Reprinted from the Journal of Nervous and Mental Disease, November, 1896 
An Initial Report from the Neuro- 
logical Laboratory of the 
Philadelphia Polyclinic. 
UNDER THE DIRECTION OF 
ALOYSIUS O. J. KELLY, A.M., M.D. 
Pathologist and Clinical Assistant to the Neurological Department. Keprmteii from the Journal ok Nervous and Mental Disease, November, 1896. 
An Initial Report from the Neuro- 
logical Laboratory of the 
Philadelphia Polyclinic. 
UNDER THE DIRECTION OF 
ALOYSIUS O. J. KELLY, A.M., M.D. 
Pathologist and Clinical Assistant to the Neurological Department AN INITIAL REPORT FROM THE NEUROLOGI- 
CAL LABORATORY OF THE PHILADELPHIA 
POLYCLINIC.1 
I'NhKR THE DIRECTION OK 
ALOYSirS O. J. KELLY, A.M., M.I)., 
Pathologist ami Clinical Assistant to the Neurological Department. 
The Neurological Laboratory is a part of the Department of Diseases 
of the Mind and Nervous System in charge of Professors Chari.fs K. 
Mii.i.S and Chari.ES \V. Burr, who furnish most of the specimens. 
LESIONS OF THE BRAIN FOUND IN A CASE 
OF ACUTE YELLOW ATROPHY OF THE 
LIVER. 
By CHARLES W. BI RR, M.D. and ALOYSIUS <J. J. KELLY, M.I). 
clinical history of the case is as follows : B. D., 
I male, aged forty years. His previous health had 
always been good. Having felt poorly for about 
one month, one week prior to his death he began to com- 
plain of chilliness, sweats and vague gastro-intestinal 
symptoms. His wife then noticed that he was slightly 
jaundiced. The jaundice rapidly increased in intensity, 
until before his death it was extreme. On the second 
1 Presented at the Joint Meeting of the Pathological Society of 
Philadelphia and the Philadelphia Neurological Society, held in Phila- 
delphia, Mav 28, 1896. 4 
day of his illness he began to be delirious and to have 
general convulsions. The liver dulness became very 
much decreased in area. The patient vomited often, and 
his bowels were absolutely constipated. The urine con- 
tained leucin and tyrosin, but no albumin. Two days 
before his death, his delirium passed into stupor, stupor 
into coma, and in coma he died, Dec. 28, 1895. 
The clinical diagnosis was acute yellow atrophy of 
the liver. 
At the necropsy the liver was about one-third the 
normal size, brown in color, and with wrinkled capsule. 
It was peculiarly soft to the touch and cut like india rub- 
ber. On section the liver structure was indistinctly vis- 
ible in the right lobe, but absolutely abolished in the 
left. There was some oozing of bile. The gall bladder 
contained about an ounce of thick, greenish black bile, 
with a little bile sand. There was no obstruction of the 
ducts, no calculi. The stomach contained a few ounces 
of bile-stained fluid, but was otherwise normal. The 
spleen was slightly enlarged and soft. The kidneys 
were congested, the capsule stripped well ; the cortices 
were well marked off. The brain macroscopically ap 
peared normal. 
For the specimens we are much indebted to Dr. L. C. 
Peter. 
The lesions discovered by microscopical examination 
of the brain may be divided into those found in sections 
prepared according to the Golgi method and its modifi- 
cations, and those found in sections stained according to 
the Nissl methods and modifications. It is convenient 
to describe the latter first. 
Sections from the motor and praefrontal regions of the 
cerebral cortex after the usual procedures subsequent to 
hardening in alcohol, were stained with dahlia, vesuvin, 
magenta red, methylene blue and thionin. While the 
majority of the stainings with the first mentioned agents 
were very satisfactory, none of them approached in clear- 
ness and sharpness of detail those stained with thionin, 
according to the method of Lenhossek. The stainings 
were far superior to those obtained with the much 
vaunted methylene blue, which latter were, however, 
better than those obtained with the other dyes. What 
follows, therefore, refers particularly to thionin prepa- 
rations, though precisely similar changes were disclosed 
by the other stainings. 
The pathological lesions discovered affect the nucle- 
olus, the nucleus and the cell body (Fig. 1). Normally, 
PATHOLOGICAL SOCIETY OF PHILADELPHIA. Fig. i. Drawing illustrating parenchymatous degeneration of the 
cells of the cerebral cortex ; implication of the nucleolus, nucleus, and 
cell body. The cells in the upper half as in a microscopic field ; in the 
lower half, collected from various regions. N. C., normal cell for com- 
parison. Thionin preparation, x 1200 Zeiss. Fig. 2. Drawing illustrating irregular swellings or tumefactions of 
the dendrites, w’ith loss of the gemmulae, of a pyramidal cell of the 
cerebral cortex—eatly stage of degeneration. Oolgi-Berkely preparation. 
Fig. 3. Drawing illustrating atrophy and disappearance of the 
dendrites—late stage of degeneration. Golgi-Berkely preparation. PHILADELPHIA NEUROLOGICAL SOCIEIY. 
5 
the nucleolus is of a definite size, of rounded contour, 
with edges smooth and well defined, and has a certain 
marked, not very variable affinity for the stain. In our 
preparations the nucleolus is very slightly, if at all, in- 
creased in size : it is of somewhat irregular contour, 
which irregularity is not marked, consisting when deni 
onstrable of a slight and limited projection into the sub 
stance of the nucleus at one, occasionally two points, along 
its periphery ; its edges, while sharp and well defined, 
are not as smooth as normally, and its receptivity of the 
stain is markedly increased, it appearing as a jet black 
dot, rendering absolutely futile all attempts to recognize 
any structure. In its position within the nucleus we can 
recognize no deviation from the normal, it being situa 
ted here and there irregularly as normally. 
The nucleus, while apparently exhibiting no marked 
deviations from the normal variation in size, is frequent- 
ly distorted in shape, being often elongated, again quite 
irregular with projections and indentations along various 
parts of its periphery. The two 01 three larger and 
more deeply staining chromophilic particles normally 
present irregularly arranged within the nuclei, are 
no longer visible as such. They have lost their 
identity bv reason of the excessive staining which 
the other finer dust-like chromophilic particles have 
thus pathologically taken on. The normally clear 
karyoplasm evinces a decided affinity for the stain, 
being in many instances excessively stained. This 
staining of the normally clear karyoplasm and the exces- 
sive staining of the nuclear chromophilic particles in 
many instances, produces such an intense staining of the 
nucleus as a whole as to obscure the nucleolus, which, in 
other instances can be quite distinctly recognized. 
The cell body seems to be most intensely affected, 
their being present all gradations from slight implica- 
tion to almost absolute destruction of it. The chromo- 
philic particles, which normally are distributed through- 
out the cell body with a certain regularity usually in 
rows, are in our preparations very irregularly arranged, 
often showing very curious figures. We notice in some 
cells but a slight deviation from the normal, the 
chromophilic particles having disappeared fiom but 
a small area, and being possibly more densely aggre- 
gated in another region. From this slight change 
there are visible all gradations of destruction until there 
remains but the nucleus deeply stained, surrounded by a 
few particles still stained along the periphery of the cell 6 
PATHOLOGICAL SOCIETY OF PH I I.A DELPHI A. 
body. In many instances the chromophilic particles are 
excessively large. One is inclined to think of a coales- 
cence of smaller ones, as high magnifications (1200) fail 
to reveal any distinction into parts. In cells manifesting 
all grades of destructive changes, there is usually ar- 
ranged around the nucleus a layer of fine, stained dust- 
like particles, between which and the nucleus, there is 
always a clear unstained zone. 
In some instances the nucleus and cell contents have 
been entirely destroyed, or the nucleus has dropped out 
of the cell, and all that is discernable are a few fine 
stained particles along what was the periphery of the cell. 
In many cells which are not so excessively affected by 
the destructive process, there is an appearance extremely 
suggestive of fat globules and detritus. The fat there- 
from may unfortunately have been removed during the 
process of hardening. 
The protoplasmic processes as far as they are stained 
present in some instances changes similar to those de- 
scribed as affecting the cell body. In most instances, 
however, they exhibit no deviation from the normal. 
The pathological changes described affect all varieties 
of cortical cells. We have been unable to discover that 
any one variety is more affected than another. In 
spots, however, the destructive process has been more 
marked than elsewhere. In certain regions all the cells 
in a quite eonsiderable area are more or less destroyed, 
while in others but few cells are implicated. This applies 
to all the layers of cortical cells. Again, in a few places 
it seems as though the more superficial cells were more 
intensely affected than those of the deeper layers. These 
instances, however, are very few. 
Other pieces of cortex after hardening in Muller’s 
fluid were stained according to the silver phosphomolyb- 
date method of Berkely. The difficulty of determining, 
by this and the ordinary Golgi method of staining, the 
number of cells affected is very great owing to the un 
certainty of the impregnation and to the fact that of all 
the cells of the various layers of the cortex but a very 
few are at any one time stained. This latter fact is, how- 
ever, a great advantage, as we are thereby enabled to 
study much more readily the changes affecting the in- 
dividual cells and their prolongations. This method of 
staining is inappropriate for detecting the finer changes 
in the cell body, and in our preparations gave negative re- 
sults. The changes affecting the prolongations are, how- 
ever, quite definite. They are of two kinds, or, as we PHILADELPHIA NEUROLOGICAL SOCIE'JY. 
7 
prefer to say, two stages of one process. The first con- 
sists of a swelling (Fig. 2), the second of an atrophy of 
the processes (Fig. 3). 
The first are more numerous. They consist of irreg 
ular swellings or tumefactions which extend along the 
dendrites for a variable distance, and are of variable 
thickness. Some are very minute, others quite large. 
The apicai process itself is very frequently affected close 
to the cell body proper. In other instances the parent 
dendrite and its finer branches abruptly become thick- 
ened, and as abruptly resume their normal calibre. As 
a rule, throughout the course of these tumefactions the 
gemmulae are absent, though occasionally one still de- 
tects a few projecting from the periphery of the swell- 
ings. Along some of the finer dendrites not the subject 
of such pathological tumefactions, the gemmulae have 
also disappeared. In other instances they themselves 
appear somewhat swollen. The varicosities normally 
present at the point of branching of the dendrites appear 
in many instances to be excessively large. 
The further stage of this destructive process has al- 
ready been alluded to as an apparent atrophy. The gem- 
mulae have entireiy disappeared from the dendrites—a 
very few may occasionally still persist. The dendrites 
themselves have become thinned and shortened. That 
they have not been broken or cut off during the process 
of preparation, is evident from the fact that at their dis- 
tal extremities they appear rounded and well defined. 
Further, many of the dendrites have entirely disappeared. 
In some of these latter instances, as well as in some of 
the former, the apical process is still quite thick. 
This destructive process affects apparently indiscrim- 
inately the various cells of the several layers of the cere- 
bral cortex. The determination of the number of the impli- 
cated cells is, however, as before stated, impossible. We 
could detect no pathological changes in the axis-cylinders 
or collaterals. 
The study of the cerebellum led to very indefinite re- 
sults. Aside from variations in the intensity of the 
staining of the Purkinje cells, nothing of any note was 
discovered by the use of the aniline dyes. The impreg- 
nation of the cells of the cerebellum by the Berkely mod- 
ification of the Golgi method was less satisfactory than 
was that of the cells of the cerebrum, but the alterations 
found in the Purkinje cells were practically the same as 
those described affecting the cells of the cerebral cortex. 
We detected no change in the neuroglia elements of 8 
PA THOL OGICA L SOCIE T J' OF PHIL A DEL PH IA. 
either the cerebrum or cerebellum, and no disease of the 
blood-vessel walls. 
To sum up we have found evidences of a marked de- 
structive process affecting- the bodies and the processes 
of the nerve cells of the cerebral cortex. The lesion is 
parenchymatous affecting the nerve cells primarily, and 
is not secondary to any disease of the blood vessels. We 
are entirely ignorant of the primary cause of this de- 
structive process. It is more than probable, it is almost 
certain, that acute yellow atrophy of the liver is caused 
by a poison, and that it is not a local but a general con- 
stitutional disease, a toxemia. And since cerebral symp- 
toms, delirium, perhaps mania, general or local convul- 
sions and coma form no small part of its clinical history, 
we should expect to find distinct signs of disease in the 
cortex whether such signs be the result of penetrated 
function or its cause. The fact that heretofore micro- 
scopic study of the brain in conditions of delirium, acute 
mania, and the acute infectious fevers has frequently 
been fruitless or indefinite, proves nothing, since we are 
only now beginning to learn methods of research com- 
petent to show any of the finer microscopic changes. As 
methods have improved, the number of so-called func- 
tional diseases has steadily decreased. Granting that 
acute yellow atrophy of the liver is a toxemia we are 
confronted with the question as to whether the brain 
lesions found are due to the same poison or whether they 
are due to another or to others produced by disturbance 
of any of the body functions. We cannot answer it. We 
have, of course, assumed that the lesions found by us in 
this one case are not accidental, but essential. 
Whether this be so can only be proven by the study 
of other cases. The lesions found are, of course, not 
claimed to be characteristic of acute yellow atrophy of 
the liver. Indeed, we should expect to find similar 
changes in the acute infectious fevers accompanied by 
similar brain symptoms. As a matter of fact the lesions 
found in this case by using Berkely’s modification of 
Golgi’s method correspond to those found experiment- 
ally by Berkely in ricin and alcohol poisoning and are 
not unlike those described by Andriezen and others as 
occurring in certain types of insanity, notably alcoholic 
dementia. 
That the case was one of acute yellow atrophy of the 
liver is proven not only by the clinical historv and the 
necropsy, but also by the microscopical examination of 
the liver, spleen and kidneys. SENILE PARAPLEGIA. 
Bv aloysius o J. KELLY, M I). 
HE clinical history of the case is as follows : G. B., 
aged 79 years, widower, white, native of Scotland, 
jeweller by occupation, was admitted to the out- 
wards of the Philadelphia Hospital, May 3, 1895, and to 
the men’s nervous wards of the same hospital, February 
13, 1896, and the following notes obtained : 
No history of any hereditary disease. He was treated 
in the surgical wards of the Philadelphia Hospital during 
September, 1895 for urethral stricture, and subsequently 
again transferred to the out-wards He has been a mod 
erate drinker: syphilis is denied. About three months 
prior to his admission to the nervous wards, he noticed 
that he was weak in the legs. He never had had any 
distinct apoplectiform attack. Two days before his ad- 
mission, on attempting to arise in the morning he found 
that he was paralyzed from the waist down. He had re 
tention of urine and incontinence of feces. 
Examination on admission from the out wards re- 
vealed complete paralysis of all the muscles below the 
waist. There were no areas of amesthesia. The third 
day after the paralysis came on, bed sores began to form 
over the sacrum and heels. Although he was put on a 
water bed, these bed sores rapidly became worse. Ex- 
amination of the urine showed a trace of albumin and a 
large number of granular casts. Symptoms of uremia 
began to develop and spots of consolidation in both lungs 
could be detected. The fourth day after his admission 
he became delirious. The temperature never went 
above normal. He became rapidly weaker, and died 
seven days after admission, apparently of uremia (Feb- 
ruary 20, 1896, 5 P.M.) 
Post-mortem examination by Dr. Jamison, February 
22. 1896. 11 a.m. Body of well-nourished old man, a small 
bed sore over the left heel and a large one over the sac- 
rum. Bladder distended and inflamed. Kidneys show 
parenchymatous and interstitial nephritis. Heart nor- 10 
PATHOLOGICAL SOCIETY OF PHILADELPHIA. 
mal. Lungs emphysematous; a few spots of senile pneu 
monia. No gross lesions of the brain or spinal cord, ex- 
cept a chronic leptomeningitis. 
For the specimen (spinal cord) and the above 
notes, I am very much indebted to Dr. Charles K. Mills. 
Microscopical examination of the cord revealed 
changes which, though intimately associated in a causal 
relationship, it will be convenient to describe under two 
headings, first, those affecting the nerve fibres; second, 
those affecting other tissues. 
Upper cervical region: In the postero-median columns, 
close to and parallel with the posterior two thirds of the 
median fissure, there is a narrow area in which the nerve 
fibres are diminished in number and in thickness. There 
is a quite marked degeneration of conical shaped area 
with base inward, bounded by the anterior one third of 
the posterior fissure, the posterior commissure, and the 
posterior cornua, and extending pointedly into the pos- 
tero-external columns almost to the periphery. In the 
lateral columns not strictly localized to the pyramidal 
tracts although there much more marked, the nerve 
fibres are degenerated in part. 
Cervical enlargement: The degeneration in the pos- 
tero-median columns along the posterior fissure is more 
marked than in the previous section, while the conical- 
shaped area alluded to, is larger. The degeneration in 
the lateral columns is marked, but is not limited to the 
pyramidal tracts While these tracts are much more af- 
fected than are other regions, the degeneration extends 
forwards into the anterior ground fibres. 
Lower cervical: The degeneration in the posterior 
columns, while more marked along the posterior median 
fissure is distributed to some extent throughout the col- 
umns. The degeneration in the lateral columns as here- 
tofore affects particularly and more markedly the pyra- 
midal tracts, though it is not confined to them. 
Upper, middle and lower thoracic regions: The de- 
generation in the posterior columns is much more gen 
eral and much more marked than in previously described 
sections The degeneration in the lateral columns is of 
about the same extent as in the last mentioned section. 
Lumbar cord : The degeneration in the posterior col- 
umns is very marked. In the lateral columns as hereto- 
fore. 
Sacral: The fibres along the lateral margin appear 
fewer in number and narrower than elsewhere FlO. i. Drawing showing the excessive intra-spinal overgrowth of 
connective tissue and its sources of origin, the sclerosis of blood vessels 
and pia mater. Ammonio-carmine preparation. * 
Fig. 2. Photograph showing the blood-vessel sclerosis, the associ- 
ated perivascular connective tissue overgrowth, and the numerically 
increased and much thickened trabecula? of connective tissue and the 
numerous islets of sclerosis in connection therewith. Weigert-Pal 
preparation. Fig.3- Higher magnification of Fig. 2. 
Fig. 4. Photograph showing changes similar to those evident in 
Figs, r., 2. and 3. Haematoxylin—Picric Acid—Fuchsin preparation. PHIL A DEL PH I A NE UROL OGICAL SOCIE 7 Y. 
11 
When not otherwise stated, the nerve fibres of the 
various tracts appear normal. 
Throughout the cord at all levels, but especially in 
the regions noted as revealing nerve fibre degeneration 
that is, in the posterior and lateral columns—there is a 
great increase of the connective tissue. This connective 
tissue overgrowth is intimately associated with changes 
in the blood vessels and pia-mater. With the exception 
of the very minutest ones, the blood-vessels are every- 
where distended, and all have greatly thickened walls. 
This applies to vessels of all calibres, from minute spinal 
ones to larger pial vessels. The smallest spinal vessels 
have greatly thickened walls and the lumen of many of 
them has apparently become obliterated. Careful exam- 
ination of somewhat larger ones, reveal slight prolifera- 
tion of the intima and great increase in the thickness of 
the media, which is poor in nuclei, concentrically lami- 
nated, and apparently somewhat hyaline in structure. 
Surrounding this latter is a layer of variable thickness of 
less homogeneously staining connective tissue. These 
changes are very marked in some of the median sized 
and larger vessels, which themselves are occasionally the 
seat of some round cell infiltration. 
The pia-mater is very greatly thickened, contains a 
very few nuclei, and has become united with the arach- 
noid. The peripheral layer of the spinal neuroglia is 
dso greatly thickened. From this greatly thickened pia 
and neuroglia, and from the blood-vessels with thickened 
walls as noted above, there extend throughout the cord 
numerous connective tissue trabecula;. These are very 
greatly in excess in number and much thicker than nor- 
mally, and while present throughout the cord, are much 
more in evidence in the areas already referred to as re- 
vealing nerve fibre degeneration. 
These trabeculae are frequently very thick, inclosing 
within their confines bundles of nerve fibres, whereas, 
again they are finer and surround only individual fibres, 
leading thus to degeneration of single fibres. The blood- 
vessel sclerosis is, of course, not confined to the vessels 
of the white matter of the cord, but implicates of neces- 
sity those supplying the gray matter, which latter is not, 
however, appreciably altered. The central canal is filled 
with proliferated epithelium. 
The most evident and important pathological altera- 
tion discovered in these sections is, therefore, the exces- 
sive overgrowth of connective tissue; the nerve fibre 12 
PATHOLOGICAL SOCIETY Oh PHILADELPHIA. 
degeneration being very properly considered secondary 
thereto. The intimate association of this sclerosis with 
the blood-vessels is very patent. The blood-vessels 
themselves are the seat arteritis and endarteritis, and 
around them as foci proceed trabeculae of connective tis- 
sue encircling in places numbers, in others,fewer nerve 
fibres. The neurolgia along the periphery of the cord is 
also greatly thickened, and from it proceed also into the 
cord, trabeculae of fibrous tissue, much increased in thick- 
ness and in number. . 
This sclerosis originating around the vessels and peri- 
phery of the cord, while marked in all regions of the 
cord, is, however, much more intense in the posterior 
and lateral columns, especially in the area of the pyra- 
midal tracts, and is more marked in the thoracic region 
than elsewhere. In areas slightly affected, more particu- 
larly where the sclerosing tissue surrounds groups of 
nerve fibres, rather than individual ones, the fibres for 
the most part appear normal. In other regions, however, 
in which the sclerosing connective tissue envelops fre- 
quently individual fibres, these have suffered greatly 
therefrom and have become atrophied, axis cylinder and 
medullary sheath in many instances, having disappeared, 
in others being much narrower than normally. There 
remain, therefore, in consequence, many minute islets of 
fibrous tissue. In places where several larger vessels 
are in close opposition there are quite large spots of 
sclerosis. 
There was discovered no embolic, thrombotic, hem 
orrhagic, or other process to account particularly for the 
acute manifestation of the severe symptoms. The case 
is simply an illustration of one of the many instances 
with which the neuropathology abounds in which defin- 
ite lesion are for a long time devoid of any very manifest 
symptoms. These when they do come on, frequently 
make their appearance abruptly. 
That the patient, however, was not entirely without 
symptoms prior to the acute attack of paraplegia, is evi- 
denced by the weakness of his legs. And, in the light 
of the microscopical examination, and reasoning a priori, 
one may very safely assume that there were present 
other symptoms, unfortunately overlooked as is but too 
frequently the case in the gradual and progressive weak- 
ness which attends old age. One cannot, therefore, but 
regret imperfect history. 
The designation “ Senile Paraplegia,” is admittedly PHILADELPHIA NEUROLOGICAL SOCIETY. 
13 
ill-chosen, but has been selected because of its concise- 
ness, and because it is sufficiently expressive of the clini- 
cal condition. We do not, however, desire to be under- 
stood as suggesting that the changes described are essen- 
tially senile in nature. They are distinctly pathological, 
and while frequently an accompaniment of old age, they 
are to be considered apart from changes of a purely sen- 
ile character. It will hardly be appropriate to here enter 
upon the discussion of this subject in detail. For the 
photographs I am much indebted to Dr. Schively. THE SPINAL CORD LESIONS IN A CASE OF 
FRACTURE OF THORACIC AND LUMBAR 
VERTEBRAL 
By ALOYSIUS O. J. KELLY, M.D. 
THE clinical history of the case is as follows : W. T. 
A., male, aged 33 years, mason by occupation, was 
admitted to the Orthopoedic Hospital under the 
charge of Dr. Wharton Sinkler, March 28, 1895. He had 
had gonorrhoea when he was 25 years of age, but syphi- 
lis was denied. December 30, 1891, a scaffold on which 
the patient was working, gave way, causing him to fall 
twenty feet to the ground. He struck on his heels, then 
on his back. A brick standing on end struck him in the 
lumbar region to the right of his spinal column, causing 
a bruise which persisted for some time. On attempting 
to arise he could not move his legs. He began to imme- 
diately experience a sensation as of “ pins and needles ” 
from his waist down. For four days after the accident 
his legs were painful and felt cold. He had complete 
loss of control of his bladder and rectum. His sexual 
function was abolished. 
Examination on admission to the hospital: No erup- 
tion or oedema ; deep bed sores over the sacrum, on 
each heel, and on the calf of the left leg. No movements 
in the legs, no rigidity. Loss of control of the bladder 
and rectum. Complete anaesthesia below the crests of 
the ilea; touch, pain and temperature sense all abol- 
ished. No girdle pain. No tenderness on pressure over 
the nerve trunks. Elbow jerks equal on both sides; 
muscle jerks in arms normal. Knee jerks absent, not re- 
inforcible. Tendon achilles jerks absent ; plantar jerks 
absent; cremasteric jerks present but much retarded. 
Abdominal reflexes present. Urine contains a trace of 
albumin. 
Electrical examination (Dr. Willets): No reaction to 
the faradic current in any of the muscles of the legs. 
Galv. ancle. > Kclc. 35 ma. required to secure reaction in 
tibialis anticus ; calf muscles 30 ma. Galvanic qualita Fig. 1. One cm. above lesion. Photograph showing distortion"of 
the cord, and complete degeneration of all the nerve fibres, except a few 
of those of the anterior column. Weigert-Pal preparation. 
FlG. 2. Thoracic Cord, three cm. above lesion. Photograph show- 
ing degeneration of the nerve fibres of the posterior column and of those 
along the antero-lateral periphery (direct cerebellar and antero-lateral 
ascending tracts). Weigert-Pal preparation. 
Fig. 3. Thoracic cord, nine cm. a1>ove lesion. Photograph show- 
ing degeneration of the postero-median. jiostero-extenial (partial), 
direct cerebellar and antero-lateral ascending tracts. Weigert-Pal prepara- 
tion . Fig. 4. Lower cervical cord, sixteen cm. above lesion. 1 lioto- 
graph showing degeneration of the postero-median, direct cerebellar and 
antero-lateral ascending tracts. Weigert-Pal preparation. 
Fir s Cervical enlargement, twentv-two cm. above lesion. Pho- 
tograph showing degeneration of the postero-median, direct cerebellar 
and antero-lateral ascending tracts. Weigert-Pal preparation. PHILADELPHIA NEUROLOGICAL SOCIETY. 
15 
tive and quantitative change. Pupils equal and react 
well to accommodation and to light. 
October 7, 1892, the patient died. The autopsy re- 
vealed a fracture dislocation of the first lumbar on the 
last dorsal vertebra ; the dura mater adherent to the 
bodies of the vertebrae at the seat of fracture ; the entire 
lumbar cord and the lower dorsal cord much flattened ; 
chronic cystitis ; slight dilatation of the ureters ; pyeli- 
tis; abscesses in the kidneys. 
For the specimen (the spinal cord) and the above 
notes, I am very much indebted to I)r. Charles W. Burr. 
Microscopical examination(Weigert-Pal preparations): 
A section through the centre of the area of disease re- 
veals total destruction of the cord, it being impossible to 
recognize any of its various constituents. What was the 
cord is now a mass of fibrous connective tissue, through 
which run a few partially degenerated nerve fibres. The 
nerve fibres of the cauda equina, particularly the most 
external ones, still retain their myeline sheath. Sur- 
rounding the structures of this region is a thick mass of 
dense fibrous tissue. 
A section through the cord one centimetre above the 
former, shows great distortion of the cord, particularly 
of the postero-lateral regions, the component parts of 
which cannot be separately recognized. The cord is 
flattened from before backward, the posterior cornua be- 
ing apparently displaced laterally, the posterior and late- 
ral columns being crushed antero-posteriorly. The 
normal configuration of the anterior cornua and columns 
is well retained. There is complete degeneration of all 
the nerve fibres in this region of the cord, with the ex- 
ception of a few along either side of the anterior median 
fissure, a few of the most centrally located of the ante- 
rior columns, a few skirting the medial and anterior bor- 
der of the anterior cornua, and a few of the anterior 
commissure (Fig. 1). 
A section through the cord 3 cm. above the first, 
shows the cord to be about normal configuration. Along 
the antero-lateral periphery there is a degeneration of 
the nerve fibres of varying extent, being greatest just a 
little external to the posterior cornua. With the excep- 
tion of a few fibres bordering the tips of the posterior 
cornua, the fibres of the posterior columns are degenera 
ted in their entirety (Fig. 2). 
A section through the cord 9 cm. above the first re- 
veals a complete degeneration of the fibres of the postero- 16 
PA THOLOGICAL SOCLE 1 Y OP PHILADELPHIA. 
median (Goll’s) column, and some degeneration of the 
medial peripheral fibres of the postero-external (Bur- 
dach’s) column. There is some degeneration of the fibres 
along the periphery of the cord between the anterior 
and posterior cornua of both sides. This degeneration 
is most marked about midway between the cornua, at 
which place it penetrates some distance into the sub- 
stance of the cord (Fig. 3). 
A section (lower cervical) 16 cm. above the first, shows 
complete degeneration of the posterior median columns, 
which degeneration towards the posterior commissure 
spreads out fan-shaped. The postero-external columns are 
otherwise unaffected. The degeneration along the lateral 
periphery noted in the previous section is more marked, 
and about midway between the anterior and posterior 
cornua extends quite a considerable distance into the 
substance of the cord (Fig. 4). 
A section (cervical enlargement) 22 cm. above the 
first reveals the same general characteristics as those evi- 
dent in the last described section (Fig. 5). 
Below the seat of manifest lesion—in the conus—it is 
absolutely impossible to recognize any spinal cord struc- 
ture. There is present a mass of connective tissue 
through which run a few partially degenerated nerve 
fibres. 
When not otherwise mentioned the tracts are normal. 
There is, therefore, complete disorganization of the 
cord at the seat of fracture, and above this region 
throughout the cord, ascending degeneration of the pos- 
tero median, direct cerebellar, and antero-lateral ascend- 
ing (Gower’s) tracts ; and for a short distance, degenera- 
tion of the postero-external columns. In other words, 
we find the anticipated spinal cord lesions of a fracture 
in this region. To be mentioned only is the degeneration 
of the direct cerebellar tract in conjunction with a frac- 
ture of the vertebrae so low down. 
For the photographs, I am very much indebted to Dr. 
Schively. A CASE OF PRIMARY COMBINED COLUMN DIS- 
EASE. 
Bv JOHN H. W. KHEIN, M.D., 
Instructor in Nervous Diseases, Philadelphia Polyclinic. 
MRS. L , aged 59 years, presented herself for exami- 
nation, complaining of unsteadiness in walking 
and numbness from the waist downward. Her 
family history reveals a decided neurotic taint. Her 
grandmother and three au: ts had paralysis agitans, a 
sister nystagmus, and her mother an attack of apoplexy. 
She herself had enjoyed excellent health prior to the on- 
set of the present affection, which began, she stated, 
suddenly, about two years previously. 
There was an attack of unconsciousness preceded by 
stiffness in the neck and nausea. No paralysis followed, 
but shortly afterwards distinct insecurity in walking, 
with progressive weakness in both legs developed. She 
became emaciated and extremely pallid. 
When examined by Dr. Frances Janney, eighteen 
months after the onset, she presented the following 
symptoms : 
The patient was exceedingly anaemic, and moderate- 
ly emaciated. There was no paralysis, though the legs 
were weak. The wasting was general and did not sug 
gest atrophy from central trouble. The station was poor 
with feet together and eyes open or closed. The gait 
was distinctly ataxic. The knee jerks were decreased on 
both sides, but reinforcible The plantar reflex was re- 
tained. There was no change in sensation except parses 
thesia of the legs and trunk to the waist. A vaginal ex 
amination revealed the presence of a large tumor involv- 
ing the fundus of the uterus. Its existence had hitherto 
not been suspected. 
Some months later a second examination was made 
and the above condition confirmed. The knee jerks were 
irregular. On the right the response was slightly below 
normal, on the left almost normal, on both sides reinforc- 18 
PATHOLOGICAL SOCIETY OF PHILADELPHIA. 
ible. There was no clonus or ankle jerk. The elbow 
jerk and chin jerk were present. Muscle reaction was 
good. Pain sense and sensation to touch and heat were 
normal. The paraesthesia was still present. 
There was no disturbance of the bladder or rectal 
functions. A fine rythmical tremor in both hands was 
observed. This had existed for years and was not made 
worse by voluntary effort. An examination of the blood 
made by Dr. James E. Talley, showed 2.464,000 red blood 
cells and 40$ haemoglobin. Dr. A.G. Thomson reported 
the eye condition as follows : Pupillary reaction normal, 
form fields and fundi normal. Clear media, margins of 
discs hazy. The patient died a year later from exhaus- 
tion. Her exact nervous condition at the time was not 
studied. 
The necropsy revealed the following facts : In the 
uterus, involving the whole body of this organ, was a 
large, hard tumor, which microscopic section proved to 
be a fibro-sarcoma. Some few masses, small in size and 
scattered, were seen in the liver, which was normal in 
size. The examination otherwise proved negative, ex- 
cept the spinal cord, which was the seat of a lesion pre- 
senting the greatest interest. Microscopically the cord 
appeared smaller than normal. There was no menin- 
gitis. The brain and its enveloping membranes showed 
no change. Unfortunately, the brain in the process of 
hardening, underwent decomposition, hence a report of 
the microscopical condition of this organ is impossible. 
Macroscopically there was demonstrated degeneration in 
the posterior and lateral columns of the spinal cord, as 
seen by the distinct paling of these tracts. The process 
involved the whole extent of the cord and was most in- 
tense in the lower dorsal region. The degeneration in 
the lateral tracts was not so extensive as in the posterior 
columns at any of the levels. 
The cord was hardened in Muller’s fluid, imbedded 
in celloidin, and stained by the Weigert-Pal method and 
with ammonio-carmine. 
Microscopical.—After staining, a sclerotic change was 
seen in the posterior and lateral pyramidal tracts through- 
out the whole extent of the cord, almost systemic in char 
acter. I11 the posterior columns the degeneration is most 
intense in the dorsal region, least in the lumbar region, 
while in the cervical region it is considerably more than 
moderate. There is always a strip of healthy tissue sur- 
rounding the degenerated area in the posterior columns Fig. i. Cervical cord showing degeneration of the postero-median, 
the postero-external (in part), and the crossed pyramidal tracts. 
KiO. 2. Thoracic cord showing degeneration in the posterior and 
lateral columns. 
plC 3> Lumbar cord showing degeneration in the posterior columns. PHILADELPHIA NEUROLOGICAL SOCIETY. 
19 
and the columns of Goll are more intensely involved than 
the columns of Burdach. 
The ganglion cells in the anterior horns show slight 
change in places, chiefly in the upper dorsal region. The 
posterior roots and Clark’s column show no signs of in- 
volvement. 
In the upper cervical region, the degenerated area in- 
volves the columns of Goll in their entirety, except a 
few fibres medianward and cervically, which take the 
stain well. Though to a much less degree, the columns 
of Burdach are markedly involved. Centrally there re- 
main a number of healthy fibres, while peripherally but 
a few well-stained fibres can be seen. The root zones are 
present. In the lateral pyramidal tracts there is begin 
ning degeneration, but to a much less degree than is 
seen in the posterior tracts. The anterior pyramidal 
and cerebellar tracts are intact. The anterior horns and 
posterior roots as well as the remaining tracts of the cord 
are normal. 
In the cervical development, the same condition exists 
save that the degeneration in the postero-external col- 
umns and in the lateral pyramidal tracts is more in- 
tense. 
In the dorsal region the process has so far progressed 
that few healthy fibres remain in Goll’s columns. In the 
columns of Burdack a narrow strip along the posterior 
horns alone is stained, the process growing more intense 
from above down wards. In the anterior pyramidal tracts 
a very moderate degree of degeneration is observed. 
There is marked degeneration of the crossed pyramidal 
tract. In the upper levels a few ganglion cells have lost 
their prolongation, but there seems to be no lessening in 
the number. The process involved to : very slight de- 
gree the antero-lateral ascending tracts. 
In the lumbar region the degeneration is less marked, 
especially marginally. In the posterior columns healthy 
fibres in increasing numbers are observed. A band of 
well-stained tissue encircles completely the degenerated 
area. 
In the lumbar enlargement, only traces of the pro- 
cess in the lateral columns are seen. In the posterior 
columns are two wedge-shaped areas of degeneration on 
either side of the posterior fissure, surrounded by healthy 
tissue. 
The degeneration now rapidly becomes less in extent 
and degree, until in the sacral cord there is no trace of 20 
PA THOL OGICA L SOCIE TV OF PHIL 4 DELPHI A. 
the process visible. Clark’s columns and the posterior 
roots are intact. 
The carmine specimens show smaller axis-cylinders ; 
in places many entirely disappeared ; a marked increase 
in connective tissue. To a very moderate degree is there 
increase in the blood vessels. There were seen no granu- 
lar cells in any of the sections. 
This is evidently one of a group of cases which has 
been variously described as combined tabes, postero-lat- 
eral sclerosis, spastic tabes (Grasset), ataxo-paraplegic 
tabes (Dejerine*, ataxic paraplegia (Gowers'), combined 
fascicular disease, progressive spastic ataxia ■ Dana), true 
combined system disease (Babinski and Charrin) and pri- 
mary combined column disease (Rothman). 
In 1871 Prevost described the post-mortem findings 
in what was probably the first case belonging to this 
group. Later, Babesin, Striimpell, Siali, Westphal and 
others added cases to the literature of the subject. In 
1886 Grasset collected 33 cases with autopsies and called 
the disease combined tabes (ataxo-spasmodique). The 
evidence did not point to a mere systemic lesion. He 
believed with Gowers that while the lesion in the pos- 
terior columns was systemic, in the lateral columns it 
tended to be diffuse, and concluded that the process was 
a diffuse myelitis. 
A study of the autopsies in the cases above demon- 
strates clearly that the disease is one with a most varied 
morbid anatomy, different columns in varying degrees 
of intensity being involved. The gray matter may or may 
not be diseased ; the peripheral nerves have been found 
involved; Clark’s columns and the posterior roots as 
shown by Rothman, Mayer and others are often affected. 
On the other hand, a number of cases show a noteworthy 
unanimity in the distribution of the lesion in the poster- 
ior columns With moderate constancy the lesion is 
more intense in the lower dorsal region, less in the cer- 
vical region and least in the lumbar and sacral regions. 
As a rule there is a band of healthy fibres surrounding 
the diseased areas adjacent to the posterior horns. In 
the lateral columns the degeneration is not strictly sys- 
temic as Gowers, Dana and others have proven, and 
which is shown in the case under discussion. 
In some cases the lateral mixed columns are en- 
croached upon, and the direct cerebellar tracts are not in- 
frequently involved. In Strumpell’s case, reported in 
1880, there was systemic degeneration of the pyramidal PHIL A DEL PIII A NE UROL OGICAL SOC1E 7 V. 
21 
tracts, posterior columns, cerebellar tracts with atrophy 
of Clark’s columns. The anterior horns and peripheral 
nerves escaped. 
This variability in the morbid anatomy, together 
with the irregularity in the clinical history, suggests 
that the lesion is not truly systemic, but rather diffuse, 
beginning as a primary disease of the column of the cord, 
the posterior and lateral pyramidal tracts most usually, 
and developing as the process progresses into a diffuse 
one. It is not a systemic lesion, as Striimpell, Hochhaus 
and others maintained. It may, if the patient succumbs 
early, show a limitation to certain tracts in the cord, but 
when the disease is of long duration the process takes on 
an increasingly diffuse character. Striimpell believed 
that the further extension of the disease by continuity is 
improbable. Certainly, at first the limitation to certain 
columns, and the freedom of the parts immediately ad- 
joining the diseased areas, inclines to this view, but later 
there little doubt that continuity plays at least some 
part in the extension of the lesion. 
The presence in the case under discussion, of a mal- 
ignant tumor of the uterus is interesting in connection 
with the recent reports of spinal degeneration in consti- 
tutions with morbid blood states. Lichtheim, Nonne, 
Minniek’ Burr and others have described characteristic 
lesions of the cord in pernicious anaemia. Babes and 
Kalindero, in 1890, reported a case of Addison’s disease, 
with lesions in the posterior and lateral columns with a 
distribution which suggests to no slight degree that found 
in many of these cases of combined sclerosis. Fleiner 
quotes Abegg’s case of spinal degeneration in a case of 
Addison’s disease. There was change in the posterior 
columns in two of his own cases. 
Minnich mentions spinal change in three cases of 
chronic icterus, in one case of leukaemia, in a case that 
died of tumor of the “ vermis inf. cerebri,” in two cases 
of chronic nephritis, and finally, a case of carcinomatous 
cachexia with hydraemia. Lastly, spinal lesion has been 
found in hypnotismus, pellagra, lathyrismus, and lead and 
alcohol poisoning. This clearly demonstrates some re 
lation between toxic blood conditions and spinal degene- 
ration, but just what that relation is, it is impossible in 
the present light of our knowledge to decide. In perni- 
cious anaemia, the origin of the blood state remains as 
obscure as the cause of the spinal lesion. The theory 
that the two conditions are common results of the same 22 
PA THOLOGICAL. SOCIETY OF PHILADELPHIA. 
cause, probably a toxine seems the most plausable ex- 
planation, one is justified at present in making. 
Since the exact duration of the tumor of the uterus is 
not known, we are inclined to place no importance upon 
its presence, and all the more likely to consider its pres- 
ence a coincidence. 
In studying the etiology of the affection it will be 
seen that nervous heredity plays an unimportant part; 
that syphilis is rarely an antecedent; that it is more fre- 
quent in males; that it is a disease of adult life ; that ex- 
posure and excesses, exercise, predispose, and lastly, it 
follows spinal injury according to Rothman. The symp- 
toms are characteristics. The onset is gradual, the first 
symptom being unsteadiness in walking. Soon there is 
added stiffness in the muscles, though this may be ab- 
sent. Romberg’s symptom is present and the gait is dis 
tinctly ataxic, though differing from the walk of true 
tabes. The high raising and flopping down of the feet 
is not prominent. It is a minglingof the gaits of spastic 
paralysis and true tabes—when spastic symptoms are 
present. Lighting pains are almost always absent owing 
probably to the freedom of the root zones. Other sen- 
sory symptoms are rare. The reflexes show a wide dif- 
ference from the tabes. The knee jerks are usually much 
exaggerated or spastic at first, while towards the last 
they may be almost or quite absent. The plantar reflex 
is present, as well as the remainder of the superficial re- 
flexes. The sexual power is early lost. The eye symp- 
toms sometimes, but rather exceptionally, resemble 
those found in true tabes. The iris reflex to light is us- 
ually preserved and optic atrophy is the exception. Pro- 
gressive weakness ushers in the final symptoms. 
The disease has little tendency in itself to cause death 
according to Gowers and Dana, and usually is of long 
duration. Rothman’s experience, however, leads him to 
conclude that the duration of the disease is but three 
years. In our own case the patient expired just three 
years after the appearance of the first symptoms, but the 
case was not uncomplicated, and had the malignant 
tumor been absent we are warranted in supposing that 
the patient would have survived a longer period. 
In conclusion, thanks are due Dr. Frances Janney for 
her kindness in permitting this report and for the oppor- 
tunity of making the necropsy. To the kindness of Dr. 
Schively are we indebted for the photographs. PHILADELPHIA NEUROLOGICAL SOCIETY. 
23 
Literature. 
Prevost: Arch, de physiolog., 1871-72, IV., p. 316. 
Westphal: Arch, de psychiat , 1878. 
Striimpell: Arch. f. psych, u. Nervenk , 1880-81, p. 275. 
Sioli: Arch. f. psychiat., 1881, XI. 
Zacher: Arch. f. psych., 1883. XIV.; 1884, XV. 
Damaschino: Gaz. d. Hop , 1883, p. 1. 
Dejerine: Arch. d. physiolog., 1884 and 1885. 
Westpl al: Arch. f. psych, u. Nervenk., 1884. 
Luekling: Lancet, London, 1S86, No. 13, p. 224. 
Gowers: lancet, London, 1886, p. 3. 
Grasset: Arch. d. Neurol., 1886. No. 11, p. 156 
Babinski and Charrin: Revue de Med , 1886, No 6, p. 962 
Lichtheim: Cong f. innere Med , 1887. 
Dana: Med. Record, N Y.. 1887, p. 1. 
Habesand Kalindero: Bull.de l’Acad. de Med., 1889, No. 20, p. 277 
I Mitchell Clark: Brain, 1890, p. 356 
Ladame: Ibid., p. 530. 
Clark: Ibid., 1890. 
Gowers: Dis of Nervous Systun, 1891, p. 453. 
Noorden: Charit. Annalen, 1891-92. 
Kleiner: Deutsche Zeit. f. Nervenk., 1892, No. 2, p 4 
Minnick: Zeit. f Klin. Med., 1892, No. 22. 
Leyden: Ibid., No 21, p 1. 
Arnold: Viren. Arch., 1892. p. 18. 
Hochhaus: Deutsche. Zeit. f Nervenheilk., 1893, p. 474. 
Nonne: Arcliiv f Psych.. 1893, XXV. 
Mayer: Deutsche Klinische Wochenschrift, 1894. 
Bowman: Brain. 1894, p. 198. 
Burr: Univ. Med. Mag., April, 189s. 
Rothman: Deut. Zeit. f. Nervenheilk., 1895, No. 7, p. 171 
Babesin: Virch. Arch., No 76, p. 74. SPINAL CORD FROM A CASE OF POTTS’ DIS- 
EASE. 
By HENRY D. BOYER, M.D. 
following case was under the care of Dr. J. P. 
Willits in the Germantown Hospital in the spring 
of 1894. 
Unfortunately he was an Italian who spoke no lan- 
guage other than his own, and his previous history could 
not be ascertained. 
When brought to the hospital he was a middle-aged 
man, with the objective symptoms of a chronic myelitis. 
And no direct cause for the cord disease could be found. 
He had evidently been in bed for some time. There were 
much emaciation, complete paraplegia, and contractures 
of the thighs and the legs with fibrous anchylosis at the 
hips and the knees. The sensation was completely lost 
from the umbilicus down. The knee jerks could not be 
tested on account of the contractures. There was full 
control over the bladder and the bowel sphincters. The 
arms were in no way affected, except by the general 
weakness. The back was perfectly straight. There was 
no point of especial tenderness along the spine, nor any 
pain in any other part of the body. The temperature 
was at times hectic, but no focus of pus could be found. 
This condition remained much the same for some 
five months, the symptoms of myelitis becoming grad- 
ually worse until death occurred. Towards the latter 
part of this time, the control of the bladder and the 
bowels was lost, and a bed sore developed on thesac rum 
and right heel. 
The post-mortem was made by Dr. Burr, who gave 
me the following notes of it and the spinal cord. 
At the time of the man’s death, there remained the 
paralysis and the contractures of the leg as before 
noted. There was no angularity of the spinal column 
and no prominence looking like an abscess near the 
surface. On cutting dbwn on the spine, there was 
opened a large pocket holding almost a pint of pus. pHIL A DEL 1 'HIA NE UROL 661C AL SOCIE T Y. 
25 
This was found under and to the inner side of the right 
scapula. The pus had burrowed into the posterior media- 
stinum, but not into the pleural cavity. The laminae of 
the dorsal vertebrae from the fifth down were carious. 
The bodies of the same vertebrae were markedly carious 
and filled with cheesy matter. The most marked de- 
struction of bone was in the fifth, sixth and seventh dor- 
sal vertebrae. The meninges of the cervical portion of 
the cord were normal. Those of the lumbar region were 
almost free of deposit. In the dorsal region, the dura 
was greatly thickened. At the point of most disease, 
from the fifth to the eighth dorsal vertebra, the cord was 
completely surrounded by a thickened dura, at some 
places one-half of an inch in thickness. The brain was 
normal. The lungs showed miliary tuberculosis with 
pleural adhesions. 
The microscope shows the extreme dural thickness 
to be due to an inflammatory process in the dura itself, 
with new cell formation, and to a cellular and a cheesy 
deposit on the outer side of the dura. 
The cord is greatly pressed upon by this new tissue. 
It is distorted and nearly destroyed at this site by both 
the mechanical and some inflammatory processes. Sec- 
ondary degenerative lesions are found both above and 
below this point. At the place of greatest pressure, 
there is shown some inflammatory changes. Many new 
cells are present where only nervous tissue should exist. 
There is no distinct line of demarcation between the 
gray and the white matter. Both being almost totally 
destroyed. The cells in the anterior horns of the gray 
matter are few in number. Some are destroyed. Others 
are not perfect, having lost some of their processes. 
The central canal is filled by new epithelial cells. The 
white matter is mostly degenerated in all portions of the 
cord at this level. Most of the axis cylinders and the 
myelin sheaths are totally destroyed. Other myelin 
sheaths are undergoing destruction, being swollen or 
narrowed, according to the degree of degeneration. 
Small particles of myelin, not in cylindrical form, are 
everywhere found through the section. There are a 
few of both myelin sheaths and axis cylinders that are 
normal. These are found near the centre of the section, 
and around the remains of the gray matter where least 
pressed upon. 
The secondary degeneration both above and below 
the point of most pressure shows the same kind of 26 
PA THOLOGICAL SOCIE'I V OF PH l LA DELPHI A. 
change as above described,but to a less extent. It follows 
fixed columns. In none of these is the degeneration so 
marked as at the transverse myelitis. 
In the cervical enlargement, the posterior median 
tracts of Goll are almost totally destroyed. The columns 
of Burdock are a very little affected. There is another 
small degenerated area in the lateral ascending columns. 
This is close to the margin of the cord and in the ex- 
treme lateral part. 
A section very high, near the medulla shows the de- 
generation in the posterior median columns. That in 
the ascending lateral tract is not so wide as in the cer- 
vical enlargement. The other lateral tracts are normal 
above the lesion. 
Below in the lower dorsal region all the lateral 
columns are involved, except the lateral fundamental 
zone lying near the anterior gray matter. The direct 
pyramidal tracts are also marked by the degeneration. 
In the lumbar region, the antero-lateral tracts all 
show more or less destruction, except immediately 
around the anterior gray matter. The degeneration is 
greatest near the surface. 
Below the lesion the posterior columns are not af- 
fected. 
I wish to thank Drs. Burr and Willits for the privi- 
lege of presenting this case. v Fig. i. Drawing showing the gross lesions: a. right third nerve ad- 
lierent to fibroid m*ss ; b, right internal carotid plugged by a thrombus ; 
c fibroid mass filling the Sylvian fissure and extending backward to the 
crus • d, chiasm ; e, left internal carotid containing recently organized 
thrombus ; f left third nerve ; g. left postcommunicant at junction with 
postcerebral ; h, basilar giving off postcerebral. * 
* This illustration is used throu (h the courtesy of the publishers of the 
Medica' News. Fig. 2. Section of right oculo-niotor nerve, showing complete de- 
generation : and almost total disappearance of the nerve fibres. Low' 
magnification. 
Fig. 3. High magnification of Fig. 2. CEREBRAL SYPHILIS.1 
By MARY ALICE SCHIVELY, M I). 
case under examination presented the follow 
I ing clinical history: L. S., single, aged 29 years; 
a seamstress by occupation. The family history 
was negative. She had a history of alcoholism and 
syphilis, with sore throat, skin eruption and loss of hair. 
In July, 1894, she began having persistent frontal head- 
ache ; at the same time her eyesight began to fail. 
Upon awakening one morning early in September, she 
noticed for the first time that her right eye turned up- 
ward and outward. Upon attempting to rise she was 
unable to stand, and discovered that her left leg was 
useless. She afterwards regained some use of her leg, 
but continued to be subject to occasional attacks, during 
which it would suddenly give way. 
The patient was admitted to the Nervous Wards of 
the Philadelphia Hospital in December, 1894. 
At this time she had a stupid expression of coun- 
tenance, and wandered about aimlessly, speaking but 
little. She constantly complained of headache which 
was relieved somewhat at intervals, by repeated doses of 
potassium iodide. She had periods of marked irritabil- 
ity, which were followed in turn by mental hebetude, 
after which she would remain in bed and during which 
she could not easily be aroused, and would not answer 
questions. Her gait was of a shuffling character ; knee- 
jerk was plus and there was slight ankle-clonus of the 
left side. 
Examination of the eyes was made by Dr. Oliver 
The conditions were as follows : There was complete 
ptosis of the right eyelid ; this eye itself was directed 
outward, and all movements of the globe were lost, ex 
cept outward and a slight movement upward and out- 
ward ; the pupil was immobile, four mm. in diameter. 
1 For a short report of this case, exclusive of the results of the micro- 
scopical examination, consult Mills: “ Some Phases of Syphilis of the 
Brain," Case V., Medical News, December 7, 1K95. 28 
PATHOLOGICAL SOCIETY OF PHILADELPHIA. 
The left pupil responded to light. Both pupils were oval 
and both optic discs gray. 
On February 28, 1895, the patient went to bed in a 
spastic condition similar to that of previous attacks, but 
more marked. The left side of the face was flushed and 
swollen and she spoke only in monosyllables. During 
the night she had a convulsive attack followed by gene- 
ral muscular twitchings. After this the oculo motor 
paralysis became deepened and she would not answer 
questions, although she appeared to understand what 
was said to her. 
During the next day the mental dullness deepened 
gradually into coma. On the following day there was 
stiffness of the right arm, but relaxation of the left arm 
and both legs; K. J. was exaggerated on the left side. 
The left eye remained open and fixed, the pupil being 
contracted. Later there was Cheyne-Stokes breathing. 
The patient remained in an apoplectic condition, dying 
on the evening of the second day. 
The post mortem examination revealed the following 
conditions: The dura was normal and not adherent; the 
pia free from inflammation, but much thickened ; the 
meningeal vessels showed distinctly on the surface, the 
vessels over the hemisphere were distended. The right 
internal carotid was free until within two or three mm. 
of the penetration of the dura, and contained a flesh- 
colored, well organized thrombus. (Fig. 1). The fight 
posterior communicating artery was a mere filament 
while the left was much enlarged. The right anterior 
cerebral was very small; the left anterior cerebral, very 
large. To the right side of the chiasm and the begin- 
ning of the optic nerve, there was found a dense yellow 
mass surrounding the internal carotid and adherent to 
the oculo-motor and optic nerves; this mass fairly oblit- 
erated the Sylvian fissure in which it was lying. The 
left internal carotid contained a recently organized 
thrombus in the region from which the posterior com- 
municating and anterior and middle cerebral form ; this 
thrombus extended into the middle cerebral artery for 
about one half its length. The cerebellum, pons and 
medulla showed on section nothing abnormal. Upon 
section of the right hemisphere, the head of the caudate 
nucleus, the anterior extremity of the striate body and 
the lenticular nucleus were found to be softened. The 
material in this softened cavity was yellow and about 
the appearance of pus. Fig. 4. Section of right optic nerve, showing new fibrous forma- 
tion, round cell infiltration, and some degeneration of the nerve fibres. 
Fig. 5. Section of the left internal carotid artery, showing a re 
cently organized thrombus, and arteritis proliferate nodosa. I'lG. 6. Section of the right internal carotid artery, showing obli- 
terating endarteritis, thrombus formation, and subsequent caseation of the 
entire structure. 
Fig. 7. Section of the right posterior communicating artery. PHILADELPHIA XL! KOLOGICAL SOCIETY 
29 
Through the kindness of Dr. Mills, 1 obtained the 
above notes of the case from the Philadelphia Hospital 
Records, and also the specimen for microscopic study. 
The brain was hardened in Muller’s fluid, and the sec- 
tions were stained with haematoxylin and eosin ; haemat- 
oxylin, picric acid and fuchsin; and according to the 
Weigert-Pal method. As a result of the microscopical 
examination, I offer the following facts illustrated in the 
accompanying drawings and photographs. 
The oculo motor nerve of the left side shows in sec- 
tion the presence of scattered regions of small, round- 
celled infiltration, and some tendency to fibrous forma- 
tion. The small, round-celled infiltration follows the 
course particularly of the endoneurium, separating the 
nerve tracts into smaller bundles, and that of the blood 
vessels. The blood vessels themselves are dilated : their 
walls thickened and surrounded frequently by groups of 
these small cells. 
In one portion of the margin of the nerve nearest to 
the median line of the brain, there is some evidence of 
degeneration of the nerve fibres. Elsewhere the struc- 
ture proper of the nerve is normal ; the axis cylinders 
being distinct. 
The oculo motor nerve of the right side shows com 
plete degeneration and almost total disappearance of 
the nerve fibres. (Figs 2 and 3). Only the remnants of 
a few degenerated nerve fibres are seen, the nerve tissue 
being replaced by fibrous tissue which is, in turn, in 
various stages of caseation. The caseous remnants of a 
few minute blood-vessels can be detected. The position 
of the groups of partially degenerated nerve fibres is 
central and lateral. The epineurium is infiltrated with 
small, spheroidal, densely staining cells, and this forma- 
tion is continuous with the gummatous mass which sur- 
rounds the nerve. This gummatous structure consists 
partly of fibrous tissue which is very dense, and is infil- 
trated with small cells (similar to those seen in the 
epineurium), while other portions consist of more or less 
homogeneous substance without nuclei or cellular infil- 
tration. 
The left optic nerve exhibits changes similar to those 
affecting the left oculo motor. While there is present 
very little degeneration of the nerve fibres, the round- 
ceiled infiltration and fibrous formation are more evi- 
dent than in the other nerve. The epineurium, peri- 
neurium and endoneurium, even to the finest divisions 30 
PA'l HOLOCICAL SOCIETY 01 III I LA DELPHI A. 
of the latter are similarly affected. The round-celled 
infiltration follows also the minute arteries whose walls 
are thickened. 
The right optic nerve (Fig. 4) shows a greater extent 
and a more advanced stage of changes similar to those 
observed in the left. Particularly on the side of the 
nerve nearest to the gummatous mass (which invades 
this region of the brain), there is an interstitial infiltra- 
tion of small spheroidal cells. In places these have pro- 
gressed to spindle shape and fibrous formation. In some 
regions, especially on the side above referred to, there is 
in addition marked degeneration of the nerve fibres. 
There are present also scattered areas of degeneration 
in neighboring regions, but none so distinctly marked as 
those above described. 
The left internal carotid artery (Fig. 5) shows upon 
examination a recently organized thrombus, which fills 
up the whole lumen of the vessel. There are present 
evidences of arteritis proliferans nodosa, the adventitia, 
muscular coat and intima being much enlarged upon 
one side, while on the opposite side there is relative 
thinning of the walls which are, however, thicker than 
normal. The adventitia is extensively infiltrated by 
small spheroidal deeply staining cells, which are here 
and there collected into dense masses. In some places 
there is a tendency toward caseation ; this being shown 
by an indistinct staining of the nuclei; but the general 
tendency is not in this direction. The elastic lamina is 
intact. Evidences of obliterating endarteritis are shown 
by the increased thickness of the intima due to increase 
in size and number of the endothelial cells in addition 
to the spheroidal cells. 
In the right internal carotid artery (Fig. 6) are seen 
the conditions of obliterating endarteritis, thrombus 
formation and subsequent caseation of the entire struc- 
ture. The vessel-walls and the tissues in their im- 
mediate neighborhood are caseous for a considerable 
distance. The distinction of vessel-walls into adventitia, 
media and intima cannot be recognized, and there is no 
elastic lamina visible. In the periphery of the adventitia 
there is an invasion of small, deeply staining spheroidal 
cells on that side of the artery, which is nearest to the 
surrounding gummatous mass. This gummatous growth 
filling up the Sylvian fissure extends about half-way 
around the artery, and consists peripherally of dense 
granulation tissue ; of small round cells with more cen- Pig. 8. Section of the left posterior communicating artery. 
Pig. g. Section through the right Sylvian fissure, showing gum- 
matous formation and caseati' n, endarteritis and periarteritis, and in- 
volvement of the meninges and brain substance. hiG. io. Section through the right Sylvian fissure, showing changes 
similar to those in Fig. IX. 
biG. II. Section through the left Sylvian fissure, left carotid arterv, 
and optic chiasm, showing thrombus in left carotid arterv and minor 
grades of other changes seen in Figs. IX and X. PHILADELPHIA NEUROLOGICAL SOCIEI Y. 
trally located fibrous tissue, inhitrated here and there 
with spindle and round cells; the centre being a great 
mass of caseated tissue. The small cells are arranged in 
definite areas in some portions, but for the most part 
irregularly scattered. 
The right (Fig. 7) and left (Fig. 8) posterior com- 
municating arteries exhibit earlier stages, and minor 
degrees of changes similar to those affecting the carotid 
arteries. 
A section through the right Sylvian fissure and the 
gumma (Figs 9 and 10) of that region, scarcely permits 
of a distinction between brain cortex, meninges and ves- 
sels. Obliterating endarteritis and periarteritis have 
progressed in this region until the vessel and its throm- 
bus form the centre of a caseous gummatous mass, 
around which are regions of fibrous and granulation tis 
sue. There are numerous other foci of caseation of 
lesser extent alike surrounded by fibrous tissue, spindle 
and small round-celled infiltration. The portion for- 
merly meninges, is now a layer of densely packed small 
round cells, and partly spindle-celled and fibrous or 
caseous. The infiltration extends a varying distance into 
the cerebral cortex in places, there being no area of 
limitation between cortex and meninges. The blood- 
vessels of the cortex are dilated, the walls thickened and 
surrounded by the same small, round celled infiltration. 
A section through the left internal carotid and the 
optic chiasm (Fig. 11) reveals changes similar to, although 
less marked than those present upon the opposite side. 
The chiasm exhibits the already described disease of the 
support structures and some disease of the nerve ele- 
ments. The implication of the blood vessels is marked. 
The pons Varolii shows evidences of gummatous 
formation, with caseation in the region of the pyramidal 
tract of the right side. The vessels of the pia mater in 
this region are enlarged and surrounded by spheroidal 
cells; the walls of these vessels are much thickened. 
There is some degeneration of the fibres of the pyra- 
midal tract of the right side. In other respects the pons 
is normal. 
In conclusion, the leading clinical features of the case 
may be summarized as follows: right oculo motor paraly- 
sis; paresis of the left leg; mental symptoms (aphasia, 
irritability, stupor) and a long apoplectiform period with 
convulsions preceding death. Pathologically, the case 
illustrates most beautifully the multiplicity and divers- 
31 32 
PATHOLOGICAL SOCIETY OF PHILADELPHIA. 
ity, both in nature and distribution, of the lesions of 
cerebral syphilis. The multiplicity of the lesions is 
evident in the various involvements of the blood-vessels, 
meninges, nerves and brain substance. The diversity in 
the nature of the lesions is manifest, when we review in 
detail the arteritis proliferans nodosa, or again the 
arteritis obliterans simplex leading in places to multiple 
thromboses and localized softenings; the interstitial 
neuritis with degeneration of the nerve fibres, or the 
absolute syphilitic destruction of the nerve; the menin- 
geal implication progressing in places to simple round- 
cell infiltration or fibrous transformation and fusion with 
the brain substance, in others to caseation ; and the in- 
volvement of the minute vessels of the brain, which 
tissue is itself in places slightly implicated, again exten- 
sively so, as evidenced by softening, or loss of normal 
limitations and involvement in large gummatous forma- 
tions, as in the pons and Sylvian fissure. There is 
hardly a manifestation of syphilis, possible in the struc 
tures examined, that does not here find its exemplifica- 
tion. Press of RAFF & CO., 
512, 514 & 516 West 41st Street. 
NEW YORK.