Reprinted from The Journal of Nervous and Mental disease, Dec, 1888. 
A CASE OF ACUTE FATAL NEURITIS OF 
INFECTIOUS ORIGIN ; WITH POST- 
MORTEM EXAMINATION. 
By JAMES T. PUTNAM, M.D., 
OF BOSTON. 
The following case is one of generalized neuritis, of 
inflammatory and disseminated character, involving the 
nerves to a greater or less extent from their roots to their 
terminations, and associated with changes in the muscles 
on the one hand, and with alterations in the central axis on 
the other, which may have had a slight share in produc- 
ing the symptoms. 
Death occurred from asphyxia on the seventh day ; and 
at the autopsy, besides the signs of neuritis, the lungs were 
found crowded with small nodular haemorrhages, and the 
spleen enlarged. 
The patient was under the care of Dr. M. A. Morris, of 
Charlestown, who kindly asked me to see him in consulta- 
tion. This I did once only, and that at the beginning of 
his illness. 
The notes which Dr. Morris has kindly placed at my 
disposal, supplemented by my own, cover most of the 
essential points. I did not have conveniences for making 
an electrical examination, and was partly deterred by the 
agitated, restless state of the patient from investigating cer- 
tain symptoms as thoroughly as I ought to have done. 
At that time, however, while the diagnosis seemed clear, 
the fatal issue of the case was not anticipated. 
The patient was a man twenty-eight years of age, in good 
health in all respects, and free from constitutional disease 
of every kind. He was of a highly nervous temperament, 
and his father and mother are reported as having been also 
of nervous temperament, but otherwise well. The patient 2 
himself had been formerly laid up with what was called 
nervous prostration, but at the time of his illness was in his 
usual health. He did not use liquor to excess. 
On Friday evening, November 28th, 1886, he rode from 
Boston to his home in Charlestown on the front platform of 
a horse-car, in a heavy rain storm, and got thoroughly 
drenched. Before morning he awoke with pain in the left 
shoulder and across the back. 
On the following day he complained of a feeling of stiff- 
ness in his muscles all over the body ; his gait was weak 
and unsteady, and he felt a general sense of feebleness in 
all his movements. 
The next day he was only with difficulty able to stand or 
walk. In the evening of this day (the third of his illness), 
he was first seen by Dr. Morris, who found him complaining 
of pain, not only in the left shoulder, but also in the ante- 
rior muscular mass of both thighs and of numbness in the 
toes of both feet. He had also noticed that he had had no 
early-morning erection of the penis since his illness began, 
which had previously been habitual. 
I will here remark that the patient had been excessive 
in sexual intercourse,during his married life of several years 
duration, but not so for the period shortly preceding his ill- 
ness. 
There was no pain in the back, nor girdle sensation, nor 
any weakness of the sphincters ; the pupils were normal ; 
his gait was very unsteady, the legs tending to cross one 
over the other, so that he nearly fell to the floor ; the heart 
was beating regularly; temperature and respiration were 
normal; heart sounds normal. Dr. Morris ordered 5 grs. 
of sodium salicylate every two hours, for the relief of the 
pain. 
The next morning he found the patient perspiring freely, 
and without pain, except in the hip-joint when he rolled 
over in bed. He was unable to walk, falling forward on 
the floor when he attempted to do so. The numbness of 
the feet had increased, but there was no noticeable loss of 
sensation to ordinary tests ; there was pain on pressure over 
both sciatic nerves and also on deep pressure over both post. 3 
tibials. The pulse was 80, temperature normal, respiration 
20. 
On the 29th (the fourth day of his illness), the symptoms 
had still further increased, but were of the same character 
as before. The pulse was 80, temperature 990 F., respira- 
tion 20. The patient was feeling anxious and restless. 
On the following day the pulse and temperature were 
still nearly normal. The patient found it difficult to raise 
his legs from the bed, but could with some effort draw them 
up and push them down. 
On December 1st (the sixth day of his illness), the pulse 
was 84, temperature 99.30 F. The patient had been 
unable to draw the legs up since the previous night; he 
could not raise his left hand to his head, but could raise the 
right with moderate effort; the grasp of the left hand was 
much weaker than that of the right ; he could flex both 
arms ; the calves of both legs were tender to deep pressure ; 
there was some strangling on attempting to drink, and slight 
cough with expectoration of frothy mucous ; the patient was 
talkative and restless. 
On December 2d the pulse was 86, temperature 99.2° F. 
The patient had been delirious the night before and had 
not slept; he coughed and raised a great deal of frothy mu- 
cus ; coarse moist rales were heard over both upper fronts; 
there was complete paralysis of both legs ; pain on pres- 
sure over both facial nerves ; the conjunctive were con- 
gested ; he had a good deal of difficulty in swallowing 
fluids, but took, on the whole, a good deal of nourishment. 
During the afternoon of this day (the seventh of his ill- 
ness), the paralysis of the upper extremities increased nota- 
bly ; the cough and expectoration and the injection of the 
conjunctivae also increased ; swallowing became very diffi- 
cult. 
At about seven in the evening, while propped up in bed 
and taking some nourishment, he suddenly began to cough 
and strangle, and became insensible. His wife, who was 
feeding him, thought that a small bit of soft bread soaked 
in chocolate which he was trying to swallow might have 
entered his trachea. On Dr. Morris’ arrival, forty-five min- utes later, the pulse was found to be 120, quite strong and 
regular; respiration barely perceptible, slow and regular ; 
tongue swollen and discolored. There was no evidence 
that any foreign body had entered the trachea. He died 
half an hour later, to all appearance from paralysis of the 
respiratory functions. 
I saw the patient on the fourth day of his illness, and 
obtained essentially the same history as has been given. 
The sequence of symptoms was reported to be as fol- 
lows : 
On the night following the exposure, he had pains in 
thighs on motion, pain in the left shoulder and back, numb- 
ness of the toes of both feet. 
The next day he found it difficult to raise the left arm at 
the shoulder, and had weakness in walking. The day fol- 
lowing he began to have numbness in the fingers. At the 
time I saw him all motions were possible, but most of them 
very feeble. He could still raise the foot about six inches 
from the bed with the leg extended, but only by the aid of 
a sudden impulse. The movements of extension at the 
knee were fairly good. The muscles of the legs were flabby 
and the patient was unable to stand alone, but from weak- 
ness rather than loss of co-ordinating power, and closure of 
the eyes did not increase the difficulty. Deep pressure in 
the regions indicated was painful, but there was certainly no 
marked loss of sensibility to touch or pricking, though only 
rough tests were used, the patient’s restless condition not 
inviting to more critical investigation. 
In view of the paraesthesia, local tenderness, steady in- 
crease and wide-spread bilateral distribution of the muscular 
symptoms, and yet the absence of complete paralysis, the 
diagnosis of multiple neuritis seemed to be justified, but 
there was no indication at the time of my visit of paralysis 
of the heart or lungs. 
The autopsy was made on the day after death, Decem- 
ber 3d, by Dr. R. H. Fitz, who has kindly given me the 
following notes : 
“ Right side of heart distended with liquid blood ; both 
lungs injected and moderately cedematous ; punctate ecchy- 
4 5 
moses throughout the lungs in every part; spleen enlarged 
to nearly three times the normal size, soft, injected ; liver 
and kidneys deeply injected ; nothing abnormal in the 
appearance of the brain or spinal cord. 
“ Pathological diagnosis ; nodular, pulmonary haemor- 
rhages ; acute splenic hyperplasia.” 
A portion of the anterior §rural, the iliolumbar, and vagus 
nerves, and part of the left axillary plexus, a portion of the 
diaphragm with filaments of the phrenic, part of the deltoid 
muscle, and a piece of one lung, were removed for subsequent 
examination. 
It is to be regretted that these nerves and others were 
not removed in their whole length, especially in view of the 
fact that in the closely similar case reported by Rosenheim, 
which came to my notice within a few days after this exam- 
ination, localized haemorrhages were here and there found 
in the course of the nerves. 
The appearances, however, in such portions as were re- 
moved, leave no doubt as to the general character of the 
process. 
The nerves were examined both fresh, in osmic acid, and 
after hardening in Muller’s fluid. The same pathological 
appearances, though varying greatly in degree, were found 
in all ; but the best specimens were obtained from the axil- 
lary plexus and the anterior crural, and the description will 
therefore be based mainly upon these, so far as the exam- 
ination of the hardened specimens is concerned. 
The vagus nerve was not examined after hardening. In 
the fresh state the most marked appearance was a strikingly 
beaded arrangement of the myeline, due to an accentuation 
of the markings of Schmidt. I should hesitate to regard 
this as certainly pathological, were it not that it occurred in 
connection with further changes. 
The myeline was eaten out near the annular constrictions 
of Ranvier, but this may have been a purely passive, post- 
mortem change (v. below). Here and there the myeline 
was swelled and had wholly lost its characteristic markings, 
and in spots there was an infiltration of cells such as will be 
described further on. 6 
Of the phrenic, only a few terminal filaments could be 
examined, and these looked perfectly healthy. Had a more 
extensive examination been practicable, changes would 
doubtless have been found, because a certain proportion of 
the muscular fibres of the diaphragm had wholly lost their 
transverse striation, and looked lustreless and granular. 
The osmic acid appearances in the other nerves were of 
the usual kind, but the larger number of the fibres exam- 
ned looked fairly healthy. 
Sections of the anterior crural nerve, obtained after 
hardening and stained with carmine, showed under a low 
power a streaked or mottled appearance, as if a number of 
nerve tubes here and there had been blotted out and a new 
formed substance, taking the carmine stain, had taken their 
place. When the sections were examined with higher 
powers, the outlines of nerve fibres were seen more or less 
altered in the affected parts ; yet, nevertheless, the spots 
seemed of a uniform red color. 
The axis cylinders in many of the nerve bundles were 
to all appearance normal, or nearly so, except in the spots 
above described ; but in some bundles, on the other hand, 
the same series of striking changes had taken place, which 
will be described more at length in connection with the ax- 
illary plexus. 
Here and there were foci of cell formation or infiltration, 
but on the whole the changes were less marked than in the 
left axillary plexus. 
The lesions met with in the axillary plexus were of the 
following character: 
i. Infiltration of small round cells with granular con- 
tents, together with an admixture of cells of other kinds, 
especially a number having a nucleus of about the size 
of a leucocyte, and granular contents, but with a distinct 
body of a pale, homogeneous protoplasm, giving to the 
whole cell a spherical or oblong shape. 
These were by far the most numerous toward the periph- 
ery of the nerve bundles, and especially between the sheath 
and the fibre, and next, around the blood vessels, where 
they often formed a well-marked ring, spreading thence 7 
outward among the nerve fibres. They were also met with, 
however, remote from either sheath or vessels, following 
the course of the nerve fibres themselve ; so much so, that I 
have some preparations of isolated fibres surrounded, at a 
part of their course, by quite a mass of these cells. Some- 
times they were collected into columns which lay between 
and parallel to the nerve fibres. 
I was not able to make out that any of these cells 
lay actually inside the nerve sheath, except possibly in one 
or two instances ; nor did the nuclei of the nerve fibres ap- 
pear to be increased in number. Some of the cells were 
evidently in process of multiplication, the nucleus being 
divided by a sharp line into two parts. Of these I saw 
perhaps, three or four well-marked instances. 
The degree of this cell-infiltration varied greatly in dif- 
erent sections from the same nerve. 
Besides the cells described, there were numerous spindle- 
shaped cells belonging to the connective tissue, whether 
increased in number or not, I am not prepared to say, and 
also here and there larger granular masses which may have 
been protoplasmic with particles of myeline, or may have 
been simply altered masses of myeline. 
There were also large and highly granular cells, with a 
large nucleus and irregular, oftentimes flattened border, 
which I took to be endothelial cells, normal or more or less 
altered. 
I searched for so-called “ Mast-zellen” with various ani 
line colors, as indicated by Rosenheim, but succeeded in 
finding only one or two that seemed to be characteristic. 
2. The next most striking change affected the axis- 
cylinders, which were in some places greatly enlarged, in 
others more or less atrophied, in other, again, entirely 
destroyed. 
The distribution of these changes was largely by nerve 
bundles ; that, is, one bundle might show nearly normal 
axis-cylinders, while in the next bundle they were greatly 
altered. In some sections there were whole (secondary) 
nerve bundles, in which scarcely a single axis-cylinder was 
to be seen ; in others all the different changes were repre- 8 
sented, showing that the swelling, atrophy, and disappear- 
ance were parts of the same process of destruction. 
The changes were also much greater in some strands of 
the axillary plexus than in others. 
PLATE I. 
Section from axillary plexus, illustrating the alteration and destruction of axis-cylinders. 
Some of these swelled axis-cylinders occupied the entire 
thickness of the nerve tube, and even the nerve tube itself 
seemed sometimes to be distended. In other cases, the sec- 
tions of the swelled axis-cylinders appeared not round but 
crescentic, occupying half or two-thirds of a nerve tube. 
In order to study more closely the position and character 
of these changes in the axis-cylinder, I made a series of 
longitudinal sections, and also of isolated nerve-fibre prep- 
arations. Through these it became evident that the swell- 
ing occurred here and there in the course of the fibre, and 
that its most common position was at or near the “annular 
constrictions ” of Ranvier (or “connecting disk”of Schieffer- 
decker). 9 
In some cases it was obvious what had taken place. 
The axis-cylinder had become swelled into a bulbous en- 
enlargement, and this had finally burst on one side, leaving 
half of the shell to give rise to the crescentic sections. In 
Nerve fibres with alterations in the axis-cylinders near the constrictions of Ran vier. Hart- 
nack Immersion, one-tenth. 
PLATE II. 
other cases the appearance suggested more or less liquefac- 
tion of the altered axis-cylinder (perhaps the myeline as 
well); for the disk at the annular constriction and the ad- 10 
joining walls of the nerve tube seemed to be, as it were, 
plastered with a substance coloring strongly with carmine, 
and evidently formed of the products of degeneration. It is 
interesting to observe that, as a rule at any rate, the disk 
had not been broken through, but remained clear and dis- 
tinct, although, as is shown by the experiments of Boll, 
Hesse, and Schiefferdeckcr,1 on the action of water and other 
substances upon the fresh nerve, the osmotic or capillary 
current setting through the nerve fibre is quite competent 
to break down the connecting disk. 
It is worthy of note that these changes of the axis-cylin- 
der, though almost always near the connecting disk, are not 
always most marked exactly at that point, but often at a 
little distance back. 
The question arises, Were these changes which have 
just been described wholly or in part post-mortem in char- 
acter? In one sense I think this question can be confidently 
answered in the affirmative. That is to say, it is highly 
probable that the swelling, etc., occurred after the death of 
the particular nerve fibre ; but, on the other hand, it is 
equally probable that they did not occur in the process of 
the hardening of the preparation. My reason for that con- 
clusion is, although the same kind of change—that is, swell- 
ing and vacuolization—is said sometimes to take place to a 
certain degree during the hardening of healthy nerves in 
solutions of chromic salts, yet I have never seen nor read 
of any change approaching to this in degree, from that 
cause. 
On the other hand, Schiefferdecker describes, as the re- 
sult of the treatment of fresh nerves with water and dilute 
acids, a localized swelling of the axis-cylinder, and even- 
tually bursting of the relatively fluid contents through its 
envelope, which seems to be quite analagous to that which 
has here taken place. 
It is probable that the swelling observed in such cases as 
this, is of similar origin with that seen in acute inflammation 
and acute anaemia of the spinal cord. 
1 Arch f. Microsc. Anat., 1887, Bd. xxx., 435. 11 
The character and position of the myeline sheath were 
also of interest. 
In some of the cross-sections, stained with picro-carmine, 
the nerve tubes could be seen to be still filled with the re- 
mains of myeline, even though no axis-cylinders were vis- 
ible. At times the myeline seemed to have been changed, 
so that it took up the coloring matter of the carmine to 
some extent, and it was doubtless in part to this change 
that the mottled appearance of the cross-sections was due. 
Here and there a tube would be entirely empty of myel- 
ine for a considerable distance, both in those cases where 
the axis-cylinders were preserved and in those where they 
had been destroyed. This may have been partly due to 
mechanical violence, or to changes during hardening, but it 
seems hardly possible that it should be entirely accounted 
for in this way. 
The myeline at the annular constriction was, in the 
bichromate of potash preparations,almost always absent for a 
certain distance, and this, also, was partly coincident with 
the alteration in the axis-cylinder at that point, and partly 
independent of the latter change, occurring in some places 
where the axis-cylinder ran through the constrictions, as it 
sometimes did, uninterruptedly and with clear and parallel 
outlines. So marked was the displacement of myeline at 
these points that some of the longitudinal sections seemed 
to be dotted over, under a low power, with vacuole-like 
spaces. 
It will be remembered that Neumann, in his classical 
paper upon nerve degeneration, points out that the neigh- 
borhood of the annular constriction was one of the places 
where the degenerative changes in the myeline were earli- 
est observed. 
Dr. Webber, of Boston, has noted the same fact in some 
unpublished experiments of his own. 
To a certain extent the changes in the myeline at the 
annular constrictions are probably of post-mortem origin. 
It is well known that Ranvier long ago pointed out that 
when nerves were exposed to the action of water and other 
fluids for an hour or so after death, the myeline on either 12 
side of the connecting disk would be found rarified and ap- 
parently eaten away, and that he considered this change to 
be an evidence of the fact that nutritive fluids probably 
enter the nerve at these points. 
Schiefferdecker, in the interesting paper above alluded 
to, while expressing his agreement with Ranvier as to the 
fact that coloring matters, and probably nutritive fluids, 
find their way into the axis-cylinders at these points, does 
not admit that the myeline is dissolved out by these fluids 
as Ranvier suggested, but considers that it is displaced by 
the slight mechanical violence in removing the nerve from 
the body, or of putting it slightly on the stretch, as Ranvier 
was in the habit of doing as a preliminary to the immersion 
in osmic acid. 
The reason that the displacement of the myeline took 
place at these particular points is believed by Schieffer- 
decker to be because the delicate membranous sheath of the 
nerve, which follows the outline of the fibre and dips down 
into the narrow portion at the annular constrictions, exerts 
a lateral pressure where the angle occurs, when it is put 
upon the stretch. 
In other words, the stretched membranous sheath tends 
to assume the form of a cylinder, the end of which is as 
large as the connecting disk, but not larger. Consequently, 
that part of the myeline which occupied the neighborhood 
of the tapering end of the cylinder is compressed and dis- 
placed. 
This explanation entirely concurred with the results of 
some experiments which I had been making, and which will 
be given elsewhere in detail. 
In order to test the point further, I made a number of 
careful observations upon the nerves of a frog, stretching 
some of them with a weight of three grammes, and leaving 
others unstretched. 
The results of the experiments were such as to entirely 
confirm the view taken by Schiefferdecker. 
The unstretched nerves, if removed with care, did not 
show these changes in the relation of the myeline to the 
connecting disks, either after one hour’s immersion in water 13 
or other fluids, or on exposure to the fluids of the body after 
■death for twenty-four hours ; whereas the nerves stretched 
with a weight of three grammes showed the changes very 
•clearly, as Ranvier described them. 
Occasionally, even in the unstretched nerve, a fibre is 
seen in which these changes are observed, but not with 
sufficient frequence, I think, to invalidate the explanation 
offered. I believe that there is also reason to think that the 
putrefactive changes which go on during the twenty-four 
hours or so after death may make this change occur more 
rapidly, but this point is still under investigation. 
The nerves in the present case were not exposed to any 
special stretching other than was necessary in their removal, 
.and it is therefore probable that the results were partly the 
effect of pathological change, and only in part of mechani- 
cal violence. 
I have, however, seen a similar change, though not 
nearly to the same extent, in a healthy nerve removed from 
the body at an autopsy and treated with the same reagents 
that were used in this case. 
One other point should be mentioned in this connection, 
namely, that the membranous sheath in the neighborhood 
•of the connecting disk, as seen in the hardened specimens, 
looked as if it had been exposed to pressure from within, 
making it bulge slightly outward. I have no explanation to 
offer of the exact manner in which this effect was brought 
about; but this influence, whatever it may have been (pos- 
sibly the result of decomposition), may have had its share 
in the displacement and destruction of the myeline as well. 
Changes in the Deltoid Muscles and Diaph ragm.—Pieces 
of the deltoid muscle were examined, both in a fresh state, 
with and without osmic acid, and after hardening in Muller’s 
fluid. In the fresh specimens the only change observed was 
that now and then a fibre was seen that had entirely lost its 
transverse striation, the rest of the fibres being apparently 
perfectly healthy. The examination of the hardened speci- 
mens was more fruitful. The cross-sections showed the 
size of the fibres to be uniform and normal. There was no 
trace of the vacuolization or so-called serous atrophy, and 14 
apparently no deposition of fat either within or between the 
muscular fibres. 
The morbid changes were the following : 
First, loss of transverse striation, limited in 
sometimes occupying only a small part of a fibre, the ap- 
pearance presented being that of fine granulation, some- 
times with traces of transverse striation here and there in 
the midst of the altered substance. 
Second, marked infiltration of cells in the connective 
tissue and around the vessels. 
Third, a localized increase in number of the muscle- 
nuclei, which sometimes, but not always, appeared to be 
more marked at the place where the transverse striation was 
wanting. 
Fourth, the intra-muscular nerves, as far as could be 
judged from the few which appeared in the sections, were 
almost entirely destroyed. 
Out of the whole number of fibres making up a small 
nerve bundle, one or two atrophied axis-cylinders might be 
seen, as dark, shining points, in picro-carmine sections, the 
rest of the bundles being represented by altered fragments 
of myeline with numerous granular round cells lying amongst 
them. 
Fragments of the diaphragm were examined, fresh and 
with osmic acid, and granular fibres without transverse stri- 
ation were here and there noted. 
Of the central nerve system, the medulla and spinal cord 
were examined. The brain was preserved, but has not 
been examined. 
In the medulla and spinal cord the following changes were 
observed: First, in the membranes and in many of the 
nerve roots, both anterior and posterior, there was an infil- 
tration of round cells both around the vessels and amongst 
the fibres, and in other respects the nerve roots were more 
or less changed, the degree of alteration being less than in 
the peripheral nerves. 
This infiltration was rather greater in the lower dorsal 
region of the cord than in the lumbar or cervical region, or 
most parts of the medulla. 15 
The blood vessels, both of the membranes and of the 
central axis, were everywhere crowded with blood. This I 
take to have been, in part, the result of the asphyxia with 
which the patient died ; in part the sign of an inflammatory 
process. 
Within the substance of the cord the vessels were sur- 
rounded here and there with a moderate number of cells 
contained in the peri-vascular sheath, and the central canal 
was filled with similar cells. 
The nerve cells, so far as I could judge, were essentially 
normal. Here and there was one with a shrunken or other- 
wise altered nucleus; but there was nothing, in my opinion, 
that might not be accounted for by post-mortem changes. 
The only other pathological appearance in the cord was 
that here and there at the periphery, especially in the lat- 
eral column near the post, cornua, and in the ant. column 
in the nerve root zone, greatly enlarged axis-cylinders 
staining feebly with carmine. 
The condition of the medulla was carefully examined, in 
the hope of finding a satisfactory cause for the multiple 
pulmonary haemorrhages. There was a general filling of 
the vessels, large and small, and here and there an accumula- 
tion of lymphoid cells in the peri-vascular sheaths, and 
occasional slight haemorrhages from the capillaries and 
smaller vessels. 
These disturbances of circulation were, in most of my 
sections, more marked in and near the sensory nucleus of 
the vagus and glossopharyngeus than elsewhere, and the 
haemorrhages were in fact only seen in this neighborhood. 
It could not be asserted, however, that the nucleus appeared 
to have been materially injured. 
The vagus nerve roots were affected in varying degrees, 
and one section, shows a more excessive infiltration than 
perhaps any other nerve root that I have seen. 
It is easy to arrange this case in its proper pathological 
position up to a certain point. It evidently belongs with 
such cases as were reported by Eichhorst in Virchow’s 
Arch., vol. 69, 1876, and Rosenheim in the Arch. f. Psych., 
vol. 18, which the latter has discussed so ably; and with the other acute, fatal cases of multiple neuritis, none 
of which, I think, have been of shorter duration than this. 
In Rosenheim’s and Eichhorst’s cases, to be sure, haem- 
orrhoids existed in the nerves, visible to the naked eye, in- 
dicating a more intensely active process than here. On the 
other hand, nothing could be more intense than the con- 
gestion in this case ; and the evidences of minute haemor- 
rhages and cellular infiltration were more extensively present 
than in most of the other cases, involving the muscles, 
spinal roots, membranes, and even the central nervous axis 
to a certain extent, as well as the nerves. 
It would be interesting to know whether, if the patient 
had not died, the spinal changes would have assumed a 
greater prominence, and a poliomyelitis or a diffuse myelitis 
have developed itself. 
Certainly the topography of the lesions suggests this 
possibility ; but it is to be noted, as regards the question of 
poliomyelitis, that the posterior nerve roots were quite as 
much affected as the anterior. The fact that the changes 
in the white columns (enlargement of axis cylinders) were 
mainly confined to the periphery, and more marked in the 
neighborhood of the nerve roots than elsewhere, but they 
did not seem to occur in the posterior columns. The 
amount of accumulation of lymphoid cells in the peri-vascu- 
lar sheaths of the central gray matter was perhaps not great 
enough to count as the first step in an inflammatory pro- 
cess, though it may have been of that character; but, 
to say the least, one can hardly doubt that it would have 
taken little more to precipitate such an event, especially in 
view of the fact that in the medulla minute haemorrhages 
had actually occurred. 
The questions of chief importance in connection with 
this case are : first, as to its etiology, and especially if we 
can gain through it any light upon the supposed toxic origin 
of generalized neuritis ; next, as to whether these acute, 
fatal cases exhibit clinical features which will enable us to 
detect them at their onset. 
With regard to the first point, the reasoning, as clearly 
expressed by Rosenheim, and endorsed by Leyden in his 
16 17 
recent address before the Militar-artzliche Gesellschaft of 
Berlin, is that the great majority of these cases are truly of 
toxic origin, the source of the poison being the bacteria of 
tuberculosis or other constitutional disease, or some mineral 
or other poison. The bacteria are, however, not supposed 
to themselves be present in the nerve, but only the poison- 
ous substances to which their growth gives rise. 
In this way the distinctly infectious cases are brought 
into a parallel with the cases due to metallic poisoning. 
Strumpell, moreover, in a recent paper upon degener- 
ative changes in the spinal cord, although not speaking 
especially of neuritis, suggests another method in which 
these processes of poisoning may be started or propagated, 
namely, through the action of the products of decomposi- 
tion of the nervous tissues themselves. Dr. Spitzka sug- 
gested last year a similar cause for the outbreak of delirium 
grave. 
In Rosenheim’s case it was believed that the primary 
source of the infection was tuberculosis, with which the 
patient was affected, although at the time of his attack in 
good nutrition ; and he further remarks that, in his opinion, 
scarcely a case of multiple neuritis has been observed in 
which no infectious constitutional disease was present. With 
this view I cannot wholly agree ; nor is it maintained, so 
far as I can see, by Leyden, who himself reports the onset 
in one of his rapidly fatal cases as being apparently due 
solely to a condition of exposure and fatigue. 
In my case the patient was not the subject of any con- 
tagious disease, so far as could be ascertained, and the 
wetting to which he was exposed was the only cause which 
could be discovered. Nevertheless, the pathological signs 
of infection are even stronger in my case than in Rosen- 
heim’s and others. In them those signs consisted almost 
solely in the acute onset and generalized character of the 
disease, together with the fact that haemorrhages were 
present in the nerves. In my case, a marked hyperplassia 
of the spleen was also present, such as has been observed 
in several cases of Laudry’s disease, but not often and never 
to this extent, so far as I know, in cases of multiple neu- 18 
ritis. In Rosenheim’s case the spleen was reported as 
measuring twelve centimeters in length, and being soft in 
consistency. 
To what cause to attribute the multiple and nodular 
haemorrhages scattered through both lungs, in the present 
case, I am unable to decide. In view of the absence of 
haemorrhages in other regions of the body it would be 
hardly probable that those were due to the local action of 
the toxic agent, although this is not to be set aside. It 
seems more probable that they were of the same origin 
with the multiple haemorrhages described originally by 
Brown-Sequard as due to certain injuries of the medulla, 
and probably of vaso-motor origin. It is possible that the 
neuritis of the vagus nerve may have given rise to them, 
although, so far as I know, such a result has not previously 
been demonstrated. 
It is noteworthy that in this, as in the other important 
cases of similar kind, the toxic agent, whatever its char- 
acter, has not given sign of its presence in a diffuse way, 
but only here and there in foci of limited extent. This is 
very likely due to the fact that the means of examination 
at our command do not enable us to detect the first signs 
of toxic influence. Even if we had any such evidence as 
that afforded by the examination in Laudry’s disease, which 
seems to be universally considered as most probably of 
infectious origin, to show that loss of function may precede 
noticeable alteration in structure, yet we should still, from 
abundance of facts, be ready to consider that this was 
possible. 
The fact that such a large proportion of the nerve fibres 
in the affected districts preserved a healthy appearance 
cannot be taken as a proof that they were performing their 
functions in a normal manner. 
It would not be out of place, before leaving the subject 
of infection and its possible sources, to refer to the group 
of symptoms characterized as a new infectious disease and 
described recently by Weil and others in the Deutches 
Arch. f. Klin. Med., 1887, 1888. 
Taken as a whole, this is not to be confounded for a 19 
moment with neuritis, the high temperature and the jaun- 
dice characterizing it as belonging in a different category. 
It is, however, noticeable that in seVeral of the cases, 
severe muscular pain and other signs of alteration of the 
peripheral nervous system were present. 
As regards the clinical aspects of the case, I would only 
mention one or two points. 
In the first place, the absence of fever throughout the 
sickness is noteworthy. This was also noted in Rosen- 
heim’s case, and referred to by him as being sometimes 
present and sometimes absent in the other cases that he 
describes. 
The mode of death seems to have been by respir- 
atory, rather than cardiac paralysis. At any rate, the res- 
piratory symptoms were the striking ones, and although 
shortly before death the pulse had risen to 120, it is reported 
by Dr. Morris as having been full and regular, while the 
respiration was scarcely perceptible. 
The distribution of the muscular symptoms deserves a 
moment’s comment. Pierson has advanced the opinion 
that the paralysis of the cranial nerves is characteristic of 
the acute cases. This, however, is not endorsed by Rosen- 
heim, who points out, very properly, that these paralyses 
are seen also in chronic cases, and not necessarily in acute 
cases only, although when present they indicate a wide 
generalization of the disease, and may be of bad import. 
In the present case, the signs of paralysis of the cranial 
nerves which was noticed, consisted in the difficulty in swal- 
lowing and the tenderness over both facial nerves. 
The fact that the left shoulder muscles were so early 
and so severely affected was to me of special interest, 
because I have been recently collecting cases in order to 
test the diagnostic value of this distribution of symptoms. 
There seems to be no doubt that although the extremities 
are usually the first to be involved, in the multiple neu- 
ritis of every cause, yet the larger muscles uniting the 
limbs and trunk are sometimes affected very early. 
Finally, I would call attention to a point which should, 
perhaps, have guided us to the recognition of the serious 20 
import of the case, which was early presented, namely, the 
restless, anxious and agitated mental condition of the 
patient, which seemed at first to the 
severity of his symptoms. 
Notes.—I. Valuable remarks relative to the significance of this acute swell- 
ing of the axis-cylinder, may be found in the Arch. f. Psychiatric, etc., 1887, p. 
263, (Auhang), Zur activen Verand, der Axen-cyl., bei Entzundungen, Dr. M. 
Friedmann; and Bd. XCVI. der Sitzb.der Kais. Akad. der Wissensch. III. Abth. 
Nov. Heft. 1887, Ueb. die Verand. am Ruckenmark n. Zeitweiser Verschliessung 
der Banchaorta. J. Singer (Reprint, p. 12). 
2. Otto Dees, (Arch, fur Psych., etc., 1888, p. 97), the latest writer on the 
anatomy and physiology of the vagus nuclei, mentions, incidentally as his opinion 
that the large “ dorsal ” nucleus is vaso-motor in function. It cannot, unfor- 
tunately, be stated, whether in the present case the fibres and ganglia of the sym- 
pathetic system were healthy or diseased.