmus of central origin arises from disease
of the cerebellum and its peduncles.
It also frequently occurs in cerebellar tumours,
multiple sclerosis, and more rarely in locomotor ataxia.
Albinos nearly always suffer from nystagmus.
Miners' nystagmus is also well known.
The movements of the eyelids and the share
taken by the globes in these movements must be
understood to appreciate the alterations observed
in exophthalmos. Dr. Gowers, in the " Medico-
Chirurgical Transactions" (Vol. LXIL), has fully
described and explained the lid movements.
In hysterical ptosis the upper lid is depressed
by a gentle contraction of the orbicularis ; if the
THE CRANIAL NERVES. 45
patient is directed to look upwards the levator
contracts with the superior rectus, and the patient
is obliged to contract the orbicularis strongly to
prevent the lid being raised, the nature of the case
being thus disclosed.
The third and fourth cranial nerves have not yet
been traced to the motor convolutions.
The third nerve has its superficial origin on the
inner side of the crus, immediately in front of the
pons ; hence its implication in tumours of or near
the crus, a crossed paralysis being produced, the
third nerve being paralysed on the same side as the
lesion, the hemiplegia being on the opposite side.
The nucleus of the third nerve is situated on the floor
of the aqueduct of Sylvius, and is the seat of three
centres. From before backwards these are—
I. — The centre for accommodation.
2. — The centre of the reflex contraction of the
iris to light ; and
3. — The centre regulating the external muscles
of the eye.
Lepine localises the cortical centre of the motor
division of the fifth nerve in the lower third of the
ascending frontal convolution. Dr. Gowers is of
opinion that the fifth nerve is the sole nerve of taste,
and that the glosso-pharyngeal has nothing to do
with this function.
The chorda tympani is the nerve of taste to the
anterior two-thirds of the tongue, but it is probably
derived from the fifth nerve by the vidian.
46 THE CRANIAL NERVES.
Dr. Gowers has published a case where there
was paralysis of one fifth nerve only, due to disease
at the surface of the pons, in which taste was entirely
lost on that side, not only at the front of the tongue,
but also at the back, on the soft palate, and on the
palatine arches.
The cortical centre for taste is not yet known in
man.
Certain trophic affections are met with in the
area of distribution of the fifth cranial nerve.
I. — Herpes zoster frequently occurs, and when in
the area of the ophthalmic nerve may destroy sight.
2. — Glaucoma probably in some cases depends
upon irritation of the fifth nerve, increase of tension
being frequently observed in trigeminal neuralgia.
3. — Neuro-paralytic ophthalmia takes place in
irritation of the fifth nerve by intra-cranial tumours
or meningitis, the cornea quickly becoming cloudy.
In severe cases ulceration followed by perforation of
the cornea and collapse of the globe occurs. These
changes are not due to anaesthesia of the eyeball,
rendering the organ liable to injury from dust, &c.,
for in complete anaesthesia of the conjunctiva
ophthalmia tnay be absent, and, moreover, oph-
thalmia may be present without anaesthesia. It is
most probabie that the phenomena are due to
lesion of trophic fibres, which descend from the
Gasserian ganglion,
4. — Unilateral progressive facial atrophy is sup-
posed to be due to a lesion of the trophic fibres of
the fifth ner\^e.
THE CRANIAL NERVES. 47
The sixth nerves running on the under surface
of the pons parallel to the basilar artery are very
liable to be compressed by tumours of the pons.
The sixth is close to the fifth, and both these nerves
on one side are apt to be compressed by tumours of
the lateral lobes of the cerebellum which grow
forwards.
Lesions of the nucleus of the sixth nerve give
rise to paralysis of the external rectus on the side of
the lesion, and of the internal rectus on the opposite
side, thus causing a conjugate deviation of the eyes
away from the side of the lesion.
The facial nerve is connected, as Ferrier has
proved, with the lower extremities of the ascending
parietal and ascending frontal convolutions ; the
fibres pass from these convolutions through the
internal capsule to the pons, where decussation
occurs.
Dr. Gowers thinks it probable that those fibres
of the facial nerve which supply the orbicularis oris
muscle arise from the hypoglossal nucleus ; in this
way the implication of the lips in bulbar paralysis is
readily explained. From clinical evidence, also.
Dr. Gowers believes that the facial nerve has no real
origin from the nucleus of the sixth.
Facial paralysis may be due to lesion of the
nerve at its nucleus or beyond its superficial origin
— that is, it may be peripheral, or it may be due to
implication either of the cortical centre or of its path
between this centre and its nucleus of origin.
48 THE CRANIAL NERVES.
Peripheral facial paralysis is characterised by
the following symptoms : —
I. — The paralysis is complete, all its external
branches being implicated.
2. — The conjunctival reflex and associated move-
ments are lost.
3. — Qualitative electrical changes are present.
4. — There is inability to close the eyelids
(lagophthalmos).
In cerebral facial paralysis the branches to the
upper part of the face are not implicated, the asso-
ciated movements being preserved ; and there are no
qualitative electrical changes.
Spasm may occur in the area of distribution of the
facial nerve (convulsive tic). Any direct or reflex
irritation of the nerve may occasion it, and the spasm
may affect all the muscles or be limited to one or
more. Trigeminal neuralgia and carious teeth are
common causes. It may also result from cold and
emotional disturbances, worry especially being a
powerful factor in its production. The spasm may be
tonic or clonic. The tonic form may be mistaken for
facial paralysis of the opposite side, or for contracture
resulting from previous paralysis. But the immobility
is on the side to which the face is drawn, the opposite
being the case in paralysis; moreover, the electrical
reactions are normal in mere spasm.
The auditory nerve has its cortical centre in the
superior temporo-sphenoidal convolution. Destruc-
tion of this convolution on both sides is necessary to
THE CRANIAL NERVES. 49
produce complete deafness, as they are bilaterally
associated ; dest ruction of the le ft convolution cau ses _
word deafness. The auditory nerve fibres can be
traced tofour nuclei in or close to the floor of the
fourth ventricle. Decussation takes place beyond these
nuclei, and fibres pass ; some to the cerebellum which
The nerve nuclei being diaeraromatically reptesented, the Roman
numerals marking the situation of the corresponding nerve nuclei.
probably are concerned with equilibriation, and others
through the internal capsule to the superior temporo-
sphenoidal convolutions.
50 THE CRANIAL NERVES.
Tlie spinal accessory nerve, — Spasm of the
muscles supplied by the spinal portion of the spinal
accessory nerve constitutes wry neck. The spasm
may be clonic or tonic, and the clonic form unilateral
or bilateral. The bilateral variety (eclampsia nutans)
is chiefly observed in children, the body and head
being constantly flexed and immediately relaxed.
There is a tendency for this variety to pass into
epilepsy and idiocy. I have met with three cases of
unilateral clonic spasmodic wry neck. One patient, a
woman, became maniacal, and had to be sent to the
asylum. In another case Mr. Jordan Lloyd excised
a portion of the nerve, a cure resulting. The third
was unrelieved by medical treatment, and refused to
be operated on. The spasm frequently extends to
the muscles of the face and upper extremity.
These cases, when of several months' duration,
are most obstinate and difficult to remedy. Excision
of a portion of the nerve offers the best chance of
recovery.
It occasionally occurs in children, especially in
girls, when it is usually amenable to treatment. Two
cases recently under my care were cured by Fara-
disation.
The pne7imogastric nerve has a more extensive
distribution than any other cranial nerve.
It leaves the medulla in company with the
glossopharyngeal and spinal accessory nerves, arising
from a nucleus situated on the floor of the fourth
ventricle, just external to the hypoglossal nucleus.
• *
THE CRANIAL NERVES. 5 I
The cortical connections of this nerve are as
yet unknown. It transmits sensory impressions from
the larynx, lungs, heart, oesophagus, and stomach.
Its cardip-inhibitory fibres and probably all its
motor fibres are derived from the spinal accessory nerve.
Paralysis of the pharynx is caused by disease
at the base of the brain, by lesions of the pons and
medulla, and is also observed as a sequel of
diphtheria.
Laryngeal paralysis sometimes occurs from
disease of the medulla, or in cases of haemorrhage
into this organ.
It occurs in bulbar paralysis, and occasionally in
multiple sclerosis and locomotor ataxia.
In locomotor ataxia, paroxysms of coughing,
something like those of pertussis, may occur (laryn-
geal crises), and may prove fatal. - In severe cases,
symptoms of asphyxia and unconsciousness occur.
These crises, which usually appear early in the
course of this disease, are pi'obably caused by irrita-
tion of the nuclei of the vagi, or of the spinal
accessory nerves, in the medulla.
In all cases of locomotor ataxia the larynx
should be examined, for bilateral paralysis of the
abductors, which may give rise to sudden asphyxia,
may be present.
The hypoglossal nerve is connected with the
lower extremity of the ascending frontal convolu-
tion, lesion of this area causing paralysis of the
opposite side of the tongue.
52 THE CRANIAL NERVES.
The fibres of the nerve pass from this centre
through the internal capsule in the situation pre-
viously described ; thence to the nucleus of the
hypoglossal ner\^e in the medulla, decussation taking
place between the cortical centre and the nucleus in
the medulla.
In hemiplegia, the tongue, when protruded,
points to the paralysed side, being tilted over by the
action of the sound genio-hyo-glossus ; when in the
mouth the raphd is concave towards the sound side.
The tongue is paralysed in bulbar paralysis and
may also be affected in locomotor ataxia.
Paralysis of the tongue by itself most commonly
results from disease of its cortical centre ; but it ma)'
be caused by a small lesion in the internal capsule.
When paralysis of the tongue is complete, it
falls back in the cavity of the mouth, and may close
the glottis ; this accident frequently occurs in deep
narcosis from inhalation of chloroform.
When one hypoglossal nerve or its nucleus of
origin is diseased, atrophy of the half of the tongue
occurs, in some cases being well marked.
CHAPTER III.
SYMPTOMS OF BRAIN DISEASE.
*
Paralysis — Hemiplegia^ Monoplegia,
In the diagnosis of diseases of the nervous
system, as in fact in the diagnosis of all diseases —
I. — You should observe the symptoms, and
notice which are the most prominent.
2. — You should enumerate the different causes
which might give rise to these symptoms, and
3. — Eliminating them one by one, determine the
most probable cause in the case under notice.
Hemiplegia.
In hemiplegia the movements most paralysed
are those most highly specialised or most volitional.
The muscles of the trunk, and those muscles of the
upper part of the face which are habitually bilaterally
associated in their action, usually escape.
Dr. Broadbent explained the escape of the
trunk muscles by supposing that when those on one
side were shut off from the motor area of the cortex
by a lesion in the internal capsule, they could still
be set in action by the opposite side of the brain,
there being a free communication bet\vee.x\ ^.Vs&x-^
I
54 SYMPTOMS OF BRAIN DISEASE.
corresponding nuclei in the cord. But Mr. Horsley
has recently determined the seat of the trunk centre
on the tentorial surface of the convolutions, the
fibres from this centre passing through the internal
capsule behind the leg fibres. The order of the motor
paths in the internal capsule from before backwards is
tongue, lips, face, arm, leg, trunk; a haemorrhage from
the lenticulo-striate artery involves these fibres from
before back, laceration occasioning a permanent, and
mere pressure a temporary paralysis. The order of
recovery is first the trunk, then the leg, then the arm
as absorption of the clot takes place ; the diminution
of pressure occurring first at the part most removed
from the seat of haemorrhage. Thus the usual escape
of the trunk muscles, and their rapid recovery when
affected, in haemorrhage into the internal capsule are
readily explained by the anatomical arrangement of
the fibres in the internal capsule. The trunk muscles
are affected in hemiplegia if the haemorrhage is large
I enough to implicate the trunk fibres. Hemianaes-
thesia is present when the clot compresses or destroys
the posterior third of the posterior half of the internal
capsule. This portion of the capsule is supplied by
the posterior cerebral artery, so that while hemian-
aesthesia does occasionally occur in haemorrhage
from the lenticulo-striate branch of the middle
cerebral artery, obstruction of this artery by an
embolon or thrombus does not cause hemianaesthesia.
Hemiplegia occurring in early life is characterised
by the following features : — (i) the leg nearly always
SYMPTOMS OF BRAIN DISEASE. 55
recovers ; (2) aphasia is transitory, and so is any
sensory loss that may be present ; but (3) the limb
may be stunted in its growth ; and (4) the intellect
may be affected.
To perceive paresis in the lower facial muscles,
we ask the patient to show his upper teeth by
elevating the upper lip. One side may be elevated
before the other, or to a greater extent. It would
not do to tell the patient to smile, for emotional
movements may be present while voluntary move-
ment is lost. Emotional movements are probably
innervated from either hemisphere. If deep coma
is present, it is sometimes difficult to tell which side
is paralysed. We must then look for conjugate
deviation of the eyes, which is usually present and is
away from the paralysed side. Or pinching the skin
may cause movement on one side. The skin reflexes
may be abolished or diminished on the paralysed
side. The paralysed side may be rigid or flaccid.
Rigidity may come on immediately with the
onset of hemiplegia ; this is called initial rigidity, and
is due to irritation of the motor tract ; or it may
come on within a few days — early rigidity, which is
probably due to inflammatory changes. In a few
weeks, if the lesion be a severe one, late rigidity due
to descending degeneration of the crossed pryamidal
tract supervenes. It is accompanied with exaggera-
tion of all the deep reflexes, and usually also of the
skin reflexes. The occurrence of ankle clonus within
a few days of the onset of hemiplegia is a bad si^tv.
56 SYMPTOMS OF BRAIN DISEASE.
The flexor and adductor muscles being more
powerful than the extensors and abductors,
adduction and flexion prevails in the arm and leg.
After late rigidity has lasted some time structural
changes occur in the muscles — structural rigidity.
The onset of late rigidity can be deferred, and its
severity mitigated by appropriate Faradisation of
the extensor and abductor muscles. In hemiplegia
from syphilitic thrombosis, late rigidity is usually
very marked ; and such a paralysis in a young man,
if embolism is excluded, is almost invariably due to
syphilitic thrombosis.
Various trophic and vaso-motor changes may be
present in hemiplegia. Elevation of the temperature
of the paralysed iirtib may be observed within the
first few days ; oedema, blebs, acute bed sores, and
occasionally joint lesions, may be present These
phenomena probably depend on the irritative char-
acter of the cerebral lesion.
The leg usually recovers first, but the extensors
of the toes are especially affected, the feet being
dropped, and the patient having difficulty in lifting
the toes off* the ground, scraping the floor as he
walks. Cerebral paralysis may be partial, the arm,
leg, face, or tongue being separately paralysed, the
lesion being usually situated in the cortical centres.
The arrangement of these centres in the cortex
explains the grouping of the paralyses ; why, for
instance, the tongue and arm cannot be affected by a
single lesion without the face. In these cases the
SYMPTOMS OF BRAIN DISEASE. 5/
paralysis is usually not absolute, and the extremities
of the limbs are especially affected. Cortical lesions
too, are liable to be attended with partial epilepsy.
A cerebral monoplegia may be due, not only to a
lesion in the cortex, but occasionally, though rarely,
to a lesion in the internal capsule, as I have already
mentioned.
Various disorders of movement may appear as the
paralysed limbs recover or mend, either tremor, chorei-
form movements, or slow continual spasm (athetosis).
Athetosis (^aOerog without position or place), first
described by Hammond, is in the great majority of
cases a sequel of hemiplegia, and especially of hemi-
plegia occurring in early life and due to softening.
It may, however, be bilateral and independent of
hemiplegia.
Spastic Iiemiplegia of infancy is due to injury
sustained by the motor areas of the brain during
birth in difficult and tedious labours. It may,
however, be due to thrombosis following specific
fevers in early life. There is frequently in these
cases idiocy or imbecility, and often epilepsy. The
bones are shortened and the limbs atrophied. This
disease is at once distinguished from paralysis due to
polio-myelitis anterior acuta : —
I. — By the history of its presence from birth.
2. — By the presence of rigidity.
3. — By the increase of reflexes.
This hemiplegia may be bilateral and the child's
four extremities rigid and paretic. The trunk
58 SYMPTOMS OF BRAIN DISEASE.
muscles being affected the child is unable even to
sit up. I recently had a well-marked case at the
Queen's Hospital of bilateral spastic hemiplegia, in
which the patient was imbecile and unable to stand
or sit up. These cases of bilateral spastic hemiplegia
are somewhat confusing, but the history of the illness
existing from birth, together with the presence of
rigidity of the limbs and exaggeration of the deep
reflexes, and generally also some degree of imbecility,
enable us to make the diagnosis. Spastic paraplegia
may be congenital and due to injury to the leg
centres or to the spinal cord at the time of birth.
These conditions are frequently met with at
workhouse infirmaries and at children's hospitals.
Cases of Spastic Hemiplegia.
Case i. — Josiah Withers, aged 24, was admitted
to the workhouse infirmary in April, 1875. He has
one sister and one brother, who are in perfect health.
His father says the paralysis came on after convul-
sions when a few months old. He is decidedly an
imbecile, but can understand perfectly what is said
to him, and can look after himself to the extent of
eating and drinking, but little more. He has spastic
hemiplegia on the right side. The right side of the
face is slightly contracted, the angle of the mouth
being elevated and the naso-labial furrow increased.
The eyelids on the right side are mere separated
than on the left, so that the right eye seems to be
slightly larger than the left. He cannot close this
SYMPTOMS OF BRAIN DISEASE. 59
eye completely. The right side of the tongue is not
atrophied, and the movements of this organ are
perfect. There is much wasting and rigidity of the
right upper and lower extremities. The arm is
abducted instead of being adducted as is usually the
Fig. II.
Spastic Hemiplegia op Infancy.
case. The forearm is flexed and pronated, and the
tendon of the biceps stands out prominently. The
wrist is preternaturally extended. The fingers are
flexed strongly over the thumb, which is adducted
across the palm. The fingers are flexed at a.lL
6o SYMPTOMS OF BRAIN DISEASE.
three joints, though usually in this disease the
metacarpo-phalangeal joints are extended, the middle
and distal joints flexed. He walks with the thigh
and knee much flexed, but he can straighten them ;
the rigidity is more marked in the upper extremity
than in the lower, and it increases towards the distal
end of each extremity ; thus the wrist and fingers
are more rigid than the elbow and shoulder. Also
the ankle is far more fixed than the knee or hip.
There is a condition of extreme talipes equino-
varus, with partial dislocation of the astragalus, the
patient walking on the balls of his toes, and being
obliged to bend his thigh and knee to a considerable
extent. There is a well-marked rotation inwards of
the limb in progression, due chiefly to the gluteus
medius. There is marked atrophy both of the
muscles and bones on the right side. The bones are
diminished both in circumference and in length.
The circumference of the right arm is 7^ins. ; of
left, 8^ins. ; of right elbow joint. Sins. ; of left, gins. ;
Around the centre of the forearm the measurement
is, on the right side Sins. ; on the left, 6j4ins,
Circumference of centre of thigh on the right side is
I3i^ins. ; of left, i6ins. Around centre of calf, on
the right side, Sins. ; on the left side, logins. The
right collar bone is S^ins. in length; the left, 6ins.
Right humerus loins. ; the left, logins. The ulna
on the right side is Sins, long, on the left is pj^ins.
The metacarpal bones of the right hand measure
21/^ins. ; of the left, 2^ins. There is also slight
SYMPTOMS OF BRAIN DISEASE. 6 1
shortening of the phalanges of the right hand.
There is no appreciable shortening of the bones of
the lower extremity. The reflexes, both superficial
and deep, are much exaggerated. The olecranon
reflex is much increased on the right side. The
patellar reflex is much exaggerated, and there is a
well marked front-tap contraction on the right side.
The plantar, cremasteric, abdominal, and epigastric
reflexes are all present. Ankle clonus cannot be
obtained, from the great rigidity of the ankle joints.
Sensation is perfect.
The patient, apart from his paralysis and imbe-
cility, is in very good health. The atrophy is mainly
due to disuse, partly also, most probably, from
extension of degeneration of the pyramidal tracts to
the multipolar nerve cells in the anterior cornua.
The latter, however, are not much affected, or the
rigidity and increase of the reflexes would not be
present. No asymmetry of the skull can be made
out, but the forehead is low and receding. The
patient suffers from the severe form of epilepsy, and
is very passionate at times.
Case 2. — Spastic Jiemiplegia, with epilepsy and
imbecilityy and with choreiform movements of the
hand (athetosis), — Patrick . Lawley, aged 38. The
patient states that his disease dates from early
childhood. He has three brothers and two sisters in
good health. His father and mother are both dead ;
he does not know anything of the cause of their
death. He says he was always told that he was
62 SYMPTOMS OF BRAIN DISEASE.
paralysed when a baby. His brother tells me that
he was paralysed after convulsions, when a few
months old. There is spastic hemiplegia of the
right side. The right side of the face appears
smaller than the left, with the naso-labial fold more
marked. The tongue when protruded is projected
to the right. There is no shortening of the clavicle
or humerus on the right side ; but the right ulna is
^in. shorter than its fellow. The metacarpal bones
are slightly shorter than those of the left hand.
The measurement around the centre of the right
arm is 8^ins., on the left side Q^ins. The move-
ments of the shoulder are a little stiff, but there
is no marked rigidity ; the elbow is in the same
condition. There is preternatural flexion of the
right wrist, adduction of metacarpal bone of thumb,
with extension of its phalanges. The voluntary
movements of the fingers and thumb are slight,
and the grasp of this hand is very feeble. There
is a slow continuous rhythmical movement of the
fingers and thumb, consisting of alternate flexions
and extensions, the fingers also being separated
from each other and then approximated ; he cannot
control these movements. There is evident vaso-
motor disturbance on the right side of the body,
for on drawing the finger nail along the skin a blush
appears far more quickly and lasts much longer
than on the left side. The hand is also very cold
compared with the opposite one, and is livid. The
right hand is decidedly atrophied, but the muscles
SYMPTOMS OF BRAIN DISEASE. 63
of the palm are hypertrophied from the continual
motion. The olecranon reflex is much better
marked on the right side than on the left. The
right lower extremity is much weaker than the
left. The bones do not seem to be shortened,
although there is decided muscular atrophy. He
can walk on the sole of the right foot, but there
is a little talipes equino-varus. The patellar reflex
is greatly exaggerated, but ankle clonus is obtained
with difficulty owing to the rigidity of the muscles."
The plantar reflex is exaggerated, and the cre-
masteric is present. The epigastric and abdominal
cannot be obtained. The muscles respond pretty
normally to Faradisation and Galvanisation, the
alteration being only a slight diminution of response
without qualitative changes. The ophthalmoscope^
shows nothing abnormal.
The patient is an epileptic, with imbecility, and
is very passionate at times when irritated. Local-
isation of sensation in the affected hand is much
impaired ; although the patient can tell when
he is touched, he cannot properly localise the
point of contact.-
Case 3. — Spastic hemiplegia of the left side^
with imbecility and epilepsy^ and choreiform move-
ments of left hand. — M. S., aged 34, a female, has
been paralysed on her left side from birth. She
suffers from the severe form of epilepsy, which
she says she was frightened into when young.
There is a great degree of imbecility, and the patient
64 SYMPTOMS OF BRAIN DISEASE.
has the characteristic expression of imbecility, with
a low receding forehead. The left side of face is
much smaller than the right, and she cannot close
the left eye as well as the right, but there is not much
rigidity. There is marked atrophy of the muscles
of the left upper extremity, except of those of the
hand. There is only slight shortening of the bones
of the forearm. The left hand is much smaller than
the right, although the muscles are hypertrophied.
There is hyperextension of the middle-phalangeal
joints, and there is a slow continuous movement of
the fingers and hand. This movement is very similar
to that observed in the case of Patrick Lawley, but
is not so pronounced. The movement only comes
on at times, and when it does she has no power of
controlling it. The hand is cold and livid, and the
grasp very feeble. There is slight rigidity of this
extremity, and increase of olecranon reflex. Sensa-
tion is normal. The muscles of the left lower
extremity are also much atrophied, but I cannot
make out any shortening of the bones. The patellar
reflex on this side is much exaggerated. There
is no front-tap contraction, but Unkle clonus is
well marked, and the plantar reflex exaggerated.
There is slight talipes equino-varus. Stiffness is
present to a slight degree, and is exaggerated at
times. There is diminished vaso-motor tone on the
left side ; on drawing the finger nail along the surface
a blush quickly appears, and lasts some time. The
electrical reactions are normal.
SYMPTOMS OF BRAIN DISEASE. 65
Case 4. — Hemiplegia of tlie right side^ with
epilepsy and imbecility, and peculiar movements of
the hand, — Ed. Webster, aged 16. His father, a very
intelligent man, gives me the following history : —
His son was a fine child till he reached the age of
sixteen months ; about this time he was seized with
convulsions from teething. The fits were very severe
and affected the right side especially. After the con-
vulsions ceased the child was found to be paralysed
on the right side of the face, and in the right arm
and leg. And from being a bright boy he became,
as his father expresses it, " a baby again," and had to
be carried about, and was dull and stupid. He was
not able to speak for several months after the con-
vulsions, although well able to before, and had to be
taught over again. Epilepsy followed the fits, and
he now suffers from the severe form. He is imbecile,
but not to a great degree. His face looks intelligent
and his memory is good, and he answers questions
perfectly coherently ; but his schoolfellows call him
**^ silly Teddy." Two years ago he took four or five
sheep from a field, drove them to the Smithfield
market, and sold them for half-a-crown ; he was " let
off" on account of his mental defect.
He has right hemiplegia, and there is marked
atrophy. There is talipes equino-varus. The rigidity
is not so marked as in the three previous cases, but
it is present. There is increase of olecranon and
patellar reflexes. No alteration of sensation. The
right side of the face is atrophied as vw XXvi^ ^xesfvoN^'s*
66 SYMPTOMS OF BRAIN DISEASE.
cases, and the tongue points to the right side when
protruded. He has almost entirely lost power in
his right hand ; slow movements are observed at
times, but they are not so marked as in the case
of Patrick Lawley. There is a remarkable illustra-
tion of the bilateral association of the movements
of the extremities in this case. If the boy opens
his left hand and straightens his fingers the right
hand is observed to slowly open and the fingers to
straighten, and if he closes his left hand the right
follows suit. He has no power at all over the right
hand by itself, but can control it through the medium
of the left. His father says he observed this him-
self; in fact, he drew my attention to it The
recovery of speech, after what must have been a
severe injury, is explained by the youth of the patient
The right side of the brain having been educated and
taken on itself the duties of the left side. Apart from
his epilepsy, the patient's general health is excellent.
His father tells me that he is bad tempered and ready
to fight on the most trivial provocation. He frightens
the children by the expression of his face when angry.
In the diagnosis of the nature of a hemiplegia, as
in the diagnosis of all varieties of paralysis, the first
question to be answered is: — Is the paralysis functional,
or is it due to organic lesion ?
Hemiplegia may be present after epileptic
attacks, or it may precede or follow chorea, or be
hysterical or simulated.
SYMPTOMS OF BRAIN DISEASE. 6/
In hysterical hemiplegia (i) there is nearly
always loss or impairment of sensation, and the
motor loss is rarely complete. Hemianaesthesia with
implication of the special senses on the same side,
there being amblyopia of the eye on the affected
and slight visual impairment on the opposite side,
is almost invariably due to hysteria.
(2) The face and tongue are not affected, and
the leg frequently suffers more than the arm.
(3) Hysterical anaesthesia and paralysis are apt to
vary and appear or disappear from trivial causes, as by
the application of metals to the skin(Burq's treatment).
(4) In hysterical paralysis the sphincters are
unaffected, and no trophic lesions or bed sores occur.
Having decided that the hemiplegia is due to
organic causes, is it cerebral, spinal, or peripheral? Of
course, in the vast majority of cases it is cerebral.
A lesion of the brachial, lumbar, and sacral plexuses
on one side would cause paralysis of the arm and
leg, but there would be electrical changes proving
damage to the peripheral nerves ; also sensory dis-
turbances with rapid wasting and trophic changes.
In spinal hemiplegia due to polio-myelitis
anterior acuta, the electrical changes would at once
show that the lesion was not cerebral. A tumour
high up pressing on the spinal cord might cause a
hemiplegia, but our attention would be arrested by
the absence of implication of the face and tongue,
and by sensation being blunted on the opposite side,
not on the same side as the motor paralysis.
68 SYMPTOMS OF BRAIN DISEASE.
Having decided that the hemiplegia is cerebral,
what IS the exact situation of the lesion ? The pre-
sumption is that it is in the internal capsule, this
being the most common seat of the lesion in hemi-
plegia of the ordinary type. The presence of partial
epilepsy would indicate that the lesion was cortical.
If the third or facial nerves were affected on the
opposite side we should localise the disease in the
crus or pons.
Vomiting. — Vomiting is a reflex act, the centre
being placed in the medulla and afferent impressions
being conveyed by various nerves, the chief of
which is the vagus. Undue irritation of the termina-
tions of this nerve in the stomach is the cause of the
vomiting in gastric ulcer and other diseases of the
stomach. Irritation of the centre in the medulla
may cause vomiting, the centre being affected either
by the quality of the blood or by the presence of
growths or inflammatory products. The vomiting
of anaemia is caused by the action of the impure
blood upon the centre.
Vomiting may be caused by psychical impres-
sions, as is well known, and also by disease in any
part of the encephalon, but is especially common
when the disease is in or near the medulla.
Tumours of the cerebellum are very constantly
attended with vomiting at some stage.
In hysteria the irritability of the vomiting
centre is exalted and the reflex act is too readily
brought about, food being at once rejected. This
SYMPTOMS OF BRAIN DISEASE. 6g
increased irritability is present in cases of cerebral
disease, and vomiting may occur independently of
the ingestion of food. But it must be remembered
that in cerebral disease vomiting frequently follows
the taking of food, and so may simulate vomiting
due to stomach mischief
Cerebral vomiting is usually unattended with
nausea, which is commonly present when the vomit-
ing is due to stomach mischief In cerebral disease
we should probably have other symptoms pointing
to brain disturbance, such as headache or vertigo, but
these might be caused also by stomachic disorders.
Cerebral is usually much more intractable than
stomachic vomiting, and in the latter a furred tongue
and tenderness or discomfort at the epigastrium are
usually present. Vomiting in children, frequently
occurring, without a furred tongue or complaint of
pain or discomfort at the stomach, should always
excite suspicion of cerebral disease.
In all cases of obstinate vomiting examine the
urine and the fundus oculi. The vomiting in cases
of cerebral tumour may be frequently checked by
counter-irritation by blisters or iodine at the nape
of the neck or by a seton.
Temperature. — The temperature is frequently
abnormal in cerebral disease. There is evidence
which goes to prove that somewhere in the con-
volutions around the fissure of Rolando there is a
heat-controlling centre, impressions from which pass
through the crura, pons, and medulla to the cord.
70 SYMPTOMS OF BRAIN DISEASE.
Lesions in the pons are especially characterised
by the remarkable variations which they may cause
in the temperature. Probably four-fifths pf cases
of pontine disease, either acute or chronic, are
attended with pyrexia. Lesions, also, below the
pons in the medulla and cervical region of the
cord may cause fever, which may amount to severe
hyperpyrexia, the temperature rising even to iio°F.
This hyperpyrexia is probably explained by loss
of the controlling influence of the centre above
mentioned over heat production. Towards the end
of tubercular meningitis hyperpyrexia is occasionally
observed.
In cerebral disease it must be remembered that
fever may be absent in inflammation, that elsewhere
would certainly raise the temperature, and also that
the pulse rate may not be increased as it usually is
with fever. For example, in an early stage of tuber-
cular meningitis a slow pulse may be observed, with
considerable fever ; this is due to irritation of the
vagi ; the same phenomenon is observed to a less
extent in enteric fever, probably also from irritation
of the vagi, but of their peripheral, not of their
proximal extremities. In enteric fever, however,
though the pulse rate does not increase proportionately
to the fever, yet the pulse is much more frequent than
in health. The chronic degenerative diseases of the
brain, e.g.^ general paralytic dementia and multiple
sclerosis, are apt to be attended with occasional
pyrexia, which is not caused by any inflammatory
SYMPTOMS OF BRAIN DISEASE. J\
mischief, but is probably due to interference with the
nervous heat-controlling mechanism.
At the onset of cerebral haemorrhage, except
when pontine, the temperature is depressed, but
afterwards there is an elevation due to surrounding
inflammatory changes.
Respiration. — Respiration is often disturbed in
cerebral disease. Lesions in or near the respiratory
centre, or large haemorrhages elsewhere, may cause
quickening, slowing, or irregularity in the breathing,
or the peculiar rhythmical variation called the
"Cheyne- Stokes'" breathing may be present, in
which the pulse is often quick during the period of
apnoea, and slow during the period of dyspnoea.
"Cheyne-Stokes'" breathing is a sign of great gravity,
and is in the great majority of cases a forerunner of
death. I have seen recovery where this modification
of the breathing had been present both in uraemia
and cardiac cases. A man was recently in the Queen's
Hospital suffering from aortic regurgitation and
dyspnoea, the respiration being of the " Cheyne-
Stokes'" type. His breathing became normal as
his condition improved, and when he was discharged
all respiratory trouble had disappeared. He died
suddenly, however, a few weeks after. I have
observed " Cheyne-Stokes ' " breathing in cases of
cerebral haemorrhage, tumour, and tubercular men-
ingitis. In various forms of heart disease and in
uraemia it is frequently met with.
72 SYMPTOMS OF BRAIN DISEASE.
Coma. — Coma is a symptom frequently present
in coarse brain disease. In coma the loss of function
is from the highest to the lowest, the mental processes
being first affected, the automatic and purely reflex
centres continuing in action and being lost late.
There is loss of power over the sphincters.
Stupor is incomplete coma, in which the
reflex actions and the power of swallowing are
preserved, and the patient may put out his
tongue when told to, but is unable to carry on any
conversation.
In deep coma the pupils may be widely dilated
and immobile. Loss of the conjunctival reflex, or loss
of the power of swallowing and the presence of stertor,
are of grave omen. Any sudden lesion of the brain
may occasion coma, but haemorrhage is by far the
most common cause ; hence the term ." apoplexy " is
generally used to indicate haemorrhage, although
this condition, which strictly means the sudden onset
of unconsciousness, is much more common in epilepsy,
and rarely present in cerebral haemorrhage. In the
diagnosis of cerebral haemorrhage as the cause of
coma we must carefully examine for any paralytic
symptoms, such as dilatation of one pupil, conjugate
deviation of the eyes, alteration of the reflexes on
one side of the body. The pulse is generally slow
and full and the breathing slow, occasionally of the
''Cheyne-Stokes'" type ; this form of respiration and
irregularity of the pulse are of fatal omen in cerebral
haemorrhage.
SYMPTOMS OF BRAIN DISEASE. Jl
In the diagnosis of coma we shall have to bear
in mind all the other causes of this condition, such
as uraemia, diabetes, alcohol, opium, epilepsy, and
hysteria. In all doubtful cases we ought to draw
off and examine the urine, and use the stomach
pump. The presence of albumen might lead you to
consider the case as one of uraemia, while it really
might be one of cerebral haemorrhage ; but uraemic
coma is rarely complete, and is usually characterised
by great restlessness. Hemiplegia may occur in
uraemia, and, coinciding with coma, may exactly
simulate cerebral haemorrhage. Chauternesse and
Tenneson in the " Revue de Medicine," November,
1885, relate cases of partial epilepsy and hemiplegia
in Bright's disease.
I recently had under my care in the workhouse
infirmary a man, 40 years of age, with cardiac
hypertrophy, a pulse of high tension, and with slight
albuminuria. The albumen was not present con-
stantly, but was often absent for weeks. He was
admitted in a semi-comatose condition, with right
hemiplegia, and after being bled he quickly recovered
consciousness, the hemiplegia also quickly passing
off. After his admission he had five similar attacks,
which were always preceded by mental symptoms,
delirium, and restlessness, and by violent convulsion
of the right side of the face, right arm and leg, and
conjugate deviation of the eyes to the right. Now,
these attacks could not be due to haemorrhage, for
recovery was complete within a few hours of Kls
74 SYMPTOxMS OF BRAIN DISEASE.
being bled, and they are best explained by the
supposition that they were due to local oedema of
the brain, as has been proved by Chauternesse and
Tenneson in their own cases.
In uraemia, convulsions usually precede coma,
and recur frequently during its continuance. At the
onset of apoplexy a convulsion may occur, but is
usually single and not repeated. In uraemia the
temperature is always depressed ; in apoplexy the
temperature falls at first, but there is usually some
increase later on. Elevation of temperature would
negative uraemia. The diagnosis is of the highest
importance, since the treatment for uraemia is one of
active interference, while the treatment for apoplexy
is one of non-intervention.
In coma, as I have previously stated, the eye-
balls are divergent ; this I have found a constant
symptom, and one that might be useful in detecting
cases of hysteria and malingering.
Headache. — Headache is a symptom produced
by many causes apart from organic disease of the
brain. The pain of organic brain disease is usually
very severe, constant, and diffused.
In migraine and hysterical headache the pain
may often be, as the patients say, covered with a
finger. Headache should always attract our atten-
tion to the eyes, errors of refraction being a common
cause, especially hypermetropia and astigmatism. In
obstinate cases always examine the urine for albumen,
and the fundus oculi for optic neuritis or retinal changes.
SYMPTOMS OF BRAIN DISEASE. 75
The following forms of headache may be
distinguished : —
I. — The anaemic ' headache ; relieved by the
recumbent, exaggerated by the upright posture.
2. — The congestive headache ; aggravated by
the recumbent posture.
3. — Clavus, or hysterical headache ; the pain
being frequently limited to one spot, so that it can
be covered by the finger.
4. — The toxic headache; caused by alcohol,
tobacco, uraemia, &c. ; may be frontal or occipital.
5. — The febrile headache, occurring in typhoid
and other fevers, usually frontal.
6. — The rheumatic headache, accompanied with
tenderness of the scalp.
7. — The gouty headache.
8. — The dyspeptic headache, which is generally
frontal.
9. — The syphilitic headache, which is very
severe, especially at night, often causing transient
mania at this time.
10. — The headache of organic brain disease,
which is usually very severe, diffuse and constant.
II. — Hemicrania, migraine, periodical, or sick
headache. In the attacks, of which we can dis-
tinguish three stages, in the first stage ocular distur-
bances occur, such as hemianopia and scintillating
scotoma ; occasionally also other sensory and motor
affections are present, such as deafness, aphasia,
transitory paresis of one limb or of some oculax
76 SYMPTOMS OF BRAIN DISEASE.
muscle ; the second stage of the attack is marked by
headache, which is gradual in its onset, very severe
and localised, and followed by the final stage of
nausea and vomiting, after which the patient rapidly
recovers. In the intervals, the subjects of this
neurosis are usually quite free from pain and
perfectly well.
Vertigo^ or Giddiness, — In this condition the
patient feels uncertain as to his position with regard
to surrounding objects, sometimes seeming to move
himself (active vertigo), sometimes feeling as if
objects were moving round him (passive vertigo).
Vertigo is constantly associated with impairment of
equilibriation, the patient usually falling or staggering
in the direction in which there is a subjective sense
of falling. The power of equilibriation is guided and
depends upon impressions derived from the periphery
that give information as to the relation of the body
to surrounding objects. The senses which subserv^e
equilibriation are touch, sight, the muscular sense,
together with special organs, the semi-circular canals
of the internal ear. Sight is especially important in
guiding equilibriation, a patient suffering from loco-
motor ataxy in an advanced stage being quite
helpless when his eyes are shut. Recent ocular
paralysis is attended with severe vertigo.
Flourens first discovered the function of the
semi-circular canals, and showed that animals lost
their power of equilibriation after section of these
organs. More recently Goltz and Cyon have
SYMPTOMS OF BRAIN DISEASE. 77
shown that it is the pressure of the endolymph
within these canals that gives rise to sensory impres-
sions which inform us as to the position of our heads
in space. If an), of these sources, namely, the ocular
muscles and vision, the semi-circular canals, &c., from
which we derive our information as to the position of
our body in space, be disordered, vertigo results.
Before we conclude that vertigo is due to
organic brain disease, we must exclude ocular defects
and disease of the middle and external ear ; we must
also exclude stomach disorder, the pneumogastric
nerve being intimately concerned with equilibriation.
Vertigo is common in uraemia and in disturbances
of the cerebral circulation, and is frequent in
minor epilepsy, sometimes constituting the entire
attack.
Meniere's disease, or labyrinthine vertigo, is
characterised by three symptoms, viz. : — (i) Vertigo,
which is severe and paroxysmal ; (2) tinnitus, and
(3) deafness ; but it is important to remember that
all these symptoms may be caused by accumulations
in the external meatus. The symptoms of Meniere's
disease may be caused by a blow on the head, being
probably due to haemorrhage into the semi-circular
canals. I had such a case recently in the Queen's
Hospital. It is important also in all cases of vertigo
to examine the nasal cavities for polypus or other
disease. In locomotor ataxy, vertigo may be present^
but usually only when there is paralysis of the
ocular muscles.
78 SYMPTOMS OF BRAIN DISEASE.
Vertigo arises from a great variety of intra-
cranial conditions, but it is most constantly associated
with cerebrellar disease, especially with disease of the
middle peduncle of this body. In disease of the
pons, of the corpora quadrigemina, or of the crura
cerebri, vertigo is often present. It is a common
symptom in cerebral anaemia and congestion. I find
that vertigo is very common in old people, and in
those affected with it the arteries are always markedly
degenerated. The bromides and hydrobromic acid
relieve such cases. Dr. Handfield Jones has recom-
mended the bichloride of mercury in small doses for
senile vertigo. Vertigo may be produced by psychical
causes, and also from toxic causes, such as tobacco
and alcoho).
A curious form of vertigo, called agoraphobia,
is sometimes met with, the subjects of this affection
experiencing giddiness whenever they attempt to
cross a wide market place or a road, while they can
walk quite well in a narrow passage, or when they
keep on the footpath. Westphal described this
variety of vertigo in 1872. I have met with it in
myxoedema in one instance, and have known it to
occur after childbirth where there had been con-
siderable loss, the patient being seized with intense
vertigo, and falling whenever she attempted to go
out of doors, but being quite well while indoors.
Deliritim, — Delirium, a perversion and excess of
mental activity, in contrast with stupor in which there
is diminution of mental activity, is frequently observed
SYMPTOMS OF BRAIN DISEASE. 79
in all conditions which cause defective nutrition of the
brain. It is essentially the same as insanity, but the
term delirium is used when the mental condition is
evidently secondary to and depends upon some
organic disease of the brain, or on some morbid state
of the blood. We rarely get fixed delusions, and
the patient is usually more incoherent than in
insanity. Pyrexia is a far more common cause of
delirium than organic brain disease. In all cases of
delirium, then, take the temperature, and if there is
fever carefully search the chest and abdomen for
signs of disease.
It is well known that people addicted to
alcohol are rendered delirious by slight causes.
Pneumonia in drunkards is nearly always accom-
panied with early delirium, and occurs frequently
without fever.
Hallucinatio?is, illusions, and delusions are
varieties of perverted consciousness. We may have
hallucinations of hearing, of vision, of taste and
touch, the patient hearing voices, or seeing things
which have no objective existence whatever, in fact
hallucinations are entirely subjective. Hallucinations
of hearing are very dangerous, the patient hearing
his neighbours abusing him is apt to resort to
violence. Illusions are incorrect interpretations of
objects which do exist, a patient mistaking the nurse
for his wife, for example. Hallucinations and illu-
sions, then, refer to the special senses ; delusions are
insane ideas of any kind.
8o SYMPTOMS OF BRAIN DISEASE.
Mental debility is markedly present in many
acute diseases, as well as in softening and various
degenerative diseases of the brain and after apoplexies.
The faculty of attefition may be impaired, and
memory may be lost ; loss of memory for recent
events is especially characteristic of general paralytic
dementia.
Apoplectiform attacks occasionally occur in the
course of the chronic degenerative diseases of the
brain, namely, in general paralysis of the insane,
and in multiple sclerosis. There is usually con-
siderable fever during these attacks. They come on
suddenly, and may last for days ; weakness of one
side of the body may remain for a few days after
the attack, soon, however, passing ofif. Aphasia may
also be present. The cause of these attacks is not
known, but in all probability they are due to local
oedema of the brain, similar to what Chauteraesse
and Tenneson have described as the cause of uraemic
epilepsy and hemiplegia.
Convulsions, — These spasmodic movements are
frequent in diseases of the brain ; they are supposed
to depend upon an abnormal discharge from unstable
grey matter.
Convulsions may be partial or general. In
children, the common cause is reflex irritation, or
the circulation of unhealthy blood through the
brain, as in uraemia, or at the commencement of
fevers. The prognosis is far more favourable in
children than in adults. Convulsions in children
SYMPTOMS OF BRAIN DISEASE. 8 1
may be due to irritating lesions of the brain, such
as tubercular meningitis, or to increase of the intra-
cranial pressure, as in chronic hydrocephalus. Sud-
den lesions of the brain, such as haemorrhage or
softening, are apt to be attended with convulsions.
General convulsions have no localising value. The
partial or local convulsions indicate disease in or
near the motor centres of the cortex. When organic
brain disease is present a trivial cause may excite
convulsions. Irritating and progressive lesions any-
where in the brain, but especially when in or near
the cortex, may cause convulsions. Stationary lesions
only cause convulsions when in or close to the
cortex.
In all cases of convulsion we should carefully
look for symptoms of organic brain disease and
examine the fundus oculi, and also exclude uraemia,
before concluding that the case is one of epilepsy
or due to reflex irritation.
Deafness may be caused by disease of the audi-
tory centres in the superior temporo -sphenoidal
convolutions, but this is rare ; more commonly it
is due to lesions of the auditory nerve itself beyond
its superficial origin. By means of the tuning fork
we can generally distinguish between deafness due
to lesions of the nerve and that due to mischief in
the conducting apparatus.
In all cases of deafness or of tinnitus the
external auditory meatus and the Eustachian tube
should be examined. Deafness from disease of the
82 SYMPTOMS OF BRAIN DISEASE.
nerves of hearing is often observed in the subjects
of inherited syphilis.
Occasionally hearing is lost in some people
during periods of mental excitement. Deafness of
nervous origin is observed in the course of and
after specific fevers, as typhus, typhoid, and mumps.
Tremor, — The division of the various forms of
paralysis into the atrophic and spasmodic varieties
is an important one. In paralysis from cerebral
lesions and in that due to lesions of the lateral
columns of the cord, spasm is a prominent feature
sooner or later. In paralysis due to lesions of the
anterior cornua of the cord, or to lesions of the
peripheral nerves, flaccidity with wasting is present.
Tremor is the mildest form of clonic spasm ; it
consists of slight contractions of particular muscles
or groups of muscles, causing a rhythmical oscilla-
tion of the limbs and trunk.
Tremor is observed in various pathological
conditions, as for instance: — In (i) alcoholism, (2)
debility, (3) mercurialism, (4) plumbism, (5) hysteria,
(6) multiple sclerosis, (7) paralysis agitans, (8) sen-
ility, (9) post- hemiplegia, (10) in all cases in which
the pyramidal tracts are the seat of disease or are
compressed. A tumour anywhere in the region of
the pyramidal tracts either in the brain or cord may
cause tremor, so that this symptom is one of con-
siderable localising value. (\\) Tremor of the
facial muscles and tongue is a constant feature of
general paralytic dementia. The tremor of multiple
SYMPTOMS OF BRAIN DISEASE. 83
sclerosis is coarser than that of paralysis agitans and
affects the head and trunk, the body during walking
being frequently lurched to one side, while the head
is held stiffly. The tremor in the former disease,
moreover, ceases when the muscles are at rest, being
present only during exertion.
Fibrillary Contractions consist of alternate con-
traction and relaxation of individual bundles of
muscular fibres visible under the skin. These are
usually present in progressive muscular atrophy, in
which disease they are readily evoked by filliping
the skin.
Fibrillary contractions • are, however, by no
means confined to this disease, but they are readily
evoked in all wasting diseases, the irritability of the
muscles in such diseases being exalted In phthisis
and in the typhoid state they are constantly present.
Cramp is a form of tonic spasm, causing painful
contractions of a muscle or group of muscles. It
most commonly affects the calf muscles after excessive
exertion. The cramps of diarrhoea, cholera, and
tetanus are well known ; severe cramps are also
present in extra-medullary growths, implicating the
nerve roots. I have such a case in which the cramps
can only be relieved by large and frequent hypo-
dermic injections of morphia.
Contracture, — By this term is meant any persis-
tent shortening of a muscle or group of muscles,
occasioning persistent deformity.
84 SYMPTOMS OF BRAIN DISEASE.
Contracture may be due : —
I. — To changes in the muscles themselves —
myopathic contracture.
2. — To paralysis of a group of muscles, their
opponents contracting, and ultimately causing con-
tracture — paralytic contracture.
3. — To spasm of a group of muscles, their oppo-
nents not being paralysed, but being overcome.
4. — To hysteria.
Whenever the origin and insertion of a muscle
remain approximated for a considerable time the
muscles become permanently shortened, causing con-
tracture. The contracture accompanying the late
rigidity of hemiplegia is well known. In hysteria,
contracture may accompany paralysis, or may exist
by itself, affecting any limb. These hysterical
contractures may last for years, and then suddenly
cease.
I have met with several cases of hysterical
contracture, and have found them most difficult cases
to cure.
In all cases a careful examination must be made,
in order that no mistake as to its hysterical nature
occurs.
Affections of Speech. — Aphasia,
Mental processes may be expressed (i) by
speech, (2) by writing, and (3) by gesture.
The expression of mental processes by gesture
is the most simple and elementary, and is the first
N
SYMPTOMS OF BRAIN DISEASE.
to be acquired by the child ; but it has little value it
expressing propositions, being more especially used
in expressing the emotions.
The faculty of speech is not innate, but is
acquired with difficulty and after much trouble.
A child understands what is said to him long
before he can speak, the sensory processes being
developed earlier than the motor.
Language possesses a subjective or sensory
aspect, and an objective or motor aspect.
Impressions derived from the eye, from the
ear, and the other senses ; but more especially from
the ear, are essential to the acquirement of speech.
If a child either before or shortly after it has
learned to speak becomes deaf, it becomes mute also.
Complete loss of speech, however, from defect in
the peripheral sensory organs, is rare, for a deaf mute
may be taught to speak by gesture.
The impressions derived from the organs of
special sense are reduced to order in the cortex.
The following diagrammatic scheme (Fig. 12,
page S6)y used by Dr. Grainger Stewart, will help
you to understand the main facts to be known about
aphasia.
The seeing centre is situated in the occipital
convolutions, and possibly in the angular gyri also.
The word-seeing centre is situated in these
convolutions on the left side of the brain. A
lesion, softening or tumour, of these parts causes
word-blindness, the patient being ur\^.b\^ \.o x^-^A -a.
y
86
SYMPTOMS OF BRAIN DISEASE.
o-a
SYMPTOMS OF BRAIN DISEASE. 87
letter, or to name any object he sees; though he may
be able to write and talk, but usually incorrectly.
The hearing centre is situated in the superior-
temporo-sphenoidal convolutions, and the word-
hearing centre in the same convolution on the left
Fig. 13.
Diagram of Probable Course of Fibres from Motor:
Speech-Centre (Gowers).
A., hand centre ; A. ;//., fibres from this to internal capsule ; S.,
motor speech-centre; S. C, fibres from this to corpus callosum ;
and S.m.f to the internal capsule; S.A., fibres from speech-centre
to hand centre. A lesion at m. m. causes transient aphasia only ;
the speech processes being able to pass by S. C. A lesion at x
causes permanent aphasia, since it involves both the fibres to the
corpus callosum and internal capsule, but would not abolish expres-
sion by writing, the fibres S.A. (connecting the speech and hand-
centres) escaping.
side. A lesion in the superior-temporo-sphenoidal
convolution on the left side causes word-deaf 7iesSy
the patient being unable to understand anything that
is said to him, although he is not deaf to sounds.
88 SYMPTOMS OF BRAIN DISEASE.
The posterior portion of the third frontal con-
volution and the lower part of the ascending frontal
convolution contain the centres for the muscles con-
cerned in articulation. Motor processes for words
leave the cortex in this region on the left side. The
left side of the brain in right-handed people, and
the right side in left-handed people being chiefly
concerned with voluntary speech.
According to Hughlings Jackson the right hemi-
sphere is concerned only with emotional and auto-
matic utterances.
A lesion of the operculum causes motor
aphasia, the patient being able to understand what
is said to him and to read, but being unable to speak
or to write. When the lesion is in the sensory part
of the cortex, there being word-deafness and word-
blindness, the aphasia is called sensory. Disease of
the convolutions of the operculum, or immediately
beneath them, causes permanent motor aphasia. But
if the lesion is some distance below the cortex the
aphasia may pass off, the left convolutions being
then able to communicate with the nerves of arti-
culation through the right hemisphere by the corpus
callosum. If, however, a lesion damages the fibres
of the corpus callosum which connect the third
frontal convolutions of the two sides; as well as those
which connect the third left frontal convolution with
the internal capsule; then permanent aphasia, simi-
lar to that produced by destruction of the third left
frontal convolution, is produced.
SYMPTOMS OF BRAIN DISEASE. 89
Occasionally in motor aphasia, a patient may
be able to express himself by writing, though he
cannot do so in words (aphemia). In this case the
lesion has not destroyed the speech centre, or the
fibres from it to the hand centre, but has interrupted
the connection between the speech centre and the
motor tract, and its connection with the opposite
frontal convolution. Loss of memory of words (verbal
amnesia), there being great difficulty in naming
objects, is always present where there is word-
deafness or word-blindness, and is much more
frequent in sensory than in motor aphasia. Intelli-
gence is nearly always affected in sensory, less
commonly so in motor aphasia.
The term "dysarthria" is used when the defect
in speech is due to defects of articulation, and must
be carefully distinguished from true aphasia.
Cases of Aphasia.
Case i. — Sensory Aphasia due to Embolism
(Word-blindness and Word-deafness). — R. S., aged
19, a stamper, was admitted on September 26th,
1885, suffering from what was said to be "brain
fever." Six years previously he had suffered from
rheumatic fever, but had since remained well up to
September 2 ist, except for occasional attacks of severe
pain in the chest (angina). On this date, while at
work, he was suddenly affected with pain in the head,
and it was noticed that he talked nonsense. He was
taken home, but his friends could not understand
90 SYMPTOMS OF BRAIN DISEASE.
him, neither could he understand them. He put up
his hand to the left side of his head, and made signs
of being in pain there. On examination, double
aortic and mitral systolic bruits with considerable
cardiac hypertrophy were found. The second sound
was replaced by a diastolic bruit. Capillary pulsation
was observed. The patient did not answer questions,
but continually put his hand to the left side of his
head. Verbal deafness was complete ; when told to
hold up his arm he put out his tongue, and answered
questions by saying, " I can't hardly think of it,
hardly," which he frequently repeated. He talked
a great deal, but used wrong words, and little sense
could be made out of what he said. At the same
time he acted in a perfectly rational way, was quiet,
and understood signs to take his food. He under-
stood nothing printed but figures and letters ; figures
he easily recognised and could add them together
correctly (the knowledge of figures being greatly
automatic). He could spell words aloud, but evi-
dently did not understand their meaning. He could
write his name, but nothing else ; could copy from a
book, but did not understand what he wrote ; could
not copy from dictation. He had great difficulty in
naming objects and always described them. When
showed an ^^'g he could not name it, but pointed to
the fire and said " it takes about two minutes." He
assented when the proper name was mentioned to
him, but could not repeat the name. When shewn
a leaf, he said, "It grows;" "Will do for a Sunday;"
SYMPTOMS OF BRAIN DISEASE. 9 1
and similarly with many other objects. He signed
an I.O.U. for ;^ioo, and allowed me to take it with-
out showing in the slightest that he understood
what he had done. The temperature was raised to
loi*^ Fahr. (due to softening). There was no hemi-
plegia, but slight paresis in the buccal region of the
right side of the face. The case was a typical one
of sensory aphasia, there being loss of understanding
of spoken and of written language, loss of faculty of
repeating words, of writing to dictation, and of
reading aloud ; with preservation of power of writing,
copying words, and of volitional speech. The lesion
was in all probability in the area of distribution of
the posterior terminal branches of the left middle
cerebral artery, and due to embolism ; the convolutions
affected being the supra-marginal or angular and the
superior-temporo-sphenoidal. The patient improved
daily, being able to name objects, which the day pre-
viously he had failed to name. It was noticed that
when asked to name an object, he would look in a
book till he came to the name in print and then would
be able to say it. On October 29th the patient was
much better. He understood all that was said to
him ; could read short sentences, but failed to under-
stand many words ; he was quite unable to copy
from dictation, except monosyllables, and still
suffered from considerable difficulty in naming
objects. His mother informed me that before his
illness he could read well and had taken prizes at
his Board school.
92 SYMPTOMS OF BRAIN DISEASE.
Case 2. — Word-deafness, — J. M., a man, aged
70, when seen in July, 1885, complained of tinnitus
in the left ear, deafness, vertigo, and falling to
the left side. He had had two slight attacks of
hemiplegia on the right side, which had quickly passed
off. There was no albuminuria, but the arteries were
very extensively diseased. On October 15th he
asked the nurse to let him see the doctor, as he did
not feel well, and had pain in the left side of the head.
When the resident medical officer saw him he found
that the man could not answer any questions. I
discovered that the patient suffered from complete
word-deafness ; he could not understand anything
that was said to him, but spoke rationally and freely.
He could read and understood what he read, and
could copy from print, evidently understanding what
he copied. He could hear when spoken to but could
not understand. Verbal amnesia was also present ;
he could name none of the several articles shown
him, but described them well. The next day the
verbal deafness had passed off, and he understood
what was said to him, and could name various
articles. The case is interesting in connection with
the symptoms of Meniere's disease previously ob-
served, and indicates that they were probably due to
central mischief The lesion was in all probability
thrombosis of the branch of the left middle cerebral
artery to the superior-temporo-sphenoidal convolu-
tion.
CHAPTER IV.
THE DIAGNOSIS OF THE SITUATION
OF THE LESION IN DISEASES OF
THE BRAIN.
*- —
In the diagnosis of the situation of the lesion in
diseases of the encephalon, an intimate acquaintance
with the anatomy and physiology of the brain is
essential.
The brain is remarkably tolerant of disease ; a
large tumour or abscess may be present without
symptoms, unless it be situated directly in or near the
motor or sensory tracts.
In acute lesions, such as haemorrhage and em-
bolism, we must wait till indirect symptoms have
passed off, before we can accurately localise the
mischief.
The prcefrontal area of the brain, that portion
in front of the ascending frontal convolutions, is
psychical in function ; a lesion may exist here
without causing any symptoms, but psychical changes
are often present.
Lesions of the orbital surface of the frontal lobes
are usually latent.
94 SITUATION OF THE LESION.
I recently had a man under my care with frontal
headache and stupidity gradually deepening into coma,
without any motor or sensory paralysis. Tenderness
on percussion existed in one spot over the frontal
bone, and the post-mortem examination revealed a
gumma of the surface of the brain immediately under
this spot.
In general paralysis of the insane the greatest
changes are found in the praefrontal area.
A lesion of the motor region of the cortex causes
motor paralysis, depending upon the centre affected.
Convulsions are exceedingly common, the grey
matter of the convulsions being less tolerant of
disease than the white matter of the brain. Disease
of one centre causes irritation in neighbouring centres,
and convulsions in the limbs may result from disease
near but not actually in the motor region.
Local paralysis is a more certain indication of
the exact situation of the lesion than are convulsions,
though usually, when convulsion attacks the whole of
one side of the body, it commences in the limb in
whose motor centre the lesion is situated. Irritative
lesions of the motor area of the cortex are characterised
then by unilateral convulsions or monospasms. The
pathology of these spasmodic affections w^as first
clearly recognised by Dr. Hughlings Jackson, who,
from the study of these partial epilepsies, first
suggested the existence of motor centres in the
cortex ; hence the term " Jacksonian epilepsy."
SITUATION OF THE LESION. 95
There may be brachial, crural, facial, oculo-
motor, or lingual convulsion. In the oculo-motor
form there is conjugate deviation of the eyes and
rotation of the head and neck.
These cases of Jacksonian or partial epilepsy
are distinguished from ordinary epilepsy by the
following features : — -
I. — The convulsions are limited to one limb,
or rather always begin in one limb, though they
may ultimately spread all over the body.
2. — An aura is always present and is very
distinct.
3. — Consciousness is either not lost or is lost
late in the attack, after the convulsions have become
general.
It is the local commencement of the convulsion
that is especially characteristic. These partial epi-
lepsies are of great localising value, they indicate
organic disease in or near the motor region of the
cortex, either softening or tumour. It is in these
partial epilepsies that we can often check the
progress of the attack by painting a ring of iodine
or blistering fluid just above the extremity whence
the aura starts.
For exact localisation of a tumour in the motor
region of the cortex three factors are required : —
I. — Lx)cal persisting paralysis.
2. — Local epileptiform convulsions.
3. — Double optic neuritis.
SITUATION OP^ THE LESION.
It is only in this region of the brain that surgical
incx^.ference with cerebral tumours is likely to prove
successful.
Extensive disease of the outer surface of the
hemisphere may cause hemianaesthesia, but this is
/ never complete.
A lesion of the angular gyrus probably causes
crossed amblyopia ; and if on the left side it causes
word blindness also.
A lesion of tJie occipital lobe causes hemianopia
towards the opposite side. Irritating lesions cause
convulsions, which may commence with a visual
I
aura referred to the opposite eye.
A lesion of the superior-temporo-sphenoidal con-
volution on the left side causes word-deafness, but
there is not absolute deafness unless the convolutions
on both sides are diseased.
A lesion of the centrum ovale causes symptoms
like those brought about by disease of the corres-
ponding portion of the cortex, except that Jacksonian
epilepsy is not present, the symptoms varying with
the seat of the lesion, and the fibres injured.
If aphasia is present, it is transitory unless the
disease is immediately beneath the cortex, so that the
fibres crossing by the corpus callosum from the third
left frontal convolution to its fellow on the opposite
side are interrupted.
\ A lesion of the corpus striatum^ if the grey matter
only is affected, causes no lasting symptoms. It is
SITUATION OF THE LESION. 97
only when the internal capsule is affected that hemi-
plegia is produced.
A lesion of the optic thalamus also causes no
symptoms unless the capsule be affected, or the crus
compressed. Cases of athetosis have been published
where the lesion was located in the optic thalami.
In a child, who presented the usual symptoms of
cerebral tumour, slight hemiplegia on the left side,
with tremor of both upper limbs on effort was
observed during life. At the autopsy caseous
encapsuled masses were found in each optic
thalamus ; the paresis and tremor being due to
pressure on the motor portions of the internal
capsules.
A lesion of the corpora qtiadrigemina does not
cause loss of sight, but loss of ocular movements,
especially of the upward movement of the eyes and
elevation of the lid. (Gowers.)
A lesion of the pons causes alternate or crossed
paralysis. Since the facial nerves decussate about
the centre of the pons, a lesion in the upper part
of the pons will cause paralysis of the face and
hemiplegia on the opposite side, but a lesion of
the lower half will cause paralysis of the face
on the same side and hemiplegia on the opposite
side.
In tumours of the pons not only the facial but
the fifth and sixth nerves may be paralysed on the
side of the lesion, there being hemiplegia on the
opposite side.
/
98 SITUATION OF THE LESION.
In haemorrhage into the pons and other acute
lesions of the upper portion of this body the pupils
are often strongly contracted from irritation of the
nuclei of the third nerves.
If the lesion be in the centre of the pons there
is bilateral hemiplegia, but generally little loss of
sensation, the sensory tract being deeper. In a lesion
of the lateral half of the pons, causing hemiplegia on
the opposite side, conjugate deviation of the eyes
towards the paralysed side may be present from
paralysis of the sixth nerve on the side of the lesion.
While in lesions of the internal capsule, the con-
jugate deviation is away from the paralysed side.
A tumour outside tlie medulla may paralyse the
hypoglossal, spinal accessory, and glossopharyngeal
nerves on one side ; and by pressure on the anterior
pyramid cause hemiplegia on the opposite side.
Acute bulbar paralysis from haemorrhage or
softening is usually rapidly fatal ; there being
paralysis of the lips, tongue, palate, pharynx, and
larynx.
A lesion of the middle peduncle of the cerebellum
causes intense vertigo, nystagmus, and forced move-
ment of the trunk on its longitudinal axis. Accord-
ing to Gowers, disease of the lateral lobes of the
cerebellum, per se, causes no definite symptoms, and
staggering does not occur unless the middle lobe is
compressed. The gait of cerebellar ataxy is reeling
like that of drunkenness, the feet being placed wide
apart. If the lesion is in the right lateral lobe the]^
SITUATION OF THE LESION. 99
patient staggers to the right side, if in the left lobe j
to the left side, if in the median lobe he staggers
either forwards or backwards. Vertigo, vomiting,
and double optic neuritis are almost invariably
present.
A tumour of the cerebellum is apt to compress
the veins of Galen, or to press on the side of the
pons and cause hemiplegia with or without paralysis
of the fifth and sixth nerves. These symptoms are
of value in localising the growth. Loss of the knee
jerk has been observed in cases of cerebellar tumour.
I have observed its loss in two cases.
Tumours of the middle lobe of the cerebellum j
are apt to cause tonic spasm of the spinal muscles, \
the head being drawn back and fixed, **^the cerebellar \
rigidity " of Hughlings Jackson.
Convulsive seizures are common in cerebellar
tumour, as also is tremor of the limbs.
Tremor or other form of spasm may be caused by
pressure on the pyramidal tracts and is a sign of
considerable localising value in tumours of the
encephalon.
I recently saw a child with tremor of both upper
extremities on exertion. Now both pyramidal tracts
must have been compressed, and the only situation in
which one lesion could cause bilateral tremor is either
in the pons or in the cerebellum. On investigation
I found that there had been vomiting and headache,
and the child had a staggering gait, the case being
one of cerebellar tumour.
lOO SITUATION OF THE LESION.
In lesions of the internal capsule in its posterior
half the hemiplegia which occurs is accompanied with
paralysis of the face and tongue, and this is the case
also when the lesion is in the crus or pons. If the
face and tongue escape, the disease is probably in the
cortex. In monoplegia due to brain disease the
great probability is that the seat of the mischief is in
the cortex, though as I have already stated it may be
in the internal capsule, the fibres from each centre
remaining separate. Hemiplegia with well-marked
hemianaesthesia and hemianopia indicates disease of
the posterior portion of the internal capsule, and
damage to the corpus geniculatum or optic
thalamus.
Paralysis of both sides of the tongue is usually
due to disease of the nuclei in the medulla and the
lips suffer with the tongue.
In paralysis of the face; if (i) only the lower part
is affected and there are (2) no electrical changes,
and (3) no loss of conjunctival reflex, the lesion is
above the nucleus and probably cortical ; otherwise
the lesion may be in the nucleus, in the pons or any-
where in its course beyond its superficial origin.
Bilateral facial paralysis is sometimes met with
but it is very rare. I lately saw a case under the care
of Mr. Oakes, of this town, in which first one side of
the face and then the other was paralysed, the lesion
being evidently peripheral on both sides. A tumour
at the base of the brain in the region of the pons
might cause bilateral facial paralysis. But it may be
SITUATION OF THE LESION. lOI
produced by exposure to cold or by the other causes
of neuritis.
Paralysis of the fifth and sixth nerves generally
indicates disease outside the pons ; but I lately
removed a brain with a glioma of the right half of
the pons where the conjunctiva was insensitive
on the right side and the right sixth nerve was
paralysed.'
Paralysis of the sixth and facial nerves^ according
to Gowers, means disease within the pons. Paralysis
of one ocular nerve generally means disease at the
base of the brain. Bilateral paralysis of the ocular
nerves means disease of their nuclei.
Crus cerebrL — Lesions of or near the crus cerebri
are apt to cause what is called a crossed paralysis,
there being hemiplegia and facial paralysis on the
opposite side with paralysis of the third nerve on the
same side. Hemianaesthesia may also be present if
the tegmentum or deeper portion of the crus be
implicated. Paralysis of the third nerve with hemi-
plegia of the same side cannot result from a single
lesion.
By crossed or alternate hemiplegia is meant
hemiplegia on one side of the body with paralysis
of a cranial nerve on the opposite side. It is apt
I
to occur — j
I. — In lesions of or near the crus cerebri. \
2. — In lesions of the pons, or outside the pons
but compressing it. /
3. — In lesions near the medulla.
I02 SITUATION OF THE LESION.
Cerebellar growths may compress and paralyse
the hypoglossal and other nerves passing from tb.e
medulla and at the same time compress the pyramidal
tract of the medulla. . The body is thus affected on
the opposite side ; the nerves on the same side. A
cerebellar growth may also compress one lateral half
of the pons causing hemiplegia on the opposite side ;
and at the same time by compressing the fifth nerve
paralyse it on the same side.
Cases of Alternate Hemiplegia.
Case i. — Right hemiplegia, with complete facial
paralysis on the right side, and paralysis of the third
nerve on the left.
George Wood, aged 51, a soldier, was admitted
into the Infirmary on the 9th of January. His
previous history cannot be obtained fully, the patient's
memory being defective. He said that he had gone
through twenty years' service in the Royal Artiller}-
in India ; that he had had syphilis ; and that six
months before admission he had had a stroke on the
right side.
There was paresis of the right arm and leg, and
the toes scraped the ground in walking. The muscles
responded to both Faradic and Galvanic currents, but
the intensity of the contractions was below normal.
There was paralysis of the right half of the soft palate,
the uvula pointing to the left, and the faucial pillars
were broader on the right than on the left. There
was also slight dysphagia from the affection of the
SITUATION OK THE LESION. IO3
palate. The deep reflexes on the right side were
increased. The patient retained his faeces but had no
control over his bladder.
There was complete facial paralysis on the right
side ; absence of conjunctival reflex ; and not the
slightest response to cither Galvanism or Faradism.
Sensation was perfect. There was no alteration
in hearing. There was paralysis of the third
nerve on the left side, as shown by external
strabismus, ptosis, and dilatation with immobility
of the pupil.
There were no changes in either fundus. The
patient was very quiet, in a somnolent condition, and
answered questions decidedly slowly ; but there
seemed to be no intellectual impairment except slight
loss of memory and slowness in comprehension. The
patient lived for a few weeks, gradually becoming
more feeble and indifferent ; and before his death,
conjunctivitis and sloughing of the cornea occurred.
He died quietly from asthenia.
He was treated with iodide of potassium in large
doses, and highly nutritious food. The disease was
considered to be syphilitic. The facial paralysis was
evidently peripheral. The right hemiplegia with
paralysis of the left third nerve was undoubtedly due
to some lesion in the neighbourhood of the left crus,
implicating the lower and inner fibres (crust) of the
crus, and the third nerve beyond its superficial origin.
Autopsy. — The head only ivas examined. The
dura mater was tense and could not be pinched up.
I04 SITUATION OF THE LESION.
Over the frontal and left parietal lobes it was thickened
and blended with the other membranes, and could
not be separated except by tearing away the brain
substance. The dura was also adherent along the
margins of the longitudinal fissure. The arachnoid
was opaque, with excess of fluid beneath it ; the
veins of the pia turgid, and the cerebro-spinal fluid
increased in quantity. A yellowish caseous mass
was found around the internal auditory meatus, com-
pressing the facial nerve, and apparently arising from
the dura. A nodule about the size of a marble,
yellow and soft, was also found on the left side on the
edge of the tentorium, projecting from its under
surface, and in a situation to compress the left crus
(and left third nerve) as it passed through the
opening in the tentorium. Two nodules were also
found close together, situated in the posterior
extremity of the right superior temporo-sphenoidal
convolutions. There were two small cysts at the
genu and posterior third of the internal capsule on
the left side, with yellowish contents ; these were
probably the remains of small haemorrhages
The autopsy completely explained and cor-
roborated the symptoms and diagnosis. Microscopical
examination showed the growths to be gummata.
In this case it will be observed that the
nodules in the right temporo-sphenoidal lobe were
not suspected to be present, for they gave rise to no
symptoms. Lesions of the temporo-sphenoidal lobe
are often latent. Ferrier localises the auditory centre
SITUATION OF THE LESION. IDS
in the superior temporo-sphenoidal convolutions, but
a unilateral lesion would be unlikely to cause deaf-
ness ; hearing being bilaterally associated. 1
Case 2. — Left Jiemiplegia with right facial
paralysis,
E. B., aged 63, a widow. There is no history of
paralysis in the family, but her father died from
diabetes. The patient has been a healthy woman
till three years ago, when she had a stroke which
slightly affected her left side ; from this she entirely
recovered. On the 9th of May; while standing, she
was suddenly seized with giddiness ; she did not fall
nor lose consciousness. On trying to move she found
she had lost the use of her left arm and leg, but since
then has gradually recovered the power in them. She
did not notice that her face was affected.
She has marked facial paralysis on the right side,
being unable to close her lids. The naso-labial furrow
is obliterated, and the angle of the mouth on the left
side drawn up. She has the usual difficulty in masti-
cation, the food getting between the gums and cheek.
There is paresis of the right half of the soft palate ;
no alteration in her sense of taste ; nor is the fifth
nerve in any way affected. The conjunctival reflex
is abolished, and there is slight conjunctivitis, but the
response of the muscles both to Faradism and
Galvanism is perfectly normal. The sequence of the
polar contractions and their intensity is normal.
There is paresis of the left side of the body, and the
left arm and leg are slightly wasted. There is
I06 SITUATION OF THE LESION.
increased patellar reflex on the left side ; no front tap
contraction, and no ankle clonus. . Sensation on the
left side is unaltered. The heart shows no signs of
disease, but the arteries are markedly atheromatous.
The patient suffers from vertigo, and there is a trace
of albumen in the urine, but no casts. The ophthal-
moscope shows that both fundi are normal.
The lesion is most probably a small haemorrhage,
and its situation is in the lower part of the right half
of the pons just below the decussation of the facial
nerves.
Case '^.—Cerebellar Disease ivith Crossed Paralysis*
W. H., a man aged 48, a fitter ; has been a
soldier, and has served in India. He had syphilis
when a young man, but was otherwise quite well
until about two years ago, when he suffered from
headache and giddiness, with obstinate constipation-
He suffered occasionally with shooting pains in the
right arm, and also had deficient control over his
rectum and bladder. The patient has been gradually
getting worse up to the present time (Feb. 25th,
1884). He sleeps badly, and his memory is not as
good as it was. His intellect appears to be clear.
The bowels are confined. His appetite is good, but
he has suffered from persistent vomiting for the last
six weeks. He always vomits after he takes food ;
but also, independently of food, especially in the
morninsf. The vomitinsr is not attended with nausea
He suffers from headache, which at first was occipital
but is now frontal. The headache is severe and
SITUATION OF THE LKSION. ID/
paroxysmal, and the patient has a wearied look
indicative of suffering. He suffers from active ver-
tigo ; objects appearing to move to. the right. He
cannot walk without help, and his gait is reeling ;
the patient staggering and always falling to the
right side. He has paresis of the right side ; the
grasp of the right hand being much weaker than
that of the left. The triceps and biceps reflexes are
exaggerated on the right side, clonus being obtained
by tapping the lower end of the right radius. The
patellar reflex is exaggerated on the right side, and
there is also ankle clonus, but no front tap con^
traction. The gluteal, lumbar, and scapular reflexes
are absent. The plantar, cremasteric, and epigastric
well marked. Sensation is perfect. The pupils respond
to accommodation freely, but not so readily to light.
Both arms tremble, but especially the right, all the
movements of which are attended with tremor. The
tongue points to the opposite side, i.e., to the left ;
whereas in ordinary hemiplegia it points to the same
side. The deflection of the tongue is marked, and
the left half is smaller than the right. The tongue
also is tremulous. The optic discs are normal, only
a few white lines along the vessels being observed.
The patient was admitted into the Queen's
Hospital on the 25th of February. He suffered
severely from cerebral vomiting, which was
checked by hourly drop doses of vin. ipecac, and
has not recurred since. He also was much con-
stipated. The patient was treated with iodide of
I08 SITUATION OF THE LESION.
potassium (gr. xxv. twice a day), and improved
greatly. His gait became steadier ; the headache
ceased ; and the grasp of the hand was stronger.
It was noticed that there was a periodicity in the
attacks of headache, and the stagger to the right
was well seen when he was ordered to turn round
quickly. The patient was kept in six weeks, and
then discharged much improved. He is still under
treatment as an out-patient, and still shows the slight
hemiplegia and the deflection of the tongue.
As to the diagnosis : — The cephalalgia, vertigo,
and vomiting, point to cerebral tumour ; and
were there double optic neuritis the diagnosis of
tumour would be positive. The staggering gait
indicates that the lesion is in the cerebellum. But
he has also a crossed paralysis, for there is paresis
of the right side of the body, and paralysis of the
left half of the tongue. We can explain this by
supposing that the lesion in the cerebellum has
compressed or invaded the motor tract in the
medulla on the left side above the decussation of the
motor fibres, thus causing hemiparesis and descend-
ing degeneration of the crossed pyramidal tract
in the right side of the cord, and has compressed
the trunk of the left hypoglossal nerve also. There
is no sign of any lesion of the vagus, glosso-
pharyngeal, or spinal accessory nerves.
As to the nature of the lesion : — It is probably
gummatous, for there is a distinct history of syphilis,
and the man improved greatly under the influence
of iodide of potassium.
CHAPTER V.
THE NATURE OF THE LESION IN
BRAIN DISEASE.
^
Diseases of the Brain,
I.— ORGANIC DISEASES.
of the Diira-Pachymeningitis-lf^/^^"^-
"' ** Interna.
{^A.) Of the MembranesH
of the Pia
f Acute I ^'"VP'^- ,
( Tubercular.
Chronic.
{B.) Of the Brain proper —
(i) Diffuse Diseases.
Anaemia and Hyperaemia.
Cerebritis or Encephalitis | Locaf^'
Chronic Degenerative Diseases.
(2) Focal Diseases.
Tumour.
Haemorrhage.
Softening.
II.— FUNCTIONAL DISEASES.
no DISEASES OF THE BRAIN.
In diagnosing the nature of the lesion in diseases
of the nervous system, we must carefully enquire as
to the mode of onset of the symptoms ; whether the
onset was immediate, rapid, or gradual. .
In the first case, where the symptoms develop
in a few minutes or hours, the lesion is probably
vascular. A sudden onset, excluding functional
disorders, means a vascular lesion.
Where the onset of the symptoms is rapid,
occupying from a day or so to two or three weeks,
the lesion is in all probability inflammatory.
Where the onset is chronic, occupying more
than three or four weeks, the lesion may be a chronic
inflammation, a degeneration, or a growth.
Meningitis,
I The general rule that inflammation of a viscus
■ is attended with little pain, while inflammation of
its coverings or capsule is attended with great pain,
holds good in the case of the brain and its mem-
branes.
Encephalitis is accompanied with little pain,
while in meningitis pain is the prominent symptom.
Inflammation of the membranes of the brain
causes two sets of symptoms : —
I. — In an early stage those due to irritation of
the cranial nerves and surface of the brain, and
2. — Later on those due to compression, and loss
of function, of the cranial nerves and brain.
DISEASES OF THE BRAIN. Ill
In meningitis, the phenomena of irritation are
more marked and more lasting than in cerebritis — in
the latter the phenomena of irritation are less marked,
fever and pain are less, and mental loss is usually
more profound.
The symptoms of meningitis vary with the
situation of the inflammatory mischief, whether at
the base or convexity of the brain.
In both varieties (i) headache is the prominent
. symptom, with (2) vomiting, (3) pyrexia, and (4)
delirium.
If at the base, the cranial nerves are at first
irritated and finally paralysed ; so that at an early
stage we find photophobia, spasmodic squint,
contracted pupils, irritability of temper and rest-
lessness.
Vomiting, a slow pulse, hyperaesthesia of the
special senses, and optic neuritis may also be present.
Retraction of the head is very constantly present,
especially in children.
Later on the inflammatory eff'usion which occurs
compresses and paralyses the nerves, and we find
paralytic squint, dilatation of the pupils, an irregular
and perhaps rapid pulse (from paralysis of the vagus),
with blindness and deafness. Irritability giving way
to somnolence and coma.
Tubercular meningitis is, as is well known, often
with difficulty distinguished from typhoid fever.
In one of my cases a young man, about 18 years
of age, was admitted in a delirious condition. No
112 DISEASES OF THE BRAIN.
account could be obtained either of his family history
or of the mode of onset of his illness. There was
considerable fever, a pulse not increased in ratio with
the fever, and a brown tongue. No spots could be
found, but there was marked tenderness in the right
iliac fossa, and enlargement of the spleen with
\ signs of bronchitis. The stools were not examined,
the patient only living a few hours after admission.
I pointed out to the students with me that the
case was 'either one of general tuberculosis or of
typhoid, and summing up the pros and cons, con-
cluded that the case was probably typhoid ; at the
autopsy, however, general tuberculosis was found,
the tenderness in the iliac fossa being due to
tubercular ulceration of the ileum.
In another case, that of a child, there was a
history of vomiting, loss of flesh, and constipation.
On admission the child was found to be emaciated ;
there was fever, no rash, a markedly retracted
abdomen, and symptoms of cerebral irritation, the
child lying curled up in bed with its head buried
in the pillows, and crying out when disturbed.
Photophobia was marked, and the spleen was not
enlarged. The case was thought to be one of tuber-
cular meningitis ; the next day, however, after the
application of an ice bag to the head, the child was
perfectly conscious, all the irritative phenomena had
disappeared, the retracted abdomen had become
swollen, and diarrhoea with typhoid stools had
supervened.
DISEASES OF THE BRAIN. II3
It is necessary, then, to be very careful in the
' diagnosis of the cause of delirium and cerebral
irritation in children. In many cases it is simply
the result of pyrexia.
Another condition which may simulate menin-
gitis in children has been called the hydrocephaloid
condition by Marshall Hall. It occurs in young
children exhausted by diarrhoea. The patient -may
become somnolent or comatose. Convulsions, strabis-
mus and dilatation of the pupils may be present, but
after death no change is found in the brain. This
condition may be distinguished from meningitis by
the history of severe diarrhcea preceding the cerebral
symptoms, and by depression of the fontanelle,
whereas in meningitis the fontanelle bulges.
In distinguishing between tubercular meningitis
and typhoid fever, it is of great importance to learn
the history of the case. An enlarged spleen and
diarrhcea point to typhoid fever. Spots, if present,
are conclusive of typhoid. Optic neuritis or tubercles
in the choroid are conclusive of meningitis. The
diagnosis in some cases cannot be made with
certainty.
Meningitis of the convexity of the brain does
not, of course, affect the various cranial nerves, nor
does it cause papillitis ; but headache, vomiting,
delirium, and pyrexia are present. Tremor of the
limbs, followed by paralysis, may be present from
implication of the cortical motor centres. The
temperature is higher, and the disease more acute
114 DISEASES OF THE BRAIN.
and less liable to remission, than in tubercular menin-
gitis, which is almost invariably basilar.
Pachymeningitis,
Pachymeningitis of the cerebral dura mater may
be divided into the following varieties : —
I. — Pachymeningitis externa, which is produced
by
(«.) Injuries which separate the dura from the
skull and occasion extravasation of blood between
them. The clot may compress the brain and cause
death, or inflammatory changes may be set up.
(^.) Extension of inflammation from the neigh-
bouring bones, the most common of such cases being
caries of the petrous portion of the temporal bone.
External pachymeningitis probably always arises
from causes such as those above mentioned. The
symptoms vary with the seat of the mischief, but
severe pain in the head is nearly always complained
of, the dura mater being freely supplied by the
fifth cranial nerve. If the brain is compressed con-
vulsions followed by hemiplegia may result.
2. — Pachymeningitis interna hcemorrhagica occurs
most commonly in old age, and always in adult life.
It may be caused by injury or by any condition con-
ducive to continued hyperaemia of the dura mater ;
such as alcoholism, sunstroke, and various cachectic
conditions. The symptoms vary greatly with the
seat of the lesion, but headache is the most constant.
Motor disturbances are common. There may be
DISEASES OF THE BRAIN. II5
twitchings of one or both sides of the body, or
paresis following a transitory loss of consciousness.
The course of the disease is chronic ; and the first
symptom may be a transient loss of consciousness
with hemiplegia, due to a slight haemorrhage, which
is usually followed by two or three others. These
attacks resemble cerebral haemorrhage, but are usually
not accompanied by such profound coma, and the
hemiplegia is usually transitory. In severe cases,
however, the symptoms cannot be distinguished from
those of ordinary apoplexy.
Encephalitis,
Encephalitis or cerebritis, except from injury or
in connection with disease of the bones in the form
of abscess, is rare; and can rarely be distinguished
from meningitis, with which, indeed, it is frequently
combined.
The phenomena of irritation and implication of
the cranial nerves are less frequent and less pro-
nounced than in meningitis, while the symptoms of
mental impairment and loss of cerebral functions
are more prominent. Headache, loss of memory,
impairment of speech, imbecility, and coma are
commonly observed, the symptoms depending, of
course, upon the situation and extent of the inflam-
matory softening.
In cerebritis the headache is less violent and the
fever not nearly so high as in meningitis.
Il6 DISEASES OF THE BRAIN.
Abscess of the brain is very commonly due to
suppuration in the tympanum and necrosis of the pet-
rous bone, it also frequently follows injuries to the head.
The symptoms of abscess are very much the same as
those of tumour of the brain. Optic neuritis and
headache may be present in both. Abscess of the
brain is usually attended with much greater emaciation
and impairment of the general health than is the
case in tumour. The focal symptoms will depend
upon the situation of the abscess, and these alone
enable us to localise the lesion.
Abscess of the brain is more often latent than
tumour, and grave symptoms may supervene sud-
denly from rupture of the abscess, either into the
ventricles or on the surface of the brain. Abscess,
moreover, usually runs a more rapid course than
tumour, and is accompanied with fever.
Caries of the mastoid cells causes abscess
most frequently in the cerebellum. Caries of the
tympanum causes abscess in the temporo-sphenoidal
lobe ; this rule as to the different situation of the
abscess in disease of the mastoid and petrous
portions of the temporal bone was laid down by Mr.
Toynbee. The presence of paralysis or of spasm on
one side of the body would indicate that the abscess
was in the temporo-sphenoidal lobe near the motor
convolutions.
In cases of ear disease with cerebral symptoms,
look for pain and tenderness over the mastoid
process, and if there is in addition redness or
DISEASES OF THE BRAIN. II7
pitting upon pressure, suppuration of the mastoid
cells is certain, and a free incision is urgently called
for, with subsequent trephining of the mastoid cells.
It is not always easy to distinguish between cases of
ear disease alone and those cases where purulent
meningitis and abscess have been set up.
The subjects of chronic otorrhcea often suffer
from symptoms of cerebral irritation, lasting a few
days and then passing away, being due to changes
in the dura covering the petrous bone. If paralytic
symptoms are present, or if there is optic neuritis,
we may be sure that either purulent meningitis or
abscess, or both are present.
Tumour.
Tumour of the brain is more common than
abscess, and may be of almost every variety. Tuber-
cular tumours are the most common, then come
syphilitic growths, and thirdly gliomata.
Syphilitic tumours are characterised by their
multiplicity. Tubercular tumours also may be
multiple. Gliomata occur singly, they invade the
brain tissue, and are liable to be the seat of haemor-
rhage from their highly vascular structure. A fall
or a blow upon the head may cause the development
of a glioma in the brain.
I recently removed the brain of a little boy who
had injured his head in falling a few months previously,
and since then had suffered from headache, other
symptoms of cerebral tumour gradually supervening.
I found a large glioma of the left side of the i^oxvs..
Il8 DISEASES OF THE BRAIN.
The characteristic symptoms of cerebral tumour
are — (i) headache, (2) vomiting, and (3) double optic
neuritis. But optic neuritis may be absent and so
may vomiting. Stupor is a common symptom of
tumour of the brain. Cerebral tumour, like abscess,
may be latent for a considerable period. The situa-
tion of the tumour can only be diagnosed by the
presence of paralysis or spasm in various situations,
or by a staggering gait. In cerebellar tumour tonic
convulsive seizures may occur in addition to the
symptoms previously mentioned, and are due to
pressure on the pons or medulla. The successive
invasion of cranial nerves is very suggestive of
cerebral tumour.
Case of Tubercular Tumours of t/ie Optic Thalavii.
W. P., a boy, aged 3 years and 9 months, was
admitted into the Queen's Hospital on the i8th
of June, with left hemiplegia and tremor of the right
upper extremity. The father and mother are healthy,
and there is no history of consumption on either
side; but of the six children they have had, the eldest
died from chronic hydrocephalus, the second died at
the age of nine months from diarrhoea and convulsions,
and one daughter is under treatment for strumous
glands of the neck. The boy has always been
weakly and ailing ; when he was about three months
old he had bronchitis, and since that time has never
been really well. About two months before admis-
sion he complained of pain in the right side of the
DISEASES OF THE BRAIN. II9
head, and his mother noticed that his right arm and
leg were occasionally convulsed, and that the left
side was paralysed. The child used to vomit about
every third day, and on those days would refuse
all food and drink. The vomiting would come
on suddenly without evident cause, and without
retching. The vomiting has ceased since about the
4th of June. Constipation has been marked during
the last two months. On admission the boy was
found to have left hemiplegia, the face being affected,
with rigidity and increase of the deep reflexes.
Tremor of the right hand of a fine character was
present on exertion. The boy was in a torpid,
somnolent condition, and had the vacant expression
of amaurosis. The right pupil was the larger, but
both responded to light and accommodation. The
mother gave a distinct history of fits, in which, she
said, he always put his hand to the right side of his
head, and then uttered shrill short screams, and
his left arm would be convulsed and then the leg.
Double optic neuritis was found to be present in a
marked degree, with some haemorrhages into the
retina. There was no sensory disturbance, and no
paralysis of the ocular muscles. No fits occurred
while the patient was in the hospital, but the drowsy-
ness gradually deepened into coma, and he died on
the 26th June, the temperature rising before death to
105° F.
Autopsy. — The membranes and convolutions of
the brain were healthy. On removing the corpus
I20 DISEASES OF THE BRAIN.
callosum and fornix, two tumours were seen side by
side, occupying the anterior portion of each optic
thalamus ; that in the right thalamus being the
larger, and about as large as a pigeon's egg. The
velum interpositum was separated with difficulty
from these tumours. The third ventricle was almost
obliterated, the growths being adherent in front.
The tumour on the right side extended out into the
internal capsule, and some circumscribed yellow
softening was found around. On section each
tumour was composed of a soft yellow material.
The lungs contained caseous masses, and the bron-
chial glands were considerably enlarged and caseous.
The mesenteric glands were caseous and enlarged.
This case was of course easily diagnosed as one
of cerebral tumour. The nature also of the growth
was foretold by the markedly scrofulous history in
the other children. The boy's sister is still under
my care with scrofulous enlargement of the cervical
glands. The mother's account of the boy's fits led
me to suppose they were of the Jacksonian type,
and indicated mischief in the motor area of the
cortex.
Tubercular tumours also far more frequently
occur on the surface than in the interior of the brain.
I therefore imagined that there was a tubercular
mass in the convolutions around the fissure of
Rolando on the right side ; this supposition, however,
did not account for the tremor on the right side
which was observed for a few weeks before death.
DISEASES OF THE BRAIN. 121
The hemiplegia in this case was due to pressure
upon the internal capsule, the paralysis having
supervened late in the course of the symptoms. The
tremor of the right upper extremity was also
probably due to pressure upon the left internal
capsule. The movements were not at all like those
of po'st hemiplegic chorea or athetosis, in which
affections the lesion is nearly always situated in
the posterior and external part of the optic thalamus.
Tumours of the optic thalami are by no means
common.
Aneurisfn,
Aneurisms of the cerebral arteries give rise to
the symptoms common to most cerebral tumours,
and focal symptoms according to their situation.
Embolism is a cause of aneurism, so that the
presence of heart disease in a case of tumour of the
brain should excite suspicion as to its being an
aneurism.
In rare instances a bruit has been detected over the
cranium.
Atheroma, syphilitic, and fibroid degeneration
of the vessels are common causes of aneurism.
Aneurism of the cerebral arteries may occur in
youth and in both sexes.
The miliary aneurisms first described by Char-
cot give no symptoms until they rupture.
Softening,
The term softening is used in medicine in its
literal sense, and ought not to be loosely applied to
122
DISEASES OF THE BRAIN.
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DISEASES OF THE BRAIN. 1 23
all cases where there is mental defect ; where, in fact,
there is frequently no softening.
The two most common causes of softening are
inflammation and occlusion of the blood vessels.
The blood vessels may be occluded either by an
embolon or by a thrombus.
Embolism and thrombosis of the cerebral arteries
produce symptoms, of course, varying with the artery
affected.
The middle cerebral artery is frequently the
seat of these lesions, hemiplegia resulting.
Hemiplegia occurring suddenly may be due to
(i) haemorrhage, (2) thrombosis, or (3) embolism.
Charcot and Bouchard showed long ago that miliary
aneurisms are common on the small branches of the
cerebral arteries of old people, and that these miliary
aneurisms precede rupture of the vessels.
They give no symptoms themselves, and are
most numerous on the antero-lateral group of per-
forating arteries.
The following are the chief features of cerebral
hcemorrhage^ cerebral thrombosis and cerebral embolism.
The commonest seat of haemorrhage is the
corpus striatum, the lenticulo-striate artery especially
being the one that ruptures. Haemorrhages are rare
in the cortex, softening being more common in this
situation. Cerebral haemorrhage frequently occurs at
night, the recumbent position not being so favourable
to the return of venous blood from the brain as the
erect.
124 DISEASES OF THE BRAIN.
The striking symptom of the apoplectic con-
dition is coma, the loss of consciousness depending
on the rapidity of the haemorrhage, as well as upon
the extent of haemorrhage. The loss of conscious-
ness is not immediate, but in the great majority of
cases is gradual, being preceded by paresis of the
side, headache, numbness, &c.
Deep coma is nearly always due to haemorrhage,
not to softening.
A small haemorrhage, however, may not cause
coma.
In old people softening may be attended with
coma.
Haemorrhage is rare under the middle period of
life ; embolism occurs at all ages.
Thrombosis is very common in the aged, but its
occurrence in young adults from syphilis is common,
and it also occurs in children exhausted by specific
fevers or diarrhoea.
In haemorrhage and thrombosis prodromata are
usually present in the shape of headache, vertigo,
attacks of numbness and tingling in the limbs, which
later on became paralysed.
Complete recovery is rare after haemorrhage,
common after thrombosis.
Coma is usually absent in thrombosis and
embolism, except in a mild degree, but thrombosis
of the basilar artery and of the sinuses is usually
attended with coma.
DISEASES OF THE BRAIN. 125
In thrombosis (i) contractures are not so com-
mon as after haemorrhage and embolism, except in
syphih'tic thrombosis; (2) the development of the
paralysis is usually gradual and recovery often rapid ;
(3) there is also usually a history of several attacks.
High arterial tension and cardiac hypertrophy
point to haemorrhage.
Albuminuria also indicates haemorrhage.
In embolism there are (i) no prodromal head
symptoms; (2) there is usually valvular disease or
aneurism.
In old cases of embolic hemiplegia the murmur
may have disappeared, and we must rely on the
history of rheumatism in diagnosing its cause.
Embolic hemiplegia is most common on the
right side, the left common carotid coming off directly
from the aorta, affording a more direct course for an
embolon.
Embolism of the central artery of the retina,
or of the spleen, or kidney, may occur at the same
time as the hemiplegia, and thus positively indicate
its nature.
Cerebral haemorrhage occasionally occurs in early
adult life. I have at present a young man, aged 21,
of very fine physique, who is suffering from right
hemiplegia. I find he has considerable cardiac
hypertrophy and a very hard pulse. The hemiplegia
occurred at night, and I have no doubt that it was
due to haemorrhage. He enlisted as a soldier at 1 8,
and had a good deal of heavy work and athletic
126 DISEASES OF THE BRAIN.
exercise to perform, the strain causing cardiac hyper-
trophy and finally cerebral haemorrhage.
Chronic Degenerative Diseases.
There are three chronic degenerative diseases of
the brain — (i) general paralytic dementia, (2) multiple
sclerosis, and (3) bulbar paralysis.
Cases of general paralysis of the insane, one of
the most fatal of all diseases, are occasionally seen
among the out-patients of hospitals. At the Bir-
mingham Workhouse Infirmary there are invariably
two or three cases in the wards.
This disease is frequently overlooked in its early
stage, and several of my cases had attended at
hospitals without their true condition being detected.
As seen in the out-patient room, the patient is
usually a young man, looking robust and in good
health, but you are told by his friends that he has
been unable to follow his employment for some time
on account of his mental failure.
The symptoms in the early stage arc : —
I. — Loss of memory and optimism.
2. — Inequality of the pupils.
3. — Tremor of the lips, tongue, and facial
muscles, when put in action.
Maniacal outbreaks, apoplectiform attacks, and
attacks of hemiplegia are common.
Epileptiform convulsions are of frequent occur-
rence.
Spinal disease may precede or follow the cere-
bral symptoms. The two most common forms of
DISEASES OF THE BRAIN. 12/
cord disease associated with general paralytic de-
mentia being locomotor ataxia and lateral sclerosis.
It must be remembered that there are cases of
pseudo-paralytic dementia characterised especially
by optimism, but the symptoms mentioned above
are not all present.
When the disease has advanced the diagnosis is
easy. The remarkable condition of well-being (bien-
etre), the patients generally expressing themselves
as feeling well and happy, and the characteristic
delusions, with debility and slurred speech, rendering
the diagnosis easy.
The characteristic features of multiple sclerosis
are : —
I. — The tremors, supervening on exertion ceasing
during rest, and accompanied with paresis. The
tremor implicates the head and trunk.
2. — When the brain is affected — an alteration
in speech, the syllabic utterance, is frequently
observed.
3. — Nystagmus is also often observed when the
eyes are moved in any direction so that the muscles
are strained.
4. — Mental changes are usually present, such as
loss of memory for recent events, unnatural cheerful-
ness, and imbecility.
5. — Vertigo is also commonly present.
6. — The gait is unsteady, the head being held
stiffly, and the patient is apt to lurch violently to one
side.
128 DISEASES OF THE BRAIN.
7. — Apoplectiform attacks frequently occur.
This disease may be mistaken for paralysis
agitans, general paralytic dementia, and cerebellar
tumour.
I. — The tremor of disseminated sclerosis only
occurs with voluntary movement ; that of paralysis
agitans, while the muscles are at rest. The tremor
of disseminated sclerosis is much coarser than that
of paralysis agitans.
2. — Disseminated sclerosis occurs in early life,
paralysis agitans is a disease of advanced life.
3. — Nystagmus, mental symptoms, vertigo, and
alteration of speech at once distinguish disseminated
sclerosis from paralysis agitans.
From cerebellar tumour, multiple sclerosis may
be distinguished by the absence in the latter com-
plaint of (i) optic neuritis, (2) vomiting, and (3)
headache.
Tremor may occur in cerebellar tumour from
pressure on the motor tracts, but is rare.
4. — Convulsive seizures are common in cerebellar
tumour, rare in disseminated sclerosis.
In bulbar paralysis or glosso-labio laryngeal
paralysis the tongue, palate, and vocal cords arc
paralysed bilaterally ; the lips and pharynx being
also involved. Defective articulation is the first
symptom, the lingual consonants being especially
articulated with difficulty. The patient finally is
unable to speak. Swallowing becomes difficult,
liquids regurgitate into the nose, and food may get
DISEASES OF THE BRAIN. 1 29
into the larynx. The aspect of the patient is very
characteristic. He is apt to attract attention in the
streets by his open mouth and silly appearance.
The tongue soon becomes completely paralysed
and lies like a log in the mouth.
Glosso-labio laryngeal paralysis is a chronic
progressive paralysis which may be primary or
supervene on progressive muscular atrophy.
Bulbar paralysis may be acute, as when it is
due to haemorrhage into the medulla, or to plugging
of its vessels.
Glosso-labio laryngeal paralysis in its initial
stage simulates general paralysis of the insane, but
the condition of the pupils and mental symptoms
readily distinguish the latter, and, moreover, the
tremor of the lips and tongue, which is usually well
marked in general paralysis of the insane, is absent
in bulbar paralysis.
Functional Affections of the Brain.
Among the functional disorders of the brain
are included such diseases as (i) epilepsy, (2) chorea,
(3) hysteria, (4) hypochondriasis, (5) delirium tremens,
(6) neurasthenia, (7) catalepsy, (8) trance.
Hysteria,
Hysteria in women and fteurasthenia in men is
nearly always the outcome of failing health, especially
from worry and mental strain. Cases of hysterical
paralysis and contracture rarely recover suddenly^ a.=> v=*
(
.' DISEASES OF THE BRAIN.
ipposedjbut recovery is generally gradual and
> with difficulty, relapse being common. Iso-
,) good feeding, and Faradisation are the agents
to jfe relied upon in the treatment of hysteria and
its manifestations, but even these agents may fail
entirely. A woman, aged 25, whose husband had
deserted her, came under my care suffering from para-
plegia with rigidity, but with no loss of sensation.
I have no doubt that the paraplegia was hysterical,
but I was unable to do any good. When the patient
was isolated and Faradised, she commenced to have
severe convulsive seizures of the left arm, and her
condition became worse. Paralysis depending upon
yjea, on the other hand, may get well immediately.
Neurasthenia in men takes the place of hysteria in
women. In America especially, where competition
is very keen, this disease is common, and it is getting
more prevalent in our own large cities. It occurs
amongst the brain-workers especially. I have met
with a large number of such cases. The following
is a typical illustration of the disease: — A young
man, who had greatly overworked himself in the
service of an important company, and had gained
for himself a very responsible position by his hard
work, gradually became nervous and irritable. When
I saw him he was suffering from what is called clau-
strophobia — a dread of being in narrow and closed
places. He could not travel in a railway carriage,
and although a season ticket holder, was obliged to
walk or ride a tricycle. The dread of being shut up
DISEASES OF THE BRAIN. I3I
in a railway carriage was so great that he could not
go to London on some important business, which
occasioned him great loss. He was also afraid of
going to any place of public n^eeting, and felt a
constant dread lest he should do something which
would disgrace and ruin him. These are very
distressing symptoms and the patient is always
depressed and miserable.
No drug will cure this neurasthenic state. Abso-
lute rest from mental work and worry, with change
of scene, especially a sea voyage, and good feeding
are the remedies. The patient should be encouraged
and should be told that there is no organic mischief
present and that he will recover.
Such cases as the one I have recorded are very
common and are on the increase. They are apt to
pass into melancholia, and, in fact, are closely allied
to insanity.
Mental depression should always be looked upon
as a grave symptom ; this fact has been impressed
upon me by two cases of suicide in which there was
depression of spirits only, without delusion or mental
loss.
I find that medical men are apt to take too
little notice of this symptom, and thus the patients
are left unattended and the friends unsuspicious.
Whereas in all cases where mental depression is
marked the patient ought to be watched, and the
friends advised as to the danger of suicide.
132 DISEASES OF THE BRAIN.
Hypochondriasis.
Hypochondriasis is a chronic mental disorder far
more frequently met with in men than in women. It
is closely allied to and frequently terminates in
melancholia. The patient is morbidly anxious about
his health. He may always complain of the same
trouble, either of his stomach or liver, &c., or he
constantly changes his complaint ; as soon as you
convince him that his liver is all right, he complains
of his heart, and so on. The symptoms in these
cases are always subjective, and it is often impossible
at one examination to come to the conclusion that
the case is one of hypochondriasis.
At the Workhouse Infirmary I have had several
cases under observation for some months at a time.
In these cases the symptoms were subjective, and I
could never find any cause for the loudness and
persistence of their complaining. They always talked
of their sufferings to their fellow-patients ; were con-
stantly writing long lists of questions for me to answer ;
and always wanted me to see them whenever I went
in the ward.
All these cases finally showed unmistakable
symptoms of melancholia, and were sent to- an
asylum.
Case of Hypochondriasis terminating in Melancholia.
W. P., a man aged 47, came to me in June, 1886^
complaining of flatulency and of a sinking sensation
at the epigastrium. He has always been of an anxious,.
DISEASES OF THE BRAIN. 1 33
worrying disposition, but has been .much worse since
he was overworked a year ago, and was very frightened
by spitting a little blood. His sister is in an asylum,
but no other history of insanity in his family can be
obtained. He told me that he felt he was going
to die ; that food turned sour on his stomach ; and
that he was going out of his mind. When assured
that there was no organic disease whatever, and
nothing of consequence was wrong with his stomach>
he began to complain of his heart — was sure that it was
seriously diseased. He was obliged to give up his
employment for he could not settle to work. His
companions said that he was continually talking to
them of his ailments, and telling them that he was
going to die. His wife said that it was wretched
to live w^ith him on account of his complaining.
After seeing me he would be better for a few
hours, but would shortly find something he had not
asked me about, and would worry about it all night
and come again the next day.
After leaving me he would frequently return in a
few minutes to ask some other question, and always
brought a paper full of written questions for me to
answer. He had a great dread of catching cold, and
was afraid to use a comb for fear it would injure him.
He soon began to show distinct delusions, became
very depressed, and talked of killing himself.
Finally, his friends were obliged to send him to
an asylum.
134 DISEASES OF THE BRAIN.
CJiorea.
Chorea must be differentiated from multiple
sclerosis, paralysis agitans, and hysteria.
The movements of chorea are disorderly, the
great characteristic of the movement being \S\^ jerk\
while in multiple sclerosis and paralysis agitans the
characteristic movement is tremor^ which is rhyth-
mical and fine.
In hysteria the movements are more co-ordinated
and regular than in chorea.
The term " habit chorea " has been used by
Weir Mitchell for a light form of the affection,
consisting of some grimace or shrugging of the
shoulders only. Hemiplegia may precede or follow
chorea, and muscular weakness is always present.
Chorea may be periodic, especially in malarious
districts, and there is a great tendency to relapse
either in the Autumn or Spring.
Chorea, occurring in men after rheumatism, is
very fatal.
I have met with two cases : — One man was
treated for acute rheumatism in the Queen's Hospital,
and later on came up as an out-patient with chorea.
He was admitted again and rapidly became maniacal
and died.
The other case was sent into the Workhouse
Infirmary. He had chorea and acute mania. I sent
him to the asylum, but he died there a few days after
admission.
DISEASES OF THE BRAIN. 1 35
Epilepsy.
The characteristic feature of epilepsy is loss of
consciousness, attended or unattended with convulsive
movements. We may distinguish four varieties : —
I. — Epilepsia gravior — in which the attacks are
severe and convulsion is a prominent feature.
2. — Epilepsia mitior — in which the attacks are
mild and convulsion absent or slight, there being
transient loss of consciousness only.
3. — Abortive epilepsy — in which consciousness is
not completely lost. These attacks usually occur in
the course of ordinary epilepsy; the patient, being in a
purely automatic condition, performs eccentric actions,
sometimes running along the street or going up into
a corner of a room and micturating, &c.
4. — Partial epilepsy (Jacksonian epilepsy). This
variety has been previously described.
Epilepsy must be distinguished from uraemia,
hysteria, syncope, and malingering.
Uraemic convulsions are usually preceded by
drowsiness ; dropsy may be present and the urine is
albuminous. In all cases in which convulsions occur
and in which the heart is enlarged and the arterial
tension high, examine the fundus oculi and the
urine.
Attacks of syncope may simulate petit-mal, but
spasm is not present and the pulse is feeble.
Epilepsy must be carefully distinguished from
hysteria ; the two diseases frequently occur together
in the same individual.
n6 DISEASES OF THE BRAIN.
J
In epileptic women an hysterical attack frequently
follows the fits, and such women are at all times
liable to hysteria.
Biting of the tongue, incontinence of urine and
faeces, and sudden loss of consciousness are peculiar
to epilepsy. In hysterical attacks the patient is
noisy, talks during the attack, and does not completely
lose consciousness.
In hystero-epilepsy^ a disease distinct from
epilepsy, and which was first clearly recognised by
Charcot, convulsive movements are markedly present.
There is a prodromal stage of the attack, in
which ovarian hyperaesthesia, globus, and clavus are
present.
In the actual attack the first stage is characterised
by tonic convulsion — the entire body being rigid,
and respiration suspended ; in the next stage
tetaniform and clonic spasms occur, respiration being
irregular and stertorous.
Finally, delirium appears, the patient assuming
various attitudes expressive of her emotional con-
dition, and having hallucinations ; hemianaesthesia
and contracture are of frequent occurrence.
In these cases hysterogenic zones have been
described, consisting of limited cutaneous areas,
which when pressed upon, blistered, or Faradised,
often give rise to or check an attack.
In epilepsy, when the fits are frequently repeated,
the patient not recovering consciousness between
DISEASES OF THE BRAIN. 1 3/
them, the temperature may rise to a high degree, even
to io6°F. more; this condition is called the "status
epilepticus," and is very dangerous.
In hystero-epilepsy, even when the attacks are
exceedingly frequent, the temperature, according to
Charcot, rarely attains a height of lOO^F., and this he
considers to be a very important diagnostic sign of
hystero-epilepsy as contrasted with epilepsy.
A malingerer cannot assume the pallor and the
wide dilatation of the pupils present at the commence-
ment of an epileptic attack.
CHAPTER VI.
THE USE OF ELECTRICITY IN
DIAGNOSIS.
■*-
Three varieties of electricity are employed in
medicine : —
I. — Static or friction electricity — Franklinism.
2. — The constant current — Galvanism, Voltaism ;
the current always flowing in the same direction,
from the positive to the negative pole, and being
produced by chemical action.
3. — The induced or Faradic current, which is
momentary in its action, constantly changing in
its direction, and produced from voltaic or magnetic
source.
The Galvanic and Faradic currents alone are
useful for diagnostic purposes.
The motor points, or the exact spots where the
nerves enter the muscles, must be borne in mind ;
USE OF ELECTRICITY IN DIAGNOSIS. 1 39
irritation here causes totally different effects from
stimulation of the muscular fibres themselves, the
whole muscle in the former case being thrown into
contraction.
Diagrams of these motor points are given in
works on medical electricity, such as those of Dc
Watteville or Hughes Bennett.
Electrical Reactions in Health,
In health, if the motor nerve be irritated with
the Farad ic current, each shock produces a contraction
of the muscles supplied by the nerve, and as the
interruptions rapidly follow one another a tetanus of
the muscles is produced.
If the nerve be irritated with Galvanism, muscular
contractions take place only at the make and break ;
the contractions are short, sudden (not tetanic), and
quickly relax.
While the current is passing without any great
variations in its strength there are no contractions.
The muscular contractions vary according to the
direction of the current : —
With one electrode on the back or sternum and
the other on the nerve (the polar method), it will be
found that the cathode (negative pole) always pre-
dominates over the anode in its power of inducing
contractions.
With currents of gradually increasing intensity,
C C C, or the cathodic closure contraction (the anode
I40 USE OF ELECTRICITY IN DIAGNOSIS.
being placed over the sternum and the cathode over
the nerve) is obtained with a weak current ; with a
stronger current we obtain not only C C C, but also
A C C (the anodic closure contraction), the cathode
being on the sternum.
With still stronger currents we obtain three con-
tractions, C C C, A C C, and A O C (A O C being the
anodic opening contraction).
And with very strong currents four contractions,
C C C, A C C, A O C, and C O C (C O C being the
cathodic opening contraction).
The practical fact to be noted is that in health
C C C exceeds A C C.
When the Galvanic and Faradic currents are
applied to the muscles in health, contractions are
produced exactly as when the nerves are irritated, but
are less extensive ; only those portions of the muscles
contracting which are in the immediate neighbour-
hood of the electrodes. If a muscle, however, be
deprived of its nerve influence by curare, Faradism
applied to the muscle causes no contraction whatever.
Galvanism causes an increased contraction, a weaker
current producing a contraction than is necessary to
do so when the nerve is intact. But so long as the
muscle is healthy the sequence of the polar contractions
remains the same. The mode of the contraction is
altered, for when the nerve is intact the contraction
is sudden and short ; when the nerve is removed the
contraction is delayed and prolonged.
USE OF ELECTRICITY IN DIAGNOSIS. I4I
Faradism acts on nerves alone. Galvanism acts
on both nerves and muscles. There is no true farado-
muscular irritability.
Electrical Reactions in Disease.
It is found that after section of a motor nerve,
corresponding with the degenerative changes which
occur in the nerve below the section and in the
muscles supplied by the nerve, important modifications
in the electrical reactions ensue.
First, as to the nerve, — the response to both
currents is increased for a few days, then diminished
without alteration in the sequence of the polar
reactions, and in from one to two weeks the excita-
bility of the nerve to both currents is abolished. A
nerve may regain its power of conducting voluntary
impulses long before it regains its electrical
excitability below the seat of injury.
Secondly, as to the muscle, — the Faradic excita-
bility rapidly diminishes, and is lost in about two
weeks ; this is due to the degeneration of the intra-
muscular nerve fibres.
With Galvanism we obtain the so-called "reaction
of degeneration" (Erb), which indicates degenerative
changes in the muscle. There are serial and modal
changes in the contractions. During the first
fortnight, galvanic irritability of the muscles is
diminished ; then their excitability to slowly inter-
rupted currents is increased, and serial changes
occur ; instead of C C C predominating, A C C does,
142 USE OF ELECTRICITY IN DIAGNOSIS.
the anode taking the place of the cathode ; and the
order of the contractions with gradually increasing
currents is
A C C
C C C
CO C
A O C
instead of
The modal changes are very important, and
indicate degeneration of the muscle ; the contraction
wave is sluggish and prolonged, and apt to become
tetanic. If the galvanic irritability is lost then the
muscle is destroyed.
The diminution or loss of Faradic irritability in
a nerve indicates its degeneration ; in a muscle,
degeneration of its nerve only.
Increased response of muscle to Galvanism with
reaction of degeneration means degeneration of the
muscle.
Total loss of galvanic reaction means complete
destruction of the muscle.
In disease, if the lesion is above the nucleus of
the motor nerve, then we either have normal electrical
reactions or slight increase or diminution. But when
the lesion suddenly destroys the nucleus, or damages
the nerve trunk, then we get not only quantitative but
also qualitative changes — the reaction of degeneration
as just described — the qualitative changes being both
modal and serial.
In cerebral paralyses^ then, we have no qualitative
electrical changes, no loss of Faradic irritability in the
USE OF ELECTRICITY IN DIAGNOSIS. 1 43
nerves of the paralysed limbs, and no modal or serial
alteration in galvanic reactions.
If the reaction of degeneration is present in the
area of distribution of a cranial nerve we know at
once that the lesion is either in its nucleus or in the
trunk of the nerve.
In diseases of the spinal cord no qualitative
changes occur unless the trophic nuclei of the nerv^es
and muscles in the anterior cornua are affected. So
that it is only in polio-myelitis anterior acuta, and in
myelitis implicating these centres, that the reaction
of degeneration occurs ; when the lesion in the anterior
cornua is a chronic one the reaction of degeneration
is not usually present, e.g,^ progressive muscular
atrophy.
In lesions o{ the peripheral nerves the reaction of
degeneration occurs in its typical form. But in these
cases, if the lesion is slight, there may be only
slight diminution in the Faradic irritability without
qualitative changes. If then, in paralysis due to
peripheral neuritis from any cause, the reaction of
degeneration is not present, the injury is slight and
recovery will quickly ensue. If the reaction of
degeneration is present then the injury is severe ; the
case will be a tedious one, but may recover. If the
galvanic irritability of the muscles is lost, then the case
is hopeless.
We can at once see the great use of electricity
in the diagnosis of the seat of the lesion. The
reaction of degeneration at once tells us that the
144 USE OF ELECTRICITY IN DIAGNOSIS.
lesion is either in the nerves, or in the anterior cornua
of the cord, or in the trophic nuclei in the case of the
cranial nerves.
Electricity is also of immense service in enabling
us to form a prognosis as above indicated. If we find
qualitative electrical changes we are sure of organic
disease, but of course organic disease may be present
without any alteration in the electrical reactions.
We can distinguish trance from death by the use of
electricity, for in the latter condition Faradic irrita-
bility is lost in two or three hours.
Qualitative electrical changes may precede
paralysis, and exist without it ; in cases of plumbism
electrical changes are often present before drop wrist
occurs.
The reaction of degeneration (R D) is charac-
terised both by qualitative and quantitative altera-
tions. The following changes constitute it : —
I. — As the nerve undergoes degeneration its
Faradic and Galvanic excitability diminishes, and at
the end of about fourteen days is entirely lost.
2. — The Faradic current applied to the muscle
causes no contraction, the intra-muscular nerves
having degenerated, and there being no idio-muscular
Faradic irritability.
3. — During the first ten days from the onset of
the disease, or from the time of injury, the galvanic
irritability of the muscles is diminished ; then it is
increased to slowly interrupted currents ; and
USE OF ELECTRICITY IN DIAGNOSIS. 145
Fi
;. 15
e
,
-'1
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1
1
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146 USE OF ELECTRICITY IN DIAGNOSIS.
4. — The following serial qualitative changes are
observed : — The sequence of the polar reactions is
altered, the anode taking the place of the cathode,
and the order of the contractions with currents of
increasing intensity is
I.— A C C ) f I.— C C C
3.-C O C f ^" P^"^^ ^^ ) 3.-A O C
4.— A O C J ( 4.— C O C
5. — The following modal changes are also
observed : — The character of the contractions is
modified ; instead of being short, sharp, and sudden,
they are slow, prolonged, and apt to become tetanic ;
and the contractions are produced only by slow
interruptions of the current
The reaction of degeneration only occurs when
the trophic centre of the nerve, or the nerve itself, is
injured. Hence it is present — (i) In lesions of the
anterior cornua of the cord ; (2) In lesions of the
peripheral nerves, from injury, plumbism, alcohol, &c.
A variety of R D has been described by Erb
where the muscles alone display quantitative and
qualitative galvanic modifications, whilst their Faradic
excitability (through the intra-muscular nerves) is
preserved, and the nerve continues to respond nor-
mally or subnormally to both currents. The nerve
remains intact, while the muscles rapidly degenerate.
Trophic changes may occur either in the nerve or
muscle alone. This variety of R D is present in many
cases of facial paralysis and in pseudo-hypertrophic
paralysis.
USE OF ELECTRICITY IN DIAGNOSIS. I47
In using Galvanism and Faradism for diagnostic
purposes we usually compare the contraction produced
on the diseased with that produced on the healthy
side, the electrodes, condition of moisture, and points
of application being the same. If both limbs are
affected we compare the reactions with those obtained
on a healthy individual, but it must be remembered
that the resistance offered by the skin and tissues
may vary on the two sides of the body, and is
different in different individuals. The only way in
which we can measure this resistance, and so
distinguish between a diminished response due to
increased resistance and one due to disease, is bv
the Galvanometer ; by its use we can ascertain the
strength of current circulating in any given circuit.
CHAPTER VII.
TROPHIC DISORDERS.
Trophic disorders of the various tissues frequently
occur in diseases of the nervous system, there being
a nervous mechanism presiding over the nutrition of
the tissues.
Trophic disorders of the skhi^ such as patches
of erythema, herpetic eruptions, bulloe, and oedema,
are frequently present in lesions of the peripheral
nerves. Zoster may occur in locomotor ataxia or in
meningitis.
Purpura is frequently observed about the legs of
tabetic patients, more especially when the pains arc
severe. The acute bed-sores that occur over the
sacrum in acute myelitis and over the buttock in
hemiplegia are well known.
Glossy skin, first described by Paget, is observed
after severe lesions of the peripheral nerves. When
it affects the fingers they are tapering, smooth, shiny>
hairless, and often hyperaesthetic.
Pigmentation or bleaching of the skin may also
occur in lesions of the peripheral nerves.
\
TROPHIC DISORDERS. I4i
Raynaud's disease is symmetrical gangrene and
local asphyxia, affecting the fingers and toes, tips of
the nose and ears.
The extremities are habitually cold, and the
circulation feeble. Acute attacks occur in which the
extremities become white, cold, and bloodless ; the
fingers and toes looking like wax. After a time
the parts become congested and painful ; bullae
containing blood and ulcers form on the affected
parts, and gangrene with loss of the terminal
phalanges may occur. This disease is supposed to
consist in ischaemia of the smaller arteries, produced
by irritation of the vaso-constrictor nerves, but in
many, cases the peripheral nerves are diseased. Dr.
Barlow recommends Galvanism of the affected
extremities in the subjects of this neurosis.
Perforating ulcer of the foot occurs in tabes
dorsalis and in diseases of the peripheral nerves, in
fact in the former disease a peripheral neuritis is
probably the cause of this affection. A large corn
nearly always precedes the ulceration. The skin
around the sinus is very often anaesthetic, but not
always so, and the sinus frequently leads down to
dead bone, the joints of the great toe being often
destroyed and the phalanges necrosed. The
favourite seat of perforating ulcer is on the under
surface of the metatarso-phalangeal articulations,
and both feet may be affected. Similar ulcers have
been observed on the hands in cases of tabes, where
the cervical region was most affected. Perforating
ulcer of the foot may be the first sym^tci^xv ^S. \3^a^^-
I50 TROPHIC DISORDERS.
In a case at the Queen's Hospital a young girl
had lost the terminal phalanges of the toes of one
foot successively. She had a perforating ulcer on
the under surface of the metatarso-phalangeal joint
of the great toe, and anaesthesia of the peripheral
half of the foot. Disease of the sciatic ner\'e was
diagnosed, and this was confirmed, for when the
nerve was exposed for the purpose of stretching, it
was found to be much atrophied.
The nails may fall off in peripheral ner\*e disease
and in tabes; they are, moreover, frequently dis-
coloured, ridged, and brittle.
The hair has been known to turn grey suddenly,
in a single night, after severe emotion.
Perspiration may be excessive or arrested.
Occasionally there is unilateral perspiration. These
disturbances depend upon lesion of the sympathetic
nerve or of the cerebro-spinal centres connected with
the sympathetic.
The trophic nerves to the skin are distributed
with the sensory fibres, for it is in such diseases as
locomotor ataxia where pains are severe that these
lesions occur ; moreover, in lesions of the anterior
cornua, where there is no sensory^ disturbance, the skin
is unaffected. Just as the nerve cells in the anterior
cornua of the cord stand in trophic relation with the
muscles and joints, so the posterior cornua of the
grey matter exert some influence over the nutrition
" the skin.
TROPHIC DISORDERS. 151
Trophic disorders of the viscera are occasionally
observed.
Lesions of the vagus nerve are said to give rise
to pneumonia and fatty heart.
Cerebral haemorrhage is said to be frequently
associated with pneumonia of the lung on the side
opposite the lesion. I have twice observed pneu-
monia on the side of the hemiplegia after cerebral
haemorrhage. Acute cystitis and renal congestion
commonly occur in acute myelitis.
The joints and bones have a trophic relation,
it is supposed, with the anterior cornua of the cord.
Lesions of the peripheral nerves of an irritative kind
are apt to cause acute inflammation of the joints
supplied by the nerves, and anchylosis may result.
Trophic disorders of the joints and bones
frequently occur in tabes dorsalis, and are attributed
by Dr. Buzzard to disease in the medulla oblongata
from their frequent association with gastric crises.
Acute synovitis may occur at the onset of an attack
of poliomyelitis anterior acuta.
Fractures of the bones, produced by the slightest
movements, have been observed by Charcot in tabes
dorsalis.
In spastic hemiplegia occurring in early life the
growth of the bones is often arrested, the limbs
being stunted. It is important to remember that
the bones of the insane undergo morbid changes,
rendering them so brittle that they are readily
fractured from trivial causes. We frequently hear of
152 TROPHIC DISORDERS.
inquests in these cases, and the attendants might suffer
unjustly unless medical men know of this change.
A man suffering from locomotor ataxia or
insanity should be handled, therefore, with the
greatest care.
The teeth are also occasionally affected in tabes.
A man in the workhouse infirmary suffering from
tabes went insane, and used to pull out his teeth and
throw them about the ward. He died in an asylum
after having many of his ribs broken.
The various glandular organs of the body are
greatly influenced by disorders of the nervous system.
Unilateral progressive atrophy of tJie face is a
remarkable trophic disorder, probable depending
upon disease of the trophic fibres of the fifth nerve.
It is more common in women than in men, and more
commonly affects the left side of the face. All the
tissues, except the muscles, atrophy on one side of
the face ; namely, the skin, fat, hair of the head,
beard, eyelashes, bones, and occasionally the muscles
of mastication. The disease may be mistaken for
congenital asymmetry of the two halves of the face ;
but the atrophy of the skin, hair, and bones, with
diminished bulk, and its supervention years after
birth, distinguish it.
Case of Progressive Unilateral Facial Atrophy,
E. C, a woman, aged 42, attended at the Queen's
Hospital for treatment for dyspepsia a few weeks
ago. Observing that there was marked facial
TROPHIC DISORDERS.
deformity I enquired as to its commencement
stated that up to her 17th year she was all right, but
that after that age the face became gradually affected,
the left side being observed to be different from the
154 TROPHIC DISORDERS.
She has suffered much from tooth-ache, many of the
teeth of the upper jaw being carious, but there is no
difference in the teeth on the two sides. There is no
history of spasm, hyperaesthesia, or neuralgia of the
left side of the face, and her general health has
always been excellent. There is marked asymmetry
of the face, the contrast between the right and left
halves being very pronounced. The left half is
altogether smaller, there being an abrupt line of
demarcation running vertically down the centre of
the face, the contrast on the chin being especially
apparent, the right half ending in a distinct ridge.
There is no alteration in the colour of the skin
or of the hair, but the eyelashes on the left side are
scanty. There is alopecia over the left half of the
front of the skull, extending to the middle line in
the one direction, and to the temporal ridge in the
other, and as far backwards as the vertex ; the alopecia
being confined to the area of distribution of the fifth
nerve. The fat seems to have completely disappeared
on the left side, the eye being sunken and the
palpebral fissure smaller than on the right side.
The malar bone is very prominent, and the fossae
above and below very deep. The tongue, soft
palate, and vault of the hard palate are unaffected.
There is no paralysis, but the left masseter seems
much smaller than the right, though the patient has
no difficulty in masticating on the left side. The
bones are much atrophied, the left malar bone being
about half the size of the right. On the left side
TROPHIC DISORDERS. 155
the measurement from the angle of the lower jaw to
the symphysis is 2j^in., on the right side 3j5^in^
The depth of the jaw, from the summits of the molar
teeth to the lower margin, on the left side is i^in.,
on the right side 2in.
On the left half of the forehead are two vertical
grooves separated by a ridge, these grooves being in
the situation of the supra-trochlear and supra-orbital
nerves.
There is no alteration in sensibility. The
temperature of the left side of the face is 97*2° F.,
of the right side 96*4° F.
The patient brought her photograph, taken when
she was 17 years of age, and in this there was no
trace of any deformity. The Faradic response on
the left side is considerably greater than on the right,
but this is undoubtedly due to the diminished resist-
ance on this side, the skin being thin and without
subcutaneous fat. This affection is a rare and
interesting one, and is supposed to depend upon a
lesion of the trophic fibres of the fifth nerve. It is
slowly progressive and incurable, but does not affect
the general health.
CHAPTER VIII.
DISEASES OF THE SPINAL CORD.
•^«e-
Tlie Anatomy and Physiology of the Spinal Cord.
The spinal cord, the great conductor of motor
impressions downwards from the brain and of sensory
impressions upwards to the brain, may be said to
consist of a series of superimposed segments ; each
segment having a pair of spinal nerves attached to it,
and consisting of two exactly symmetrical halves.
A transverse section of the cord is seen to be divided
into two halves by the anterior and posterior median
fissures, each half being again divided by secondary
fissures into certain columns. The anterior columns
of the cord extend laterally from the anterior median
fissure to the anterior roots of the nerves. The inner
portions of these columns constitute the direct pyra-
midal tracts which contain those fibres of the motor
tract from the brain which have not decussated in the
medulla. Some believe that the fibres of the direct
pyramidal tract decussate in the cord, so that there is
DISEASES OF THE SPINAL CORD.
Fig. iS.
: Representation of Transverse Section of the
SriNAi, Cord.
A. P. R., [interior primary nerve tools. P. P. R., posterior primary
nerve roots. D. P. T., tlie direct pytadmidal tracts. C. P. T., (lie crossed
pyramidal tracts. P. I. C., tlie posleto-inteinal columns, or thecolumns of
GoU. P. E. C, the poslero-exlernal coiumns, or the too* zones, itavetsed
by fiiires of the posterior nerve toots. A. C., anterior cornua of the grey
matter, G., ganglion on the posterior roots of the nerves. C, the
cetebellar tracts. A., region of lateral column conlainiiuj sev.wivi S4«ss..
B., region of unknown function sepai&Vni^ ifet ctcreasi. vi"'™^'^ '•svs.
yrom ibe grey malter.
158 DISEASES OF THE SPINAL CORD.
finally a total decussation of the motor fibres from
the brain. Dr. Hughlings Jackson, however, believes
that the direct pyramidal tracts do not decussate, but
that the fibres pass to the cells in the anterior comua
and thence to the motor nerves. The direct pyramidal
tracts cease about the middle of the dorsal region.
The lateral columns of the cord extend from the
anterior roots of the nerves to the posterior roots,
and are divided into four distinct areas by Flechsig.
A tract on the surface, the cerebellar tract, conducts
fibres upwards from the muscles to the cerebellum,
for this tract undergoes upward degeneration, after
lesions of the posterior nerve roots, the degeneration
implicating the cerebellum. The most important
tract in the lateral column is the crossed pyramidal
tract, which is formed by upwards of 97 p. c. of the
fibres of the motor tract of the opposite side of the
brain. This tract is separated from the surface of
the cord by the direct cerebellar tract It diminishes
in size as it passes downwards, and comes to the
surface in the lumbar region, where it is situated
external to the apex of the posterior horn of grey
matter. There is a layer separating the grey matter
from the crossed pyramidal tract, whose function is
unknown, and another layer in front of the pyramidal
tract, which is probably sensory, for ascending de-
generation in this region is said to occur after lesions
of the posterior nerve roots. Dr. Gowers thinks that
sensations* of pain are conducted upwards in this
layer.
DISEASES OF THE SPINAL CORD. 159
Fig 19.
Si'iN-AL Cord (Flechsig).
The leiiered poilions are the four regions of the lateral columns.
l6o DISEASES OF THE SPINAL CORD.
The posterior columns extend from the posterior
roots to the posterior median fissure; each posterior
column is divided into an inner portion, the postero-
internal column (column of Goll) which conducts
tactile impressions upwards and which undergoes
ascending degeneration after lesions of the sensory
roots ; and an outer portion, the postero-extemal
column or root zone of Charcot, which is of great
importance, in that it contains fibres of the posterior
roots of the nerves passing on to the grey matter, and
is the seat of the lesion in locomotor ataxia.
The fibres of the posterior roots of the nerves,
after leaving the ganglia, in great part pass directly
into the posterior cornua of the grey substance ; some,
however, pass through the postero-external columns
on their way to the grey substance.
The sensory fibres decussate in the spinal cord
almost immediately in the cervical and upper dorsal
regions, but not immediately in the lower dorsal and
lumbar regions, as has been pointed out by Gowers.
A transverse lesion of one half of the cord in the
lower dorsal or lumbar region may cause anaesthesia
in the lower extremity of the same side.
According to Ferrier, the fibres concerned with
the function of muscular sense also decussate in the
cord, but in a well-marked case of hemilateral myelitis
recently under my care, muscular sense was impaired
on the side of the lesion, thus upholding Brown
S^quard's dictum.
DISEASES OF THE SPINAL CORD. l6l
The large multipolar nerve cells in the anterior
corniia are —
I. — The centres for the various reflex actions of
the cord ;
2. — The trophic centres for the motor nerves
and muscles ; and possibly
3. — Preside over the nutrition of the joints.
The rest of the grey matter probably exerts a
trophic influence upon the skin and the viscera.
As in the brain, so in the cord, the sensory tract
is much less defined than the motor, and probably a
very thin strand of grey matter is sufficient to
conduct sensory impressions upwards. In a trans-
verse myelitis, motor power is sooner and more
completely lost than sensation. Sensation is more
rapidly recovered than motion.
Vaso-motor centres, vaso-constrictor, and vaso-
dilator nerves exist in the cord, but their situation
is unknown.
The centre for the dilatation of the pupil is
situated in the lower cervical region of the cord.
The fibres of the pyramidal tracts have their
trophic centre in the motor convolutions of the brain.
Lesions severing this connection will be followed
by descending sclerosis of the pyramidal tracts,
both crossed and direct ; there are, therefore, four
tracts in which descending degeneration occurs after
a transverse lesion of the cord.
The fibres of the posterior roots of the nerves
have their trophic centres in the ganglia \ V^^s^va^ ^S.
1 62 DISEASES OF THE SPINAL CORD.
these fibres between the ganglia and the cord, or in
their passage through the postero-external columns,
as in locomotor ataxia, is followed by ascending
degeneration of the postero-internal and cerebellar
tracts, and also of the anterior region of the lateral
columns.
The two halves of the cord, though to a great
extent independent, especially in the cervical region,
are yet in intimate relation with one another. In
cases where hemiplegia has occurred in early life it is
frequently found that the patient cannot open or close
the sound hand without the one on the affected side
following suit, and in old cases of hemiplegia where
the leg does not recover the opposite leg suffers also.
There is no doubt an intimate connection between
the multipolar nerve cells on the two sides of the cord.
The Reflex Actions.
The reflex actions may be conveniently arranged
in three divisions —
I. — The organic reflexes.
2. — The superficial or skin reflexes.
3. — The deep or tendon reflexes.
The organic reflexes have their centres in the
spinal cord and medulla oblongata.
In the medulla are situated the respiratory, the
vaso-motor, the cardio-inhibitor>', the deglutition, the
vomiting, the diabetic, and salivary centres.
In the lumbar region of the cord very important
organic centres are situated, namely — the micturition.
DISEASES OF THE SPINAL CORD. 163
the defoecation, the sexual, and parturition centres,
which are reflex processes.
The vesical reflex is a hiighly important one, and
it is frequently deranged in diseases of the spinal cord.
When the bladder becomes full of urine the sensory
nerve endings in the mucous membrane are stimu-
lated, and impressions are conveyed along the
sensory nerves to the micturition centre in the
lumbar region of the cord. Impressions are also
conveyed to the brain, which excite the desire to
micturitate.
The brain may inhibit or set in action the
micturition centre.
If micturition occurs, that part of the centre
which controls the sphincter vesicae is inhibited, and
that which controls the detrusor stimulated ; the
abdominal muscles are also made to contract.
The proper performance of the act of micturi-
tion requires then the integrity of —
I. — The sensory nerve endings in the mucous
membrane of the bladder.
2. — The sensory nerves from the bladder to the
cord.
3. — The micturition centre in the cord.
4. — The efferent nerves to the sphincter and
detrusor muscle (fourth sacral).
5. — The integrity of these muscles.
6. — The connections between the brain and the
micturition centre.
164 DISEASES OF THE SPINAL CORD.
In lesions of the brain impairing consciousness,
incontinence of urine is observed, but this incon-
tinence is intermittent; the reflex function goes on,
micturition being brought about whenever sufficient
urine collects in the bladder to sufficiently stimulate
the sensory nerves ; but there is lack of cerebral
control.
The involuntary discharge of urine in coma
does not imply any paralysis of the bladder.
A transverse lesion in the cord above the lumbar
region does not paralyse the bladder, but by breaking
the connection between the micturition centre and
the brain causes the act to be purely reflex and
involuntary.
Lesions, however, in the lumbar region of the
cord destroying the reflex centre cause paralysis of
the bladder.
The detrusor and sphincter muscles have
separate centres, and one only may be partially or
completely paralysed.
The fibres connecting the micturition centre
with the cerebral convolutions probably pass along
the lateral columns, for in primary lateral sclerosis
the patient has little power to initiate or arrest the
act of micturition, the process becoming a purely
involuntary reflex action. The same remarks apply
to the other organic reflexes situated in the spinal
cord, although more is known concerning the process
of micturition than is known of the other reflex
actions.
DISEASES OF THE SPINAL CORD. 1 6
«•
Tlie superficial and tendon reflexes y like the
organic, are of great importance in the diagnosis of
diseases of the spinal cord. Their presence indicates
the integrity of their reflex paths through the cord,
but disease may of course be present in the cord .
outside the reflex path (which is formed by the
posterior nerve root fibres, the grey matter and
anterior nerve root fibres) without abolishing the
reflexes.
The lateral columns, the postero-internal, and
the anterior columns may be destroyed without any
injury to the reflex tract.
Absence of a reflex is not a certain indication of
disease of the cord for —
{a.) Many reflexes, such as the gluteal, epigastric,
and interscapular may be absent in health.
{b.) Disease anywhere in the reflex path outside
the cord, either of the motor nerves and muscles or
of the sensory nerves, will abolish the reflex.
The different reflexes pass through the cord at
different levels, so that we may test the integrity of
the cord throughout its length. If a reflex be absent,
the one immediately below and that immediately
above being present, then we have strong evidence of
disease in the area of this reflex, either in the cord
or peripheral nerves.
Loss or diminution of the reflexes may be due to
(i) disease in the reflex path; (2) to increase of
cerebral controlling influence ; (3) to diminution or
abolition of muscular irritability.
l66 DISEASES OF THE SPINAL CORD.
Increase of the reflexes may be due (i) to
increased irritability and diminished resistance in the
reflex arc, as produced by strychnia ; (2) arrest of
cerebral controlling influence conducted down the
. lateral columns, hence the exaggeration of all the
reflexes observed in lateral sclerosis ; (3) increase
of the irritability of the muscular fibres ; hence
the exaggeration of the reflexes in wasting
diseases.
The stiperficial reflexes are true reflexes. They
are produced by stimulation of the skin or mucous
membranes.
I. — The plantar reflex obtained by irritating the
skin of the sole, the muscles of the foot contracting,
passes through the lower end of the cord. In cases
of neuritis of the great sciatic nerve this reflex is
absent on the affected side. I have met with two or
three cases of chronic neuritis of this nerve for which
I could discover no cause.
2. — The gluteal reflex consists in contraction of
the gluteal muscles, brought about by irritating the
skin over the buttock. It passes through the cord
at the level of the fourth and fifth lumbar nerves.
This reflex is rarely to be obtained in the healthy
subject.
3. — The cremasteric reflex by which the testicle
is drawn up when the skin on the inner side of the
thigh is irritated, passes through the cord at the level
of the first and second lumbar nerves. This reflex is
pretty constantly present in health. It is, however,
more lively in hoys than in men.
DISEASES OF THE SPINAL CORD. 167
4. — The abdominal reflex consists in contraction
of the abdominal muscles upon irritating the skin on
the side of the abdomen in the nipple line. This
reflex passes through the cord from the eighth to the
twelfth dorsal nerves. It is frequently absent in
health.
5. — The epigastric r^^A' consists in the dimpling
of the epigastrium* caused by contraction of the upper
fibres of the rectus produced by stimulation of the
side of the chest in the fifth and sixth spaces. This
reflex passes through the cord between the fourth
and sixth dorsal nerves. It may be absent in health.
6. — The erector spince reflex consists in a con-
traction of these muscles caused by stimulation of
the skin from the angle of the scapula to the iliac
crest. This reflex is rarely present in health, but is
frequently present in wasting disease, and its pro-
duction depends upon the integrity of the cord in the
dorsal region.
7. — The interscapular reflex is produced by
stimulation of the skin between the scapulae, and
consists in contraction of some of the scapular
muscles. This reflex is frequently absent in health.
It passes through the cord at the level of the upper
two or three dorsal and lower two or three cervical
nerves.
8. — The palmar reflex^ consisting of a contraction
of the flexors of the fingers induced by stimulating
the skin of the palm, and is only obtainable in young
infants. It is not obtainable during the waking hours
l68 DISEASES OF THE SPINAL CORD.
after this period of life, the hand being much more
under cerebral control than the foot. This reflex
passes through the cervical enlargement of the cord.
9. — Cranial reflexes. The chief reflexes of the
cranial nerves are : —
{a.) The conjunctival reflex caused by irritating
the conjunctiva. This is lost in peripheral lesions of
the facial nerve and of the ophthalmic division of the
fifth nerve.
{b.) The reflex contraction of the iris to light.
(r.) The palatal reflex, the soft palate being
elevated when the mucous membrane covering it is
stimulated. This reflex is lost in paralysis of the
soft palate on one or both sides, according as the
paralysis is uni- or bi-lateral. It is also frequently
lost after diphtheria without actual paralysis.
The act of sneezing is a reflex caused by irritation
of the mucous membrane of the nose.
These cranial reflexes unlike some of the skin
reflexes are constantly present in health and their
absence implies disease.
The deep reflexes consist of contractions of
muscles produced by striking their tendons or by
suddenly stretching the muscles in other ways.
The knee-jerk and ankle clonus are the best
known of the tendon percussion contractions.
The knee-jerk^ or patellar-tendoji-refleXy or the
knee-pheno7nenon (so named by Westphal, who first
perceived its great importance), is probably not caused
by reflex but by direct action, and is due to a sudden
DISEASES OF THE SPINAL CORD. 169
Stretching of the muscle, but the integrity of the reflex
loop through the lumbar region of the cord is
essential for its production.
Dr. Gowers has proposed the term " myotatic
contraction," as being more appropriate than the
term "deep reflex." For all practical purposes we
may regard the knee-jerk as a reflex, for a lesion
anywhere in the reflex path through the lumbar
region of the cord will abolish the phenomenon.
In obtaining the knee-jerk it is important to
uncover the knee and to percuss the bare skin. I
have once or twice found the knee-jerk to be present
where medical men had supposed it to be absent
because they had percussed the tendon through the
clothes.
The knee-jerk when diminished, but not entirely
abolished, can be more easily obtained by telling the
patient to clench his fists tightly at the moment the
tendon is struck, or to link the fingers together and
pull energetically.
In 1883, Dr. Ernst Jendrassik, of Buda Pesth,
showed that muscular exertion, as lifting weights,
clenching the fists, &c., increases the response to a
blow on the patellar tendon. It has since been
found that every muscular exertion increases the
tendon reactions. This increase is explained by
supposing that the will force is not confined to one
channel, but that there is an overflow affecting all
the spinal ganglia and momentarily increasing the
I/O DISEASES OF THE SPINAL CORD.
muscle tone, a single muscular contraction bracing
up every other muscle in the body through the
overflow it sets in movement.
Loss of the knee-jerk is pathological, and
indicates disease somewhere in the reflex path. The
knee-jerk is rarely if ever absent in health, and is
never absent in hysteria.
In a case of hysterical anaesthesia of both legs»
recently under my care, the knee-jerk was lost. The
patient, a woman, was in the infirmary for two years,
and all my efforts to remove the anaesthesia were
unavailing. However, after leaving the infirmary
she applied leeches to her legs, and returned with the
anaesthesia gone, but still having loss of knee-jerk
and other symptom.s of locomotor ataxia.
The knee-jerk is absent —
I. — In locomotor ataxia, the lesion here inter-
rupting the reflex in the root zone. Loss of the
knee-jerk may be the first symptom of this disease,
and may precede all other symptoms for years.
Simple loss of the knee-jerk should always excite
grave anxiety as to the future.
2. — In lesions affecting the lumbar region of
the cord, in meningitis, myelitis, tumour, or other lesion
implicating the anterior or posterior nerve roots or
the grey matter ; and in lesions of the anterior
cornua, as in infantile paralysis.
3. — In disease of the afferent and efferent nerves
of the reflex ; hence in peripheral neuritis, when the
DISEASES OF THE SPINAL CORD. 171
branches of the lumbar nerves are involved. The
knee-jerk is lost, e.g.^ in —
(^.) Alcoholic paralysis.
(^.) Diphtheria, even without actual paralysis.
(r.) Diabetes.
(rf.) Peripheral neuritis from other causes, such
as injury, cold, gout, lead poisoning.
4. — In pseudo-hypertrophic paralysis when the
disease is advanced.
5. — In cases of tumour of the cerebellum, it is
occasionally lost on one or both sides.
6. — In those rare cases of progressive muscular
atrophy in which the wasting commences, and is
mostly marked in the legs, the lesion here probably
being in the peripheral nei-ves. The knee-jerk is
lost somewhat early in this form of progressive
muscular atrophy long before the atrophy is extreme.
The knee-jerk is occasionally, but very rarely,
present in cases of locomotor ataxia, and in cases df
combined sclerosis of the postero-external and lateral
spinal tracts, it is exaggerated.
I have a case of locomotor ataxia at present
under observation with myosis and Argyll -Robertson
pupils, gastric, urethral and rectal crises, and slight
ataxy without loss of knee-jerk. The knee-jerk
once lost in locomotor ataxia never returns. In
peripheral neuritis it may, and its return in diphtheria
is hastened by the administration of strychnia.
The knee-jerk is exaggerated (i) in disease of
the lateral columns, either primary or in the form of
172 DISEASES OF THE SPINAL CORD.
descending degeneration ; (2) in all other lesions by
which the cerebral controlling influence is shut off;
(3) in all cases in which the muscular irritability is
exaggerated, or in which the irritability of the grey
substance of the cord is increased.
In cases of myelitis (above the lumbar region)
or tumour pressing upon the spinal cord and leading
to contracture of the lower extremities, the knee
being flexed to a marked degree and the rigidity
being extreme, the knee-jerk may appear to be
absent, but careful observation will show that the
rigidity is increased when the tendon is percussed.
Ankle clomis consists of a rhythmical clonic
spasm of the foot due to rhythmical contraction of
the calf muscles. To obtain it the foot must be
suddenly flexed at the ankle, the Achilles tendon being
thus forcibly stretched.
Ankle clonus is not present in health or in
disease of the extreme end of the cord implicating
the roots of the nerves or the grey matter. Its
presence denotes disease, or, at any rate, diminution
or loss of cerebral control.
The great cause of ankle clonus is (i) sclerosis
of the lateral columns, but it may be present in (2)
hysterical paralysis and (3) even in pressure on the
cord without actual disease, as is observed in cases of
spinal caries, where ankle clonus may disappear
after rest or the application of a Sayre's jacket.
Wrist clonus, — Other forms of clonus mav be
obtained, for instance, in cases of hemiplegia, where
DISEASES OF THE SPINAL CORD. 1 73
descending degeneration has taken place to a marked
degree, a wrist clonus may be obtained by sudden
hyper-extension of the wrist.
A patella clonus^ produced by sudden depression
of the patella, may be observed under the same
conditions as ankle clonus.
Muscular contractions may also be induced by
tapping the bones.
The masseteric reflex or jazv-jerk has been inves-
tigated by Dr. Watteville. It is only slightly marked
in health. To obtain it the lower jaw should not be
fixed by any voluntary muscular contraction ; a flat
object, such as a paper knife, is placed over the molar
teeth, and a blow, with a percussion hammer or with
the finger, struck near the teeth.
In some cases a regular clonus has been obtained,
as in the case of amyotrophic lateral sclerosis, pub-
lished by Dr. Beevor, in " Brain," Vol. VIII.
The latent period of this reflex is very short, too
short for the phenomenon to be a true reflex.
I have seen the jaw-jerk well marked in a case
of trigeminal neuralgia.
Periosteal and fascial reflexes. — The front tap
contraction^ first described by Dr. Gowers, and con-
sisting of contractions of the quadriceps femoris,
produced by tapping the inner surface of the tibia,
is a delicate test of morbid irritability, and is not
present in health. It depends for its presence upon
the same conditions as does the production of ankle
clonus.
174 DISEASES OF THE SPINAL CORD.
Bicipital reflex. — In the late rigidity of hemi-
plegia, tapping the lower end of the radius is followed
by contraction of the biceps, the bicipital reflex ;
tapping of the ulna, by contraction of the triceps.
Tapping the clavicle causes contraction of the
deltoid and pectoralis major.
Tapping the spine of the scapula causes con-
traction of its muscles.
Tapping the lumbar fascia may cause con-
traction of the erector spinae muscles.
The early occurrence* of these deep reflexes in
hemiplegia is of grave omen, indicating extensive
damage to the motor tract.
In contrast with the deep reflexes, where we
find muscles contracting when put on the stretch, a
peculiar conditio first observed by Westphal, occurs
occasionally in locomotor a axia, and has been
observed in paralysis agitans ; it consists in the con-
traction of a muscle induced by suddenly approxi-
mating its points of origin and insertion. It is best
seen in the tibialis anticus.
If dorsal flexion of the foot be either
suddenly or gradually produced, this muscle, though
greatly relaxed, gets into a state of contraction, its
tendon becoming prominent. This contraction may
persist for several minutes. Contraction produced
by relaxing a muscle was named by Westphal
the "paradoxical contraction." It may afiect other
muscles on the front of the leg in addition to the
tibialis anticus.
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CHAPTER IX.
DISEASES OF THE SPINAL CORD
(CONTINUED).
•r«-
By extra-medullary disease is meant disease,
outside the cord itself, of the bone, membranes, or
nerve roots, the spinal cord suffering secondarily ;
and by intra-medullary disease is meant primary
disease of the cord.
By system disease is meant the limitation of
disease to definite physiological spinal tracts, the
lesion being bilateral and symmetrical, and extending
a considerable distance along the cord. An indis-
criminate lesion affects any part of the cord, and is
not limited to any definite tract.
Functional Affections of the Spinal Cord,
Spinal irritation is a functional affection of the
spinal cord occurring in women, rarely in men. The
subjects of this complaint present various hysterical
symptoms, and there is little doubt that the spinal
symptoms are manifestations of hysteria also.
■fji
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5 5
DISEASES OF THE SPINAL CORD. 1 7/
The characteristic symptom in spinal irritation
is pain in the back, and extreme tenderness on even
lightly tapping the spinous processes of the vertebrae;
with various motor and sensory disturbances in the
area of distribution of the nerves given off from the
cord in the region corresponding to the tender points.
The tenderness may be so great that the patient
cannot bear the pressure of her clothes. The
patient often complains of neuralgic pains in the
limbs. Menstrual disturbance is almost invariably
present.
It is important to remember that pain in the
back is not a prominent symptom in organic disease
of the spinal cord ; it is present in disease of the
bones and membranes, but it is never so marked as
in spinal irritation.
The exquisite hyperaesthesia over the spinous
processes, and the pain elicited by the lightest touch,
are pathognomonic of spinal irritation, a purely
functional disorder.
Hysterical paraplegia is by far the commonest
form of hysterical paralysis. It is of the highest
importance to remember that paralysis from organic
cause may be present in an hysterical subject, and
that in all organic affections of the nervous system
in women hysterical symptoms are apt to supervene.
It must be remembered that the brain really is
the seat of whatever lesion there may be, the power
of the will being in abeyance; as Paget has well said,
"she cannot will."
xt
178 DISEASES OF THE SPINAL CORD.
In the diagnosis of hysterical paraplegia the
following facts must be borne in mind : —
I. — Paralysis of hysterical origin maybe gradual
or sudden in its onset, often far too sudden to be
due to any organic disease of the cord, except intra-
medullary haemorrhage, which is exceedingly rare;
and it frequently follows a trivial injury or emotional
shock.
2. — The sphincters are unaffected.
3. — No trophic lesions, such as local muscular
atrophy, bed sores, cystitis, &c., occur. CEdema,
however, is occasionally seen in the paralysed or
contracted limbs of hysterical subjects, but this
oedema, unlike that observed in paralysis from
organic causa, varies from time to time, is apt to
disappear and recur about the menstrual periods or
on emotional disturbances.
4. — Qualitative electrical changes are never met
with, but there may be electrical anaesthesia and
delayed muscular response.
5. — The symptoms will be found to be incon-
gruous. For instance, there may be complete anaes-
thesia as well as paralysis, and yet no wasting, no
cystitis or paralysis of the sphincters, which would
most certainly be present if the anaesthesia were due
to organic disease of the cord. The patient may be
quite unable to move her legs in bed and yet be able
to stand when out of bed.
DISEASES OF THE SPINAL CORD. 1 79
6. — In hysterical paraplegia there is nearly
always rigidity and exaggeration of all the reflexes,
both superficial and deep, ankle clonus being well
marked.
Primary lateral sclerosis, the symptoms of
which 'are frequently exactly simulated in hysteria,
is rare, and very rare indeed in women ; moreover it
commences insidiously and lasts for years before
complete paralysis ensues, while in hysterical para-
plegia the onset is frequently sudden and the
paralysis complete. It is important to remember
that in time hysterical rigidity may end in sclerosis.
Charcot has reported cases of this kind.
Case of Locomotor Ataxia ivitli Hysterical Ancesthesia,
M. C, a woman aged 32, a pen maker, unmarried,
was admitted on May 5th, 1883, complaining of
difficulty in walking. No family history of nervous
disease could be obtained, except that her father had
hemiplegia. Three years before she came to the
infirmary she had been an in-patient of a large hospital,
suffering from severe pains in the legs, which used to
occur paroxysmally ; these pains still occasionally
occurred. No distinct history of syphilis could be
obtained. The patient had great difficulty in walking,
the gait being very ataxic ; her body swayed from
side to side, and she had to cling to surrounding
objects for support ; the ataxy affected the body far
more than the legs. The ataxy was rendered worse
by closing the eyes, swaying being then well marked
l8o DISEASES OF THE SPINAL CORD.
(Romberg's symptom). In the dark she was quite
unable to get about. She complained of a sensation
of " pins and needles" on placing the feet to the
ground. The knee-jerk was abolished on both sides;
the plantar reflex was also absent. There was com-
plete loss of sensation in both lower extremities up
to the middle of each thigh, analgesia and anaesthesia
being absolute ; sensation elsewhere was normal.
Co-ordinating power in the upper and lower extremi-
ties was normal, and she could accurately tell the
position of her limbs. She suffered from shooting
pains in the legs, and pain in the back. There was
no paresis or rigidity of the legs ; no spinal or
ovarian tenderness. The pupils were unequal ; they
responded normally to accommodation, but not to
light (Argyll-Robertson pupil). Faradisation of the
skin of the legs caused no pain, but Faradisation of
the muscles caused normal contractions and slight
pain. She had recently suffered from attacks of
vomiting. She was very emotional, giving considerable
trouble during the investigation of her case, and being
careless in her replies. She had a typical " facies
hysterica" and nictitation. There was no ischaemia
in the anaesthetic area, and no vaso-motor or trophic
change. There was no history of clavus, globus, or
fits. Micturition, defoecation, and menstruation were
normal. This case was diagnosed as being one
of locomotor ataxia, and the anaesthesia was supposed
to be hysterical. For two years the patient was
under observation in the infirmary ; and isolation^
DISEASES OF THE SPINAL CORD. l8l
Faradisation, blisters, and Burq's treatment were tried
without any influence upon the anaesthesia. Vertigo
was occasionally complained of. On May nth, 1885,
she took her own discharge, and returned to the
infirmary on August 26th, 1885. On re-admission it
was found that the anaesthesia of the legs had quite
disappeared. The knee-jerk was still absent, and the
Argyll- Robertson pupil and ataxy with vertigo and
occasional pains were still present. She said that
while out of the infirmary it struck her that " leeches
would make the blood circulate." She applied a leech
to each knee and ankle, with the result that sensation
was completely restored. The scars of the leech
bites could be seen. Localisation, discriminative
tactile sensibility, and perception of pain and heat
were normal. Faradisation of the skin occasioned
pain, but there was some loss of muscular sense.
The patient is still under observation with the above
mentioned symptoms of locomotor ataxia.
The above case illustrates the important truth
that in all organic affections of the nervous system
in women hysterical symptoms are apt to appear,
and that organic disease of the nervous system may
be present in an hysterical subject. Such a group of
symptoms as loss of the knee-jerk, the pupil pheno-
mena, pains, ataxy, and vertigo could not be ascribed
to hysteria. Loss of the knee-jerk I have never seen
or read of in hysteria. On the other hand, the
anaesthesia in this case was far more extensive and
complete than that usually met with in tabes, 1.^%
1 82 DISEASES OF THE SPINAL CORD.
hysterical nature was proved by its disappearance
immediately after the appHcation of leeches.
Paraplegia depending upon idea. — This affection
was first described by Dr. Russell Reynolds. It is a
purely functional afiFection of the brain, in which the
patient gets the idea that she is paralysed, and
remains so until this idea is negatived.
In both cases an injury was the exciting cause.
The subjects of this form of paralysis belong to
the neurotic class of individuals, and not to the
hysterical class, the distinctions between which are
well marked, and have been graphically described by
Dr. Clifford Allbutt
Ideal paralysis is cured immediately the diag-
nosis is made, in this respect widely differing from
hysterical paralysis, in which the cure is always
difficult.
The diagnosis is made by the paralysis super-
vening in a highly nervous individual after a trivial
injury, all signs of organic disease being absent.
Cases of Paralysis Depending upon Idea.
Case i. — John Riley, aged i6, was sent to me
on March 25 last, by Mr. Jordan Lloyd, complaining
of complete paralysis of the left leg, from which he
had sufiered for two years.
The patient is a bright, intelligent boy, and,
according to his mother, is very emotional, good
tempered, unselfish, and very well-behaved. The
DISEASES OF THE SPINAL CORD. [1 83
mother tells me that all the family are "nervous,"
but I can obtain no history of organic disease. The
boy was most particular in relating his case to me,
and evidently took notice of the slightest ache or
twitch. He attributed the paralysis to an accident
two and a half years ago, when he was hit on the
inner side of the left ankle by a cricket ball. The
joint did not swell, and he was able to walk about
after the injury. Two or three weeks after this he
knocked his left knee against a chair very slightly ;
he had pains in the left calf immediately after this
injury, and tucking of the left leg, which he says
was straightened by a medical man under ether, but
which returned with the return of consciousness.
He was able to walk about after the second injury
until the tucking of the leg came on, when he took to
his bed, and one night found that he had lost all use
in the limb, the leg, which previously was stiff and
tucked, becoming completely flaccid He never lost
control over the urine or faeces. There was no loss
of feeling in the limb, but some pain. The paralysis
continued unchanged up to the time of my seeing
him. He used to see objects green, and at times
double. He had never had any previous illness, but
was always a nervous and apprehensive boy. Had
never had fits or suffered from headache. On exami-
nation, the left lower extremity was found to be
completely paralysed and flaccid, he could not even
move the toes, and there was absolutely no move-
ment at any joint in the limb. The left foot was a
184 DISEASES OF THE SPINAL CORD.
little bluish, but only very slightly colder than the
right, the rest of the leg was just as warm as the
right. The limb was evidently wasted, but there
was no local atrophy.
The circumference of the right leg two inches
below the tubercle of the tibia was 1 3 inches ; of the
left, ii^in. The circumference of centre of calf on
right side, I2in. ; left, 11 ^in. Circumference of
thigh 6in., above patella on right side I5^in. ; left,
I3^in. The plantar reflexes were absent on both
sides ; there was no ankle clonus ; the knee-jerk was
rather excessive on both sides ; there was no front
tap contraction ; 'the cremasteric reflexes were well
marked ; there was a general slight increase in the
reflexes, except that the plantar were absent. Sensa-
tion in the paralysed limb was perfect ; there were
no traces of bed sore or any trophic mischief; no
spinal tenderness or deformity ; no cerebral symp-
toms ; and no twitchings of the muscles of the face.
He had acne on the face, and was evidently anaemic,
there being pallor of the mucous membranes, and
soft systolic bruits at the base and apex of the heart.
He never had suffered from rheumatism. Bowels
were constipated.
On testing the nerves, motor points, and muscles
of the left limb with a powerful Farad ic current, the
muscles responded well, only very slightly less than
those of the sound side ; great pain being caused by
the current. With weaker currents contractions were
DISEASES OF THE SPINAL CORD. 1 85
obtained, only slightly less in intensity than those on
the sound side.
After informing him that I should continue
giving him the battery till he could move his toes
and raise his heel from the ground sufficiently to
enable me to pass my fingers under it, he quickly
moved them and wriggled his foot till he got his heel
on my fingers. Another fact observed greatly aided
me in the diagnosis. I made him support himself
entirely on his crutches, letting his legs hang freely ;
I then pushed the right leg backwards away from the
vertical position, making a considerable deflection
backwards ; the left leg went back with the right,
and did not remain hanging perpendicularly as it
would have done had it been paralysed from organic
disease.
It will be seen that there were absolutely no
signs of organic disease except the wasting of the
muscles ; but this was slight and general, and easily
explained by the long duration of the paralysis
(over two years). I was forced then to conclude that
the paralysis was functional. But the boy was not
of the "hysterical type." He had no hysterical
symptoms, and no variation in the paralysis had
occurred; but was vivacious, good tempered, unsel-
fish, anxious, and intelligent, always nervous and
apprehensive. He was evidently of the " neurotic "
class of individuals.
Dr. Russell Reynolds has described a form of
paralysis depending upon imagination, where there is
1 86 DISEASES OF THE SPINAL CORD.
no malingering, but the patients are thoroughly con-
vinced that they are suffering from paralysis. This,
I believe, is the explanation of the above case. The
absence of signs of organic disease, the temperament
and mental state of the boy, show it to be a case of
ideal paralysis.
Slight paralysis and atrophy of extensor
muscles occur in chronic joint diseases, due to
changes set up in the cord by the local irritation.
In these cases the extensor muscles chiefly suffer,
and complete paralysis is rare. Charcot reports a
case of a young man who had received an injury to
his knee, which was followed by marked paralysis of
the extensors of the leg on the thigh. These cases
form one variety of reflex paralyses. Was this mono-
plegia, in the case under notice, of the nature of a
reflex paralysis, or was it ideal ? The slightness of
the injury, which was never followed by any evident
joint mischief, the absence of any local atrophy, and
the completeness of the paralysis show that it was
not due to joint mischief
After making the diagnosis of ideal paralysis, I
informed the boy's mother that there was no organic
disease, and that the paralysis? would get better very
soon. The boy was also told that the leg would get
all right, and that he was to use it as much as
possible. After one application of a powerful
Faradic current, he was able to flex the toes and
move the ankle. He attended daily to be Faradised,
and in a week was ordered to leave off the use of
DISEASES OF THE SPINAL CORD. 1 87
crutches and to use a stick. In a few days the stick
was also dispensed with. On April loth (about a
fortnight after I first saw him) he walked to the
Queen's Hospital without any support, a distance of
about two miles. For a few days he limped
slightly with the left leg, this was due partly to the
wasting, but chiefly to the disuse for the last two
years, the various movements of the extremity
having to be re-acquired. The patient resumed his
employment, and has been perfectly well since.
Case 2. — Sarah F., a widow, aged 46, was sent
to the Queen's Hospital, to be admitted under my
care, by Dr. Middleton, of Harborne, on the 15th of
March last, and was discharged well on March 28th.
She has led a very industrious life, having supported
her five children by needlework since her husband's
death ten years ago. On October 9th, 1885, she
tumbled downstairs, falling down twenty-one steps
on to her back. She was much hurt and "dazed,"
and very much frightened, thinking every bone in her
body was broken. She walked about after the
accident for a day or two, but suffered from pains in
the back, down the legs, and round the body ; these
pains were intermittent, very severe, and lasted
altogether three weeks. Two days after the accident
she took to her bed, and a day or two later found
that she was paralysed in both her legs, and had lost
all feeling in them. Since the accident she had
suffered from constant headache and backache.
Upon examining her I found that she had a little
l88 DISEASES OF THE SPINAL CORD.
power over the legs, but very little. Slight ankle
clonus could be elicited on the left side. The plantar
and abdominal reflexes were lost, but the knee-jerk
was well marked. There was complete analgesia
and thermal anaesthesia in both legs up to the knees.
She was unable to localise tactile sensations below
the knees, the anaesthesia not being complete. When
touched with a sharp-pointed instrument she said she
felt as if she were being pushed. Muscular sense
was unaffected. There was superficial tenderness
over the lower dorsal spines, but no pain on firm
pressure or on percussion, and no irregularity of the
spine. The bladder and rectum were unaffected, and
I was informed by Dr. Middleton that she had never
lost control over the bladder, nor had any sign of bed
sore during her illness. There was no oedema of the
legs, no alteration of temperature, and no change in
the colour or aspect of the skin or nails. In fact,
there were absolutely no trophic changes whatever.
The response of the muscles to Faradisation of their
nerves was normal, but there was considerable
electrical anaesthesia. In summing up the symptoms
present, I of course observed their incongruity, if we
supposed the case to be one of myelitis, or, in fact,
as due to any organic lesion. If the anaesthesia were
due to actual lesion of the grey matter, how could
the bladder and rectum escape? How was it that
there was no sign of bed sore, no oedema, or other
trophic change, such as muscular wasting? I
diagnosed the case immediately as being purely
DISEASES OF THE SPINAL CORD. 1 89
functional, and, the woman being of the neurotic
type, as one of paraplegia depending upon idea. I at
once acted upon this diagnosis, and told the patient
that I should give her the battery, which I said would
at once remove the loss of sensation and enable her
to move her legs as well as she ever did. She was
delighted to hear this, and after a minute's Faradisa-
tion sensation was completely restored, and she had
full command over her legs. I then told her that on
my next visit I should expect to see her walking
about the ward, for I was sure that she would be able
to do so. I instructed Mr. Whittindale, my house
physician, to see that she got up after I left, and to
apply the Faradic current whenever she displayed
any hesitancy. On my next visit, two days later, I
found her up and able to walk and run about the
ward perfectly well. She was quite delighted at her
recovery, and had been most industrious with her
needle since getting up. She expressed deep grati-
tude, and hoped to be able to repay our kindness.
I may add that I saw the patient six months later^
and she was quite well.
How was the cure effected in this case?
Undoubtedly, I think, it was by the mental state of
faith or expectation, or both, on the patient's part.
She fully believed what I told her, and thus I was
able to remove the idea she had that she was para-
lysed. The essential thing, then, in these cases is to
make a correct diagnosis, and then the patients can
safely and with success be told that they will ajivckV^
I90 DISEASES OF THE SPINAL CORD.
recover. Now, had this been an hysterical woman, I
should in all probability have failed to cure her, or
at any rate, the cure would have been more tedious.
I have previously recorded the case of a woman
under my care siffering from locomotor ataxy with
hysterical anaestheo. \ For two years I did all I could
to cure the anaesthesia, and ailed ; but when she left
the infirmary she applied leeches to her legs, and
returned with the anaesthesia gone. Isolation, so
useful in hysterical cases, is not needed in these.
In the same ward with my case of ideal paralysis
there was a young woman suffering from hysterical
neuralgia, and the contrast between the two patients
was very marked. The hysterical woman was listless
and apathetic, did not manifest any desire to be
cured, and would scarcely allow that she was any
better than when admitted. When told that she
was well enough to go back to her duties as a teacher
she seemed disappointed, and said that she did not
intend to begin work again for some months. The
neurotic woman, on the contrary, wanted to leave the
hospital immediately she could walk. The hysterical
woman was observed to be always sitting opposite
the neurotic woman, contemplating her with her
hands idly folded in her lap, watching the other
busily working.
Such cases as these illustrate the enormous
influence of the mind over the body. It is with
these cases that the so-called faith healers work
pretended miracles. What an opportunity for a faith
DISEASES OF THE SPINAL CORD. IQI
healer my two cases would have afforded ! Just as the
mind has an enormous influence in causing disorders
of sensation, of motion, and also of the organic
functions, so also its influence can be used as a
practical remedy in disease. As Dr. Wilks has well
observed, " the practice of medicine is not only one
of physic, but of psychology also.'*
Reflex paraplegia is paraplegia due to irritation
of peripheral nerves acting reflexly.
Paralysis, like spasm, may be brought about by
irritative diseases of various organs, but especially of
the urethra, bladder, or rectum.
The paralysis which is apt to be associated with
disease of the bladder or rectum is not always
functional or purely reflex.
I. — In some cases myelitis is present, caused by
ascending neuritis of the nerves of the diseased
organ.
2. — In some cases there is neuritis of the branches
of the lumbar and sacral plexuses spreading from the
nerves of the diseased organ.
3. — In a third class of cases there is no myelitis
or other change in the cord, and no affection of the
nerves. These are the cases of true reflex paralysis.
We can only diagnose reflex paralysis when there are
no signs of organic disease of the cord or nerves and
when removal of the peripheral irritation at once
cures the paralysis.
The term reflex paraplegia was first used by
Brown-S^quard, who supposed that the paralytic
193 DISEASES OF THE SPINAL CORD.
phenomena were due to reflex spasm of the vessels of
the spinal cord.
Malarial paraplegia is said to be intermittent,
and to occur at inter\'als, often taking the place
of a paroxysm of ague. It is said to be a
functional affection of the cord and to be cured by-
quinine.
Ancemic paraplegia, — The arrangement of the
blood vessels in the lower end of the cord fully
explains the occurrence of paraplegia in severe cases
of anaemia.
The branches from the ilio-lumbar and lateral
sacral arteries to the spinal cord are very long and
small, and pass along the branches of the cauda
equina to the conus medullaris. Hence it is that
the extreme end of the cord suffers in anaemia,
the blood supply being weakest here. The late
Dr. Moxon first pointed this out a few years
ago in his lectures on cerebral anaemia and hyper-
aemia.
A woman who had been confined several weeks
previously was admitted into the Queen's Hospital
under my care. She had sufi'ered from severe
haemorrhage after her confinement, and the day after
getting up, about the tenth day after confinement,
she felt numbness and tingling in the feet, and
gradually lost the use of the legs.
The paralysis was complete in the feet, much
less in the legs and thighs, with flaccidity. Sensation
was only slightly affected, and the reflexes were
DISEASES OF THE SPINAL CORD. I93
normal with the*exception of the plantar which were
abolished.
The sphincters were unaffected and no trophic
lesions were present, the preponderance of the
paralysis in the feet being fully explained by the
feeble vascular supply to the conus medullaris.
This patient only stayed in the hospital a few
days, but she recovered some months after.
CHAPTER X.
DISEASES OF THE SPINAL CORD
(CONTINUED),
Organic Affectmis of the Spinal Cord,
«
PoliO'inyelitis A?iterior Acuta,
This IS a system disease affecting the anterior
cornua of grey matter in the cord. There are two
varieties —
I. — That occurring in infants, and
2. — That occurring in adults.
This disease is well known under the name of
infantile paralysis or essential paralysis of children.
The following are its characteristic features : —
I. — The onset of paralysis is sudden and attended
with fever.
2. — The maximum of paralysis is at once reached,
and subsequent changes are in the direction of
improvement.
3. — The paralysed limbs are flaccid.
4. — There are no sensory disturbances except in
rare cases, and no bed sores.
DISEASES OF THE SPINAL CORD. I95
5. — Qualitative electrical changes are present,
varying in degree according to the extent of the
damage to the motor cells in the anterior cornua.
6. — Rapid wasting of the paralysed muscles
occurs.
7. — The bladder and rectum are unaffected.
8. — The reflexes are abolished.
9. — In the infantile variety the bones are arrested
in their growth ; deformities and contractures are
common.
This disease occasionally occurs in adults, and in
them deformities, contractures, and arrest of develop-
ment of the long bones seldom occur.
Nearly all cases of paralysis in children are apt
to be put down to this disease.
The following diseases must be carefully dis-
tinguished from polio-myelitis anterior acuta : —
I. — Peripheral neuritis. — After specific fevers or
from other causes neuritis of certain nerves may
occur, which may lead to wasting. I have met with
several such cases.
If sensory disturbances, in the case of a mixed
nerve, are absent the only way in which a differential
diagnosis can be made is by accurately observing the
distribution of the paralysis.
If the distribution of the paralysis is an
anatomical one ; that is, if the muscles supplied by
certain nerves only suffer, the lesion is in the
peripheral nerves.
196 DISEASES OF THE SPINAL CORD.
If, on the other hand, those muscles suffer which
are physiologically associated or functionally related^
then the lesion is in the anterior cornua.
Take for instance the muscles that flex the
elbow : — Disease of the spinal cord causing paralysis
of one of these muscles causes paralysis also of the
others, although they are supplied by different nerves ;
the biceps and brachial anticus being supplied by the
musculo-cutaneous nerve, the supinator longus by the
musculo-spiral.
2. — Another affection, first described by
Duchenne, under the name of " paralysie obstetricale
infantile du membre sup^rieure," or obstetrical
paralysis, is occasionally met with in infants.
It is a paralysis of the upper extremity occurring
in children whose birth has been effected by instru-
ments or by turning, and it is due to injury to the
brachial plexus. There is not complete paralysis of
the' limb but it hangs immovable in an extended
position, and is forcibly rotated inwards. The child
can move the hands and fingers but is unable to flex
the forearm or to raise the arm.
Usually the paralysis is similar to that form first
described by Erb, in which there is simultaneous
paralysis of the deltoid, biceps, brachialis anticus, and
the long and short supinator muscles, the lesion being
one of the fifth cervical nerve.
Two years ago I showed one of these cases
before the Midland Medical Society as a case of
peripheral monoplegia due to injury of the brachial
DISEASES OF THE SPINAL CORD. \gj
plexus at birth. Such cases are to be distinguished
by their existence from birth and by the distribution
of the paralysis.
3. — Rickets. — Parents frequently bring their
children to the hospitals thinking that they are
paralysed in the legs. It is at once seen that the
child can move the limbs, and that the inability to
stand is due to the muscular weakness depending
upon the ricketty condition.
Siibaaite Inflammation of the Ajiterior Cornua,
General Spinal Paralysis. — This disease was first
described by Duchenne ; it is characterised by
weakness, first affecting the lower limbs, the feet before
the legs, the legs before the thighs ; then affecting the
upper limbs, the extensor muscles of the fore-arms
suffering first, then the arms.
The muscles of the trunk may or may not be
affected. The lesion being one of the anterior
cornua, the symptoms can be readily understood, e.g,
I. — "The reaction of degeneration " is met with.
2. — Rapid wasting of the muscles takes place,
being preceded by paralysis.
3. — There are no sensory disturbances.
4. — There is no paralysis of the rectum or bladder.
In rare cases the upper limbs are affected before
the lower. This disease can be distinguished from —
I. — Polio-myelitis anterior acuta, by its gradual
onset and by the progressive character of the
paralysis, which never reaches its maximum at oace..
198 DISEASES OF THE SPINAL CORD.
2. — Progressive muscular atrophy, by its more
rapid progress, by the qualitative electrical changes,
and especially by the fact that paralysis precedes the
atrophy, not following and being proportional to it.
3. — Acute multiple neuritis, which greatly
resembles it by the absence of sensory disturbances,
and of tenderness along the course of the nerves, and
also by the anatomical distribution of the paralysis in
multiple neuritis.
ProgressivelMtisailar Atrophy.
This is a chronic disease of the anterior cornua
of the cord, characterised by progressive atrophy
of the muscles, first usually of those of the thenar
eminences.
The following are its characteristic features : —
I. — There is no paralysis until all the muscular
fibres are destroyed.
2. — The weakness depends upon and is propor-
tional to the atrophy.
3. — The reflexes and the Farad ic response are
not abolished until all the muscular fibres are
destroyed.
4. — The bladder and rectum are unaffected.
5. — Sensation is also unaffected.
This disease leads to a peculiar distortion of the
hand called the " clawed hand " or " main en griffe,"
which is due to paralysis of the interrossei muscles.
The "clawed hand " may be caused by lesions of the
DISEASES OF THE SPINAL CORD. 1 99
ulnar nerve, which is the motor nerve to the inter-
rossei muscles, but in this case there would be sensory
and trophic disturbances also.
In addition to the common and classical form of
progressive muscular atrophy, to which in fact the
name was first applied, there are several types of the
disease marked by sufficiently constant and peculiar
features to warrant their separate consideration.
The infantile type was described by Duchenne in
1855. It occurs in childhood and affects first the
muscles of expression of the upper part of the face,
which are rendered immobile, thus imparting a fixed
expression to the face. The forehead is smooth and
free from wrinkles, and in the act of laughing the
mouth is moved laterally only, the rest of the face
being immobile (^^ rire en travers''). To this con-
dition of the face the term " facies myopathica "
has been applied.
• The muscles of mastication and deglutition are
unaffected ; the atrophy, however, affects the shoulder
and arm muscles, and late in the course of the disease
attacks the hand muscles. There is no reaction of
degeneration, and no fibrillary tremor, the disease being
probably myopathic and not neural. Heredity is a
marked feature.
T lie juvenile type was described by Erb in 1884.
This form of progressive muscular atrophy is charac-
terised by its occurrence about the period of puberty,
first appearing in the shoulder muscles, the hands
being rarely affected except in an advanced stage.
200 DISEASES OF THE SPINAL CORD.
The legs frequently suffer, fibrillary tremors do
not occur, nor is the reaction of degeneration present.
The leg type of progressive muscular atrophy has
recently attracted considerable attention.
Charcot and Marie, in the " Revue de Medicine,"
for February, 1886, contribute an article upon this
form of progressive muscular atrophy, and fully
describe five cases which they have met with.
Dr. H. A. Tooth, in a thesis, has recently fully
described and collected all the previously recorded
cases of this form of atrophy. Dr. Tooth names
this variety the peroneal type, because the atrophy
most frequently commences in the peronei muscles*
which being weakened, cause the foot to be turned
inwards (talipes varus). But the atrophy may begin
in the calf muscles or in those on the front of the
leg, and, moreover, the foot is not always turned
inwards, so that perhaps it is well to use the more
general term and call it the leg type.
The following instances of this form of pro-
gressive muscular atrophy have recently come under
my notice : —
Case i. — E. B., a woman, aged 40, was admitted
into the Queen\s Hospital on November iSth, com-
plaining of weakness of her hands and legs.
The patient remembers that her father was unable
to straighten his fingers, and that his hands were
wasted like her own. She has heard her father talk
of an uncle of his who was affected in the legs and
hands, and she says that it was looked upon as a
N
DISEASES OF THE SPINAL CORD. 201
family complaint. She has two sisters who are
affected in the same way as herself.
About three years ago she noticed that she could
not easily lift her feet. They dragged and often
caused her to trip, until to avoid this constant falling,
she got into the habit of raising her feet well off the
ground when walking. Soon she noticed weakness
in the calf muscles, with wasting, the weakness and
wasting gradually increasing up to the present time.
About twelve months ago she observed that her hands
were wasting and becoming weak.
There is effacement of the thenar and hypo-
thenar eminences ; the '* clawed hand " is present on
both sides, and the forearms are slightly wasted. The
legs are much wasted, the calf muscles being almost
destroyed, and there is a depression along the
outer side of the tibia, marking the atrophy of the
extensor muscles.
The feet are dropped, flaccid, and turned inwards,
there being no power of dorsal flexion, but she can
flex the toes and move the feet from side to side.
The soles of the feet are deeply hollowed. There is
marked wasting of the vastus internus on each side,
causing the inner condyle of the femur to appear
abnormally prominent.
The shoulder, trunk, buttock, and facial muscles
are unaffected.
There are no fibrillar contractions, nor can any
be evoked by filliping the muscles. Sensatiotv vrv
2D2 DISEASES OF THE SPINAL CORD.
unaffected but she has suffered from cramps in the
calf muscles.
The plantar reflex is lost on both sides, the knee
jerk is present on the right side, absent on the left.
The feet and hands are always bluish and cold.
With the Faradic current, in the right leg the
peronei contract very feebly. The tibialis anticus
and extensor proprius pollicis also respond very
slightly. The extensor longus digitorum does not
respond.
The calf muscles, interossei and peroneus tertius
all respond, but the response is decidedly below-
normal.
In the left leg the tibialis anticus and peronei
respond as do the calf muscles, but the response of
the extensor communis digitorum is much diminished.
With Galvanism^ the reaction of degeneration
is present on both sides, the contractions being
quantitatively diminished and sluggish, A C C pre-
dominating over C C C.
There was in this case no enlargement of any
muscles, and no history of lead or alcoholic poisoning.
The patient's two sisters came to see me at the
hospital, and I found that they were both suffering
from the same type of progressive muscular atrophy.
Case 2. — C. M., aged 41, states that her illness
commenced four years ago, and that she noticed it first
after a confinement, observing that she could not pick
her toes up ; and she often used to pitch forwards.
She has had nine children and no miscarriages.
DISEASES OF THE SPINAL CORD. 203
The muscles of the feet and legs are extremely
atrophied, and she has no power over the feet, which
are perfectly flaccid, dropped, and turned inwards.
Thecircum.of R. Ieg6in. below patella = 9in.; L. 8^in.
„ „ „ above „ = I3in.; L. I3in.
With Faradism the extensor communis digitorum
and the peronei on both sides give no response, the
gastrocnemii respond freely. With Galvanism
A C C predominates over C C C in the leg muscles.
The knee jerk is absent on the left side, feebly
present on the right side.
The gait is very characteristic, the patient having
to bend the knees to a considerable extent to enable
her feet to clear the ground, "equine gait," there
being no waddling.
Sensation is unaffected but she has suffered from
pains in the legs and from girdle pain.
The thenar and hypothenar muscles are wasted,
and the grasp is very feeble. She is unable to extend
the fingers, which are flexed at the phalangeal,
extended at the metacarpo-phalangeal joints (main
en griffe).
There is no fibrillar contraction, no muscular
hypertrophy, no pupil alterations, and no wasting of
the face, tongue, shoulder, hip, or trunk muscles.
The thighs are wasted in the lower third only. The
disease commenced insidiously, and the weakness
and atrophy are slowly progressing /^r/ passu.
Case 3. — The other sister, A. B., 49, the eldest of
the three sisters, is affected in the same way as her
204 DISEASES OF THE SPINAL CORD.
sisters, but the disease in her case is more advanced.
She states that it has been coming on twenty-nine
years. The knee-jerk is lost on both sides. The
legs and lower third of each thigh are much wasted,
the feet being in the position of talipes varus. There
is no power of dorsal flexion of the foot. The
hands are clawed and wasted, and there is marked
" high action " gait. There are no fibrillar contrac-
tions, no sensory changes, no wasting of the face,
shoulder, hip or trunk muscles. The muscles on the
front of the legs gave no response to the Faradic
current ; some pain having been given her she
refused to let us try the Galvanic current.
Case 4. — J. B., a man, aged 50, at the present
time an inmate of the Birmingham Workhouse
Infirmary, is in an advanced stage of progressive
muscular atrophy, which has completely destroyed
the muscles of the legs. The disease commenced
nine years ago, when he noticed that he was clumsy
in picking his feet up, and often used to trip. He
had syphilis twenty-five years ago, and has been an
ironworker, having had to pull up heavy melting
pots out of a furnace, there being thus a great
strain on the legs. The legs and lower third of
the thighs are extremely atrophied, the feet are
dropped, and he has completely lost all power over
them, being unable to produce the slightest move-
ment even of the toes. He can bend the knee, but
has difficulty in extending it again. The circum-
ference of the right leg three inches below the patella
DiyEASES OF THE Sl'INAL CORD.
205^^1
is iiiii., of the left at the same level ii^in. The
circumference of the thigh five inches above the
patella on the right side measures i3in., on the left
I3j^in. The gait is very characteristic, and similar
Thr Leg Tvi'E ok Pkooressive Musculak Atkopilv.
to that in the above cases, not at all waddling, but ot
the high action character. The thigh muscles are
much atrophied in the lower third, especially in the
206 DISEASES OF THE SPINAL CORD.
situation of the vastus internus, the internal condyles
projecting to a marked extent. The muscles of the
sole of the foot are much wasted, and in standing
there is complete talipes valgus. With the Faradic
current there is no response in any of the muscles on
the front of either leg, and a feeble response only of the
peronei and calf muscles. With Galvanism there is
no response of the muscles on the front of the legs.
In the peronei and calf niuscles A C C predominates
over C C C. There is a little flattening of the
thenar and hypothenar eminences in each hand, but
no clawed condition. Sensation is normal, but he
complains of coldness of the hands and feet, which
in fact are cold and bluish. There is no wasting of
the facial, shoulder, or trunk muscles, and no fibrillar
contractions. He can give me no family history of
importance.
Progressive muscular atrophy must be dis-
tinguished from
I. — Lesions of the peripheral nerves.
2. — Lead paralysis.
3. — The atrophy that is frequently present in
cases of writer^s cramp and other professional hyper-
kineses.
Paralysis and muscular atrophy due to lead
poisoning, in the absence of the blue line on the
gums, may be distinguished by the following facts: —
I. — The onset of the paralysis is usually rapid
when due to lead.
2. — The paresis is in excess of the atrophy.
DISEASES OF THE SPINAL CORD. 207
3. — Qualitative electrical changes are usually
present.
4. — There is improvement on administering
iodide of potassium internally.
In the muscular atrophy which sometimes
accompanies writer's cramp and other professional
hyperkineses the atrophy is preceded by paresis or
cramp, and partial or complete recovery ensues when
absolute cessation of the act of writing is insisted
upon and galvanism is employed. The atrophy does
not become general and endanger life.
Pseiido-hypertrophic Paralysis.
The pathology of this disease is by no means
definitely known, some authorities believing it to be
a disease of the motor cells in the anterior cornua,
others a disease of the muscles.
This disease may be confounded with progressive
muscular atrophy, for there is always atrophy of some
muscles and towards the end a condition of general
paralysis with great emaciation. But even then the
calf-muscles and the infra-spinati will be found to be
enlarged. The knee-jerk will be lost and talipes
equinus with inability to perform dorsal flexion of the
foot present.
Of course the presence of the waddling gait,
the characteristic mode of rising from the recumbent
and sitting posture, and lordosis at once distinguish
the disease.
208 DISEASES OF THE SPINAL CORD.
It is important to remember that this disease
occurs in adults. I have met with three such cases,
two of which I have recorded. All three patients
had been informed that they were suffering from
" general debility," and that they would get well.
The characteristic symptoms of the disease
are : —
I. — Enlargement of the muscles of the calves,
buttocks, and forearms, with marked weakness.
2. — Atrophy of certain muscles, especially of the
biceps and costo-sternal portions of the pectoralis
major.
3. — Marked lordosis in the erect position, a
plumb-line let fall from the most prominent part of
the spine falling three or four inches behind the
sacrum.
4. — A waddling gait and the characteristic mode
of rising from the sitting and recumbent position.
5. — In a late stage loss of the knee-jerk.
When progressive muscular atrophy commences
in the lower extremities and back it is difficult to
distinguish it from pseudo-hypertropic paralysis, but
a waddling gait is peculiar to the latter disease, while
in the former the gait is of the high action or
"equine" type.
PseiidO'Hypertrophic Paralysis m Adults,
Case i. — J. McD., aged 33, a commercial
traveller, applied on account of weakness in the
back and legs, by which he had been affected for
DISEASES OF THE SPINAL CORD. 209
nearly three years. There was no history of any
similar disease, to the patient*s knowledge, in his
family. He was perfectly strong and well up to
within three years ago, and had never noticed any
enlargement of his calves or weakness in the legs
when a boy. He could not assign any cause for his
illness ; he had never done any laborious work, and
had never worked in lead, nor been exposed to wet
or cold. He had been rather a free drinker, but
there was no history of syphilis or of rheumatism.
Three years ago, in the winter, when in South
America, he noticed himself becoming weak in the
back, and found that he could not run ; and if at any
time his foot slipped, he had difficulty in recovering
himself. At that time, his arms and legs were
unaffected, but his back kept getting worse, and in
about six or seven months he noticed his thighs to
be getting smaller and weaker, and, at the same time,
his arms wasted and became weaker. When first
seen, his height was 5ft. 63^ in., formerly it had been
5ft. 7>^in.
The patient, apart from the atrophied parts,
looked a strong, healthy man. His gait was markedly
waddling ; he walked on his toes, the heels not
touching the ground ; if he separated his legs, he
could make his heels touch the ground, but not
otherwise.
He walked with his shoulders thrown back, and
there was marked lordosis and considerable projec-
tion of the belly. The lordosis disappeared when
2IO DISEASES OF THE SPINAL CORD.
he sat down, being replaced by a convexity back-
wards. A plumb-line, dropped from the shoulders,
was about 3^in. from the sacrum. When asked to
sit down, he first jerked his body forwards, and then
went down suddenly. When going upstairs, he took
hold of the balusters, and having put one foot on the
step above, at a considerable distance from the
balusters, so as to avoid the necessity of bending
his knee, he dragged himself up by the balusters.
When lying on his back, he could not sit up unaided,
except by turning over on to his side, and pushing
himself up. If, however, his feet were fixed, and
thus his legs prevented from moving, he could bring
himself straight upwards and forwards into the
sitting posture. If he wished to stand up, he had to
turn over on his side, and then push himself upwards
to the length of the arms, and place his hands on his
knees, thus climbing up his own body.
There was marked atrophy of the muscles of
the arm, buttock, and thigh on each side. The biceps
had almost disappeared on both sides. The scapular
portion of the deltoid was much atrophied, the cla-
vicular portion little altered. The inner head of the
triceps on the right side was unduly large. The fore-
arm and hand on each side seemed to be splendidly
developed, the thenar and hypothenar eminences
being very large ; yet, when tested with the dyna-
mometer, the grasp was only forty pounds.
The scapular muscles were much atrophied. The
scapular portion of the trapezius was atrophied,
DISEASES OF THE SPINAL CORD. 211
while the clavicular portion was unaffected. The
dorsal muscles did not seem to be reduced in volume.
The pectoral muscles on both sides were markedly
atrophied, and the patient could not bring his arms
to the middle line in front — that is, he could not
clap his hands unless he flexed Tiis elbows. There
was a marked hollow between the scapulae, the
posterior borders of these bones projecting a great
deal (winged scapulae). The serrati muscles were
evidently paralysed, for the patient could not
raise his arm above the horizontal line on the
right side, and only a little above on the left side.
The buttock and thigh muscles were much wasted,
but the gluteus medius could be felt to contract
when he walked. The calves were firm and large,
and the swelling was high up. Dorsal extension of
the foot could not be produced to the normal extent.
Sensation was perfectly normal, and the bladder and
rectum unaffected. The temperature of the legs was
95° F. There was no mottling of the skin, nor could
any fibrillary contractions be evoked.
The patient was very sensitive to cold, and was
always better in warm weather. His intellect was
unaffected, being much above the average. The
patellar tendon reflex was abolished on both sides,
the other reflexes were normal. The muscles
responded to Faradism, except the latissimus dorsi,
the serrati, the pectoral muscles, and the erector
spinae, which did not respond at all. The response
of the biceps muscle on each side was much
212 DISEASES OF THE SPINAL CORD.
diminished ; Galvanism of the nerve trunks caused
contraction of the forearm and hand muscles ; but
the contraction was below the normal, while Gal-
vanism applied directly to the muscles showed a
much greater diminution of response. No response
could be obtained in the case of the pectoral muscles,
the serrati, and rhomboidei, showing that they were
totally destroyed.
Case 2. — F. B., aged 35, a married woman,
attended the Queen^s Hospital on April 21st, 1885.
She complained of weakness in the back and legs,
and instability when standing, saying that she easily
fell or was pushed over, and of occasional pains in the
joints. Her father died from consumption at th-^ age
of 35 ; one of her brothers had a "stroke." Besides
this brother no one else in the family ever suffered
from any weakness or paralysis. She has. had two
miscarriages and six children born alive, one of
whom died from whooping-cough ; of the other five
children, one little boy is weakly, all the others
perfectly well and strong. The patient has occasion^
ally had pains in her joints, but otherwise her health
has been good ; there is no history of syphilis ; .she
has not worked in lead or been much exposed ta
cold or wet. Eleven years ago she noticed weakness
and pain in the bottom of her back, the weakness
being the chief trouble. This got gradually worse,
and has extended during the last four or five years to
the arms and legs, and she has noticed that she has
been getting stouter in her limbs and body. The
DISEASES OF THE SPINAL CORD. 21 3
patient looks a strong, healthy woman, is well developed,
and rather stout. She stands with her feet apart and
her back much arched, there being very considerable
lordosis. She can, however, stand with her feet close
together, and the heels touch the ground. When
standing, a plumb-line dropped from the most
prominent part of the spine falls three inches behind
the sacrum ; when in the sitting posture the lordosis
disappears. Her gait is waddling, the body swaying
from side to side as she walks. She says that she
falls even if a child runs against her. In raising
herself from the ground when lying on her back,
she first turns over to the left, puts both hands on
the ground, gets upon her feet, then places the hands
upon the knees, and climbs up her thighs, and finally
jerks herself into the upright position. When rising
from the sitting posture she puts her hands upon the
knees and raises herself by jerking movements.
The prominence of the calf muscles is very large on
both sides and firm. On the right side there is a
well-marked abrupt ridge formed by the calf muscles;
the circumference of the largest part of the right
calf=i5^in. ; of the left, I4^in. The patellar
reflex is present on both sides, but is much diminished
on the right, and the right leg is weaker than the
left. The buttocks are also large, the glutei muscles
being felt to contract on walking. The sterno-costal
portion of the pectoralis major of the right side is
much wasted. She has great difficulty in raising her
arms vertically upwards, and she cannot hold her
214 DISEASES OF THE SPINAL CORD.
right arm horizontally forwards for more than a few-
seconds, and when she does so the posterior border
of the scapula projects markedly backwards, showing
paresis of the serratus magnus. She can place the
right hand upon the head, but with difficulty. The
right infra-spinatus muscle is very large, the biceps
on the right side is very feeble and atrophied, and
she cannot flex the elbow when the forearm is
supinated. The forearm is apparently finely developed
on both sides, and the prominence of the extensors of
the wrist is excessive, while the power of extension is
very feeble. The thenar eminence is very well marked
on both sides, and there is no evidence of atrophy in
the small muscles of either hand. Although the
upper limbs look splendidly developed, yet she
complains of great weakness in them, and speedily
wearies even by holding them out for a few seconds.
The grasp of the right hand by the dynamometer
registers /olbs. ; of the left, 75 lbs. The erector spinae
muscles are atrophied and weak. Sensation is every-
where normal, and there are no vasomotor distur-
bances, nor any affection of the bladder or rectum,
and no fibrillary contractions can be obtained by
filipping the muscles. The intellect is also normal.
Faradism to the nerves, motor points, and muscles
brings about feeble contractions ; Galvanism to the
nerve trunks causes a stronger contraction than when
the current is applied directly to the muscles. The
patient brought her little boy, whom she said was
weak in the legs, to see me. The calves in his case
DISEASES OF THE SPINAL CORD. 215
seemed large, but not markedly so. The gait was
waddling, and he complained that he was easily
upset, but there were no other symptoms of the
disease.
Pseudo-hypertrophic paralysis is very rare in
adults, except in those cases where the disease begins
in infancy, and the patient lives to adult age. Two
cases, similar to those reported above, are recorded
in the Clinical Society's "Transactions," Vol. XVI.
The waddling gait, the absence of patellar reflexes,
the talipes equinus, the hardness and increased size
of the forearms and legs, distinguish the disease
from progressive muscular atrophy. Talipes equinus
is only met with late in the disease, and the patellar
reflexes are not abolished as long as the quadriceps
extensor is not completely atrophied.
Primary Lateral Sclerosis.
This disease is a primary system disease affecting
the crossed pyramidal tracts of the lateral columns,
with the following symptoms : —
I. — It is a disease of adult life very rarely
affecting women.
2. — Weakness and rigidity, with spasmodic
twitchings of the legs, are the characteristic symptoms.
The onset is very insidious, the rigidity being present
from the first ; the paresis and rigidity commencing
simultaneously and diAwdincmg pari passu.
2l6 DISEASES OF THE SPINAL CORD.
3. — There are no sensory disturbances.
4. — The deep and superficial reflexes are exag-
gerated, ankle clonus being present.
5. — The gait is very characteristic, the patient
having great difficulty in elevating the toes, which
scrape the ground.
We must distinguish between this disease and
secondary degeneration of the pyramidal tracts
following a chronic myelitis or following compression
of the cord, as in the paraplegia which often follows
spinal caries, or in that produced by an extra
medullary tumour ; because in chronic myelitis all
sensory disturbances may disappear, leaving a con-
dition exactly similar to that observed in primary
lateral sclerosis. We must then depend upon the
history of the onset of the illness.
In chronic myelitis : —
I. — The weakness precedes the rigidity.
2. — Sensory disturbances are usually present.
3. — The bladder and rectum may be paralysed,
and these organs are always more affected than in
primary lateral sclerosis.
In compression of the cord the onset and
progress are more rapid than in primary lateral
sclerosis ; the paresis also precedes and preponderates
over the rigidity.
In disseminated sclerosis the sclerosis might
affect only the pyramidal tracts and cause symptoms
exactly similar to those observed in primary lateral
DISEASES OF THE SPINAL CORD. 21/
sclerosis, but sooner or later characteristic symptoms
of the former disease would appear, such as nystagmus,
vertigo, syllabic utterance, &c.
Amyotrophic Lateral Sclerosis,
This is a combined system disease of the crossed
pyramidal tracts, and of the anterior cornua, and was
first described by Charcot.
I. — The upper extremities are usually first
affected, the symptoms consisting in weakness, with
rigidity and contracture, followed by
2. — General atrophy of the muscles of the upper
extremity, followed by
3. — Weakness and rigidity of the lower ex-
tremities, and after a time diff'use atrophy of the
muscles of the lower extremities.
The reflexes are exaggerated, there is no dis-
turbance of sensation and no affection of the bladder
or rectum. The disease is a very fatal one, lasting
two or three years, death being produced by extension
of the disease to the medulla and the production of
bulbar symptoms.
I published in the " Birmingham Medical
Review," March, 1884, an account of a man still
in the Workhouse Infirmary, who is suffering from
this disease. The disease has not yet extended to
the medulla, but the patient is quite bedridden.
2l8 DISEASES OF THE SPINAL CORD.
The diagnosis of this disease is very easy.
From progressive muscular atrophy we can dis-
tinguish it : —
I. — By the atrophy being general and following
the paresis, for this reason Charcot called this disease
"atrophic en masse.'* In progressive muscular
atrophy it is local, a group of muscles, or even a
single muscle, being affected
2. — By the presence of rigidity and the increase
of reflexes.
3. — By the rapidity of its progress.
4. — By the signs of spastic paraplegia, which
supervene in the lower extremities.
Pachymeningitis cervicalis hypertrophica some-
what resembles amytrophic lateral sclerosis ; but the
former disease is attended —
I. — With marked sensory disturbances, severe
pains, and hyperaesthesia in the upper extremities.
2. — There is no atrophy of the muscles of the
lower extremities.
3. — The disease frequently ends in complete
recovery, and does not implicate the medulla.
Primary lateral sclerosis is easily distinguished
from amytrophic lateral sclerosis —
I. — By the absence of general atrophy of the
muscles.
2. — By its far more chronic nature.
3. — By there being no tendency to bulbar
paralysis.
DISEASES OF THE SPINAL CORD. 219
Locomotor Ataxia^ or Tabes Dorsalis,
This disease is so well known to you that it is
needless for me to enumerate its symptoms. It is a
primary system disease of the postero - external
columns of the cord or root zones. Loss of the knee-
jerk is an early symptom of this disease ; it may, in
fact, precede all other symptoms for years, although
usually it is associated with the Argyll-Robertson
pupil (loss of the pupil reflex to light only).
The various diseases in which the knee-jerk is
lost must be carefully kept in mind before the diag-
nosis of tabes is made. There is little doubt that
many supposed cases of this disease which have been
cured were cases of peripheral neuritis from alcohol
or other cause.
Primary optic atrophy may precede all other
symptoms, even loss of the knee-jerk, for years. In
one of my cases perforating ulcer of the foot was the
first symptom observed.
The combination of anaesthesia with shooting
pains and cramps, termed "anaesthesia dolorosa," is
often observed in this disease. This condition is of
considerable value as a diagnostic sign, for it shows
that the lesion is situated outside the grey matter of
the cord. It is produced by pressure on the posterior
nerve roots, or on the sensory fibres as they pass
through the postero-external columns of the cord ;
therefore it is often present in locomotor ataxia, and
is a marked symptom also in cases of extra-medullary
growths which compress the posterior nerve roots.
220 DISEASES OF THE SPINAL CORD.
The diagnosis of tabes dorsalis can be made
long before the gait becomes ataxic : —
Thus (i) loss of the knee-jerk, (2) with the
characteristic pains, and (3) the pupil phenomena
are in themselves sufficient ; or grey atrophy of
the discs, with loss of the knee-jerk, would
suffice for the diagnosis of the disease, even in the
absence of ataxy. The disease may commence in
the upper extremities. Mr. Chavasse recently sent
me a man, who complained of numbness in the
fingers and inability to use them in picking up
things. He was a hatter by trade, and he could not
hold hats in his left hand as well as usual. There
had been no pains, and there was no paralysis or
anaesthesia, but there was marked ataxy and loss of
muscular sense in the upper extremities. He could
not distinguish a half-pound from an ounce weight
suspended in bags from his fingers. He said that
he could only just perceive a pound weight
similarly suspended. There were no electrical
changes or other indications of a peripheral neuritis.
The knee-jerk was normal, and the legs were not
ataxic, nor were there any ocular symptoms. I
think there can be no doubt that this was a case of
tabes dorsalis beginning in the lower cervical region
of the cord.
Loss of muscular sense may occur —
I. — In lesions of the peripheral nerves.
2. — In lesions of the cord, especially in loco-
motor ataxia.
DISEASES OF THE SPINAL CORD. 221
3. — In lesions of the internal capsule, as previ-
ously mentioned.
I have several times seen maniacal symptoms
supervene in cases of locomotor ataxia and symptoms
of general paralytic dementia.
The joint disease occurring in locomotor ataxia,
and described by Charcot as a trophic lesion, is said
to be distinguished from chronic rheumatic arthritis
by the following features : —
I. — ^^Pain is absent in this disease, present in
rheumatic arthritis.
2. — Effusion is generally present here and absent
in rheumatic arthritis.
3. — Dislocations are common tn tabes, but rare
in rheumatic arthritis, moreover the bones are apt
to fracture very readily, and without pain in the
former.
4. — In the joint lesion of tabes there is preter-
natural mobility.
5.^In tabes the knee and shoulder are most
often affected, in rheumatic arthritis the hip and
smaller joints.
6. — There is more atrophy of bone in tabes,
more out-growth or hypertrophy in rheumatic
arthritis.
Locomotor ataxia must be distinguished from
I. — The ataxy of cerebellar disease.
2. — Hysterical ataxy.
3. — Multiple sclerosis, with implication of the
postero-external columns.
222 DISEASES OF THE SPINAL CORD.
4. — Syphilis, which may cause symptoms very-
like those of true tabes, with paralysis of the cranial
nerves and pains in the legs.
5. — Ataxia due to peripheral neuritis, from
alcoholism, diphtheria, diabetes, &c.
In cerebellar disease there is a staggering gait,
not the peculiar jerking gait of the ataxic.
The knee jerk is sometimes lost in this disease,
so that a mistake may easily occur.
But the presence of vomiting, headache, double
optic neuritis, or convulsive seizures would clear up
the case.
In hysterical ataxy the patient is able to use the
limbs with perfect order while lying down, ataxy-
being marked when she sits up or stands. Pains are
usually absent and the knee jerk is not lost.
In locomotor ataxia temporary paralysis of the
ocular muscles is common, and it is characteristic in
that the paralysis gets well of itself, contrasting with
the optic nerve atrophy^ which never recovers.
Mercury and iodide of potassium cure syphilitic
affections, but I have never observed any appreciable
improvement from the administration of iodide of
potassium, even in large doses, in locomotor ataxy.
Combined disease of the postero-external and lateral
spinal tracts.
Sclerosis of the postero-external columns of the
cord may be combined with sclerosis of the lateral
columns.
DISEASES OF THE SPINAL CORD. 223
In these cases there is weakness of the lower
extremities combined with ataxy.
The reflexes are exaggerated, the knee jerk being
excessive, and ankle clonus is present.
Pains are usually absent or slightly marked.
The pupil symptom and optic atrophy are rarely
present.
Visceral crises are also very rare.
In this disease the lesion in the lateral columns
occurs simultaneously with that in the postero-
external tracts.
In ordinary tabes weakness may supervene from
extension of the disease to the lateral columns, and
wasting from extension to the anterior cornua, but in
these cases the knee jerk, which is lost early, does not
reappear.
Dr. Gowers has recently fully described this
condition, which he calls " ataxic paraplegia " in a
clinical lecture published in the "Lancet," July, 1886,
and in "Brain," Vol. VIII., is contained a critical
digest of the subject by Dr. Ormerod.
Friedreich s Disease,
An hereditary ataxia^ first described by Fried-
reich, and hence named after him, must be dis-
tinguished from ordinary tabes.
Hereditary ataxia attacks many members of the
same generation, and runs in families.
It occurs in early life (4-18), and in both
sexes, while ordinary tabes is a disease of adult life.
224 DISEASES OF THE SPINAL CORD.
Ataxy of the lower extremities, with loss of the
knee jerk, is always present, the. ataxy soon affecting
the muscles of the trunk and upper extremities.
There are no pains, no loss of pupil reflex to
light, no transient paralysis of the ocular muscles, no
optic atrophy, no visceral crises, and no joint or bone
lesions.
But speech is usually affected, being slurred, or
there may be a mere drawl or stammering.
In some cases speech becomes unintelligible.
Nystagmus occurs late in the disease, and
Curvature of the spine may occur early or late from
defective muscular support.
The rapid spreading of the ataxy upwards is
characteristic.
The indiscriminate lesions of the spinal cord are
I. — Myelitis.
2. — Disseminated sclerosis.
3. — Haemorrhage.
4. — Tumours.
]\[yelitis may be acute, subacute, or chronic, and
may attack the whole or any part of the transverse
section of the cord, and a variable length of the
cord.
Aaite transverse myelitis or other lesion affectiiig
the whole transverse section of the cord will cause the
following symptoms :^-
I. — Paralysis of the muscles supplied by the
nerve cells of the anterior cornua in the inflamed
DISEASES OF THE SPINAL CORD. 225
segment, and of all the muscles supplied by nerves
coming off from the cord below the lesion.
2. — Anaesthesia below the lesion and in the area
corresponding to the inflamed segment.
3. — A narrow band of hyperaesthesia is usually
present at the upper level of the lesion, due to
irritation of the sensory nerve fibres at this level.
If the myelitis be in the dorsal region this
hyperaesthesia is in the form of a band round the
body and occasions the girdle sensation.
If the myelitis be in the lumbar or cervical region
then the hyperaesthesia is distributed over the limbs
according to the distribution of the sensory nerves
at the upper level of the lesion.
4. — The reflexes passing through the cord above
the lesion are unaffected, those passing through the
seat of the lesion are abolished, and those passing
below the lesion are exaggerated, cerebral control
being shut off.
5. — In the muscles supplied from the inflamed
area of the cord rapid wasting and degeneration both
of motor nerves and muscles takes place, but there
are no qualitative electrical changes or rapid wasting
in the paralysed parts supplied from the cord below
the lesion.
Trophic changes in the skin in the form of acute
bed sores also occur in the sensory area corresponding
to the inflamed portion of the cord.
6. — The bladder and rectum are always affected
but in a manner depending upon the situation of the
lesion.
^s
226 DISEASES OF THE SPINAL CORD.
If the lesion is in the lumbar region then the
sphincters are paralysed and cystitis with ammoniacal
urine rapidly supervenes.
If the lesion is above the lumj)ar region then the
reflex acts of defaecation take place without the
knowledge of the patient, and cannot be controlled
by him.
7. — Elevation of temperature in the paralysed
limbs is common, and oedema is also often present,
being due to vaso-motor paralysis.
8. — Later on, descending degeneration of the
pyramidal tracts takes place, causing rigidity and
contracture.
In the other varieties of myelitis the symptoms
will of course vary with the seat of the lesion in the
transverse section.
Case of Aaiie Myelitis.
G. C, a man aged 20, a shoemaker, admitted into
the Queen's Hospital, March 19th, died May 5th, 1884.
The patient never had any previous illness to
his knowledge, but there were scars of strumous
abscesses in his neck ; there was no distinct history
of syphih's, and anti-syphilitic treatment when tried
had no good effect, but was injurious. There was no
history of alcoholism or exposure, but his occupation
compelled him to lead a sedentary life. The family
history as far as could be ascertained was good. The
patient had been ill for eight weeks previous to
• the illness commencing as pain passing
DISEASES OF THE SPINAL CORD. 22/
round the body about midway between the umbilicus
and ensiform cartilage (girdle pain). He had also
numbness in the feet spreading quickly upwards,
with sensation "of pins and needles." He had
twitchings of the legs. He took to his bed and
rapidly lost all power over the lower part of the
body, and all sensation. There was also some diffi-
culty at this time in micturition. On admission the
patient was found to be completely paralysed in the
lower extremities.
Sensation (as to touch, pain, heat, and cold) was
completely abolished up to the level of the umbilicus,
where there was a well-marked hyperaesthetic zone.
A pin drawn over this area occasioned a cutting
sensation. In this region also there is well-marked
tache cdrdbrale. The special senses were perfectly
normal.
Reflexes. Superficial. — The plantar reflexes were
exaggerated ; the cremasteric were also well marked ;
the abdominal and the epigastric reflexes were absent.
The scapular reflex was well marked on both sides.
Deep. No ankle clonus or front tap contraction
could be obtained. The patellar-tendon reflexes
were exaggerated. The lower limbs were wasted,
but no local atrophy could be made out.
Bedsores were found over the right trochanter
and anterior part of the iliac crest. [The patient had
been lying chiefly on this side.] The skin over the
trochanter on the left side was discoloured and
evidently about to break down. There was no bed-
230 DISEASES OF THE SPINAL CORD.
change. A tubercular ulcer was found near the ileo-
caecal valve.
Kidneys. — The left weighed g}^ ounces, and
was fatty. The right 12 ounces, with yellow cheesy
deposits beneath the capsule and in the cortex. In
one place was an abscess from softening of a caseous
mass in communication with the pelvis.
Remarks. — The case was a typical one of acute
diffuse myelitis; the characteristic features of which
are the rapid loss of motion and sensation in the
parts supplied by nerves given off from the cord below
the seat of lesion, attended with fever. The stage of
irritation was first present, there being pain in the
back, and twitchings, and perverted sensations, but
this was quickly followed by complete loss of motion
and sensation. The lesion was easily localised by
means of the reflexes. i. The cremasteric reflex
passes through the cord at the level of the ist and
2nd lumbar ner\'es. 2. The abdominal through the
cord between the 8th and 12th dorsal nerves. 3. The
epigastric through the cord about the 5th, 6th, and
7th dorsal nerves. 4. The interscapular through the
cord about the two lower cervical and three upper
dorsal nerves. Now the cremasteric and interscapular
were present; the abdominal and epigastric absent;
therefore we supposed the lesion in the cord to be
situated between the 4th and 12th dorsal nerves, and
it was found between the 5th and 9th. We also
judged that the lesion was of considerable vertical
extent. The lumbar enlargement was found to be
DISEASES OF THE SPINAL CORD. 23 1
intact, thus accounting for the absence of paralysis
of the bladder and sacral bedsore. The presence of
the sores over the front of the crest of the ilium and
trochanters is explained by the fact that the skin here
is chiefly supplied by the lateral cutaneous branch of
the last dorsal nerve.
The prognosis was rendered even worse than it
usually is by the evident strumous condition of the
patient. The prognosis in acute myelitis depends
upon — (i) The situation of the inflammation, i.e., the
region of the cord affected; (2) The extent of the
transverse section of cord affected ; (3) The vertical
extent. It is always more fatal in the cervical and
lumbar regions than in the dorsal ; more serious when
the grey matter is affected, because bedsores break
out ; and more serious the greater the length of cord
affected.
In the above case the cord was found after death in
a condition of white softening; it was like cream. This
was due to the extensive fatty degeneration of the
medullary sheaths of the nerves, and also of the nerve
cells, and to the formation of masses of fat granules
This stage is preceded by red softening, when the
affected part of the cord is swollen, red, and injected,
and its consistency diminished. It was, of course,
impossible that recovery could take place after such
extensive softening, but had the patient not been
previously debilitated he would not have died so soon.
As to the cause of the myelitis in this case. It
was found that the softening of the cord exactly
232 DISEASES OF THE SPINAL CORD.
corresponded to the situation of caseous material
on the outer surface of the theca. Probably this
material, by constricting the vessels to this part of
the cord (for it extended along the nerves), was the
predisposing cause.
Hemilateral myelitis or other lesion affecting one
Iialf of tJie transverse section of the cord will cause
the following symptoms : —
I. — Paralysis on the same side of the body,
there being paralysis of all muscles supplied by the
nerves coming off at the seat of the lesion, and from
the same side of the cord below the lesion.
2. — Since the sensory nerves decussate almost
immediately on entering the cord, inflammation of
one half segment of the cord causes anaesthesia on
both sides of the body in the area of the inflamed
segment. If the lesion is in the dorsal region, then
there is a band of anaesthesia round the body ; above
this band of anaesthesia there is generally a band of
hyperaesthesia, due to irritation of the sensory fibres,
which enter the cord just above the lesion.
3. — Below the lesion there is anaesthesia on the
opposite side ; hyperaesthesia on the same side.
The sensory fibres not decussating immediately
in the lumbar and lower dorsal regions of the cord, a
unilateral lesion in these regions will cause anaesthesia,
as well as paralysis, of the leg on the same side.
4. — The reflexes passing through the inflamed
segment are lost, those passing through the same
side of the cord below the lesion are increased.
DISEASES OF THE SPINAL CORD. 233
5. — There is vaso-motor paralysis with elevation
of temperature and loss of muscular sense on the
same side as the lesion, that is, in the paralysed
extremity.
6. — Those muscles supplied by the inflamed
segment of the cord will present qualitative elect-
rical changes, and will undergo rapid atrophy.
A unilateral lesion of the cord then causes motor
paralysis, vaso-motor paralysis, and loss of muscular
sense, with hyperaesthesia on the side of the lesion>
and anaesthesia on the opposite side.
Case of Acute liemilateral Myelitis due to Syphilis,
P. C, a man aged 61, was treated for primary
syphilis in the Birmingham Workhouse Infirmary,
in August, 1884. In November of the same year
he was under my care for secondaiy ulceration
of the throat and tongue. In December he was
again admitted, and treated for syphilitic iritis.
The patient as soon as he felt relieved persisting
in leaving the infirmary. On the 28th of May,
1885, he was again admitted under my care, com-
plaining of complete paralysis of the left leg. The
loss of power, he said, had come on somewhat
gradually, and was complete in about a week. He
had had no pain in the leg or around the body.
There were several pigmented scars on the leg^
and the pupils were irregular and refused to re-
spond to light or accommodation.
234 DISEASES OF THE SPINAL CORD.
It was found that the patient was sufifering from
complete motor paralysis of the left leg, with flaccidity.
There was marked hyperaesthesia on the paralysed
side, ordinary impressions being painful. Sensations
of touch, temperature, and pain were all exaggerated.
Contacts made by the ends of a pair of compasses
coalesced and were perceived as a single sensation
when the distance between the points was less than
three inches on the right leg, but on the left the
distance between the points had to be diminished to
three-quarters of an inch before fusion of the two
impressions was produced. The discriminative sensi-
bility of the skin was, in fact, much increased in the
left leg, much diminished in the ri^ht. There was,
moreover, vaso-motor paralysis and impairment of
muscular sense in the paralysed limb, with elevation
of temperature. The temperature of the right lower
extremity was 98*4^ F., that of the left 97° F. The
patient could appreciate the difference between i oz.
and 2 oz. weights suspended in bags from the toes on
the right side, but not on the left. This experiment
was performed after the patient had recovered motor
power in the leg and could thus bring into play the
muscular sense to aid in the estimation. In the right
lower extremity there was complete analgesia and
thermal anaesthesia. As to the sense of touch, the
power of localisation was perfect, but the dis-
criminative sensibility was diminished.
The analgesia on the right side and the hyper-
aesthesia on the left extended upwards over the
DISEASES OF THE SPINAL CORD. 235
abdomen to a line drawn round the body two inches
above the umbilicus, being sharply defined at the
upper limit and ending at exactly corresponding
levels, sensation abruptly becoming normal at this
line. There were no zones of anaesthesia or hyper-
aesthesia encircling the body at the upper level of the
lesion in the cord as are described in text books to
be present in unilateral cord lesions. The plantar
reflex on the left side was excessive. There was no
ankle clonus on either side. The patellar reflex was
diminished on the right side, absent on the left. The
cremasteric reflex was well marked on the right side,
absent on the left. The abdominal reflex was also
present on the right side, but absent on the left. The
epigastric reflexes were present on both sides. He
suffered from retention of urine for a day or two after
admission, and then recovered control, but passed his
faeces in bed for some days. The pulse was 130 and
irregular, the temperature 104^ F. The urine was
acid and contained no albumen. He was at this time
delirious towards night and very stupid during the day
The patient was put upon a water bed and given
20-grain doses of iodide of potassium and half-drachm
doses of the liq. hydr. perch, twice daily, the urine
being drawn off". On June 2nd albumen in small
quantity appeared in the urine, which remained acid ;
no pus was present. On June 3rd the urine was
faintly ammoniacal; the iodide was increased to
30 grains and the liq. hydr. perch, to one drachm
thrice daily.
236 DISEASES OF THE SPINAL CORD.
June 6th. Rusty coloured sputum was ex-
pectorated, and crepitation was heard over the upper
lobe of the right lung; the lung mischief, however,
quickly subsided, the treatment remaining the same.
June 9th. Benzoate of soda in 20-grain doses
was given with each dose of his medicine; this
quickly restored the acid reaction of the urine, it
having been ammoniacal since the 3rd instant.
June I ith. The patient could move the left leg,
bending the knee and drawing up the limb without
assistance. The patellar reflex had reappeared on
the left side, but the epigastric and abdominal still
remained absent. The temperature had now fallen
to normal. Constipation was marked, and necessitated
the use of enemata.
June 24th. The patient could walk without
difficulty. The sensory disturbances in each leg were
still present but diminished. No ataxy was observed
on the return of motor power. A small bedsore
formed over the great trochanter on the left side, but
soon healed.
July 2nd. In addition to the administration of
iodide of potassium and mercury internally a drachm
of mercurial ointment was ordered to be rubbed into
the skin of the arm-pits daily.
July iSth. The patient is much improved, in
fact, he is well as regards motor power, but the sensory
disturbances are still present though to a less degree.
Brown-S^quard first thoroughly investigated the
group of symptoms observed in unilateral spinal
DISEASES OF THE SPINAL CORD. 237
lesions. The condition of the reflexes in unilateral
lesions has not bean fully investigated, but in this
case the abolition of the patellar, cremasteric, and
abdominal reflexes, and the increase of the plantar on
the paralysed side, indicate the seat of the lesion to
have extended in the cord on the left side from the
8th dorsal to the 4th lumbar nerves, and negatives
the supposition that the centripetal fibres concerned
in reflex actions have a crossed course within the
cord.
Brown-Sequard observed that there existed in
cases of hemi-myelitis a vertical space of about one
inch, near the median line, anteriorly and posteriorly,
in which hyperaesthesia is absent on the side of the
lesion, and a similar space on the front and back in
which there is an absence of any great degree of
anaesthesia on the side opposite the lesion. This he
explains by the fact that the sensory nerves of the
two sides overlap for a short distance near the median
line ; these spaces were not to be found in this case.
Dr. Broadbent has pointed out that it is in those
cases of syphilis where the secondary affections are
slight that the nervous system is especially liable to
suffer, and the tertiary stage arrives early. In this
case the secondary phenomena were well marked.
The absence of any phenomena of irritation
preceding the paralysis is characteristic of syphilitic
myelitis. The absence of the zones of hyperaesthesia
and anaesthesia at the upper level of the cord lesion is
noteworthy; but in this case localisation of tactile
238 DISEASES OF THE SPINAL CORD.
impressions on the opposite side to the lesion was
perfect, and may possibly be explained by supposing
that the lesion chiefly affected the lateral columns, grey
matter, and anterior cornua, and only slightly the
posterior nerve roots. The early occurrence in this
case of nervous disease (nine months) after the con-
traction of syphilis is interesting. In the "British
Medical Journal" for June 27th, 1885, a case is
reported by Dr. Churton where ataxy supervened
within four months of the contraction of the
chancre.
In many cases of spinal cord disease I have been
able to prevent the supervention of cystitis by giving
benzoate of soda, or by washing out the bladder.
The first indication of approaching cystitis is an am-
moniacal reaction of the urine. I give benzoate of
soda in preference to washing out the bladder unless
the cystitis be established, for there is considerable
danger in the use of catheters.
Early anti-syphilitic treatment is, of course, of
the highest importance, and iodide of potassium alone
cannot control the disease; mercury must be given
either by the mouth or by inunction. In several
instances I have found iodide of potassium to fail
unless combined with mercury. The prognosis in
these cases is favourable but should be guarded. The
recovery of motor power, the sensory disturbances
remaining, though to a less extent, is contrary to
what is usually seen in myelitis. Sensation is, as a
rule, first recovered.
DISEASES OF THE SPINAL CORD. 239
Myelitis must be distinguished from
I. — Haemorrhage outside the cord or into its
substance.
2. — Acute meningitis.
3. — Compression of the cord by tumours or by
thickened dura mater as in spinal caries.
Haemorrhage into the cord is very rare but may
complicate a myelitis, or may be due to injury. The
onset of paralysis is immediate, far more rapid than
in myelitis, and no fever and no irritative phenomena
occur, as in myelitis.
In acute meningitis and in tumours, the lesion
being extra medullary, irritative phenomena are
far more prominent and lasting than in myelitis, the
motor and sensory nerves being first compressed,
symptoms due first to their irritation and later on to
their destruction, are observed before the cord is
implicated.
Meningitis and myelitis are the only two acute
spinal diseases beginning with fever, excluding polio-
myelitis anterior acuta.
In meningitis —
I. — Pain in the back is much more prominent
than in myelitis and is aggravated by movement. V
2. — Contractures and cramps arc present.
3. — Shooting pains in the limbs are prominent
symptoms.
4. — There is rarely absolute paralysis as in
myelitis, but paresis only.
5. — The sphincters are rarely paralysed, nor is
cystitis present.
240 DISEASES OF THE SPINAL CORD.
It is in the chronic form of myelitis that difficulty
may occur in the diagnosis as to whether the lesion
is primary in the cord or results from external
pressure, and in these cases a careful examination of
the spine should always be made, for spinal caries is
frequently overlooked in cases of paraplegia.
The diagnosis of primary lateral sclerosis from
descending sclerosis of the lateral columns following
a chronic myelitis has already been mentioned, as
has also the distinction between functional and organic
paraplegias.
Acute Ascending Paralysis. — Landrfs Paralysis.
^'Progressive paralysis^^ (Graves) is a form of
progressive paralysis commencing in the feet and
passing upwards to the trunk and upper extremities,
and finally causing death by implicating the medulla.
The duration of the disease is usually only a few
days, and it is characterised by the following negative
features, there being : —
I. — No atrophy.
2. — No reaction of degeneration.
3. — No increase of reflex excitability.
4. — No contractures.
5. — No paralysis of the bladder or rectum.
This disease must be distinguished from sub-
acute general spinal paralysis and from multiple
neuritis.
The negative features of Landry's paralysis
above enumerated distinguish it from these diseases.
DISEASES OF THE SPINAL CORD. 24 1
Mtiltiple Sclerosis,
In disseminated or multiple sclerosis the cord may-
or may not be affected, and if afifected the symptoms
vary according to the distribution of the patches of|
sclerosis.
The lesion may be confined to the postero-
external columns of the cord and the case thus
simulate tabes, or to the lateral columns (simulating
lateral sclerosis), and causing a spastic paraplegia,
the latter being the commonest form of cord lesion
in this disease.
The presence of the cerebral symptoms
characteristic of the disease would at once enable the
diagnosis to be made.
Case of Disseminated Sclerosis,
A. S., a man aged 30, came to the Queen's
Hospital in December last complaining of giddiness
and difficulty in walking. He was a draper by trade
and had lived a fast life. Eleven years ago he had a
chancre of doubtful character and gonorrhoea.
There was no histoiy of nervous disease in the
family, and no history of injury or of lead or mercurial
poisoning. The present illness came on gradually
two years ago with stifiTness of the arms and legs,
and his gait gradually became afifected.
Three weeks before coming to the hospital he
suffered from diplopia, particularly when looking to
the right or left.
/
/
242 DISEASES OF THE SPINAL CORD.
He had suffered from frontal headache but had
not vomited and his memory was good.
His gait was ataxic, he could not walk without
a stick, and in walking widely separated his feet and
frequently lurched to one side, the neck being held
stiffly, and coarse tremor, especially of the head,
being marked. The gait was not like that of tabes ;
he did not jerk out his legs, bringing the heels
down violently.
He had never suffered from pains in the legs.
The pupils were unequal but they responded
normally to light and accommodation, and clonic
spasm of the iris was observed. Nystagmus was
not present during ordinary movements but when
the patient was directed to look to one side so as to
strain the ocular muscles it was marked. These
movements were taken as evidence of paresis of the
3rd nerve. There was no optic neuritis or atrophy.
The patient suffered at times from vertigo, probably
due to the ocular disturbance. The only sensory
disturbance present was slight numbness of the fingers^
i The speech was unaffected and the only psychical
disorder present was irritability and occasional loss
of self-control and inability to bear the slightest noise,
especially of children. Occasionally he had difficulty
in passing his urine. The knee jerk was increased
on both sides and there was a tendency to ankle
clonus, but no rigidity or paresis of the extremities.
There was marked tremor of the head, neck, and
body when walking, and of the head when sitting
DISEASES OF THE SPINAL CORD. 243
and standing, disappearing when lying down; also
slightly of the left arm, observed when he raised a
glass of water to his mouth.
The peculiar gait; the nystagmus with clonic \
spasm of the iris ; the coarse tremor of the head and
body ceasing during rest; together with the increase
of the deep reflexes; leave little doubt as to the
diagnosis. Cerebellar tumour, locomotor ataxy, and
paralysis agitans are easily excluded.
Extra- Medtdlary Lesions,
Extra-medullary lesions are conveniently classi-
fied by Bramwell as follows : —
(i.) Meningitis^
Leptomeningitis i ^,
^ (. Chronic
(Inflammation of the pia and arachnoid)
Pach)'meningitis
(Inflammation of
; the dura mater)
Externa
Interna | "'^"'""hagica
\ Hypertrophica
(ii.) Extra-Medullary Haemorrhage.
<iii.) Extra-Medullary Tumours.
In the diagnosis of tlie nature of a paraplegia, as
in the diagnosis of hemiplegia, the first question to
decide is: — Is the paralysis functioiml or organic ?
If organic, is the lesion spinal or peripheral ? If
spinal, is the lesion ^>//r^-medullary or extra-
medullary? Extra-medullary lesions irritate, and
compress the anterior and posterior nerve roots;
therefore pain in the back, shooting pains, hyj7
aesthesia and anaesthesia, together with spasn?'
paralysis, occur. /
242
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DISEASES OF THE SPINAL CORD. 24S
Acute spinal meningitis must be distinguished
from acute myelitis (see myelitis) and from tetanus. •
In tetanus: —
I. — There are no sensory disturbances — there is
severe pain during the exacerbations but no marked
hyperaesthesia or anaesthesia.
2. — The spasms are much more general and
constant than in meningitis and trismus is present
3. — The reflexes are much more exaggerated
than in meningitis.
4. — There is less fever than in meningitis.
Chronic meningitis resembles acute meningitis
in its symptoms except that the lesion is more
localised, the fever less,- and pressure on the cord
leading to paraplegia is common.
It may be distinguished from chronic myelitis by
the same features which distinguish acute meningitis
from acute myelitis.
Chronic meningitis occurring in the lumbar
region may cause loss of the knee jerk and pains
similar to those observed in locomotor ataxy, but the
eye symptoms are absent.
Pachyme?i ingitis.
Pachymeningitis externa chiefly occurs in disease
of the vertebrae. The inflammation is localised, the
thickened patch of dura compressing the nerves and
the spinal cord.
The surface of the cord being compressed there
is frequently paraplegia with exaggeration of the deep
reflexes without impairment of sensation or paralysis
246 DISEASES OF THE SPINAL CORD.
of the bladder. In such cases always look for Pott's
disease of the vertebrae.
Sensation may, however, be destroyed and the
bladder paralysed in bad cases.
Pachymeningitis interna hcB7norrJiagica^ like the
cerebral form, is characterised by its liability to sudden
haemorrhage with production of paralytic symptoms.
Apart from haemorrhage the symptoms would be those
of a chronic meningitis.
Pachymeningitis interna hypertrophica. This
condition where the dura mater is greatly thickened^
forming a ring around and compressing the cord, and
the nerves coming off from it, usually affects the dura
in the cervical region, and was first described by
Charcot.
As in all extra-medullary lesions, symptoms due
to irritation of the nerve roots are at first prominent,
there being shooting pains in the neck and arms and
hyperaesthesia with spasm, later on anaesthesia and
paralysis with trophic disturbances in the area of
distribution of the affected nerves.
The pressure of the thickened dura leads to a
transverse myelitis with secondary degeneration, a
spastic paraplegia being thus produced.
There is, in fact, a general paralysis, both arms
and legs being affected, but wasting and contractures
are confined to the upper extremities.
Pressure upon the cervical region of the cord
causes paralysis of the upper extremities, "a cervical
paraplegia " before the legs are affected, the nerves for
' ■* upper extremities being nearer the surface.
DISEASES OF T-HE SPINAL CORD. 247
Amyotrophic! lateral sclerosis can be distinguished
from this disease by the marked sensory disturbances
and progress to recovery, more or less complete in
the latter.
Pott's disease, which might lead to symptoms
exactly resembling this disease, is excluded by the
absence of spinal tenderness, deformity, cachexia,
fever, or signs of scrofula.
Tumour of the bones, membranes, or nerve roots
might cause some difficulty, but the symptoms here
progress steadily from bad to worse, and do not
improve.
Case of Pachymeningitis Cenncalis Hypertrophica,
W. B., a boy, aged 18, was admitted into the
Workhouse Infirmary, May 2Sth, 1883, with paralysis
and tucking of both legs.
When 5 years of age, he fell down some steps
on to the back of his head. Ever since he has had
an internal strabismus of the left eye. Another fall
two years previously to his admission, he says,
caused the paralysis ; in his opinion the paralysis
commenced shortly after.
The patient had been in the General Hospital
for twelve months before he was brought to the
infirmary, and while there, both arms and legs were
paretic and rigid. The paralysis began in the right
arm ; the onset was gradual, and attended with
numbness, tingling, and loss of sensation.
248 DISEASES OF THE SPINAL CORD.
There was great pain in the neck and scalp, for
which a seton was introduced, and the neck was
rigid, movement causing great pain. The pain was
along the great occipital and third cervical nerves,
upward towards the head, also down the shoulders.
Two or three months after the paralysis of the
right arm, the left arm, both legs and back, began to
get weaker, until the patient was completely paralysed.
The arms were rigid, with extreme flexion of
the fingers and wrists. There was no paralysis of
the bladder or rectum.
Five months before admission (in 1883) he
began to recover the use of his arms, and they have
been getting better ever since.
There was never any facial paralysis, or any
cerebral affection or disease of the cranial nerves,
no vertigo, delirium, or vomiting.
The legs were weak when the arms were affected.
At first they were flaccid, but they gradually began to
get stiff, and contracted and trembled. All four
extremities were paralysed together, but the arms
got better while the legs got stiff.
When admitted, the patient was much emaciated,
had spasmodic internal strabismus of the left eye
and torticollis, the head being twisted to the right.
He could rotate his head more to the right than to
the left.
No tenderness could be elicted by percussion
over. the cervical spines, and there was no fever or
any sign of scrofula.
DISEASES OF THE SPINAL CORD. 249
Both legs were paralysed and flexed at the
hips and knees, with adduction of the thighs.
The arms had recovered power, but were still
weak. There were no sensory disturbances.
Ankle clonus and front tap contraction were
markedly present in both legs. On account of the
contracture, the patellar reflexes could not be
obtained.
The plantar reflexes were present ; the cremas-
teric, abdominal and epigastric absent.
There was no sensory disturbance in the lower
extremities, and no marked wasting.
The optic disc and fundus on each side was
normal. The patient was treated with iodide of
potassium, and counter-irritated over the cervical
spine, and when examined in July, 1884, was much
better, could rotate the head more, could use the
right leg well, and there was little rigidity on this
side, but still ankle-clonus.
The left leg was still tucked, and wasted with
increase of reflexes.
He was well fed, and spent as much time in
the open air as possible, going about on crutches. A
shot bag was suspended to the ankle of the left
foot, to diminish the contracture. On the 14th
March, 1885, the patient, wishing to leave, was again
examined. The chin was still slightly turned to
the right, the reflexes (bicipital, &c.) in the upper
extremities well marked, but there was no rigidity,
and the grasp on both sides was very powerful.
250 DISEASES OF THE SPINAL CORD.
Ankle-clonus had disappeared, and the con-
tracture of the left leg was much diminished. He could
not, however, put the left heel to the ground, there
being talipes equinus. The left leg was considerably
wasted. The circumference of the left calf was
lO^in., of the right, I3in.
This wasting could only be accounted for by
supposing that an extension of the morbid process
in the crossed pyramidal path to the anterior cornua
had taken place.
The electrical reactions of the nerves and
muscles of the left leg were normal.
As to the diagnosis of the case : —
Amyotrophic lateral sclerosis is excluded by the
marked sensory disorders and progress of the case
to recovery.
A transverse myelitis is excluded by the great
predominance of the irritative phenomena, and absence
of anaesthesia and complete paralysis of the leg,
preceding the rigidity.
Progressive muscular atrophy, by the presence
of rigidity and sensory disturbances.
Atrophy is said not to occur in the leg in this
disease, but in this case it has occurred in the left
leg. There is no doubt that the lesion was one of
the spinal membranes, and to be certain of the
diagnosis of pachymeningitis cervicalis hypertrophica,
we must eliminate Pott's disease and tumour of the
membranes.
DISEASES OF THE SPINAL CORD. 251
Pott's disease is excluded by the absence of
spinal tenderness, deformity, cachexia, and fever;
also by the absence of scrofula.
Tumour is more difficult to eliminate, but the
gradual recovery excludes it, so that there can be
little doubt about the case. A traumatic form of
the disease has 'been described, and this case was
probably due to injury.
The position of the hands shows the lesion to
have been in the upper half of the cervical enlarge-
ment of the cord.
Spinal Hcemorrhage,
Haemorrhage may occur either in the substance
of the cord (a very rare occurrence) or outside the
cord into the membranes. Both varieties may result
from traumatic violence, and are characterised by
their sudden onset, with absence of febrile disturbance.
The one variety may be distinguished from the
other in the same way that we distinguish extra-
medullary and intra-medullary diseases generally.
Spinal Tumours.
Tumours also may be extra- or intra-medullary^
A tumour may exist in the spinal canal without
symptoms for a considerable time until it compresses
the nerve roots and the cord, when the symptoms
gradually increase in severity, paraplegia with con-
tracture and severe cramps rapidly supervening.
A tumour in the cord, according to Sharkey,
disturbs its function even from the first, but it may
252 DISEASES OF THE SPINAL CORD.
continue to grow for a long time before it produces
marked symptoms, which it does either by pushing the
cord against the bone walls of the spinal canal or by
exhausting the elasticity of the spinal membranes.
A tumour outside the cord will of course be
likely to cause symptoms due to pressure on the
spinal nerves.
The symptoms of an intra-medullary tumour
will vary with its situation and with the extent of
the transverse area of the cord involved.
CHAPTER XI.
DISEASES OF THE PERIPHERAL
NERVES.
*
PeripJieral Neuritis,
It IS only during the last few years that lesions
of the peripheral nerves have attracted the attention
they deserve, and in fact demand. Peripheral
neuritis was shown to be the lesion in alcoholic
paraplegia in 1881, by Lancereaux, and since then
Dreschfeld, Wilks, Broadbent, Buzzard, and others
have added considerably to our knowledge of this
subject.
There are many causes of peripheral neuritis in
addition to alcohol, e,g.^ lead poisoning, exposure to
cold, traumatism, and general diseases, such as diph-
theria, gout, diabetes, tuberculosis, syphilis, rheu-
matism, locomotor ataxy, and leprosy.
Peripheral neuritis occasionally occurs after
typhoid and other specific fevers, and it may also be
idiopathic.
The paralysis caused by the fumes of bisulphide
of carbon probably depends upon a multiple neuritis.
254 DISEASES OF THE PERIPHERAL NERVES.
Neuritis may be acute or chronic, of one nerve or
oi almost all the peripheral nerves, when a condition
of general paralysis is present and the disease is
termed multiple neuritis.
In the early stage of neuritis symptoms due to
irritation of the nerve fibres, such as pain, hyper-
a^sthesia, and other sensory disturbances, with cramps
and muscular twitchings, occur; and later on
symptoms due to destruction of the nerve fibres and
complete cessation of their conductivity causing
anaesthesia and paralysis.
Other symptoms are also usually present, since
the muscles are shut off from their trophic nuclei in
the cord there is muscular atrophy varying with the
degree of damage to the nerve.
Qualitative electrical changes are always present
in severe cases, the Faradic response being lost, and
the reaction of degeneration present.
Trophic changes are often observed, the nails
becoming brittle, ridged, and discoloured ; the skin of
the fingers and toes hairless and glossy.
Vaso-motor disorders are of frequent occurrence,
consisting of patches of redness on the hands and
feet, and oedema of these parts. Profuse perspiration
either of the general surface of the body or limited
to the feet also occurs.
The deep reflexes are abolished at an early
period of the disease, the knee jerk being soon lost
when the neives of the lower extremities are affected,
but the superficial reflexes may be retained. .
DISEASES OF THE PERIPHERAL NERVES. 255
The paralysis and anaesthesia resulting from
peripheral neuritis is always most marked at the
extremities of the limbs.
The extensor muscles of the fore-arm and leg
being especially affected, there is dropped wrist and
dropped feet. The latter is a very characteristic
feature, the patient being quite unable to perform
dorsal flexion of the foot, while he may be able to
flex and extend the knee.
There is frequently tenderness along the nerve
trunks and occasionally they may be felt to be enlarged.
In multiple neuritis both sides of the body are
affected symmetrically, the numbness and paresis
being always first noticed in the feet and hands*
gradually spreading upwards.
The muscles of the trunk and those supplied by
the cranial nerves may be affected and death may be
produced by paralysis of the diaphragm and inter-
costal muscles, or from paralysis of the pneumo-
gastric nerve.
The paralysed extremities are always flaccid at
first, but contracture of the unopposed healthy
muscles may occur in severe cases.
Paralysis never supervenes suddenly in peripheral
neuritis, but is gradual in its onset and requires some
time to become general, being usually preceded by
more or less severe pains in the extremities.
Before the paralysis is complete incoordination
may be marked and may exactly resemble that of
locomotor ataxy.
256 DISEASES OF THE PERIPHERAL NERVES.
Although the extensors of the legs and of the
forearms suffer most, all the other muscles are
weakened.
The lower are always earlier and more affected
than the upper extremities.
The bladder and rectum are not affected in the
majority of cases, but only in those rare instances in
which the nerves to these viscera are diseased.
Bedsores are not usually present.
Sensory disturbances are present in very varying
degrees, from total anaesthesia to the mere sensory
disorder of "pins and needles."
The mental faculties are unaffected except in
cases due to alcoholism, when there is nearly always
loss of memory or other mental symptoms such as
insomnia, delirium, &c.
Hyperaesthesia of the skin and muscular struc-
ture is generally marked, and on pinching the calf
muscles considerable pain is elicited.
We must now consider the diagnosis of peri-
pheral neuritis from lesions of the spinal cord and
brain.
Monoplegia, paraplegia, hemiplegia, or paralysis
of all four extremities may be cerebral, spinal, or
peripheral.
In a cerebral monoplegia as in all cerebral
paralyses —
I. — There are no qualitative electrical changes.
2. — Sensation is usually unaffected.
DISEASES OF THE PERIPHERAL NERVES. 25/
3. — The paralysis is followed by rigidity, with
exaggeration of the reflexes.
4. — There is no rapid ftiuscular wasting.
5. — The lesion is most commonly in the motor
area of the cortex, when Jacksonian epilepsy may
be present, but it may be in the internal capsule.
6. — We should probably have optic neuritis,
headache, vertigo, or other cerebral symptoms
present.
In a spinal monoplegia the lesion is usually one
of the anterior cornua. The onset is sudden, and
the reaction of degeneration present, but there are
no marked sensory disturbances — the reflexes are
abolished.
In a monoplegia from disease of the peripheral
nerves, as we have already seen, sensory distur-
bances are prominent, the reflexes are abolished, and
the reaction of degeneration is usually present.
Peripheral neuritis may also be distinguished
from lesions of the anterior cornua of the cord by
the fact that in the former case the distribution of
the paralysis is anatomical, the muscles paralysed
being in groups supplied by particular nerves, and
the paralysis is gradual in its onset and progressive,
while in the latter, muscles functionally associated
are paralysed and the onset is sudden, the maximum
of paralysis being quickly reached.
There is no difficulty in the diagnosis of well-
marked cases of multiple neuritis, but in some cases
there may be absolute motor paralysis without any
258 DISEASES OF THE PERIPHERAL NERVES.
sensory disturbance, and all the muscles of one limb
may be paralysed. It is a general rule that in
inflammation and injuries' of mixed nerves the motor
nerve fibres suffer far more than the sensory, and
therefore paralysis is usually far in excess of anaes-
thesia or other sensory disturbance. The nerves,
moreover, may be affected beyond the points at which
their sensory branches are given off, and thus motor
symptoms alone are present, though the nerve is a
mixed one. Moreover, in peripheral neuritis there
may be complete motor paralysis without any
electrical changes. In all cases tenderness along the
nerve trunks should be searched for.
After diphtheria absolute paraplegia may occur
without any sensory disturbance, and without elec-
trical change, and it is difficult to decide whether
the lesion is in the cord or in the peripheral nerves,
but recovery is so rapid and complete that there can
be little doubt that in these cases the lesion is in the
peripheral nerves.
Paraplegia may be cerebral, spinal, or peripheral,
as may hemiplegia, and the diagnosis can be made
on the same grounds as in the case of a monoplegia
or paralysis of one extremity only.
Peripheral neuritis must be distinguished from —
I. — Locomotor ataxia.
2. — Polio-myelitis anterior acuta.
3. — Myelitis.
4. — Meningitis.
5- — Subacute general spinal paralysis.
DISEASES OF THE PERIPHERAL NERVES. 259
6. — Acute ascending paralysis or Landry's
disease.
It is highly probable that many cases of peri-
pheral neuritis, due to alcohol or other cause, have
been diagnosed as cases of locomotor ataxia, and
their cure as that of this hopeless disease. Loss
of the knee-jerk, pains, and ataxy are present in
both diseases, but the pupil symptoms of locomotor
ataxia are not present in peripheral neuritis.
Qualitative electrical changes if present would
at once distinguish them. Before a diagnosis of
locomotor ataxia is made, peripheral neuritis from
alcohol, diphtheria, &c., must be carefully excluded.
In locomotor ataxia, peripheral neuritis occa-
sionally occurs, and is the cause of such symptoms
as perforating ulcer of the foot, optic atrophy, &c.
In paraplegia due to myelitis, bed sores, bladder
and intestinal troubles are almost invariably present,
while in peripheral neuritis these symptoms are very
rarely present.
Spinal meningitis or pachymeningitis closely
resembles peripheral neuritis, in fact, the nerv^es
themselves are affected, but the marked pain in
the back, aggravated by movement, together with
retraction of the head and muscular twitchings,
distinguish the former disease.
Subacute general spinal paralysis is not attended
with any sensory disturbances, and the distribution
of the paralysis is that peculiar to disease of the
anterior cornua; muscles functionally associated bevw^
36o DISEASES 0¥ THE PERIPHERAL NERVES.
paralysed. In this disease, moreover, the order in
which the muscles are attacked is different from that
observed in neuritis. When the spinal disease com-
mences in the lower extremity of the cord and
spreads upwards, the paralysis is first observed in
the foot muscles, and then attacks in succession the
muscles of the legs, thighs, buttocks, and trunk.
Later on the intercostal muscles are paralysed, and
the intrinsic muscles of the hand. The latter, which
derive their nervous supply from the first dorsal
nerve, are affected before the extensor muscles of the
wrist and fingers (which are supplied by the seventh
cervical nerve). Now, in multiple neuritis the
paralysis, which first attacks the feet and then the
legs and thighs, skips the trunk muscles and affects
the extensors of the wrists before the small muscles
of the hand.
Landry's disease is unattended with electrical
alterations or sensory disturbances.
Alcoliolic Paralysis.
Dr. Dreschfeld ("Brain," Vol. VII.) divides
alcoholic paralysis into two types — alcoholic ataxia
and alcoholic paralysis proper.
In alcoholic ataxia, which occurs chiefly in men,
the symptoms greatly resemble those of locomotor
ataxia, there being marked incoordination in the
lower extremities, lancinating pains, and loss of
the knee-jerk, without paralysis or atrophy. But
the history of alcoholic excess, of morning sickness
DISEASES OF THE PERIPHERAL NERVES. 26 1
or hsematemesis, and the presence of mental
symptoms, such as loss of memory, together with
the absence of myosis, of the Argyll-Robertson pupil,
of arthropathies, and of visceral crises, suffice to
enable us to distinguish between ataxia due to
chronic alcoholism and that due to tabes dorsalis.
Moreover, in the former the ataxia disappears and
the knee-jerk returns when alcohol is entirely with-
held. The symptoms in the ataxic form of alcoholic
paralysis are due to a multiple neuritis, especially of
the sensory nerves, and these cases differ from those
of the second type in the absence of hyperaesthesia,
hyperalgesia, paralysis, and atrophy.
The second type of alcoholic paralysis is the
more common, occurring chiefly in females who have
previously suffered from symptoms of chronic
alcoholism. Sensory disturbances are well marked,
there being extreme hyperaesthesia of the feet and
lower extremities, which may later on be followed by
anaesthesia and analgesia. Lancinating pains are
complained of, especially in the legs, but often in
the upper extremities also. The calf muscles are
exquisitely tender when grasped, and tenderness is
found in the course of the nerve trunks. A remark-
able perversion of the sense of temperature, has been
observed in the subjects of alcoholic paralysis, all
objects in contact with the skin appearing cold.
Paralysis chiefly attacking the lower extremities, and
always commencing and being most marked in them,
is present. The extensor muscles of the legs suffer
i
262 DISEASES OF THE PERIPHERAL NERVES.
most, SO that the feet are dropped, the patient being
quite unable to perform dorsal flexion of the feet.
The arms are affected later than the legs, and to a
much less degree, the extensor muscles here also
suffering most, dropped wrist being frequently
present. The paralysis may be general, and in
those cases where the extensor muscles only are
paralysed evidence of weakness in the other muscles
is present. Marked muscular atrophy is usually
present, together with qualitative electrical changes
constituting the R. D.
Vasomotor changes as shown by redness and
cedema of the hands and feet also occur.
Purpura has been observed.
The skin may present the glossy appearance first
described by Paget, but it is often harsh and dry.
The nails are frequently affected, being curved, ridged,
and brittle.
Emotional alterations, impairment of memory,
insomnia, restlessness, delirium, and hebetude,
together with digestive disturbances such as morning
sickness or haematemesis, are characteristic features of
chronic alcoholism; and when occurring with ataxy
or paralysis render the diagnosis of the nature of
these two symptoms certain.
Dr. Dreschfeld describes a peculiar form of
delirium present in the subjects of alcoholic paralysis;
the patient although unable to move saying that he
gets up every day or that he has been out to a certain
place.
DISEASES OF THE PERIPHERAL NERVES. 263
I can confirm this from my own experience, for
in one case of cirrhosis of the liver, with general
emaciation and debility, the patient would assure
me that he had walked several miles that morning,
and was apparently rational in all else he said.
In another case of cirrhosis of the liver the
patient used to tell me that she had just been to
the "Rose and Crown," for a "noggin." She used
to get out of bed and shake the other patients, telling
them it was " time to open."
Dr. Dreschfeld examined the spinal cord and
peripheral nerves in two fatal cases. He found that
the cord was healthy but the peripheral nerves which
were examined, namely, the two sciatics, the musculo-
spiral and the anterior crural were found to be
diseased, the myeline and axis cylinders being broken
up.
Diphtheritic Paralysis,
In many of its features diphtheritic paralysis
very closdy resembles alcoholic paralysis, but it is
rarely the case that the symptoms are so un-
equivocally the result of peripheral neuritis in the
former as in the latter complaint. There are several
degrees in the intensity of the nervous disturbance
after diphtheria, which may be grouped as follows: —
I. — The knee jerk is very frequently lost and
there may be no other symptom present.
This loss of knee jerk occurring as it does
so commonly after diphtheria and often unac-
companied by any other symptoms seems to be a
264 DISEASES OF THE PERIPHERAL NERVES.
point in favour of a peripheral lesion, especially
as in these cases the jerk reappears again in a few
weeks.
2. — In other cases, in addition to the loss of the
knee jerk, there is ataxy with more or less general
paresis without sensory alterations.
3. — In sonie cases there is absolute paraplegia
with loss of knee jerk without any disturbance of
sensation and without electrical alterations.
The symptoms in these cases being those of an
acute lesion of the multipolar nerve cells of the
anterior cornua of the cord. Since, however, recovery
is usually rapid and complete, it is difficult to suppose
that the lesion can be in the cord, for nerve cells do
not recover from injury so easily as nerve fibres, and
the former when once destroyed are not regenerated,
while the latter are readily regenerated.
4. — In other cases of diphtheritic paralysis,
sensory disturbances, hyperaesthesia, anaesthesia,
tenderness along the nerve trunks and shooting pains
are present. These cases cannot be due simply to
lesion of the anterior cornua of the cord.
In rare cases we have a condition exactly like
that observed in severe cases of alcoholic paralysis,
there being dropped feet and hands, sensory dis-
turbances, tenderness along the nerve trunks and of
the muscles, with wasting and qualitative electrical
changes, there being no doubt that in these cases the
lesion is a neuritis of the peripheral nerves.
DISEASES OF THE PERIPHERAL NERVES. 265
It is difficult to suppose that the lesion in the
cases that recover is one of the anterior cornua of
the spinal cord, while in those rare and severe cases
which often end in incomplete recovery, the lesion is
one of the peripheral nerves only.
It is more reasonable to suppose that the lesion
in all cases of diphtheritic paralysis is a peripheral
neuritis, but that in the former type of case the lesion
is a slight one, and in the latter type a severe one.
In injury to a mixed nerve it is well known that
there may be paralysis without anaesthesia or
qualitative electrical change, provided the injury is a
slight one. In more severe cases, anaesthesia, wasting,'
and the reaction of degeneration are met with.
After diphtheria, paralysis of the ocular muscles
and of the soft palate are of common occurrence,
and these paralyses are certainly in favour of the
peripheral nature of the lesion in diphtheritic
paralysis. Buzzard, Mendel, and Charcot are inclined
to the view that the lesion in diphtheritic paralysis is
a neuritis of the peripheral nerves. The cases on
record where neuritis of the peripheral nerves has
been found after death are of course very few, as
diphtheritic paralysis is rarely fatal.
A case of acute multiple neuritis following diph-
theria was sent to me by Mr. Latham, of West Brom-
wich, in July last. The patient (Samuel Westwood),
aged 23, was admitted into the Queen's Hospital,
July 19th, 1886. His father died of diabetes, but
there was no other family history of importance.
266 DISEASES OF THE PERIPHERAL NERVES.
Previous to this illness he had never had anything the
matter with him except bad colds. Thirteen weeks
before his admission, the patient's sister and niece
had diphtheria, and he himself had a sore throat with
membranous exudation.
Mr. Latham tells me that he attended the sister
and niece, the latter of whom died from diphtheria,
and that he did not see the patient, who lived in the
same house, for ten days after the. onset of his sore
throat, but that the sister saw ash-coloured spots on
the tonsils and soft palate. Three weeks after the
onset of the sore throat the patient noticed that his
legs were getting weak. He gradually became unable
to walk, and in a month completely lost all power
over his feet. As his legs began to get weak he
suffered from very severe pains shooting down them,
which occurred paroxysmally ; his legs were also
very tender and he could not bear them rubbed.
Shortly before admission his arms began to get weak
also, but he had no pains in them. On admission the
patient was found to have lost all power over his feet,
which were dropped ; he could bend and straighten
the knees, but the feet hung helplessly, being perfectly
flaccid.
There was also drop-wrist on both sides, and the
grasp was very feeble, that of the right hand tested
by the dynamometer being 8 lbs., that of the left
lo lbs. The muscles of the legs and forearms were
much wasted, and the thenar and hypothenar
eminences almost effaced. The fingers were flexed
DISEASES OF THE rERIl'HERAL NERVES. 267
slightly at all three joints and could not be
straightened voluntarily, The plantar reflex and the
knee jerk were absent on both sides. The cremasteric
g
1
1
5^
Mm, > 'H
1
)
/
-J
Acute Multiple Keuritis uue to JJii'iruiiiKiA.
abdominal and epigastric reflexes were present on both
sides. The following sensory disorders were present.
The power of localisation of tactile impressions
268 DISEASES OF THE PERIPHERAL NERVES.
was not much impaired, though the patient had
to consider a short time before he could answer.
Tactile and painful impressions were evidently
delayed in their transmission to the brain. One
prick with a pin produced about two seconds later a
sense of contact, followed after a short interval by a
sense of pain. There was decided analgesia and
diminution of thermal and muscular sense. The
patient complained of pains in his legs, with numbness
and tingling of the hands and feet. The calf muscles
were very tender, and when pinched caused him great
pain ; he could scarcely bear the contact of the bed-
clothes. There was well-marked tenderness along
the course of the great sciatic and internal popliteal
nerves. The idio-muscular contractility was increased,
fibrillary contractions being produced by filliping the
wasted muscles. The feet were cold and the skin red
and cedematous. The skin of the fingers was tense
and shining, and the nails presented several white
transverse lines. There was no paralysis of the
internal or external muscles of the eyes or of the
soft palate, but anaesthesia of the throat and larynx
was well marked, it being possible to put the finger
into the larynx without discomfort. There was no
albumen in the urine, no bedsore, and no trouble with
micturition or defaecation.
Electrical Reactions. — The Faradic current
applied to the nerves, motor points and muscles
of the legs produced a very slight contraction of
the gastrocnemii, but none of the other muscles
DISEASES OF THE PERIPHERAL NERVES. 269
either at the back or front of the legs, or of the
foot, responded in the slightest.
Galvanisation of the great sciatic nerve pro-
duced no contraction of the muscles supplied by it.
Galvanisation of the gastrocnemii with twenty cells
caused sluggish contractions, the anodic closure
contraction exceeding the cathodic closure contrac-
tion. With twenty- four cells the anodic closure
contraction also predominated in the extensor
muscles of the legs. The response of the muscles
in front of the thighs was diminished on both sides,
the anodic closure contraction exceeding the cathodic
closure contraction. The hamstring muscles responded
well, CCC exceeding AC C. Faradism applied to the
extensor muscles of the forearms caused no contrac-
tion on the right side and only a feeble one on the
left ; the supinator longus and the flexor muscles acted
well on both sides. The thenar and hypothenar
muscles and the interossei did not respond at all on
either side. With Galvanism the extensor muscles of
the forearm responded to the current of eighteen
cells, A C C exceeding CCC. The short muscles of
the thumb also presented the reaction of degener-
ation.
The patient was ordered strychnia, the dose being
gradually increased, and the galvanic current was
applied daily to the affected muscles. He could not
bear massage on account of the extreme tenderness
of the muscles, and he had restless nights from the
pain in the feet.
2JO DISEASES OF THE PERIPHERAL NERVES.
On the 26th of July it was found that the
extensor muscles on the back of the left forearm
responded well to Faradism, but there was still no
response on the right side.
On the 29th the extensor muscles on both sides
responded well to Faradism, but there still was no
Faradic response in the muscles of the legs or in
the thenar and hypothenar muscles.
On the 1st of August the drop- wrist had dis-
appeared, the patient had much greater power with
his hands and also slight voluntary movement in his
feet.
On the 5th a trace of albumen was found in the
urine. The patient was now taking twenty- two
minims of Liq. Strych. (B. P.) In the short thumb
muscles CCC now exceeded ACC.
On the 8th it was found that the hyperaesthesia
of the calf muscles was not so marked as previously,
but there was still much tenderness.
On the lOth he complained of twitching and
jumping of the legs. The tenderness formerly present
along the great sciatic and internal popliteal nerves
was not nearly so marked.
On the 20th the muscular tenderness had
disappeared, as had also the tenderness in the
course of the nerves. The improvement followed
the application of blistering fluid along the course
of the nerve trunks. He was now taking Liq.
Strych., 11130, thrice daily.
DISEASES OF THE PERIPHERAL NERVES. 2J\
On the 28th there was marked hyperidrosis
along the inner side and under surface of both feet,
and this had been present for some days. The
reflexes remained in the same condition, and there
was no Faradic response in the extensor muscles of
the legs or in those of the thenar eminences. He
was now taking Liq. Strych., iri36, thrice daily, and it
was not thought advisable to increase the dose further.
September 4th. Sweating of the feet still
continued and was accompanied with extensive
desquamation, small ulcers forming on one or two
toes, but these quickly healed.
September i6th. The hands had desquamated
like the feet. The fingers were a little flexed still
and could not be quite straightened, but the tendency
to contracture was much less than it had been. The
oedema of the feet had almost disappeared and the
sweating was much less.
On the 17th the following were the electrical
reactions with Faradism : — In the right forearm the
extensores ossis, primi and secundi responded well,
the extensor indicis, ext. com. dig., ext. carpi ulnaris
very feebly, the ext. min. dig. did not respond at all.
The muscles on the front of the right forearm
responded normally. The thenar muscles gave no
response, but the hypothenar muscles and the
interossei responded well. On the left side the
thenar muscles did not respond, with the exception
of the adductor pollicis. All the muscles on the
back of the forearm' responded. In the right leg
272 DISEASES OF THE PERIPHERAL NERVES.
there was no response of the muscles on the front
and outer side, and an almost imperceptible response
only in the calf muscles. Similarly in the left leg".
With Galvanism. — The muscles on the posterior
surface of the right forearm responded, A C C exceed-
ing C C C. The contractions of these and of the
thenar muscles were sluggish and prolonged. The
muscles of the right leg responded well, in the
extensors C C C exceeded A C C, in the peronei
A C C predominated.
October 2nd. The thenar muscles on both sides
responded feebly to Faradism. The clawed condition
of the hands was not nearly so marked as it had been.
At the present time (December 2nd) the clawed
condition of the hand is quite gone, and he can
extend the wrists. The grasp of the right hand by
the dynamometer equals 5olbs., that of the left hand
6olbs. The feet are still dropped, and there is no
Faradic response with a strong current in the extensor
muscles of either leg. The peronei on the left side
and the gastrocnemii on both sides respond feebly.
Sensation is still a little delayed but has much
improved. The knee-jerk and plantar reflexes are
still absent. The reaction of degeneration is well
marked in the thenar muscles and extensor muscles
of the forearms. In the extensor communis digitorum
and extensor proprius pollicis of both legs the re-
action of degeneration is also well marked. The
peronei respond better than the extensors, C C C
predominating.
DISEASES OF THE PERIPHERAL NERVES. 2/3
As to the diagnosis in this case. Is the lesion
spinal or peripheral? A lesion of the anterior
cornua of the cord would account for the paralysis,
rapid wasting, and electrical alterations present, but
would not explain the sensory disturbances so marked
in this case, nor the tenderness of the nerves or
muscles. Moreover, in this case it is the peripheral
portions of the extremities only which are affected,
the hands and forearms, the feet and legs ; while the
arms and shoulders, thighs and hips are unaffected.
The disease also commenced in the feet and legs,
missed the trunk, and appeared in the hands. This
is not what we should have expected in a spinal
lesion, but it is just what occurs in multiple neuritis.
In an acute lesion of the anterior cornua, more-
over, the paralysis at once reaches its maximum ; in
this case the disease was progressive, and after the
legs were affected it was some weeks before the
hands suffered ; so that polio-myelitis anterior acuta
must be excluded. Subacute general spinal paralysis
(a disease of the anterior cornua) is also excluded by
the sensory disturbances present.
In acute ascending paralysis (Landry^s paralysis)
there are no sensory disturbances and no electrical
alterations. The bladder and rectum being unaffected
and there being no bedsores, no fever, no girdle pain
or hyperaesthetic zone, we can exclude myelitis.
Spinal meningitis or pachymeningitis might give rise
to symptoms exactly resembling those of multiple
neuritis, but there was in this case no pain in the
274 DISEASES OF THE PERIPHERAL NERVES.
back, no pain on movement of the spine, no rigidity
and no retraction of the head. I think there can be
little doubt that the case is one of multiple neuritis.
Neuralgia,
Neuralgia consists in severe periodical paroxysms
of pain limited to the course of a sensory nerve, not
being due to any evident organic lesion of the nerve.
Tender spots, first described by Valleix, may be
found at various points in the course of the affected
nerves, where the nerves pierce muscles or fasciae, or
emerge from a bony canal, or where they can easily
be compressed, as when they lie in contact with bone.
Various symptoms are associated with neuralgia,
especially those due to vaso-motor changes.
Neuralgia may affect any of the sensory nerves
of the body, either of the trunk and limbs, or of the
viscera.
We must distinguish between neuralgia of
peripheral and of central origin.
In peripheral neuralgia: — (i) painful points are
present; (2) remedies applied peripherally relieve;
(3) the pain is limited to definite branches of the
nerves.
In central neuralgia tender spots are absent.
There are usually mental symptoms and the pain is
not so strictly limited to definite branches of one
nerve but affects several of the cranial nerves.
Neuralgia is usually unilateral, when bilateral
organic mischief must be suspected. The presence
DISEASES OF THE PERIPHERAL NERVES. 275
of intercostal neuralgia, especially when bilateral,
should lead you to explore the spine carefully for
Pott's disease, &c.
Sciatica is usually unilateral ; when bilateral,
suspect the presence of some organic disease of the
spinal cord, such as locomotor ataxia or ataxic para-
plegia; a malignant or other growth compressing the
Cauda equina might occasion bilateral sciatica.
Bilateral sciatica is occasionally present in
diabetes.
In all cases of obstinate sciatica examine the
patient per rectum to detect if present any swelling
in the pelvis.
In an old man who suffered from intense pain
along the left sciatic nerve a swelling was detected
on the left side of the sacrum during life, there were
no tender spots in the course of the sciatic nerve, and
the limb gradually emaciated without actual paralysis
or anaesthesia.
At the autopsy an osteo-sarcoma of the sacrum
was found, the left sacral plexus being compressed
and the left sciatic nerve extremely atrophied.
Case of Plantar Netiralgia,
H. E., a single woman, aged 38, employed as a
domestic servant, was admitted into the Workhouse
Infirmary, April 9th, 1885, complaining of pain in
the soles of the feet, and inability to walk or stand
on account of the pain.
2/6 DISEASES OF THE PERIPHERAL NERVES.
Both her parents had suffered from rheumatism,
and two of her brothers have had rheumatic fever.
The patient has had jaundice twice, otherwise
has enjoyed good health, but is not robust.
About four years ago she had pains in both her
feet similar to the present illness, but soon recovered.
Three weeks before admission she got her feet damp,
and the next day they were very gainful. There
were shooting pains confined to the soles of the
feet near the heel. The pain was much aggravated by
walking or standing, and much relieved by lying down.
When examined on admission there was con-
siderable hyperaesthesia of the soles of both feet and
tenderness. The hyperaesthetic area was close to the
heel, and measured an inch and a-half in length and
one inch in width on each foot. When the feet were
allowed to hang down the painful areas became red,
and the veins stood out, and free perspiration followed.
The same phenomena occurred after walking a few
yards. There was a tender spot behind the internal
malleolus and another over the heel. There was no
special tenderness, no pain in the back, or any sign of
disease of the spinal cord or its membranes. There
was no pain in the joints, nor any heart murmur.
The urine was normal. The patient was kept in bed,
and a blister applied behind the internal malleolus of
each foot. Simple rest in bed relieved the pains, but
she always suffered from them at night. Repeated
blistering finally caused complete cessation of the
pains.
DISEASES OF THE PERIPHERAL NERVES. 2/7
At the present time (May 9th) hanging the feet
out of bed does not cause them to become red or to
perspire, and walking does not cause pain.
For the time at any rate the patient is well.
This disease was first described by Weir Mitchell,
and is said to be rare in women.
On the 20th of May the patient left the Infirmary
perfectly well
On the 25th the patient, having tramped about
and having been much exposed, was re-admitted, the
pains having returned, but in a less degree than when
first admitted.
Neuritis of a nerve must be distinguished from
neuralgia : —
In neuritis. In neuralgia.
I. — The pain is continuous. The pain is inter-
mittent.
2. — Tenderness extends along Tenderness is present
a considerable length at certain spots
of the nerve. only.
3. — The nerve may be felt to
be thickened.
4. — Anaesthesia and paralysis
occur only in neuritis,
though paresis is some-
times present in sciatica.
Injuries of Perip/teral Nerves,
As has been elsewhere stated, the electrical re-
actions in diseases of the peripheral nerves vary
according to the extent of the lesion.
2/8 DISEASES OF THE PERIPHERAL NERVES.
When a motor nerve is divided there is total loss
of response to both currents when applied to the
nerve, and with Galvanism applied to the muscle the
"reaction of degeneration" is obtained.
The same changes are found after severe injury
to a motor or mixed nerve.
When the degree of injury is less there may be
complete paralysis with loss of Faradic irritability
but with normal Galvanic reactions.
In still a slighter degree of injury there is
paralysis but with normal electrical reactions.
The prognosis in cases of injury to nerve trunks
can thus be accurately estimated by the electrical
reactions.
Case of Division of tJte Median Nerve,
The patient, a medical student, was reaching a
bottle of soda-water out of its case, when the bottle
burst in his hand, severely cutting his right wrist in
front and in the middle line.
This occurred on the 25th of September, 1885.
At the time of the accident he perceived, as it
were, a great rush of blood into the hand, which felt
as though it was being greatly distended, and became
cold and numb.
During the dressing of the wound, and every
time the pad was used to swab up the blood so as to
look for a divided nerve or artery, the pain was most
acute, and was probably due to the pad coming in
contact with the divided nerve.
DISEASES OF THE PERIPHERAL NERVES. 279
The nerve was not seen during the treatment of
the wound. The hand was put in splints for three or
four days ; and on their removal it was found that the
muscles of the hand supplied by the median nerve
Fig. 22.
Palmar Surface Three Days after Accident.
The Shaded portion repiesenis complete An^estltesiii.
were paralysed, and that there was total anaesthesia in
the area of distribution of its sensory branches.
Three days after the accident there was total
anaesthesia of the radial half of the palm and thenar
280 DISEASES OF THE PERIPHERAL NERVES.
eminence, the anaesthetic area being sharply defined
and not gradually shading off; it extended in the palm
to a line contiguous with the axis of the ring-finger.
Dorsal Surface Thkee Days after Accident.
The Shaded poition represents complete Anjeslhesia.
There was also complete anaesthesia of the palmar
surfaces of the thumb, index, middle, and radial half
of ring-finger.
DISEASES OF THE PERIPHERAL NERVES. 28 1
On the dorsum of the hand there was total
anaesthesia of the ungual phalanx of the thumb and
of the second and third phalanges of the forefinger
and middle finger, and of the radial halves of the same
phalanges of the ring-finger.
A few days after the accident he began to feel
sharp shooting-pains in the hand and fingers, which
would come on suddenly and as suddenly disappear.
These pains frequently prevented sleep, but after
lasting about a month they gradually ceased.
When he attempted to move the fingers he was
always troubled with a sharp pain of a tearing
character, which would at times extend into the
forearm ; this was especially acute on moving the
index-finger. This pain also gradually ceased.
Since the accident there has been a great
diminution of temperature in the three and a half
fingers, and during the cold weather he had great
difficulty in keeping them warm. After exercise he
frequently noticed the little and half the ring-finger
and the inner part of the hand to be covered with
perspiration, while the rest of the palmar surface of the
hand was quite dry.
At the present time (February), nearly five
months after the accident, there is a scar in front of
the right wrist passing obliquely across the tendon of
the flexor carpi radialis and median nerve. The scar
is very sensitive when touched. A small bulla, con-
taining blood, is seen on the inner side of the terminal
phalanx of the index-finger.
282 DISEASES OF THE PERIPHERAL NERVES.
No changes in the nails are to be observed. He
has recovered power to a considerable extent, being
able to write with the right hand; but the grasp is
much weaker than on the left side.
Palmar Surface Five Months after Accident.
The portion thickly Shaded represents the Anseathesia; the thinly
Shaded portion Hyperarslhesia.
There is wasting of the thenar eminence on the
right side. The circumference of the base of the
right thumb being five inches, that of the left, five
DISEASES OF THE PERIPHERAL NERVES. 2S3
and a half. The response of the muscles of the hand
supplied by the median nerve is much diminished to
Faradism. To Galvanism the response is increased,
the contractions being slow and prolonged, the anodic
closure contraction predominating.
Dorsal SusrACE Five Months aftbr AccIDE^T.
Tha portion thickly Shaded represents the Ansesthesia ; the thitily
Shaded portion Hypersesthesia.
The distribution of the anjesthesia at the present
time, nearly five months after the accident, is as
284 DISEASES OF THE PERIPHERAL NERVES.
follows. The area of the right palm previously
anaesthetic is now everywhere hyperaesthetic, a slight
touch causing pain, the pain radiating into the fingers.
The hyperaesthesia extends over the palmar
surface of the first phalanx of the thumb and
encroaches on the first phalanges of the forefinger,
middle finger, and ring-finger.
The skin of the rest of the phalanges is still
anaesthetic on slight pressure, but hyperaesthetic on
deep pressure, the pain radiating into the fingers.
On the dorsum of the hand the following changes
have occurred : —
The anaesthesia previously present on the dorsal
aspect of the ungual phalanx of the thumb has dis-
appeared. The only alteration in the other fingers is
that the anaesthesia of the middle phalanges of the
fore and middle fingers extends now only over the
radial half of the phalanges, the ulnar half being
normal.
INDEX.
Abdominal reflex, 167.
Abclucens nerve (6th cranial nerve), 47.
Abductor paralysis of vocal cords, in locomotor ataxia, 5 1 ,
Abscess of the brain, 116.
Accommodation, centre for, 45.
Accommodative asthenopia, 34.
Achilles-tendon reaction or ankle clonus, 172.
Action — the reflex actions, 162.
Acute ascending paralysis, 240.
Acute atrophic spinal paralysis, 194.
Acute hemilateral myelitis, 232.
Acute meningitis, no.
Acute transverse myelitis, 224.
Agoraphobia, 78.
Alcoholic paralysis, 260.
Alternate hemiplegia, loi.
Am])lyopia, 27 and 30.
Amblyopia due to cortical disease, case of, 27.
Amyotrophic lateral sclerosis, 217.
Anatomy, medical, of brain, 10.
of cord, 156.
Anaemia, optic neuritis in, 31.
Anaemic paraplegia, 192.
Aneurism, intracranial, 121.
Angular gyrus, 22.
lesions of, 96.
Ankle clonus, 172.
Anosmia, 21.
Anterior cerebral artery, distribution of, 3.
Anterior grey cornua, functions of, 161.
diseases of, 176.
Aphasia, 84.
in migraine, 75.
motor, 88.
sensory, 88.
Apoplectiform attacks, 80.
Apoplexy, 122.
diagnosis of, from urismia, 74.
284 DISEASES OF THE PERIPHERAL NEP^
follows. The area of the lig^t pr*
anaesthetic is now everywhere hjrper
touch causing pain, the pain radia'
The hyperaesthesia extsr
surface of the first phakt*'
encroaches on the first* .jB^
middle finger, and rimj^
The skin c
anaesthetic or
deep pressu
Ontl
have oa <«9-
136.
.77'
P^ ^ents, escape of, in hemipl^a, 53.
app
g!? obstruction of, 6.
gjrsis (peripheral facial paralysis), 48.
i^flex, 174-
junervation of, 163.
^ to colour, 35.
word, 88.
^ophic affections of, 151.
Igl plexus, alteration in pupil in lesions of, ^y,
Erb's paralysis, 196.
jp^ abscess of, 116.
arteries of, i.
cortical lesions of, 94.
disease of membranes of, lio.
diseases of, 109.
motor centres of, 11.
motor tract in, 14.
sensory centres of, 16.
sensory tract in, 15.
softening of, 121.
tumours of, 117.
veins and sinuses of, 7.
Bright's disease, fundus oculi in, 31.
Broadbent, Dr., on bilateral innervation of certain muscles, 51.
Bulbar paralysis, 128.
INDEX. 287
Capsule, internal, 12.
anatomy and physiology of, 13 and 14.
lesions of, 100.
Case —
of acute hemilateral myelitis, 233.
of acute multiple neuritis due to diphtheria, 265.
of acute myelitis, 226.
of alternate hemiplegia, 102.
of amblyopia due to cortical disease, 27.
of aphasia, 89 and 92.
of disseminated sclerosis, 241.
of division of median nerve, 278.
of hypochondriasis terminating in melancholia, 132.
of locomotor ataxy with hysterical anjesthesia, 179.
of loss of the conjugate movement of the eyeballs down-
wards, of convergence, and of accommodation, 42.
of ophthalmoplegia externa, 41.
of pachymeningitis cervicalis hypertrophica, 245.
of paralysis depending upon idea, 182.
of plantar neuralgia, 275.
of progressive muscular atrophy commencing in the legs, 200.
of progressive unilateral facial atrophy, 152.
of pseudo-hypertrophic paralysis in adults, 208.
of spastic hemiplegia of infancy, 58.
of tubercular tumours of the optic thalami, 118.
Caudate nucleus, 13.
Central or ganglionic system of arteries, 4.
Central scotoma, 29.
Centres, auditory, 16.
gustatory, 16.
motor, II.
visual, 16.
word hearing, S7.
word seeing, 85.
Centrum ovale, lesions of, 96.
Cephalalgia, 74.
Cerebellar rigidity, 99.
Cerebellum, afferent fibres to, 158.
lesions of, 99.
middle peduncles of, 98.
Cerebral amaurosis, 27.
Cerebral arteries, i.
Cerebral facial paralysis, 100 and 48.
Cerebral haemorrhage, 123.
Cerebral hemiplegia, 122.
Cerebral veins and sinuses, 7.
Cerebral tumours, 117.
Cerebritis, 115.
Cerebrum, convolutions of, and their relations to the surface, 19.
Cheyne-Stokes breathing, 71.
Chiasma, optic, 22.
288 INDEX.
Chorea, 134.
post-hemiplegic, 57.
Ciliary muscle, paralysis of, 39.
Circle of Willis, 2.
Circulation, intracranial, i.
Claw -hand, 198.
Clonus, forms of, 172.
Colour-blindness, 35.
Columns of Goll, 160.
Coma, 72.
Conducting paths, of the spinal cord, 156.
degeneration of, 161.
of the brain, 14.
Congenital spastic hemiplegia and paraplegia, 57 and 58.
Conjugate movements of the eyes, 39.
Conjugate deviation of the eyes and rotation of the head and neck, 39.
Conjunctival reflex, 168.
Consciousness, perversion of, 79.
Contraction, paradoxical, 174.
Contracture, 83.
varieties of, 84.
Convolutions of the brain, 10.
Convulsions, 80.
Convulsive tic, 48.
Cord, medical anatomy of, 156.
diseases of, 176.
Corpora quadrigemina, lesions of, 97.
Corpus striatum, lesions of, 96.
Cortex of the brain, 10.
lesions of, 94.
motor centres in, li and 12.
sensory centres, 16.
Cortical system of arteries, I.
Cortical paralysis, 256.
Cramp, 83.
Cranial nerves, 21.
Cranial reflexes, 168.
Cremasteric reflex, 166.
Crossed paralysis, loi.
Crura cerebri, lesions of, loi.
Crust of crus cerebri, 14.
Cutaneous reflexes, 166.
Cutaneous trophic affections, 148.
Deafness, 81.
word, 87.
Decussation, of muscular sense fibres, 160.
of motor fibres, 14.
of optic nerve, 22.
of sensory fibres, 15 and 160.
Deep reflexes, 168.
INDEX. 289
Degeneration of conducting paths of brain and cord, 17 and 161.
Degeneration, reaction of, 144.
Degeneration, Wallerian, 17.
Degenerative diseases of the brain, 126.
Delirium, 78.
DeUisions, 79.
Descending degeneration, 17 and 161.
Deviation, conjugate, of eyes, 39.
Diabetes, optic atrophy in, 32.
Dimness of vision, 30.
Diphtheritic paralysis, 263.
Diplegia facialis, 100.
Diplopia, 34.
Direct cerebellar tracts, 158.
Diseases of the brain, 109.
of the peripheral nerves, 251.
of the spinal cord, 175.
Disseminated sclerosis, 241.
Double vision, 34.
Dura mater, diseases of, 114.
Dysarthria, 89.
Ear disease as a cause of abscess of the brain, 116.
Eclampsia nutans, 50.
Electrical reactions, normal, 139.
in disease, 141.
Electricity, use of in diagnosis, 138.
Eleventh nerve (spinal accessory), 50.
Embolic hemiplegia, 123.
Embolism, 122.
Encephalitis, 115.
Epigastric reflex, 167.
Epilepsy, 135.
Epilepsy, Jacksonian, 95.
Erb's paralysis, 196.
Erectores spinge reflex, 167.
Excitability, electrical, 138.
Extra-medullary diseases, 243.
Eye symptoms, in migraine, 30.
in nervous disease generally, 22.
Eyes, conjugate deviation, and rotation of head, 39.
Eyeball, paralysis of external muscles of, 40.
Eyelids, movements of, 44.
Face centre, ii.
Face, unilateral progressive atrophy of, 152.
Face, bilateral paralysis of, 100.
Facial nerve, 47.
paralysis of, 48 and 100.
spasm in the area of distribution of, 48.
Faradism, 138.
Fascial reflexes, 1 73.
290 INDEX.
Ferrier, Professor, on the cerebral centres, lo.
Fibrillary contractions, 83.
Field of vision, retina and optic tract, relation of, 25.
peripheral contraction of, 30.
Fifth nerve, 45.
paralysis of fifth and sixth nerves, loi.
trophic affections in territory of, 46.
Franklinism, 138.
Friedreich's disease, 223.
Front tap contraction, 173.
Functional and organic disease, differential diagnosis, 66 and 177.
Functional affections of the brain, 129.
spinal cord, 175.
Functions of the cortex of the cerebrum, 10.
Fundus oculi, normal, see plate (chromo).
changes in, in disease, 30, 32, and 33.
Gait, cerebellar, 98.
equine, high-action, 205.
in multiple sclerosis, 127.
Galvanism, 138.
Galvanometer, use of, 147.
Ganglia on the spinal nerves, 161.
Gangrene, symmetrical, 149.
General paralysis of the insane, 126.
pupil in, 38.
optic atrophy in, 33.
General spinal paralysis, 197.
Gesture, expression by, 84.
Giddiness, 76.
Glioma, 117.
Glosso-labio laryngeal paralysis, 128.
Glosso-pharyngeal nerve, 45.
Glossoplegia, 52.
Glossy skin, 148.
Gluteal reflex, 166.
Goll, columns of, 160.
secondary degeneration of, 162.
Gustatory nerve, 45.
Htemorrhage, into the brain, 123.
into the spinal cord, 251.
into the spinal meninges, 251.
retinal, 33.
Hyemorrhagic pachymeningitis, 114 and 246.
Hair, trophic disorders of, 150.
Hallucinations, 79.
Headache, 74.
ansemic, 75.
from eye defects, 74.
go^ity, 75.
INDEX. 291
Headache, hypersemic, 75.
hysterical, 75.
organic, 75.
pyrexial, 75.
rheumatic, 75.
syphilitic, 75.
toxic, 75.
Hemeralopia, 34.
Hemiansesthesia, 14 and 27.
Hemianopia, 22.
varieties of, 24 and 26.
Hemiatrophia facialis, 152.
Hemicrania, 75.
Hemiplegia, 53 and 122.
alternate, loi.
diagnosis of, 66.
distribution of paralysis in, 56.
hysterical, 67.
in early life, 54.
in uraemia, 73.
spastic, of infancy, 57.
spinal, 67.
Hydrocephaloid condition, 113.
Hydrocephalus, acute (tubercular meningitis), ill.
Hyperpyrexia in disease of pons or of cervical region of cord, 70.
Hypertrophic internal spinal pachymeningitis, 246.
Hypocampal region, 16.
Hypochondriasis, 132.
Hypoglossal nerve, 51.
Hysteria, 129.
Hysterical paralysis, 66.
paraplegia, 177.
Hystero-epilepsy, 136.
Ideal paralysis, 182.
Illusions, 79.
Indiscriminate lesions of the spinal cord, 224.
Infancy, spastic hemiplegia of, 57.
spastic paraplegia of, 58.
Infantile spinal paralysis, 194.
Insular sclerosis (disseminated or multiple sclerosis), 127 and 241.
Internal capsule, 12.
Interscapular reflex, 167.
Intracranial aneurisms, 121.
Intracranial circulation, I.
Intracranial tumours, II7.
Iridoplegia, 39.
Iris, nervous mechanism of, 36.
clonic spasm of, 38.
reflex movements of, 38.
292 ^ INDEX.
Jacksonian epilepsy, 95.
Jendrassik, Dr., observations of, on the influence of imisciTlar exertion
on the knee-jerk, 169.
Joints, trophic affections of, 151 •
Knee-jerk, 168, 169, 170, 171.
Labio-glosso laryngeal paralysis, 128.
Labyrinthine vertigo, TJ.
Landry's paralysis, 240.
Laryngeal crises, 5 1 .
Laryngeal paralysis in locomotor ataxia, 51.
Late rigidity, 55.
Lateral columns, 158.
Lateral sclerosis, 215.
Lead poisoning, changes in fundus oculi, 31.
paralysis from, 206.
Leg centre, 11.
Lenticulo-striate artery, 4.
Lesions of the brain, diagnosis of their situation, 93.
Lips, centres for, ii.
Local asphyxia, 149.
Local convulsion, 95.
Locomotor ataxia, 219.
Main en griflfe, 198.
Malarial paraplegia, 192.
Masseteric reflex or jaw -jerk, 172.
Median nerve, case of division of, 278.
Medulla oblongata, nuclei in, 49.
lesions of, 98.
Memory, loss of, in general paralysis of the insane, 126.
Meniere's disease, 77.
Meningitis, 1 10.
basilar, iii.
of convexity, 113.
spinal, 244.
tubercular, III.
Mental debility, 80.
Mental depression, 131.
Micturition, 163.
Middle cerebral artery, 3.
Middle peduncle of cerebellum, lesions of, 98.
Migraine, 75.
ocular disturbances in, 30.
optic atrophy in, 33.
Monoplegia, cerebral, 57 and 256.
peripheral, 257.
spinal, 257.
Monospasms, 94.
INDEX. 293
Motor centres, 1 1.
Motor points, 139.
Motor tracts, in the brain, 14.
in the cord, 156.
Multiple neuritis, 253.
Multiple sclerosis, 127 and 241.
Muscae volitantes, 30.
Muscles of the eye, paralysis of, 39.
Muscular asthenopia, 34.
Muscular atrophy, progressive, 198.
Muscular sense, loss of, 220.
Mydriasis, 37.
Myelitis, transverse, 224.
hemilateral, 232.
Myosis, 36.
Myotatic contraction, 169.
Nails, trophic disorders of, 150.
Nerves, cranial, 21.
Neuralgia, 274.
Neurasthenia, 130.
Neurasthenic asthenopia, 35.
Neuritis, 253.
Neuro-paralytic ophthalmia, 46.
Nyctalopia, 34.
Nystagmus, 44.
Occipital lobes, 16.
lesions of, 96.
Ocular muscles, paralysis of, 39 and 40.
Ocular nerves, paralysis of, 39.
Olfactory anaesthesia, 21.
Olfactory nerve, 21.
Ophthalmoplegia externa, 40.
Ophthalmoplegia interna, 39.
Ophthalmoscopic appearances in health, see plate (chromo).
in optic neuritis, 30, see plate (chromo).
in optic atrophy, 32, see plate (chromo).
Optic commissure, 22.
lesions of, 23.
Optic nerve, 22.
atrophy of, 32.
Optic neuritis, 30.
Optic thalami, lesions of, 97.
Optic tract, 22 and 24.
Organic reflexes, 162.
Osseous lesions in the insane, 151.
Osseous trophic neuroses, 151.
Otorrhoea, chronic, its connection with cerebral abscess, 117.
294 INDEX.
Pachymeningilis cerebcnlis externa, 1 14.
Pochymeningilis certhralis inletiia hasmorrh^ica, 1 14.
Pachymeningilis cervicalis hyperltophica, 246.
FacbymeningiliB 5pina.lis, 345.
Pain iibres in spinal cord. 150.
Palmar reflex, 167.
Papillitis, 30.
Poiailnxical contiacLion, 174.
Paralysis, luncLional, 66 and 177.
alternate, lOI
ctepending upon idea., 182.
Paralysis siscendens a.ciita, 240.
Paralysis, cortical, 94 and 57.
Paralytic contracture, 83.
Paraplegia, reflex, 191.
anemic, 192.
malacial, 192.
Spastic, of infancy, 58.
Patella clonus, 173.
Patella- tend on reaction, 168.
Pedujicles of the cerebrum, 14.
Perforating ulcer I49.
Periosteal reflexes, 173.
Peripheral facial [inralysis, 48.
Peripheral neuritis, 253.
Plantar neuralEia CBseof,27S,
Plantar reflex, 166.
Pneumof^ltic nerve, 50.
Pneumonia, after cerebral hsemorrhage, 15
Polio-mjelilis anterior acuta, 194.
Polio-myelitis anteria chronica, 198.
Pons vaiulii, lesions of, 97.
Posterior and lateral combined sclerosis, a
Posterior cerebral nrlcry 4.
Posterior colurcns, 160.
Post-hemiplegic moveiiienls, 57.
Pmefrontal lesions, 93.
Primary lateral sclerosis, sij.
Progressive locomotor ataxy, 219.
Progressive muscular atrophy., 198.
Progressive paralysis, 240.
Pseuilo-hy per trophic paralysis, 207.
Flosis in hysteria, 44,
Pupil, Argj-ll-Robertson, 37.
ovemenlsDf,36.
■nous rneehanisin of, 36.
:e of. 36, 37- and 38.
INDEX. 295
Pyramidal tracts, 158.
Pyrexia in diseases of the brain, 69.
Raynaud's disease, 149.
Reaction of degeneration, 144.
Reading in loss of speech, 87.
Reflex actions, 162.
abdominal, 167.
cremasteric, 166.
epigastric, 167.
gluteal, 166.
of erectores spina, 167.
organic, 162.
plantar, 166.
scapular, i67'
skin, 166.
tendon, 168.
Reflex paraplegia, 191.
Respiration, 71.
Cheyne-Stokes, 71.
Rigidity, initial, 55.
cerebellar, 99.
early, 55.
late, 55.
structural, 56.
Rolando, fissure of, 20.
Root zones, 160.
Scapular reflex, 167.
Sciatica, 275.
Sclerosis, ascending, 162.
descending, 16 1.
lateral, 215.
multiple, 127.
Sclerosis of posterior and lateral columns combined, 222.
Scotoma, 29.
Seat of lesion, diagnosis, 93.
Senses, special, 21.
Sensory tracts, in brain, 15.
in cord, 158.
Seventh cranial nerve, 47.
Sight, subjective disturbances of, 30.
Signs, expression by, 84.
Sixth cranial nerve, 47.
paralysis of sixth and fifth nerves, lOi.
paralysis of sixth and facial nerves, loi.
Skin, glossy, 148.
trophic disorders of, 148.
Skin reflexes, 166.
Skull, relation of cerebral fissures and convolutions to scalp, 19.
Smell, 21.
296 INDEX.
Softening of the brain, 121.
Spastic paraplegia of infancy, 58.
Spastic hemiplegia of infancy, 57.
Speech, disorders of, 84.
Spinal accessory nerve, 50.
Spinal cord, medical anatomy of, 156.
diseases of, 1.75.
functions of, 158.
unilateral lesion of, 232.
Spinal haemorrhage, 251.
Spinal hemiplegia, 67.
Spinal irritation, 175.
Spinal membranes, diseases of, 243.
Spinal tumours, 251.
Status epilepticus, 137.
Stupor, 72.
Subacute inflammation of the anterior cornua, 197.
Superior cerebellar artery, obstruction of, 6.
Superior temporo-sphenoidal convolution, 16.
lesions of, 96.
Superficial or skin reflexes, 163.
Sylvius, fissure of, 19.
Syncope, diagnosis of epilepsy from, 135.
Syphilis, optic neuritis in, 32.
Tabes dorsal is (locomotor ataxia), 219.
ecchymoses in, 148.
laryngeal crises in, 51.
optic atrophy in, 33.
Taste, 45.
Teeth, trophic affections of, 152.
Temperature, 69.
Tendon-reflexes, 168.
Tetanic seizures, cerebellar, 99.
Thalami optici, 97.
Third cranial nerve, 45.
Thrombosis of superior cerebellar artery, 6.
of basilar artery, 6.
of cerebral veins and sinuses, 8.
of middle cerebral artery, 123.
Tic, convulsive, 48.
Tobacco amblyopia, 29.
Tongue, centre, 1 1.
paralysis of, 52 and 100.
Torticollis, 50.
Transverse myelitis, 224.
Tremor, 82.
Trigeminus, 46.
Trophic affections, 148.
Trunk, centre, 1 1.
Tubercular meningitis, diagnosis of, from typhoid fever, 113.
INDEX. 297
Tumours, intracranial, 117.
spinal, 251.
Ulcer, perforating, 149.
Unilateral, or partial convulsions, 95.
Unilateral progressive facial atrophy, 152.
Uraemia, diagnosis from apoplexy, 73.
Urinary paraplegia, 191.
Vagus nerve, 50.
Vascular lesions, no and 122.
Veins of Galen, 9.
Veins of the brain, 7.
thrombosis in, 7.
Vertebral arteries, obstruction of, 6.
Vertigo, 76.
Vesical reflex, 163.
Vessels, intracranial, i.
Viscera, trophic affections of, 151.
Vision, colour, 35.
fields of, 26.
Visual centre, 16.
Vomiting, 68.
Wallerian nerve degeneration, 17.
Willis, circle of, 2.
Word -blindness, 85.
Word-deafness, 87.
Word -hearing, centre, 87.
Word-seeing, centre, 85.
Wrist clonus, 172.
Writing power, loss of, 88.
preservation of in aphasia, 89.
Wry neck, 50.
\^K
LIST OF CHIEF AUTHORS REFERRED TO IN
THE TEXT.
Allbutt, Clifford.
Jendrassik.
Argyll - Rober t son .
Lancereaux.
Beevor.
Bennett-Hughes.
Marshall, Hall.
Bramwell.
Mendel.
Broadbent.
Moxon.
Brown -S6qiiard.
Mitchell, Weir.
Buzzard.
Medico - Chirurgical ** Trans
'* Brain," Vols. VII.
and VIII.
actions."
Charcot.
Ormerod.
Charcot and Marie.
Chauternesse.
Paget.
Churton.
Cyon.
Reid.
Clinical Society's "Transactions."
Reynolds, Russell.
'* Revue de Medicine."
Duchenne.
Dreschfeld.
Stewart, Grainger.
Erb.
Tenneson.
Tooth.
Ferrier.
Watteville.
Gowers.
Westphal.
Goltz.
Wilks.
Hammond.
Horsley.
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