I. 
A CLINICAL CONTRIBUTION 
TO THE STUDY OF 
Post-Paralytic Chorea 
ii. 
A CONTRIBUTION 
TO THE STUDY OF 
LOCALIZED CEREBRAL LESIONS 
BY 
E. C. SEQUIN, M.D. 
Clinical Professor of Diseases op the Mind and Nervous System, in the College 
of Physicians and Surgeons, New York, ; President of the 
New York Neurological Society. 
Reprinted from the Tram-actiom of .the A nierttnn -M^urolog^al 
NEWYORK 
Gr. P. PUTNAM’S SONS 
183 Fifth Avenue 
1877 i. 
A CLINICAL CONTRIBUTION 
TO THE STUDY OF 
Post-Paralytic Chorea 
ii. 
A CONTRIBUTION 
TO THE STUDY OF 
LOCALIZED CEREBRAL LESIONS 
BY 
E. C. SEGUIN, M.D 
Clinical Professor of Diseases of the Mind and Nervous System, in the College 
of Physicians and Surgeons, New York ; President 
New York Neurological Society. Mss*! s: 
Reprinted from the Transactions of the America// Neurological 
Association, Vol. 11., iSyy 
NEWYORK 
CL P. PUTNAM’S SONS 
182 Fifth Avenue 
1877 A CLINICAL CONTRIBUTION 
TO THE 
STUDY Of POST-PARALYTIC CHOREA. 
E. C. SEGUIN', M.D., of New York. 
Haying had the opportunity of observing two well-marked 
instances of this remarkable symptom-group, and as I am able to 
bring forward one of the patients, I make bold to call the atten- 
tion of thn Association to the subject. Before reciting the cases, 
it may not be amiss to say a few words of the growth of our 
knowledge of the subject. Although the symptom-group had 
been observed a number of years ago by various physicians, yet it 
was our distinguished Fellow, Dr. Weir Mitchell, who first called 
special attention to it, and gave it a name, in 1874;* but already 
in 1873, f Professor Charcot, of Paris, had cpiite well described 
the movements, and indicated their association with hemi-ames- 
thesia. I would here beg to call attention to the fact that the 
description of the symptoms in my first case was written in 
December, 1873. Recently M. Charcot has written specially upon 
“post-hemiplegic” chorea in its relations to hemi-ansesthesia,! 
and has expressed the opinion that both these symptoms are 
caused by lesions situated at the outer and posterior borders 
of the optic thalamus, or in the posterior expansion of the corona 
radiata. Last year,§ Dr. W. R. Cowers read to the Royal Medical 
* Post-Paralytic Chorea. American Journal of the Med. Sci., Oct., 1874, 
p. 842. 
f Lemons sur les maladies du systeme nerveux, t. i., p. 279. 
\ Lemons, etc., 4me fascicule, Paris, 1877, p. 329. 
§On Athetosis and Post-hemiplegic Disorders of Movements. The Lancet, 
1876, vol. i., p. 709. 4 
E. C. SEGUIN. 
and Chirurgical Society an elaborate essay based upon a number 
of cases showing various degrees of post-paralytic incoordination, 
including athetosis, athetoid movements, and post-hemiplegic 
chorea. 
A good description of a remarkable case of this condition, also 
coincident with hemi-anaesthesia, will be found in M. Schoepfer’s 
Paris thesis.* 
I now pass on to relate the cases which have come under my 
observation. 
Case I.—H. H. H., aged eighteen years; by occupation a clerk, 
and a native of this country, was referred to me by Dr. Fisher, 
December 6, 1873. 
He was a fairly-developed boy, with apparent good general 
health. He had been well until last April, when he began to suffer 
from diffused headache, moi'e temporal, but not one-sided. One 
day in May he went down to his office feeling as well as usual, 
and began his work with full use of all his limbs. About 11 
o’clock a.m. was writing, leaning on the desk, the left arm thrown 
forward and its fingers steadying the paper. He got up to cross 
the room with a book in his left hand, but the book fell to the floor, 
and he then first became aware that his left arm was weak. There 
were at the time no subjective or sensory symptoms, cerebral or 
peripheral. The leg was not in any way affected. He was able, 
though awkwardly, to feed himself at dinner that evening. 
The paresis gradually increased until the middle of July, and 
since that time there has not been much change. 
Shortly after the attack, within a few days, patient noticed 
numbness of the left hand and forearm, and this has somewhat 
increased. 
In the early part of July convulsive movements began in the 
left hand, and have since become greater in force, and have ex- 
tended to other parts of the left side. The left leg began to 
twitch and groxv weak also in the first part of July, and since 
October slight twitching has appeared in the lower part of the 
left side of the face. Lately sight has become impaired, but 
hearing is preserved. 
There have never been any symptoms on the right side. He 
has never had any epileptic or epileptiform seizures. Memory 
has somewhat failed. / 
* Considerations sur un cas d’liemianesriiesie avec mouvements atasiques, 
succedant & une hemiplegie du mihne cote. Th&se de Paris, 1876. POST-PAEALYTIC CHOEEA. 
5 
In the middle of July there appeared double vision, which 
gradually passed away. At the same time he had severe bi-tem- 
poral headache with nausea, lasting one week. The latter symp- 
tom never recurred, and it was probably caused by diplopia. Ho 
rectal or vesical symptoms. Ho dysphagia. 
Examination reveals left hemiplegia with peculiar spasmodic 
movements of the palsied parts. The left arm and leg execute 
all movements, though feebly and awkwardly. The dynamome- 
ter shows a strength of 30° in the right hand and 10° in the left; 
can barely stand on left foot alone; no evident facial paralysis ; 
tongue points a little to the left. There is now no twitching 
in the face. The left pupil is a trifle larger than the right; 
botli are active. The ophthalmoscope shows both optic disks con- 
gested, their outlines blurred, and traces of exudation along the 
bloodvessels. There is no evident palsy of any muscle about the 
eyes, though the eyes converge abnormally. Fields of vision not 
impaired. 
There are strong choreiform (this is the word used in notes 
made at the-time of first seeing patient—lß73) movements in the 
left arm, shoulder, and leg. These parts are constantly agitated 
during waking hours, but quiet during sleep. The arm is more 
or less rigid, and its various parts perform large oscillations. The 
movement is increased by emotion or by the attempt to perform 
voluntary acts; he cannot carry a glass to his lips. Eyes being 
closed, he can, after groping a little, place fore-finger on tip of 
nose. There is, however, a marked ataxiform element in the 
spasm. The muscles of the shoulder and the trapezius are in- 
volved, but not the muscles of the trunk and neck. 
Sensibility (to contact and pain) is slightly impaired in fingers 
'and hands; the points of the aesthesiometer must be separated 
from 3 to 5 mm. to be distinguished on the finger-tips. 
January 20th, 1874.—Chorea is as before. There is much heb- 
etude, On the right side there is marked ptosis with weakness 
of the internal rectus (palsy of third nerve). 
We now have a form of crossed paralysis, i. e., third nerve on 
the right side, body on the left. The right crus cerebri is proba- 
bly involved in lesion. 
January 2Sth.—Greater evidence of palsy of third nerve on right 
side; more chorea in left limbs ; left side of face paralyzed; speech 
thick, saliva escaping from the mouth. There is marked anaes- 
thesia in range of left supra-orbital nerve. Sister states that he 6 
E. C. SEGUIN. 
lias frequent partial syncopal attacks without spasm or loss of 
consciousness. Is this petit-mal ? 
March Ist.—Much as before, hut weaker. While speaking has 
spasm in left side of face which simulates involuntary laugh- 
ter. 
This patient died during March without presenting any new 
symptoms, and I was unable to make an autopsy. 
Judging by the symptoms, the lesion must have been placed 
just above the motor tract of the right crus cerebri, acting upon 
it by pressure. 
It is probable that the lesion was hemorrhage with subsequent 
inflammation about the clot, though it may have been a tumor. 
I am in doubt on this point, because I am not disposed to at- 
tach much value to the ophthalmoscopic examination which I 
made. The certain diagnosis of neuro-retinitis would, of course, 
have strengthened the probability of there being a tumor in the 
locality indicated. 
Case II.—J. P., aged 26, a clerk, was referred to me by Prof. 
Edward Curtis, on May 24th, 1877. 
I learned that this young man had been well up to April 16, 
1876, when he had, in the street, an attack of right hemiplegia. 
He did not fall down ; was able to walk with help to a street-car, 
yet knew nothing of what afterward occurred until the next day. 
This was either late loss of consciousness, or amnesia. 
On the next day speech was much affected, he could not recall 
names and addresses of persons; his right arm was powerless, and 
there was much numbness of the right cheek and arm. “ Could 
only see with inner half of right eye.” Right leg weak. In a 
day or two speech improved. 
In three weeks he walked well, but the arm did not regain its 
strength for three months. 
During this period of improvement irregular movements ap- 
peared in the right arm, and have persisted. No jerking in face, 
leg, or on the left side of the body. Imperfect vision persisted. 
The numbness continued marked in toes, finger-tips, cheek, and 
tongue, on the right side. The numbness on the right side of 
face and tongue never quite reached the median line. 
In August (four months after attack of paralysis) had an epi- 
leptiform spasm, followed by loss of consciousness lasting until 
the ensuing morning. 
In April, 1877, had a second epileptiform attack. At times POST-PARALYTIC CHOREA. 
7 
feels queerly in his head, “asif a spasm were coming on.” Has 
not suffered from headache or dizziness. 
Inquiries into patient’s past history show that six or seven years 
ago he had several chancres, which did not heal for three months. 
Had no buboes., Never had any eruptions, strictly speaking; but his 
legs “ ulcerated,” and he has since frequently suffered from ulcer- 
ated sore throat. At no time any osteocopic pains. Sight was 
good until after attack of paralysis. Memory is a little impaired. 
Examination.—Patient’s speech is imperfect, a sort of aphasic 
stammering. It would appear that he has always had a some- 
what similar defect. The right leg has almost perfectly recovered, 
but the right hand is not quite as strong as the left, and presents 
curious abnormalities of movements. The dynamometer test 
shows for the right hand 18°-22°; for the left, 28° and 28°. 
The peculiar movements are of two sorts : 
1. While the patient is seated quietly, with his hand resting 
on his thigh, it (the hand) may be seen to be agitated by slight 
rythmical movements of the type observed in paralysis agitans. 
These are not truly constant, but seem to be provoked by obser- 
vation or by the patient’s own watching of the hand. 
2. During attempted use of the extremity, an ataxiform move- 
ment is developed; or, more properly speaking, a movement com- 
pounded of the want of combined and harmonious action of large 
muscular groups which is characteristic of the ataxic movement, 
and of the totally irregular and capricious muscular contractions 
which constitute the choreic type. On the whole, the movement 
is more like that of ataxia; i. e., more or less regularly oscilla- 
tory. 
The right leg is not the seat of any tremor, ataxia, or chorea; 
and the left side of the body shows none. 
There is no marked facial palsy, but the right naso-labial crease 
is less distinct than the left. The tongue deviates a little to the 
right. * These points make it probable that the paralytic attack 
in April, 1876, was one of common typical hemiplegia. 
There exists a degree of right hemi-anaesthesia. To slightest 
contact, according to patient’s positive statement, the anaesthetic 
district of the face begins at a point 1 cent, to the right of the 
median line. The sesthesiometer and the simple contact test 
show slight loss of sensibility on the right side of the face. On 
the finger-tips the points of the assthesiometer cannot be distin- 
guished at a less distance apart than from 5 to 8 mm. on the 8 
E. C. SEGUIN. 
right side, while on the left they are distinguished at 3 mm. 
Pricking is well felt. 
The fault in vision is in the shape of incomplete hemiopia; the 
right temporal and the left nasal halves of the fields being ob- 
scured, as shown in the cut. 
EIGHT EYE. 
The pupils are equal and normal; the ocular muscles act well; 
and the ophthalmoscope shows no lesion which I can appreciate. 
A careful examination of the throat does not reveal any cica- 
trices. The heart is normal. 
My diagnosis was slight cerebral hemorrhage just outside the 
left thalamus opticus. Yet I was unwilling not to give the pa- 
tient the benefit of the doubt that syphilis had led to arterial dis- 
ease and rupture, though the history was not one that pointed to 
the existence of syphilis at any time. Yet how often are serious 
syphilitic nervous lesions developed after equally or more incom- 
plete chains of evidence ? Consequently I have given this patient 
mercury internally, and have brought about a degree of saliva- 
tion. * 
Remarks.—These cases are strongly in support of M. Charcot’s 
proposition. In the first place, we observe in both the co-exist- 
ence of hemiplegia, hemi-anassthesia, and choreiform movements. 
In case 1., a positive symptom, palsy of oculo-motorius nerve, 
points to a lesion near the crus cerebri—probably just above it. 
In the second, there is a strong probability that the lesion is not 
far from the same part—near the thalamus opticus. 
In my second case, the occurrence of hemiopia is of great inter- 
est, because it will be remembered that Prof. Charcot has re- 
cently f denied that a lesion of the hemisphere could produce 
LEFT EYE. 
* July 1, 1877.—1 may now add that salivation, followed by the admin- 
istration of iodide of potassium in doses of 3 iii. a day, made no change 
whatever in this patient’s symptoms. I have now advised him to cease 
treatment, and hope for spontaneous improvement. 
f Lemons sur les localisations dans les maladies du cerveau. Paris, 1876, 
p. 12G. POST-PARALYTIC CHOREA. 
9 
hemiopia. In the absence of a post-mortem examination, I would 
not be understood as claiming that the case positively contradicts 
M. Charcot’s statement; yet it must be admitted, I think, that 
there is no probability that there was in this case a second lesion 
affecting one of the optic tracts. CONTRIBUTION 
TO THE 
STUDY or LOCALIZED CEREBRAL LESIONS. 
E. C. SEGUIN, M.D., of New York. 
It has fallen to my lot to observe during life and to examine 
after death a number of cases in which localized cerebral lesions 
gave rise to definite peripheral symptoms, and it has appeared to 
me that these cases might profitably be studied in the light of 
recent experimental and pathological researches upon the func- 
tions of the brain. In other words, I shall endeavor to determine 
the bearing of these cases upon the recent hypothesis of the local- 
ization of functions in the cortex of the brain. 
I shall divide my cases into three categories: Ist. Cases in 
which localized lesions gave rise to Aphasia. 2d. Cases in which 
localized lesions gave rise to Paralysis. 3d. Cases in which 
localized lesions gave rise to Spasm. 
CASES nsr WHICH A MORE OR LESS LIMITED CEREBRAL LESIOM 
PRODUCED APHASIA. 
PART I. 
Case I.—Cerebral softening from arterial degeneration: apha- 
sia, and right hemiplegia. 
A woman aged seventy-five years was admitted to the Epileptic 
and Paralytic Hospital on Blackwell’s Island, January 17th, 1873. 
The history of the case is very meagre, and only states that when 
attacked she screamed, threw up her hands, and became insensible. 
On recovering from insensibility it was found that she had com- 12 
E. C. SEGUIN'. 
pletely lost speech, and was paralyzed in the right side, face, and 
limbs. No mention is made of the state of sensibility ; but, as I 
am in the habit of always looking for hemi-anaesthesia, I feel sure 
that the case was one of common hemiplegia. I also feel very 
positive that during the six months of the patient’s stay in my 
ward she greatly regained voluntary power on the right side, 
being able to take a few steps alone, and to move her arm quite 
freely. Aphasia, however, remained complete. 
The patient died on July 13th, 1873, and careful notes were 
made at the time of the post-mortem examination on the 13th. 
I reproduce only those relating to the state of the brain, making, 
however, the-preliminary statement that the valves of the heart 
were free from disease. 
Dura mater not abnormally adherent to the skull, and healthy 
at base. Moderate sub-arachnoid effusion at the top of the brain, 
and a great deal at its base. 
Both anterior lobes have undergone more or less atrophy. The 
convolutions of the left parietal lobe, beginning at a point an inch 
and a half from the median line, bulge and form a soft and yel- 
lowish tumor. The pale yellowish color of the affected convolu- 
tions is in marked contrast with the injected appearance of the 
rest of the brain. Over these diseased convolutions there is more 
sub-arachnoid effusion than elsewhere. After removal of the 
brain, and escape of the greater part of the serum, the left parietal 
lobe appears sunken, and there results an appearance like a loss 
of substance as large as a small walnut. The basilar and other 
large arteries of the circle of Willis are open, and nearly free 
from changes. 
Careful inspection shows no externally visible lesion in the left 
frontal lobe, its third convolution, and the island of Keil. The 
depression in the parietal lobe measures six and a half cent, 
square, involving all of the lobe except the part lying next to the 
great longitudinal fissure. 
Two small old lesions are found in the right hemisphere, one 
lying at the external margin of the extra-ventricular nucleus of 
the corpus striatum, just behind the island of Reil; the other in 
the posterior part of the same (lenticular) nucleus. Both are 
small cavities, the size of large beans. 
The following is a transcript of notes which I made upon the 
state of the left hemisphere. I was very careful in studying the 
limits of the rarnollisscment, because at first sight the case seemed LOCALIZED CEEEBEAL LESIONS. 
13 
to be one opposed to Broca’s hypothesis of aphasia. The extent 
of the lesion was studied, after hardening for a few days in a solu- 
tion of bichromate of potassa, by means of transverse horizontal 
sections, and tracings made on transfer paper upon each section 
by Mr. George Wright. Each tracing was afterward carefully re- 
duced and drawn to a scale, with a sketch of the appearance of the 
unsliced hemisphere. This last drawing, Eig. 1, shows that the 
greatest destruction of tissue has taken place in the parietal lobe 
proper. Posteriorly and interiorly a degree of degeneration of 
CASB I.—PROFILE OF LEFT HEMISPHERE. TWO TRANSVERSE HORIZONTAL SECTIONS OF 
SAME. EXTENSIVE RAMOLLISSEMENT. 
the convolutions may be traced almost to the confines of the 
occipital and sphenoidal lobes; while anteriorly, after having 
destroyed in great part the ascending frontal convolution, it ex- 
tends over a portion of the second frontal gyrus. 
Sections were made through the hemisphere in the planes iudi- 14 
E. C. SEGUIN. 
cated by lines in Fig. 1, and the morbid appearances seen on each 
section were accurately traced on paper. Fig, 2 shows that the 
atrophy has destroyed a large part of the upper posterior part of 
the hemisphere. Fig. 3 demonstrates that the hinder part of the 
third frontal convolution is likewise involved. 
By this method of examination the case is restored to the cate- 
gory of common cases of aphasia, viz., those supporting Broca’s 
hypothesis. 
Remarks.—I consider this case as doubly instructive. 
First, in a positive manner, as showing that a superficial degen- 
eration of the cortex of the brain (involving Broca’s centre for 
speech) may produce aphasia of the most complete kind. 
Second, negatively; because, in spite of the destruction of gray 
matter in the regions which Ferrier makes out to include nearly all 
the motor centres for the face, arm, and leg, a great degree of vol- 
untary power was regained by the patient in a few months. Hence 
it would appear that other pfarts of the injured hemisphere had 
acquired controlling power over the limbs of the opposite 
side. 
Case ll.—Embolism of the left middle cerebral artery, soften- 
ing of the brain: aphasia, and right hemiplegia. 
Mrs. G., seen in consultation with Dr. William Pierson, jr., 
of Orange, IST. J., on May Bth, 1877. With the exception of a 
badly acting heart and a tendency to gout, Mrs. G. enjoyed fair 
health and had three children up to 1875. Late in November of 
that year she had a moderately severe miscarriage. On December 
7th, at 7.30 p. m., experienced a sudden attack of common hemi- 
plegia on the left side, without loss of consciousness. Speech was 
much impaired by defect in articulation. The palsy passed away 
rapidly, though she dragged her left foot for some days. Power of 
articulation slowly regained. Patient’s husband is an unusually 
well-informed gentleman, and states that trouble in speech was 
surely not aphasiform. There remained a want of proper action 
of muscles of throat and larynx; patient not knowing how to 
pitch her voice afterward. 
On January 13th, 1876, a second attack of left hemiplegia 
occurred. Consciousness was lost for a moment. Left leg but 
not left arm palsied. All symptoms, except a degree of excite- 
ment, passed off the next day, after a long sleep. 
On April Ist, at 1 a. m., had a first epileptic fit while asleep; 
had full spasm, slight frothing at mouth, loss of conscious- LOCALIZED CEREBRAL LESIONS. 
15 
ness, stertorous breathing, and a heavy terminal slumber. On 
April 29th, second fit; falling like a shot to the floor. Has had 
a few attacks since; only two, however, since last August. One 
was two weeks ago. 
Present paralytic attack occurred twelve days ago. On April 
36th, came down stairs, and in a few minutes was found fumbling 
a door-knob. Without apoplectic symptoms, complete right hemi- 
plegia and aphasia were developed. Possibly a little return of 
voluntary movement has taken place in the right limbs. No re- 
turn of speech. Indeed, the aphasia has been so absolute, that even 
sign-language has been lost, and patient’s friends have thought 
her deprived of her faculties, though she has been conscious at 
all times. There has been no retention of urine, no tendency to 
bed-sore. Food has hardly been taken, and patient’s respirations 
have been extraordinarily frequent. 
Examination shows complete right hemiplegia, with marked 
loss of sensibility in the paralyzed limbs. The face is hardly dis- 
torted. Absence of spoken and gesture language as above, but 
patient looks intelligent. Pupils very wide, but equal. Breath- 
ing very rapid, 50 or 60 in the minute. Pulse slightly irregular, 
beating about 90 in the minute. The heart is enlarged, apex 
in sixth intercostal; cardiac sound can be heard away from the 
patient, as far as two feet. No distinct murmur can be heard, 
but the heart-sounds are completely reduplicated. Mouth tem- 
perature 37.5° 0. No sensibility to pinching on the right side, 
and only slight on left; but this may be owing to rapid respira- 
tion. There is a marked tendency to turn eyeballs to the left, 
away from the paralyzed side. Lungs are free from deposit or 
congestion ; the optic disks are normal, 
I learn that Mrs. G-. has had pains in the small joints, with 
atrophy of hand-muscles, and, in the last few years, gouty knees. 
From childhood she has had a curious affection of the heart, 
characterized by dyspnoea, hard beating of the organ, and by 
transmission of its sound to a distance from the body of two to 
four feet. My diagnosis was embolism of various arteries in both 
hemispheres; the last attack being due to blocking of a branch, 
or branches, of the left Sylvian artery, and consequent softening 
of (probably) the third frontal and the ascending frontal convo- 
lutions. 
In spite of an attempt at supporting treatment, Mrs. G. died 
on May 11th. 16 
E. C. SEGUIN. 
For notes of the post-mortem examination, made on the same 
day, six hours after death, I am indebted to Dr. Pierson. 
“ The membranes and sinuses of the brain were normal. The 
surface of the third frontal convolution of the right side was yel- 
low in color, with a tough, elastic feel. This lesion, extending 
through the gray matter, was about one inch square and one- 
quarter inch thick. The same change was also found, but to a 
less extent, in the same part on the left side. The left middle 
cerebral artery was plugged by an embolus at a point one-half 
CASE lI.—SOFTENING IN BOTH HEMISPHERES, IN CONSEQUENCE OP EMBOLISM, 
inch from its origin. A spot of brain-tissue, about the size of a 
quarter of a dollar (one inch in diameter), supplied by this 
artery, was in a softened state; it was yellow, tinged with red, 
broken down, and of semi-fluid consistence. The situation of 
this lesion was external and posterior to the anterior cornu of the LOCALIZED CEREBRAL LESIONS. 
17 
left lateral ventricle, and corresponded to that part of the third 
frontal convolution which is known as the island of Reil. The 
softening was confined to the white brain substance, and did not 
implicate the surface. The rest of the encephalon was normal. 
“ The heart was much diseased. The mitral valves were much 
thickened, and nodules of atheroma could be felt at various points. 
The two leaves of the valve were joined together, constricting 
the auriculo-ventricular opening to such an extent that it would 
not admit the end of the finger; there was stenosis and insuffi- 
ciency.” 
Unfortunately the brain was not preserved for more minute 
examination, so that the existence of microscopic changes in the 
rest of the territory supplied by the left Sylvian artery remains a 
matter for speculation. * 
The notes and the plugged artery were brought to me by a 
student of Dr. Pierson, and I asked him to mark out for me on 
plates in Ecker’s and Luys’ books the location of lesions. The 
accompanying diagrams are constructed faithfully after this gen- 
tleman’s indications, and Dr. Pierson’s corrections. 
Remarks.—The complete aphasia in this case was undoubtedly 
due to lesion of the third convolution and of the anterior folds 
of the island of Reil. We have in this case an addition to the 
large list of cases supporting Broca’s hypothesis. It is remark- 
able that such complete hemiplegia should have existed without 
apparent lesion of those parts which are more directly connected 
with the movements of the arm and leg, viz., the ascending fron- 
tal and parietal convolutions. These convolutions are supplied 
by the artery which was plugged, and it is very probable that 
microscopic study would have shown them to be full of granular 
bodies. They may have been saved from gross softening by an 
unusually free anastomosis between the final branches of the 
plugged Sylvian artery and other arteries in the same hemisphere. 
It is also possible that a part of the hemiplegia was due to pres- 
sure upon and anaemia of parts adjacent to the softened spot; and 
that, had the patient survived, the paralysis would have disap- 
peared in a few weeks. 
Another interesting feature of the case lies in the connection 
between the very localized lesion in the right hemisphere and the 
first attack of hemiplegia. This attack, it will be remembered, 
was characterized by slight and transitory paralysis of the limbs, 
and by very great defect in articulation. Indeed, it is said that 18 
E. C. SEGUIN', 
the patient never recovered the full use of her vocal organs. 
From this we might be led to infer that the function of the third 
frontal convolution on the right side in right-handed human 
beings is intimately connected with the muscles governing the 
movements of articulation and phonation. 
Case 111. Chronic meningitis almost limited to the posterior 
art of the third left frontal convolution, extensive central cerebral 
softening : epilepsy, chronic aphasia of varying degree, right hemi- 
plegia ; death in status epilepticus. 
A male, age forty-seven years, was admitted to the Connecticut 
General Hospital for the Insane, at Middletown, on Nov. 29th, 1873. 
For a full account of the case and for the post-mortem examina- 
tion I am indebted to my friends Drs. A. M. Shew and W. B. 
Hallock, medical officers of the hospital. 
The patient was sent to the hospital because of “ dementia.” 
It was learned from his wife that he had had three “ apoplectic ” 
attacks. The first occurred in April, 1873, and consisted in loss 
of consciousness and general spasm. After this he had at short 
intervals some few slight “ spasms.” In July had a second severe 
attack of same kind as the first, followed by slight hemiplegia. 
Three weeks later had a third seizure, after which he was in a 
state of delirious mania, which still continues. 
On admission, mind is in dementia, the pupils are very small, 
articulation good, the tongue protrudes straight, and the only 
palsy apparent is in right lower limb. At times is violent and 
has insomnia. Speech very incoherent. In December it is noted 
that palsy is less, but that legs are not well co-ordinated, and that 
hands tremble. 
In middle of January, 1874, patient is calmer, and more rational, 
hut speech is imperfect. “He talks plainer, seems to have ideas, 
but has forgotten words. ” Aphasia. 
Feb. Ytth.—At two o’clock p.m. had an epileptic attack, with 
paralysis of right side; tongue deviating to the right. Four 
other spasms in three-quarters of an hour; each characterized by 
usual symptoms, foaming at mouth, stertor, upturned eyeballs. 
March 6th.—ls up and about the ward. Is more coherent than 
for some time. Hallucinations of sight in the night, 
March 30th.—Is discharged improved. For some time past the 
difficulty in speech has taken the form of amnesia, and his 
writing has shown the same characteristics. 
Ee-admitted June 29th, 1874. Aphasia still present, and he LOCALIZED CEREBRAL LESIONS. 
19 
seems to appreciate the trouble. “I like that fountain I drink 
from three times a week,” meaning, I like that medicine I take 
three times a day. He knows that he calls things hy wrong 
names, and is thereby irritated. “ I wish you would sell me,” 
meaning bleed me. “ Oh, I can’t talk.” 
July 26th.—Yesterday and last night had ten attacks of an apo- 
plectiform character, without paralysis. These must have been 
epileptic seizures. 
Sept. 29th.—Rose as usual, made up his bed nicely. At table was 
unable.to grasp knife and fork. In twenty minutes, complained 
of bad smell and dim vision, then had a general convulsion. 
Had ten attacks in the course of an hour. There was foam at 
the mouth, and more twitching on the right side of the body. 
In a few days was up again. 
Oct. 29th. —Three epileptic attacks in a few minutes. This is the 
third time that patient has had prodrornata, consisting of nervous- 
ness, a slight degree of paralysis of right side; has gone to his 
room and made signs that he was ill. 
Oct. 21st.—Ho paralysis after attacks; some excitement in 
night. 
Nov. 19th.—Is in good physical health; has hallucinations of 
sight; aphasia continues marked. 
Jan. Bth, 1875.—After dinner (1 p.m.) had an epileptic seizure, 
and at 5 p.m. the attacks followed each other rapidly. The right 
side is completely paralyzed. 
Jan. 9th.—Has been in status epilepticus all night, and must 
have had nearly four hundred convulsions. Died at 3.15 a.m. 
Autopsy Jan. 10th, thirty-two hours post mortem. Calvarium 
normal. Vessels of dura mater and of pia mater congested. 
Dura mater adherent to bone over right posterior lobe of cere- 
brum, membranes adherent to pia mater over left middle lobe of 
brain. General moderate opalescence of the arachnoid. Other 
organs in remarkably good condition. 
The entire brain was at once sent to me in a solution of 
bichromate of potassa, and I made a careful examination of it in a 
few days. 
The only externally visible lesion is on the left hemisphere. 
There a patch of dura mater adheres to the soft membranes and 
the brain, at the posterior extremity of the third frontal con- 
volution and the lower extremities of the ascending frontal and 
ascending parietal convolutions, bridging over the fissure of 20 
E. C. SEGUIN. 
Sylvius. The patch measures 33 mm. in a vertical direction, and 
15 mm. horizontally. The anterior border of the piece of mem- 
brane is 58 mm. from the apex of the frontal lobe; its upper 
edge is 58 mm. below the upper border of the frontal lobe (at the 
longitudinal fissure); aud its lower border, lying on the fissure 
of Sylvius, is 55 mm. above the lowest part of the sphenoidal lobe. 
The arachnoid and pia mater surrounding the patch, in the 
fissure of Sylvius and for 35 mm. above it, are thickened and 
whitish. 
The patch lies in a depression in the underlying convolutions, 
and a horizontal transverse section through it and the hemisphere 
shows that the three membranes are fused in the patch, which is 
3.5 mm. thick, and that the subjacent gray matter of the third 
and ascending frontal convolutions, and the ascending parietal 
convolutions, are grayish and translucent. 
The same section reveals extensive softening in the central 
parts of the left hemisphere. The lenticular ganglion (extra- 
ventricular part of corpus striatum) is soft and reddish; con- 
tains nervous debris, granular bodies, and granular blood-vessels. 
The few ganglion cells seen are filled with granulations. 
A second softened spot is in the white centre of the hemisphere, 
in its posterior half, outside and above the lateral ventricles. The 
microscope shows the same granular detritus as in lenticular 
ganglion. Abundant granular bodies are also found in the white 
centre of the frontal lobe, and in the convolutions of the island 
of Reil, deep in the fissure of Sylvius. 
The corpus striatum proper contains only a few granular gan- 
glion cells. 
Microscopic examination gave evidence of descending degener- 
CASE 111.—PATCH OF PACHYMENINGITIS ADHERENT TO LEFT HEMISPHERE. LOCALIZED CEREBEAL LESIONS. 
21 
ation in tlie motor tract through the left half of the pons Yarolii 
and medulla oblongata, and the right lateral column of the spinal 
cord. 
The ganglion cells of the anterior horns of the spinal cord con- 
tained an abnormal amount of granular matter, and the posterior 
columns contained an immense number of amyloid bodies. 
Remarks.—This case, partly from its complicated nature, and 
partly because of its imperfect record, is difficult to analyze with 
reference to the question which I have in view in this contribu- 
tion. 
In addition to epileptic, paralytic, and aphasic manifestations, 
there seems to have been actual insanity present, as manifested 
during life by hallucinations and delusions, and by incoherence 
and dementia; and post mortem, by opacity of the delicate mem- 
branes of the brain, and degeneration of the posterior columns 
of the spinal cord. 
It seems probable, however, that some of the so-called “ demen- 
tia ” in the first part of the history of the case was aphasia. 
In estimating the share of the two lesions in the production of 
symptoms, it must be admitted that, whereas the patch must have 
been ancient, the ramollissement cannot have been very old. The 
latter lesion was, however, at least six weeks old, since secondary 
descending degeneration had set in to a slight degree. Yet, as 
the chief phenomena of the disease—epileptic seizures, transitory 
hemiplegia, and aphasia—existed from the beginning of the illness, 
it is right to conclude that the older lesion, i. e., the localized 
chronic meningitis, was the cause of these symptoms. 
The thickened state of the pia mater, arachnoid, and dura ma- 
ter, acted upon subjacent parts in several ways: by pressure and 
by mechanical irritation, increased by the respiratory and cardiac 
movements of the brain, and by interfering with the blood-supply 
of the gray matter, and of the white substance for a certain depth. 
The part which was most affected by this lesion was Broca’s speech 
centre in the posterior part of the third frontal convolution. 
Consequently, it seems right to me to consider this case as 
favorable to the hypothesis of the localization of functions in 
limited parts of the cortex of the brain. 
As to the nature of the localized meningitis, nothing is said in 
the history of the case concerning syphilis, or symptoms belong- 
ing to the syphilitic category. Sections of the patch and subja- 
cent nervous tissue were very difficult to make, because of the 22 
E. C. SEGUIN. 
difference of density between the two tissues and the lax bond o. 
union between them. The specimens now passed around must 
be judged leniently because of these peculiarities. In so far as 
the thickness of the sections will permit microscopic study, it 
seems to me that the lesion is a simple hyperplastic one, having- 
resulted in the formation of dense fibrillar connective tissue. In 
no part of the specimens can I find the numerous young cells 
so characteristic of gummatous products. 
Case IV.— Constitutional syphilis, commencing caries of the 
dorsal vertebrce, acute tuberculosis, tubercular meningitis, most 
developed over left third frontal convolution and island of Reil: 
intermittent aphasia, and later, hemiplegia. 
Mr. X , aged forty-three years; a private patient of Drs. 
William H. Draper and Frank P. Kinnicutt. The latter gentle- 
man has kindly furnished me with abbreviated notes of the cases, 
and the brain was placed in my hands for examination. 
The patient was a victim of unusually severe syphilitic infec- 
tion : having had series of secondary and tertiary lesions while 
under Dr. Draper’s care. At the time of his last illness he had 
syphilitic neuralgia. In 1874-5, there was slight trouble at apex 
of right lung, but the disease seemed wholly arrested during the 
past year. 
Since two months, emaciation has rapidly advanced, and 
strength has much diminished. Since April 20th, there has 
been fever of a very irregular type; the temperature varying from 
37.1° to 39.1° 0.; the temperature not being the same on any two 
days. Pulse has been very frequent: 100 to 120. Physical exam- 
ination has revealed simply moderately fine moist rales, at first 
only in the anterior and posterior parts of the right lung ; later, 
during the last four weeks of life, in both lungs. 
On May 10th, there was suddenly developed aphasia and 
agraphia, without loss of consciousness or paralysis. [This neg- 
ative statement is not made upon the patient’s or the nurse’s 
statement, but after critical examination by Dr. Kinnicutt, whose 
accuracy in clinical observation is extreme.] This condition of 
aphasia continued about twenty-four hours, and during this time 
the patient’s mind was perfectly clear. A nearly complete inter- 
mission (return of speech) then occurred, followed in twenty-four 
hours more by a second attack of complete aphasia and agraphia, 
also without impairment of consciousness or mental clearness, 
and without paralysis. These intermissions and attacks con- 23 
LOCALIZED CEREBRAL LESIONS. 
tinned to succeed one another until within forty-eight hours of 
death, when the intermissions became incomplete. At first, there 
existed only a certain slowness of speech during the intermissions; 
bnt in the last few days there was partial aphasia; or, more properly 
speaking, aphasia would show itself after a few moments of correct 
speaking. Eight hemiplegia was almost imperceptibly developed 
(face and limbs); became marked forty-eight hours before death, 
and was complete, with a semi-comatose state at the last. 
At no time was there only pain in the head. General hyperal- 
gesia (more marked on the right half of the body) was present 
in last week of life. 
Dr. Kinnicutt diagnosticated acute pulmonary tuberculosis, with 
a cerebral complication. There was a doubt in our minds, whether 
the cerebral lesion was meningitis, tubercular or syphilitic, or 
whether it consisted in syphilitic arteritis, involving the left 
middle cerebral artery. 
The post-mortem examination was made on May , sixteen 
hours after death, by Dr. Kinnicutt, and the following lesions 
found: 
There was a cavity about three-quarters of an inch in diameter, 
filled with pus, in the right half of the body of the twelfth 
dorsal vertebra; and the pus wras seen to have made its way 
within the sheath of the psoas muscle, nearly as far as Poupart’s 
ligament. At the apex of the right lung was a dense cicatrix, 
and over one of the lower ribs on the left side, the remains of a 
gumma, which had suppurated many months. Gray tubercular 
granulations were found in abundance throughout both lungs, in 
the spleen and kidneys. There were none in the liver, and their 
presence in the peritoneum was doubtful. 
The brain, placed in a solution of bichromate of potassa, was at 
once sent down to me for examination. I did not do more at 
first than note that the left sphenoidal lobe had been damaged in 
the removal of the brain, and that there were a very few granula- 
tions, the size of tobacco seeds, or a little larger, in the pia mater 
on the convexity of the hemispheres. My reason for not cutting 
the brain while fresh was that, from the lack of consistency ot 
the left anterior lobe, Dr. Kinnicutt thought it likely that there 
was an abscess or a patch of rainollissement near the third frontal 
convolution, and I wished, if there were such a lesion, to obtain 
its exact topography. 
The brain having been completely hardened in bichromate of 24 
E. C. SEGUIN 
potassa, I proceeded to examine it by means of vertical and 
horizontal sections. Somewhat to my surprise, I found no lesion 
in the deeper parts of the hemispheres. There was only a lepto- 
meningitis of very peculiar distribution. 
In the first place, the convexity and base, and the whole of the 
right hemisphere, showed only traces of exudation alongside of the 
chief vessels of the pia mater, with here and there a granulation 
varying in size from .5 mm. to 1 mm. in diameter. 
CASE XV.—A. SHOWING FOCUS OF TUBERCULAR MENINGITIS ON EXTERNAL PART OF 
LEFT HEMISPHERE. B. THE EXUDATION IN THE FISSURE OF SYLVIUS. 
11l the second place, the lower median region of the left 
hemisphere showed very much more developed exudation. The 
vessels covering the posterior part of the third convolution as it dips 
into the fissure of Sylvius were bordered by thick bands of exuda- 
tion quite as wide as the vessel itself, and the pia mater was thick- 
ened over a space 25 mm. or more in diameter. On opening the LOCALIZED CEREBRAL LESIONS. 
25 
fissure of Sylvius, the pia lying in it was found enormously thick- 
ened, and its meshes filled with semi-solid and solid exudation. 
The focus of the meningitis was in the territory of distribution 
of the left middle cerebral artery, especially over the third frontal 
convolution, and the convolutions of the island of Red. 
Microscopic examination of the exudation showed an accumu- 
lation of young cells in the meshes of the pia mater, and more 
especially round about blood-vessels next the cortex. Around 
many of these, the exudation formed tumor-like swellings, or, 
more exactly speaking, muff-like masses. The young cells could 
be followed some distance into the cortex of the brain, lying in 
the perivascular spaces. This examination corroborates the 
diagnosis of tubercular meningitis. 
PART 11. 
CASES IN' WHICH A LIMITED CEREBRAL LESION CAUSED 
PARALYSIS. 
Case V.—Limited softening of the left ascending frontal convo- 
lution ; right hemiplegia without aphasia. 
A female, aged fifty-four years, was admitted to my ward in the 
Epileptic and Paralytic Hospital on Blackwell’s Island, on June 
20th, 1875. 
The brief history of her case is to the effect, that about Christ- 
mas, 1874, during the night, she was suddenly paralyzed on the 
right side. She did not lose consciousness, her face was not 
paralyzed, and speech was preserved. 
Examination shows that patient’s face is not paralyzed, her 
tongue points straight, the right upper extremity is palsied, hut 
there is slight voluntary motion at elbow and fingers. The lower 
limbs are without voluntary motion. There is some oedema 
about the ankles, and a superficial bed-sore on both nates. Death 
occurred June 23d. 
Post-mortem examination. The only externally visible lesion 
in the brain is a disappearance of a part of the convolution in 
front of the fissure of Rolando, within 25 m.m. of the great 
longitudinal fissure, on the left hemisphere. It is not like a 
yellow patch, but is more like an ulceration of the convolution. 
A horizontal section, made through the hemispheres above the 
ventricles, shows healthy tissue in the right hemisphere, while in 
the left it reveals a softened but not much discolored part in con- 26 
E. C. SEGUIN. 
nection with the superficial lesion above described. A vertical 
transverse section through this lesion and the lower part of the 
left hemisphere shows that the softened mass has its greatest 
diameter vertically, and extends from the roof of the lateral 
ventricle upward. 
CASE y.—LIMITED SOFTENING OF THE LEFT ASCENDING FRONTAL CONVOLUTION. 
jSTo other lesion is found in the cerebral tissue. The cerebral 
arteries show some arteritis, especially the left middle cerebral; 
but their channels are open. 
A considerable spinal lesion is found, consisting in purulent 
infiltration of the lower cervical muscles alongside the 3d, 4th, 
and sth vertebrae. On removing the posterior portion of the 
vertebrae, there is found a thick exudation, like a membrane, be- 
tween the dura mater and the bones. Between the dura mater 
and the bodies of the vertebrae there is no trace of exudation. 
The arachnoid and the spinal cord seem healthy. The only 
osseous lesion is a roughness of the arches of the cervical vertebrae 
near the exudation. 
This case is only to be made use of with reservation, because of 
its imperfect history, and because of the co-existence of a spinal 
peri-pachymeningitis. The main interest of the case is a negative 
one of unquestionable exactness. At no time was there aphasia; 
and it may be seen that the softened patch was placed quite far 
from the speech centre, above and behind it. It would seem that 
the face and tongue were not palsied; and this again is in accord 
with the location of the lesion, which is in the ascending frontal 
convolution, near Terrier’s centre, No. 6, which he* finds in the 
monkey, to co-ordinate certain movements of the arm and fore- 
arm. 
* The Functions of the Brain. New York, 1876; p. 306. 27 
LOCALIZED CEREBRAL LESIONS. 
PART 111. 
CASES IN WHICH LOCALIZED CEREBRAL LESIONS GAVE RISE TO 
LOCALIZED CONVULSIONS OR SPASM. 
Case Vl.—lnjury to the top of the skull on the right side,, 
osteitis, inflammation of the dura mater, with lesion of subjacent 
convolutions ; development of a large sarcomatous tumor in the 
right hemisphere ; epilepsy ; spasms limited to left arm, neck, and 
face ; left hemiplegia: no neuro-retinitis. 
George S., a laborer, was admitted to my service in the Epileptic 
and Paralytic Hospital, Blackwell’s Island, on April 19, 1875, for 
epilepsy. 
The following history of his case was obtained: 
On December 19, 1869, he got out of bed, in the middle of the 
night, to get some water; went to a stairway on the outside of 
the house, made a misstep, and fell to the ground. He lay in- 
sensible until morning, when he was taken care of. Paralysis of 
the left side followed the injury, but improved under treatment 
sufficiently to allow him to do his ordinary work. 
Three years later (1872), he was seized with epileptic convulsions 
of the common typical sort; sudden fall, general spasm, biting of 
tongue. These attacks ceased in December, 1874, and were then 
wholly replaced by very frequent attacks of partial or localized 
epilepsy, without loss of consciousness. 
These attacks consist of tonico-clonic spasm of the muscles of 
the left side of the face' and neck, and of left upper extremity, 
especially the thumb and index. The left upper extremity is 
strongly flexed and the mouth drawn to the left during the attack, 
which lasts from 80 to 140 seconds without nitrite of amyl, and 
from 70 to 90 seconds with it. The attacks occur with extreme 
frequency, from three to eleven taking place every hour. At night 
they are rare. The spasm begins simultaneously in the facial 
muscles and in those governing the thumb and index. Conscious- 
ness is never lost. Ho general convulsions occur. An examina- 
tion shows the left pupil to be a trifle larger than the right; the 
left cheek is paretic; the left arm and forearm absolutely 
paralyzed, and the left leg weak. The gait is characteristic of 
hemiplegia. There is marked tactile anaesthesia on the left side; 
the two points of an aesthesiometer not being distinguished at 
45 mm. on the forehead, at 40 mm. under the eye, at 40-50 mm. 28 
E. C. SEGUIN. 
on the side of the cheek and on the fingers. He feels pricking 
normally on face and fingers. 
The injury to the skull, caused by the fall in 1869, is indicated 
by an irregular depression existing on the vertex, within an inch 
to the right of the median line, in a plane passing vertically 
through the external auditory meatus. 
The attacks of limited epilepsy were much reduced in frequency, 
but not interrupted for any length of time by the systematic use 
of the bromides pushed to the limit of prudence. The partial 
hemiplegia increased. 
June 28th.—The weakness of the left leg has greatly increased ; 
patient is unable to stand or walk without help ; the fingers can 
be moved a little, and a degree of contraction has appeared in the 
elbow and hand. 
Sept. 13th.—Patient had a slight general convulsion, with loss of 
consciousness, last night. 
December 3cl.—Is growing gradually worse. The ophthalmoscope 
shows fulness of veins, but no neuro-retinitis. Patient lies on 
his back, with left arm strongly flexed ; there is some opisthoto- 
nus; complains of being deaf in right ear. Axillary tempera- 
ture 36.4° C. 
December Ith.—Complains of pain in right arm and leg, and in 
posterior part of head on the right side: pupils are ecjual and of 
medium size. There is no distortion of face, and the tongue 
comes out straight. The left upper extremity is completely par- 
alyzed ; the forearm and hand flexed and rigid. Left lower ex- 
tremity is deprived of voluntary power, and lies rigidly extended. 
The neck is rigid, with tendency to opisthotonus. During the 
examination (and at other times) patient turns his head and eyes 
away from the palsied side—deviation conjuguee. Contact and 
pinching are felt on the palsied side. Pinching produces reflex 
spasm in the left limbs, of the nature of spinal epilepsy, i. e., tonico- 
clonic spasm. The veins of the neck and forehead, especially on 
the right side, are unnaturally distended. An ophthalmoscopic 
examination shows no neuro-retinitis. Pulse 108, axillary tem- 
perature 37.1° 0. 
Localized and general convulsions recur from time to time. 
Patient is semi-conscious. 
Death occurred on December 23, 1875. 
The body is much emaciated, and rigor mortis is well marked, 
especially on the left side. On removing the scalp there occurs a 29 
LOCALIZED CEEEBBAL LESIONS. 
large escape of blood from enormously distended veins. The oc- 
cipital veins on the left side are just perceptible, while on the 
right side they are 6 mm. in diameter. The frontal veins on 
both sides are much developed, but not filled with blood, 
because the body has lain upon its back. The right frontal bone 
is the seat of marked irregularities, and is rough and fissured 
between the median line and the external angular process. On 
the top of the skull, on a line passing vertically in front of the 
external auditory meatus, and 12.5 mm. from the median line, 
are two depressions about the size of peas. One of these con- 
tains a varicose vein, and a sound passed through the aperture 
seems to strike against the dura mater. 
After sawing the skull through in the usual manner, the brain 
is divided horizontally without removing the skull-cap. The 
inferior half of the brain, examined as it lies in the fossa; of the 
skull, presents the following peculiarities: The right half of the 
brain is much enlarged, and the lateral ventricle and septum luci- 
dum are forced over.to the left. On the left side, the corpus 
striatum, thalamus, and convolutions appear healthy. On the 
right side the intra-ventricular nucleus of the corpus striatum 
alone is normal. Its extra-ventricular nucleus is undistinguish- 
able. The white matter forward and outside of the corpus stria- 
tum, and in the neighborhood of the optic thalamus, is of a creamy 
consistency. The external and posterior half of the thalamus is 
involved in this softening. The convolutions directly outside of 
the thalamus are very much crowded together. At the base of 
the brain the convolutions lying immediately over the right olfac- 
tory bulb are very much softened, as are also the convolutions of 
the right sphenoidal lobe. The inferior convolutions of the occi- 
pital lobe appear normal. The white matter of the apex of the 
right anterior lobe is so soft that it is torn through in removal. 
The upper half of the cerebrum, still lying in the skull, ap- 
pears as follows: The septum lucidum is displaced to the left of 
the median line fully one-half inch. The white substance of the 
right hemisphere is the seat of a tumor, larger than a hen’s egg, 
movable in the substance of the hemisphere, and of the consist- 
ence of glandular tissue. The opto-striate bodies of the right 
side are strongly compressed by the tumor, and so are the convo- 
lutions of the parietal region. The white matter in front and 
behind the growth is softened. 
The upper half of the brain is carefully detached from the cal- 30 
E. C. SEGUIN. 
varium, by pushing the fingers between the dura mate]’ and the 
bone. No difficulty is experienced in doing this until the neigh- 
borhood of the external depression in the bone is reached, when 
the dura mater is felt to be strongly adherent to the skull. With 
some difficulty the adhesion is broken up and the brain removed. 
A careful examination of the convexity of the brain, thus 
exposed, shows the dura mater depressed and firmly adherent to 
the convolutions on the right side of the longitudinal fissure. 
There, is some bony formation in the depressed adherent part of 
the dura. Around the patch, which is 25 mm. in diameter, the 
dura mater is moderately adherent to the anterior lobe over an 
oval space, measuring 75 mm. longitudinally, and 38 mm. trans- 
versely from the median line. The longitudinal fissure opposite 
this patch is obliterated by adhesions, and these are also present 
13 mm. to the left of the median line. 
CASE VI.—PATCH OP THICKENED DURA MATER ON TOP OP EIGHT HEMISPHERE 
Just to the right of the median line, opposite the depressed 
adherent spot in the dura, the skull presents a marked thickening 
and roughness. This tumor-like development of bone is 25 
mm. anterior to the opening in the skull above described. A 
transverse section of the bone at this point shows it to be 13 mm. 
thick, and much condensed. 
Transverse sections through the pons Varolii show ho lesion 
except hypersemia. 
The fossa; of the skull are unusually deep, and irregularly fur- 
rowed and hilly. 31 
LOCALIZED CEBEBKAL LESIONS. 
The upper half of the left hemisphere, after hardening in bi- 
chromate of potassa, is examined by means of vertical transverse 
sections. The surfaces of these sections show that the tumor is 
very much larger than would appear from an inspection of the 
convexity of the hemisphere, or of the horizontal section above 
the ventricles. In fact, almost the whole of the anterior two- 
thirds of the upper half of the right brain is occupied by the 
growth, which has partly pushed aside and partly taken the place 
-of the nervous tissue. 
A transverse vertical section made through the anterior third 
of the thickened patch of dura mater reveals that the tumor 
occupies the Avhole thickness of the hemisphere above the opto- 
striate bodies, and that these bodies.are strongly pressed upon. 
The mass of the tumor is so considerable as to press upon the 
inner surface of the left hemisphere. 
A transverse vertical section through the middle of the thick- 
ened patch of dura mater and the cerebrum shows an appear- 
ance represented in Fig, 2. The tumor, continuous with the dura 
mater, extends deeply into the substance of the right hemisphere, 
down to the level of the roof of the lateral ventricle. Besides, 
this roof and the falx cerebri are much displaced by the growth. 
Posterior to this level the tumor diminishes rapidly in size, 
though still pushing over to the left of the median line. 
CASE YI.—TRANSVERSE VERTICAL SECTION THROUGH HEMISPHERES, SHOWING RELATIVE 
SIZE AND POSITION OE THE TUMOR. 
A transverse vertical section made in the hinder part of the 
brain (beyond diseased dura mater) shows the tumor only as a 
small nodule in the upper inner part of the section-surface, lying 
wholly in the white substance. 
The great longitudinal sinus is obliterated for a space of nearly 
50 mm. in the thickest part of the patch of dura mater. 32 
E. C. SEGUIN. 
Microscopical examination showed the tumor to be an alveolar 
sarcoma in parts, and in others a common sarcoma. 
As regards the connection between these lesions and the symp- 
toms during life: 
These symptoms were at first epilepsy, for nearly two years, 
followed by partial hemiplegia on the left side of the body, by 
incomplete localized epileptiform spasms in the left cheek, neck, 
and upper extremity, and the scene closed with complete left 
hemiplegia and a few general epileptic attacks. 
It seems right to me to connect the above symptoms with the 
lesions in the following manner: 
The first manifestations, general epileptic seizures, were caused 
by the development of thickening of the skull (internal plate), 
inflammation of the dura mater, and irritation of the cerebral 
substance. 
As the pachymeningitis increased, with formation of bony 
spicules in its substance, the inflammation extended along the 
pia mater farther outward and backward, and thus reached parts 
of the convolutions which lie next to the fissure of Eolando and 
above the upper end of the fissure of Sylvius. These parts cover 
the regions numbered 2, 3, 4, and G, in Terrier’s chart of the 
probable motor centres in the human brain, as deduced from ex- 
periments on apes. 
By this irritation, there were caused the peculiar spasmodic 
movements of the muscles on the left side of the face and neck, 
and of the left hand and arm. Terrier considers the regions num- 
bered 2, 3, 4, and 6, as motor centres for the hand and arm 
chiefly. 
There was also partial left hemiplegia. Later still, sarcoma 
was developed from the pachymeningitis; the malignant growth 
rapidly extended in all directions, substituting itself for the 
nervous- tissue, and producing powerful compression-effects in 
all directions, but chiefly downward upon the opto-striate bodies. 
In this terminal stage of the disease, the phenomena were com- 
plete left hemiplegia, a few general convulsions, no localized 
spasm. 
As an additional sign of extensive lesion of the hemisphere, we 
may note the conjugate deviation of the eyes, away from the 
paralyzed side, and toward the injured hemisphere. 
Why, with such an enormous tumor, and such an increase 
of intra-cranial pressure as must have existed, there was no LOCALIZED CEEEBEAL LESIONS. 
33 
amblyopia, neuro-retinitis, atrophy of the optic nerves, diplopia 
or hemiopia, is a very puzzling question. This case is the second 
one of large cerebral tumor without choked disks or atrophy of 
the optic nerves which I observed in 1875. 
In conclusion, I think that this case may be looked upon as 
corroborative of Hughling Jackson’s, and Perrier’s theory of the 
existence of excitable motor districts, in some way connected 
with the motions of the face and forearm, in the upper median 
convolutions of the cerebrum—the ascending frontal and ascend- 
ing parietal convolutions. 
Case YII.—Pneumo-pyo-thorax ; suppurative cerebral menin- 
gitis ; abscesses in both hemispheres: localized epileptiform 
spasms in left hand, arm, and face ; no paralysis or aphasia. 
For notes of the following remarkable case I am indebted to 
my friend, Dr. F. P. Kinuicutt. 
The patient, a lad of thirteen, had been under the care of Drs. 
William H. Draper and Kinnicutt for empyema during several 
years. 
During the last year of his life, the patient had a number of at- 
tacks of what was called slight septicaemia, characterized by mod- 
erate chill, fever, and diminished secretion from the pectoral fis- 
tula. The checking of the outflow of pus was held to be the 
cause of these attacks. 
On February 18th, 1877, there occurred a severe chill, followed 
by fever, with a temperature of 37.7° and 38.8° C., lasting forty- 
eight hours. There was severe diffused headache. Dr. Kinnicutt 
was called and made the following observations : 
On February 23d, patient felt very well, and it was thought 
that this attack had terminated favorably, like the others. But 
suddenly, while engaged in play, there occurred a twitching in 
the middle finger of the left hand; the spasm soon extended to 
the forearm. The entire spasm (clonic in form) only lasted a 
few seconds, and rather amused the boy. A few hours later a 
second attack took place, and was witnessed by Dr. Kinni- 
cutt. Patient was aware of beginning of spasm by an almost 
imperceptible tremulousness of the facial muscles on the left 
side, followed, a few seconds later, by clonic spasm of the left 
middle finger and thumb (the former being strongly flexed, the 
latter adducted and flexed), succeeded by clonic flexions of the 
forearm, and evident clonic spasm of the left side of the face. 
The entire seizure lasted about 60 seconds, and during it there 34 
E. C. SEGUIN. 
was no spasm of any part but the left face, arm, forearm, and 
fingers. There was no loss of consciousness, and patient con- 
versed intelligently during the attack. The pupils and vision 
remained normal. Not a trace of local or general paralysis fol- 
lowed the spasm (contrast to Hitzig’s case). There was no 
anaesthesia or abnormal sensation (aura or numbness) in the 
affected parts before, during, or after the attack. 
The headache, of which he has complained since the 18th, has 
grown much worse; it is not localized, but is more violent in 
the occipital region; the pain extending into the nape of the 
neck. 
There were five or six of these hemiplegic spasms on the 23d. 
I saw the patient in consultation with Dr. Kinnicutt that even- 
ing, and a careful examination failed to reveal any objective 
symptom except a buccal temperature of about 37.7° 0. The pulse 
was proportionately rapid, but not irregular. Complaint was 
made of severe headache, as above, No trace of paralysis or dis- 
order of sensibility; no nausea; mind remarkably clear; patient 
not anxious. Ophthalmoscope shows only somewhat enlarged 
retinal veins. 
I agreed with Dr, Kinnicutt in diagnosticating a meningitis, 
probably of a tuberculous nature; and I advanced the view that 
there was a lesion of the convolutions on the right side, in the 
neighborhood of the fissure of Sylvius, involving the excitable 
district of the cortex, and producing the localized epilepsy. 
February 2Mh.—At 6 o’clock a.m., had a general convulsion, fol- 
lowed by vomiting; T, 37.1°, P. 108 and regular. At 2.30 P.M., 
T. 38.8°, P. 100; headache violent; vomited once. At 10 p.m., 
T. 38.5°, P. 100 regular; R. 32 and regular. 
February 25fh.—At 10.30 a.m., T. 39°, P. 100 regular. At 
5 p.m., T. 38.5°, P. 100 regular. At 10 p.m., T. 37.7°, P. 100. 
Vomited twice during afternoon ; no new symptoms; headache 
violent; urine albuminous. 
February 26th.—At 10 a.m., T. 39°. At 3.15 p.m., T. 37.7°, 
P. 94, slightly irregular. At 10.30 p.m., T. 37.5°, P. 88, slightly 
irregular. Vomited once in twenty-four hours. 
February mh.—At 2.30 p.m., T. 37.5°, P.BO, R. 20. At 10 
p.m., T. 38°, P. 88, irregular, R, 16-20, irregular. 
February 2Sth.—At 5.30 a.m., pain in head intense; no motor 
disturbance of any kind; pupils normal and symmetrical; pulse 
and respiration irregular, the latter exhibiting the Cheyne-Stokes LOCALIZED CEREBRAL LESIONS. 
35 
phenomenon typically. The mind is perfectly clear; strength 
good. 
At 6 a.m.j there occurred a general convulsion, followed by sev- 
eral others in rapid succession. There was loss of consciousness, 
and death took place quietly at 7 .40 a.m. 
The treatment employed by Drs. Draper and Kinnicutt con- 
sisted in blisters to the neck, the giving of iodide of potassium, 
and, at last, to alleviate the severe cephalalgia, morphia hypoder- 
mically. ' 
CASE VII.—ABSCESS IN LOWER TART OF SECOND FRONTAL CONVOLUTION, LEFT SIDE : NO 
SYMPTOMS. 
I made the post-mortem examination at 3 o’clock p.m. on 
March Ist, in the presence of Drs, Draper and Kinnicutt. The 
condition of the left lung and remains of the pleura was one 
of great interest, but details on this point would here be out of 
place. 36 
E. C. SEGUIN. 
As regards the encephalon, we found a meningitis most marked 
at the base and sides of the brain, with purulent exudation in 
the meshes of the pia mater. There were no tubercles to be seen, 
and no marked lesion was to be found on the surface of the right 
hemisphere. On the left side, however, on the anterior lobe in 
front of the fissure of Sylvius, was a softened spot, probably an 
abscess. On carefully slicing the brain, a second lesion was found, 
however, and that in the right hemisphere just above the poste- 
rior extremity of the fissure of Sylvius. It is well worth while 
to state precisely the location and limits of these two localized 
lesions. 
CASE VII.—ABSCESS IN RIGHT SECOND PARIETAL CONVOLUTION ; CAUSE OF SPASM IN LEFT 
HAND AND FACE. 
The first abscess, measuring 2 cent, in diameter, and lined by 
a soft membrane, nearly 1 mm. thick, lay in the lower part of 
the second frontal convolution, and the anterior border of the LOCALIZED CEEEBIiAL LESIONS. 
37 
third frontal convolution, on the left side, just in front of the 
speech-centre which has been referred to as injured in the cases 
of aphasia recorded in this essay. lam prepared to state, most 
positively, that the posterior part of the third convolution and 
island of Beil were perfectly healthy to the naked eye. The 
injured part is quite in front of Perrier’s centre, No. 9. 
During life, no symptoms, motor, sensory, or intellectual, oc- 
curred which might be connected with this large irritating and 
destructive lesion. Consequently, it seems to be fair to conclude 
that in some human brains the lower part of the second fron- 
tal convolution is not excitable, and contains no motor cell- 
groups. 
As regards the second abscess, not larger than a pea, it was 
found wholly in the white substance just beneath the cortex of the 
anterior part of the second parietal convolution on the right 
side, just above the upper extremity of the fissure of Sylvius. 
This lesion, which, in all probability, gave rise to the spasm 
in the left face and hand, is placed just behind the parts which 
Perrier considers to be centres for motions of the hand and 
wrist. 
If any conclusion is to be drawn from a study of the second 
lesion, it is that in man fibres for the face and hand pass farther 
downward and backward in the hemisphere than ivould be indi- 
cated by experiments on dogs and apes. 
A fact certainly well worthy of remark is, that a small lesion in 
an excitable district of the brain may produce well-marked symp- 
toms, whereas a much larger lesion may exist in non-excitable 
regions without giving any sign of its presence. 
Conclusions : The three cases in Part I. fully bear out Broca’s 
(and Perrier’s) hypothesis of the existence of a speech-centre in 
the posterior part of the left third frontal convolution, and in 
the anterior folds of the island of Reil. 
The case in Part 11. is unfortunately worth very little; still 
it may serve to show that a lesion of the ascending frontal 
convolution may cause paralysis of the arm (and leg) with- 
out affecting the lingual and facial muscles, or producing aphasia. 
The two cases in Part 111. appear to indicate that spasm, limited 
to one side of the face and one upper extremity, may be set up by 
irritation of quite distant parts of the cerebral cortex, extending 
from region No. sto below region d, in Perrier’s chart. In this 38 
E. C. SEGUIN'. 
particular, these cases, while not contradicting experimental re- 
sults, show that if there be such motor centres in man, they are 
not distributed quite as in monkeys and dogs. 
The only case which appears to bear against the doctrine of 
localization of motor functions in the cerebral cortex is Case 
I. In this, it will be remembered, great recovery of volun- 
tary power occurred, although a large part of the cortex of one 
hemisphere, including regions 6, 7, 11, a, b, and c, of Ferrierfs 
chart, or, in other words, the so-called psycho-motor centres for 
the hand and forearm, the angle of the mouth and platysma, and 
those for the hand and wrist, were irreparably injured, nay, de- 
stroyed. , 
FEKRIBR’S CHART.—I, centre for leg ; 2, 3, 4, for arms and legs ;5, extension 
OF ARM AND HAND ; 6, FOR BICEPS OF ARM ; 7, 8, FOR ANGLE OF MOUTH ; 9, 10, FOR 
LIPS AND TONGUE (BROCA’S CENTRE) ; 11, FOE PLATYSMA ; 12, FOR HEAD, EYES, AND 
PUPILS ; A, B, C, D (ASCENDING FRONTAL CONVOLUTION), FOR HAND AND WRIST ; 13, 13') 
14, CENTRES FOR VISION AND HEARING. 
I append a reproduction of Fender’s chart of psycho-motor 
centres to render easy the determination of the injured parts in 
the above cases. 
The problem of localization of functions in the cerebral cortex 
is a grand one, and well worthy of thorough study. I am not 
prepared to accept the hypothesis as enunciated by Perrier, yet 
it seems to me in the highest degree rash and unscientific to call 
it baseless and worthless, because a few recent negative cases can 
be brought forward against it. As for old cases bearing on these 
questions, I wholly reject them as cracked or weak links in a 
chain that must be made only of approximately perfect joints. 
It is surely the duty of all medical men to publish cases negatively LOCALIZED CEREBRAL LESIONS. 
39 
or positively bearing on this question, but only when their ob- 
servations have been made in an exact manner. 
With a large accumulation of precise autopsies, with careful ex- 
periments by physiologists, with more embryological knowledge, 
and with unbiassed comparative anatomy, some one may, in a few 
years, study and solve the problem.