THE PATHOLOGY OF 
ACUTE ASCENDING (LANDRY'S) 
PARALYSIS 
HENRY HUN, M. D., 
BY 
PROFESSOR. OF DISEASES OF THE CHEST AND NERVOUS SYSTEM 
IN THE ALBANY MEDICAL COLLEGE 
REPRINTED FROM 
THE NEW YORK MEDICAL JOURNAL 
FOR MAY 30, 1891 
NEW YORK 
D. APPLETON AND COMPANY 
1891 THE PATHOLOGY OF 
ACUTE ASCENDING (LANDRY'S) 
PARALYSIS 
HENRY HUN, M. D., 
BY 
PROFESSOR OF DISEASES OF THE CHEST AND NERVOUS SYSTEM 
IN THE ALBANY MEDICAL COLLEGE 
REPRINTED FROM 
THE NEW YORK MEDICAL JOURNAL 
EOR MA Y 30, 1891 
NEW YORK 
D. APPLETON AND COMPANY 
1891 Copybight, 1891, 
By D. APPLETON AND COMPANY. THE PATHOLOGY OF 
ACUTE ASCENDING (LANDRY'S) PARALYSIS* 
The following case of Landry's paralysis which 1 have 
recently observed seems to me not unworthy of publication, 
especially at this time when the attempt is being made on 
many sides to class this disease as one of the forms of mul- 
tiple neuritis: 
G. C., aged forty-five years, a salesman, unmarried, entered 
the Albany Hospital on April 18, 1890. His family history was 
good, and he, with the exception of a gonorrhoea contracted at 
the age of twenty-six years, had always enjoyed good health, 
and in especial he had never had either syphilis or rheumatism. 
In the winter of 1886, while skating on roller skates, he fell and 
struck his sacrum against the edge of a bench, in consequence 
of which fall he felt some soreness and stiffness in his back, 
which passed off entirely in a week, and which did not at any 
time interfere with his ordinary duties. About four months 
after this fall he felt a sudden "lightness" in the left leg, and a 
feeling as if there was a tight band about the left ankle, which 
feeling of constriction about the ankle has persisted up to the 
present time. He has had some slight pain in both legs, espe- 
cially in the left, at various times, always worse before a storm ; 
but these pains have troubled him but very little during the 
past year. In January, 1890, he had what his physicians called 
an attack of "plastic iritis" of the right eye, and since that 
time the sight in that eye has been somewhat impaired. Of 
late he has felt some stiffness in his legs and has taken walks of 
several miles daily "to limber himself up." About one week 
ago (April 11th) walking became difficult, and he felt " as if he 
was dragging weights on his feet." At this time he was ex- 
* Read before the New York Neurological Society, April 7, 1891. 4 
THE PATHOLOGY OF 
amined by Dr. H. Lyle Smith, of Hudson, who found a weak- 
ness of the muscles of the legs and diminished knee-jerks, and 
who prescribed fluid extract of ergot. The patient continued 
at work, although his walking gradually became worse, until 
the 15th of April, when he was obliged to go to bed, having 
lost completely the power of the muscles of his legs below the 
hips. At the same time he noticed a slight weakness of his 
hands and arms, and a difficulty in speech (during the past 
month he had noticed that his voice was somewhat husky and 
that mucus was excreted in excess). Since he has been con- 
fined to his bed it has been necessary to draw off bis urine with 
a catheter, and his bowels have been constipated. The muscles 
of bis body have become paralyzed so that he has been unable 
to sit up in bed. His arms have grown weaker, his voice has 
become more husky, and deglutition has grown difficult. His 
appetite has been good, and he has suffered no pain. 
Physical Examination.-Well nourished. Ptosis of right 
eyelid, which he says is voluntary and due to impairment of 
vision. This impairment of vision seems to consist of diplopia, 
one object being to the right of and lower than the other. De- 
cided paralysis of lower branch of left facial nerve. Tongue 
protruded straight, no tremor of tongue or lips, and no mus- 
cular atrophy or fibrillary contraction. Breath very offensive 
and tongue covered with a white coat. He can whistle with 
difficulty. Speech thick and indistinct. Deglutition so difficult 
that he has to be fed with a stomach tube. Mucus collects in 
the trachea and patient can eject it only imperfectly. Hearing, 
smell, and taste are normal. Grasp of left hand null. Grasp of 
right hand very feeble. Flexors and extensors of upper arm 
very feeble, but more powerful than those of forearm. Muscles 
of shoulder feeble, but more powerful than those of arm. Mus- 
cles of body paralyzed so that be can neither sit up nor move 
in bed. Absolute motor paralysis of both legs and thighs. Ab- 
sence of plantar, cremasteric, umbilical, and patellar reflexes. 
No muscular tenderness, fibrillary contraction, nor atrophy. No 
disturbance of sensibility to tactile (tested with pin-head and 
cotton), thermic, or painful impressions anywhere. No re- 
tardation of conduction of pain. Bladder and rectum inactive. 
Urine drawn off with catheter and bowels moved by injection. 
Temperature and pulse normal. His treatment consisted in a 
drachm of iodide of potassium and half a drachm of salicylate 
of sodium daily. 
April 20lh.-Patient is growing weaker. He has more diffi- 
culty in expelling phlegm by coughing and his speech is becom- 
ing more difficult. Temperature norma], pulse 85. 
22d.-Growing weaker. The left-sided facial paralysis con- ACUTE ASCENDING PARALYSIS. 
5 
tinues unchanged, and, in trying to cough, the muscles connected 
with the larynx and jaw on the right side of the neck can be 
seen to contract decidedly, while those on the left side remain 
passive. To-day the muscles of both arms are much weaker, 
and those of the right arm and shoulder are weaker than those 
of the left, so that he can scarcely move the right arm at all. 
The muscles of the legs continue absolutely paralyzed. There 
is nowhere any muscular atrophy, tremor, or disturbance of any 
kind of sensibility, and there is no muscular tenderness. All 
the muscles of both legs respond decidedly and quickly to the 
chloride-of-silver faradaic battery (the roll being shoved into 
between the marks 60 and 70). Tne difficulty of speech and of 
respiration is so great that it does not seem possible that he can 
live twenty-four hours; the coarse mucous rales in the trachea 
can be constantly heard. 
23d.-At 11.30 a. m. he seemed better than yesterday. 
The symptoms remained without change, except that his voice 
seemed somewhat stronger, although still very indistinct, but 
at 12 m. he began to fail rapidly. He first became deaf ; about 
half an hour later he became entirely blind, a quarter of an 
hour later he became comatose, and about a quarter of an hour 
later, his respirations having become steadily slower and more 
difficult, and being only three to five a minute, he died, the 
pulse being of fair quality, although rapid, almost to the mo- 
ment of death, and continuing after the respiration bad ceased. 
Autopsy, held Eight Hours after Death.-Thorax and abdo- 
men not examined. Post mortem rigidity slightly marked. 
Spinal cord seemed normal, except that the lumbar portion 
seemed to be slightly cedematous, and the outlines of the gray 
matter in this region a little less clear than normal. Brain 
seemed normal, except for a somewhat increased amount of 
subarachnoid fluid over both parietal regions. At junction of 
ascending and horizontal arm of left fissure of Sylvius was a 
patch of white thickened cicatricial pia mater (as large as a 
silver quarter of a dollar) adherent to the cerebral cortex; the 
convolution at this point seemed atrophied. About an inch 
above this point on the anterior central convolution was a small 
piece of bone, about a half by a quarter of an inch, firmly 
adherent to the pia mater. The corresponding portion of the 
dura mater was fenestrated, and the bone of the skull at this 
point was roughened and presented several deep boles filled 
with fresh blood exuding from the veins in the bone. The arte- 
ries at the base of the brain were not atheromatous, and the 
ventricles of the brain were not dilated. The nervous organs 
were placed in Muller's fluid, which was changed once after 
about three hours, and then sent immediately to Dr. Van Gieson 6 
THE PATHOLOGY OF 
for examination. His examination was so very thorough that 
I may be pardoned in presenting it at length. 
Microscopical Examination.-The brain, spinal cord, and 
peripheral nerves were hardened in a two-per-cent, solution of 
bichromate of potassium for six weeks, and subsequently in 
eighty per cent, alcohol, and finally in strong alcohol. The sec- 
tions were stained doubly by hsematoxylin and picro-acid fuch- 
sin, and by Weigert's method. 
The cerebral pia mater contains in its meshes a moderate 
accumulation of small round and cuboidal cells which appear to 
be derived partly from the connective-tissue cells of the pia 
mater and partly by emigration from the blood-vessels. This 
condition of the pia mater is quite uniform over the whole con- 
vexity of the brain, and is not more extensive over the motor 
zone than elsewhere. 
The Cerebral Cortex.-Sections from the paracentral lobule, 
from the middle of the precentral and postcentral convolutions 
of both sides, and from the lower junction of the central convo- 
lutions on the left side show nothing abnormal about the struct- 
ure or arrangement of the elements of the cortex. The large 
multipolar ganglion cells in the paracentral lobule and the prse- 
central convolution are unchanged. They are not present in 
the post-central convolution. The blood-vessels of the cortex 
are normal. Sections of the basal ganglia show nothing ab- 
normal. 
The crus, pons, and medulla are normal. The nuclei of the 
third, fifth, sixth, seventh, tenth, eleventh, and twelfth nerves 
were examined in detail for changes in the motor ganglion cells, 
but the latter are not changed in structure or deficient in 
number. 
The spinal cord was divided into thirty-one segments, cor- 
responding to the insertions of the nerve roots, and sections 
from each of these segments were thoroughly examined by 
Weigert's method, and with double staining by haematoxylin 
and picro-acid fuchsin. There are no changes in the substance 
of the spinal cord, except some slight alterations in the ganglion 
cells of the anterior horns. Some of the ganglion cells stain 
faintly, have a vitreous, homogeneous appearance, and appear to 
be swollen; but these changes in the ganglion cells are so 
slight, and affect so few of them in such an irregular way, that 
the alterations in the ganglion cells may be ascribed to the bi- 
chromate hardening, which does not preserve the ganglion cells 
perfectly. 
To eliminate the artificial changes in the ganglion cells which 
might be produced by the bichromate hardening, small portions 
from the sixth cervical and third lumbar segments were hard- ACUTE ASCENDING PARALYSIS. 
7 
ened in absolute alcohol, a better preservative agent for the 
ganglion cells. The ganglion cells in these portions hardened 
in alcohol are well preserved and seem perfectly normal. 
The ganglion cells from the hypoglossal nucleus and from 
the anterior horns of the spinal enlargements were examined in 
the fresh condition, and no changes could be found. 
The spinal pia mater contains in its meshes, especially in 
the dorsal region, a moderate number of small round cells. A 
few of the larger and smaller veins of the spina] pia mater have 
their walls infiltrated with small round cells (Fig. 3, A). 
Fig. 1, showing the infiltration and thickening of the walls of the anterior spinal 
vein. In the section A the walls have collapsed so that the lumen is arti- 
ficially closed. The lumen is nearly normal. 
The anterior spinal vein and its branches in the dorsal and 
lower cervical regions are not only infiltrated with small round 
cells, but their walls are considerably thickened in places. The 8 
THE PATHOLOGY OF 
lumen of the vein, however, does not appear to be narrowed. 
Fig. 1 shows this infiltration and thickening of the anterior 
spinal vein, which may be appreciated better by comparing 
with Fig. 2, illustrating the normal structure and thickness of 
the anterior spinal vein. (The lumen of the vein in Fig. 1 is 
very nearly normal; it looks small when contrasted with Fig. 2, 
but this is due to the fact that in Fig. 2 the sections were taken 
from a larger cord which had a correspondingly larger anterior 
spinal vein.) 
Fig. 2.-Sections showing the normal structure and. thickness of the anterior 
spinal vein. Taken from a larger cord having a correspondingly larger vein 
than in Fig. 1. 
How much interference, if any, this condition of the an- 
terior spinal vein may have made in the circulation of the gray 
matter is very questionable, and no special significance is at- 
tached to this change in the vein. The change in the an- 
terior spinal vein seems to be simply a part of the general infil- 
tration of the pia mater, which may very well have occurred 
secondarily during the course of the disease, if not during its 
latter stages. 
Hyaline thrombosis, recently described in Landry's paralysis 
by Klebs,* in the central arteries of the cord, was not found in 
this case. (In two places-in a small vein passing out of the 
* Deutsche medicinische Wochenschrift, January, 1891. ACUTE ASCENDING PARALYSIS. 
9 
hypoglossal nucleus, and in a capillary in the motor cortex- 
hyaline plugs were found, but the perfectly normal condition of 
Fig. 3.-(A) Thickened and infiltrated vein accompanying one of the anterior 
dorsal spinal nerve roots. (B) Thickened and infiltrated anterior spinal 
vein. 
the gray matter surrounding these two vessels indicated that 
the hyaline plugs were a post-mortem occurrence.) 
The Cranial and Spinal Nerve Roots.-The root strands of 
the facial, acoustic, trigeminus, vagus, and hypoglossal nerves, 
and also many of the anterior roots of the cervical, lumbar, and 
Fig. 4, showing the average number of degenerated fibers in the anterior roots 
of the cauda equina. 
sacral regions of the cord, were hardened in osmic acid. The 
cranial and cervical nerve roots show no changes except those 
due to manipulation and imperfect preservation. There is no 
evidence of degeneration or neuritis in these roots. The anterior 
roots of the cauda equina show, in a slight degree, the changes 
of neuritis or degeneration of the nerve fibers (Figs. 4 and 5). 
The degenerated fibers are not numerous, comprising about one 10 
THE PATHOLOGY OF 
tenth of the fibers of the anterior roots of the cauda equina. 
Transverse sections of the cauda equina show in places a con- 
siderable number of small round cells lying about and between 
Fig. 5, from a place selected to show the maximum number of degenerated fibers 
the nerve fibers (Fig. 6). Whether the small round and branch- 
ing cells of the cauda equina are actually increased to any ex- 
tent is difficult to determine, and for this reason, and from the 
fact that Nauwerck and Barth describe an increase of cells in 
the cauda equina in Landry's paralysis, Fig. 6 has been drawn 
to show definitely the number and distribution of cells in the 
cauda equina. The number of cells in the cauda equina is 
practically normal. 
Fig. 6.-Section showing the number and distribution of the cells in the cauda 
equina. 
The peripheral nerves examined were the median, a branch 
of the musculo-spiral, and the trunk of the sciatic. Sections of 
these nerves, stained in the same ways as the central nervous 
system, show nothing abnormal. Portions of all of these nerves ACUTE ASCENDING PARALYSIS. 
11 
were also preserved in osmic acid (one-per-cent, solution) and 
examined, without finding any alterations. 
The semi-tendinosus and biceps muscles are normal. They 
were examined in the fresh condition, and sections were made 
of the hardened muscles. 
Bacteriological Examination. - Glycerin-agar plates were 
planted from the hypoglossal nucleus, from the motor cortex, 
and from the anterior horns of the spinal enlargements, and 
nothing grew on the plates. Cover-glass preparations of the 
gray matter from the same places were stained with the simple 
aniline dyes, with Lbffler's solution, and by Gram's method, 
but no bacteria were found. Sections of the cord, hardened in 
alcohol, were stained for bacteria in various ways, and exam- 
ined with the oil-immersion lens with negative results. Sec- 
tions of portions of the peripheral nerves, hardened in alcohol, 
were carefully examined for micro-organisms, but neither the 
bacilli which Centanni* found in the peripheral nerves in 
Landry's disease, nor any other kind of bacteria, were dis- 
covered. 
The results of the microscopical examinations are: A slight 
cerebral and spinal meningitis and infiltration of the walls of 
some of the veins of the spinal pia mater, and a degeneration (or 
neuritis) of some of the fibers of the anterior roots of the cauda 
equina, the nervous system in other respects being normal. 
We have here, then, the case of a man who is suddenly 
attacked by a paresis of the legs which, in the space of four 
days, becomes a complete paralysis, and then the muscles 
of the trunk, arms, and parts supplied by the bulbar nerves 
become paretic in the order named, and this paresis be- 
comes a more and more decided paralysis until death from 
bulbar paralysis puts an end to the further extension of the 
process. The paralysis was a purely motor one, the sensory 
nerves not being involved, and the sphincters of the bladder 
and rectum were not involved, although the paralysis of the 
abdominal muscles made the expulsion of the contents of 
these viscera difficult or impossible. As a result of the post- 
mortem examination, we have a slight cerebral and spinal 
meningitis of quite recent origin, a degeneration of a few 
of the fibers of the anterior roots of the cauda equina, and 
a thickening and infiltration of the walls of the anterior 
spinal vein. 
This complex of symptoms corresponds entirely with 
* Lar ifor ma medica, July, 1889. 12 
THE PATHOLOGY OF 
the clinical picture of the disease-acute ascending paraly- 
sis-which was first clearly described by Landry * in 1859, 
and which has since been generally called in his honor by 
the name of Landry's paralysis, or by the name which Lan- 
dry himself gave it, acute ascending paralysis. The only 
unusual symptom in the case reported was the diplopia, a 
symptom which is not common in Landry's paralysis, al- 
though it has been observed by Pellegrino-Levi,-J- and the 
usual factors-i. e., exposure to cold or previous 
occurrence of some infectious disease-were not present in 
this case. It is very doubtful whether the blow on the back 
received four years previous to his death had any connec- 
tion with the disease. The slight lesions found in this case 
are altogether insufficient, both in extent and in intensity, 
to explain the severe symptoms present during life, and this 
case goes far to confirm the previously accepted view that 
acute ascending paralysis is not associated with any appre- 
ciable lesion. 
It is not a desirable thing to overburden our already 
long list of nervous diseases with additional names, and it 
is a question demanding careful consideration whether 
acute ascending paralysis can not be regarded as a va- 
riety of some other well-recognized nervous disease. In 
answer to this question we must say that there are 
only three diseases of the nervous system which bear 
any close resemblance to acute as.cending paralysis- 
viz., bulbar paralysis, myelitis of the anterior horns, and 
multiple neuritis. 
Certainly acute ascending paralysis can be easily distin- 
guished from bulbar paralysis, for in this latter form of dis- 
ease the disturbances in respiration and deglutition are the 
first, or at least very eaily, symptoms, to which the paraly- 
sis of the arms and legs is quite subordinate, and this pa- 
ralysis usually involves sensation as well as motion, while 
the tendon reflexes are not only present but are exaggerated. 
It is true that a few cases have been reported under the title 
acute ascending paralysis in which lesions have been found 
in the medulla obldngata or in the upper cervical region of 
the cord, but these cases were either not acute ascending 
* Gazette hebdomadaire, 1859, pp. 472 and 486. 
f Archives generates, 1865, i, p. 123. ACUTE ASCENDING PARALYSIS. 
13 
paralysis at all, as in the case reported by Leyden,* or the 
lesions were too small to explain the symptoms, as in the 
case of Kummel,t or, finally, the lesion was of a very inde- 
terminate nature and not found in other cases, as the patches 
of exudative matter deeply stained by carmine found by 
Eisenlohr,J and the swollen axis cylinders and minute haem- 
orrhages found by Hoffmann.* 
Myelitis of the anterior horns bears a closer resemblance 
to acute ascending paralysis, although bulbar symptoms oc- 
cur very rarely in the former disease. In both diseases 
there is a widespread motor paralysis with abolition of re- 
flexes and without any disturbance of sensibility or of the 
organic reflexes ; and the attempt has been made by Petit- 
fils, || Bernhardt,A and others, to classify acute ascending pa- 
ralysis as a form of myelitis of the anterior horns in which, 
in consequence of the rapidly fatal termination, the muscles 
do not exhibit the characteristic electiical reaction of de- 
generation during life, nor do the nerve cells in the anterior 
horns exhibit any definite changes in death. These assump- 
tions were disproved by who, in several cases of 
relatively long duration, found neither lesions after death 
nor the electrical reaction of degeneration during life. Since 
the publication of Westphal's paper the early appearance of 
muscular atrophy and that of the electrical reaction of de- 
generation have been regarded as diagnostic symptoms, and 
are sufficient to distinguish clinically myelitis of the anterior 
horns from acute ascending paralysis ; while at the autopsy 
of cases of myelitis of the anterior horns a definite lesion is 
found sufficient to explain the symptoms observed during 
life. Although in most cases there is no preat difficulty in 
distinguishing these two forms of disease from each other 
clinically, yet some cases of myelitis of the anterior horns 
simulate the symptoms of acute ascending paralysis quite 
* Ally. Zeitschrift f. Psych., 1875. 
f Zeitschrift f. klin. Med., 1881, ii, p. 273. 
J Virchow's Archiv, 1878, Ixxiv, p. 73. 
# Archiv fur Psychiatric, 1884, xv, p. 140. 
|| Considerations sur I'atrophie aigue des cellules matrices, Paris, 
1879, p. 93. 
A Perl. klin. Wochenschrift, 1871, No. 47. 
Q Archiv f. Psychiatric, Bd. vi, p. 765. 14 
THE PATHOLOGY OF 
closely, as, for instance, the cases reported by Sudeykine * 
and Immermann.f 
Multiple neuritis bears a very close resemblance to acute 
ascending paralysis, and, just as twenty years ago, when 
myelitis of the anterior horns was attracting great attention, 
the attempt was made to regard Landry's paralysis as a 
form of it, so, during the past five years, when multiple 
neuritis has been attracting much attention, the attempt has 
been made to regard Landry's paralysis as one of its forms, 
but neither attempt has been as yet successful. Certainly, 
to one who has observed cases of both diseases, there is a 
decided difference in the clinical picture of Landry's paraly- 
sis and multiple neuritis. There can be no doubt that 
many of the cases which have been reported under the name 
of acute ascending paralysis are really cases of multiple 
neuritis ; but in every such case in which the autopsy has 
revealed a multiple neuritis, even of slight degree, the 
symptoms of bulbar paralysis were absent or very slightly 
marked,J and there was present during life either a decided 
disturbance of sensibility, manifesting itself by severe pain 
or by extensive ansesthesia,* or else a paralysis of the 
sphincters, || or else the muscles presented a more or less 
well-marked electrical reaction of degeneration, and were 
tender on pressure and atrophied A-symptoms which form 
* Russk. Med., St. Petersburg, 1886. Ctrlbl. f. klin. Med., 1887. 
f Poliomyelitis Anterior Acuta, Subacuta ,et Chronica. By Charles 
Morel. Basel, 1890. 
| Difficulty of respiration due to paralysis of the intercostal or 
phrenic nerves can not be regarded as a symptom of bulbar paralysis 
in the absence of any disturbance in deglutition and speech. 
* Sensory symptoms were prominent in the cases reported by Nau- 
werck and Barth (Ziegler's Beitragez. path. Anat., etc., Bd. v, p. 1) and 
Eisenlohr {Deutsch, med. Woch., Sept. 18, 1890). 
|| Paralysis of the sphincters was present in the cases reported by 
Dejerine {Arch, de phys. norm, et path , 1873, p. 312, and 1876, p. 312 ; 
Comp, rend., 1878, Ixxxvii, No. 3 ; and Recherches sur les lesions du sys- 
tems nerveux, Paris, 1879) and Roth (Corresp.-Blatt. f. schweizer Aerzte, 
1883, No 13). 
A The electrical reaction of the muscles was altered in the cases re- 
ported by Dejerine {Arch, de physiol, norm, etpath., 1876 p. 312 ; Comp, 
rend., 1878, Ixxxvii, No. 3; and Recherches sur les lesions du systeme 
nerveux, Paris, 1879), Eichhorst (Virchow's Arch., 1876, Ixix), Eisen- 
lohr {Deutsche med. Woch., Sept. 18, 1890), Gombault {Arch, dephysiolo- 
gie, v, 1873, p. 81), and Schultz and Schultze {Arch. f. Psychiat., Bd. 
xii, p. 458). ACUTE ASCENDING PARALYSIS. 
15 
no part of the clinical picture of the disease described by 
Landry. 
It is true that cases of multiple neuritis present so much 
variation in the relative prominence of the sensory and mo- 
tor symptoms, in the completeness of the electrical reaction 
of degeneration, and in their other symptoms, that it seems 
somewhat artificial to insist on separating the complex of 
symptoms constituting Landry's paralysis from the general 
class of multiple neuritis. But if we do make such a sepa- 
ration, we can find in medical literature some two dozen 
cases of well-marked Landry's paralysis, while many other 
cases reported under this title are cases either of multiple 
neuritis or are too imperfectly reported to allow of a diag- 
nosis being made. Of these cases, six terminated in recov- 
ery ;* in twelve cases the disease terminated fatally, but 
the peripheral nerves were not examined ; f while at least 
six cases similar to the one which forms the basis of this 
paper have been reported by competent observers-such as 
Westphal, J Corni],# Bernhardt, || and Leyden A-in which 
during life the paralysis was a purely motor one, followed 
an ascending course, and extended to the medulla, there 
being no involvement of the sphincters nor any reaction of 
* These cases terminating in recovery have been reported by Mieth 
(Deutsch, med. Woch, 1885, xi, p. 67), Rendu (La France medicale, 1881, 
ii, p. 793), Sorgenfrey (Neurolog. Ctrlbl., Bd. iv, p. 198), Oppenheim 
(Wien. klin. Woch., 1890, No. 39, iii, p. 761), Ross (Treatise on Diseases 
of the Nervous System, second ed., vol. 1. p. 905), and Eiselt (Aertz. 
Bericht. des K. K. ally. Krankenhaus z. Frag [1880], 1882, p. 53). 
f These cases terminating fatally in which the peripheral nerves 
were not examined have been reported by Walford (Brit. Med. Jour., 
1853, p. 993), Chalvet (These de Paris, 1871, p. 16), Dazet (Revue medi- 
cale de Toulouse, 1881, xv, p. 225), Emminghaus ( Verhand. d. phys.-med. 
Gesellsc. in Wurzburg, 1880, N. F. xiv, p. 17), Finny (Brit. Med. Jour., 
1882, vol. 1, p. 732), Kahler and Pick (Arch.f. Psychiat., Bd. x, p. 313), 
Kiimmel (Zeitsch. f. klin. Med, 1881, ii, p. 273), Aufrecht (Path. Mit- 
theil., Magdeburg, 1881, i, p. 170), Eisenlohr (Virchow's Arch., 1878, 
Ixxiii, p. 73), Mann (Med. Chronicle, 1887, vol. vi, p. 99), Fere (Comptes 
rendus d. la Societe de biologie, 1888, vol. v, 3d s., p. 189), and Stair 
(Med. Record, 1882, vol. xxii, p. 355). 
| Arch, fur Psychiatric, 1876, vi, p. 765. 
* Case of Pellegrino-Levi, reported in Archives generales de medecine, 
1865, vol. 1, p. 132. 
|| Berlin, klinische Wochenschrift, 1871, No. 47. 
A Die Entzundung der peripheren Nerven, Berlin, 1888, p. 21. 16 
THE PATHOLOGY OF 
degeneration, and in which, after death, the most careful 
examination of the central and peripheral nervous organs 
failed to reveal any lesion. 
It must be confessed that most of these observations are 
of rather old date, and, further, it may be urged that typi- 
cal cases of Landry's paralysis run such a rapid course that 
death occurs before the reaction of degeneration and struct- 
ural changes in the nerve fibers have had time to develop. 
But in those cases which run a slower course the reaction 
of degeneration does not occur, and even at the outset of 
the disease cases of acute ascending paralysis differ from 
cases of multiple neuritis by the absence of those decided 
sensory disturbances which are so characteristic of the lat- 
ter disease. And, finally, those very acute cases of multi- 
ple neuritis which terminate fatally in the course of a few 
davs, as in the cases reported by Putnam * and Rosenheim,! 
or in a few hours, as in the case reported by Pitres and 
Vaillard, | present the well-marked lesion of a neuritis. 
Two papers have recently appeared, in which the attempt 
is made to prove that Landry's paralysis is a form of mul- 
tiple neuritis, which are so very elaborate that they demand 
especial notice. One of these papers was published in 
England by Ross, and the other in Germany by Nauwerck 
and Barth. 
Ross* makes a comparative study of a large number of 
cases of acute ascending and allied forms of paralysis. Of 
course, it is possible-by including in a list of cases of 
acute ascending paralysis a number which, by their clinical 
course and by the lesions found at the autopsy, are evi- 
dently cases of multiple neuritis, and then making a sum- 
mary of the symptoms found in all these cases-to so oblit- 
erate the lines dividing the two diseases from each other 
that acute ascending paralysis will resemble moi e and more 
closely multiple neuritis, and the greater the number of 
cases of this latter disease which are included in the list, 
the greater will this resemblance be. This is what Ross 
does in his article ; but even be agrees with the first con- 
* Boston Med. and Sure/. Jour., Feb. 4, 1889. 
f Arch. f. Psychiat., Bd. xviii, Hft. 3. 
£ Arch, de physiologic, 1887, ii, p. 150. 
* Medical Chronicle, November, 1889, p. 102. ACUTE ASCENDING PARALYSIS. 
17 
elusion of Nauwerck and Barth, that cases of typical acute 
ascending paralysis do occur in which it is impossible after 
death to discover any lesion. 
Nauwerck and Barth,* after a long discussion of the 
previously reported cases of acute ascending paralysis and 
of some allied forms of disease, arrive at the following 
conclusions: 
1. A typical acute ascending paralysis, with slight sen- 
sory symptoms, without implication of the sphincters, and 
without any diminution of the electro-muscular excitabili- 
ty, may prove fatal, and it may be impossible to discover 
any anatomical changes in either the centfal or the periphe- 
ral nervous system. 
2. No sure proof has hitherto been afforded that the 
clinical picture of an acute ascending paralysis can be pro- 
duced by disease of the medulla oblongata or spinal cord 
or of any part of the central nervous system. 
3. If acute ascending paralysis is defined so as to in- 
clude cases in which the loss of motor power is accom- 
panied by more severe sensory symptoms, by affections of 
the sphincters, and especially by diminution or loss of the 
electro-muscular contractility or the reaction of degenera- 
tion, then a considerable number of observations have been 
recorded which warrant us in assuming a disease of the 
peripheral nerves alone. 
4. It has not been proved that, even in the extended 
signification of the term, acute ascending paralysis can be 
caused by disease of the central nervous system. 
At the close of their valuable paper Nauwerck and Barth 
report under the name of Landry's paralysis a case in which, 
after death, the medulla and spinal cord were normal, but 
an interstitial neuritis, without any degenerative changes in 
the nerve fibers,f was found in the canda equina, and to a 
less degree in the anterior and posterior nerve roots through- 
out the spinal cord, while the bulbar nerve roots were nor- 
mal. The muscles and the peripheral nerves were normal 
with the exception of the sciatic nerves, which were affected 
in the same way as the nerve roots. Their case then must 
* Ziegler's Beitrage z. path. Anat. u. z. allg. Pathologic, Bd. v, p. 3, 
j- This lesion is therefore quite different from the lesion found in 
the case reported in this paper. 18 
THE P2VTH0L0GY OF 
be regarded as a multiple neuritis mainly limited to the 
nerve roots, and one factor in the production of the neuritis 
may well have been the tuberculous disease which was 
found in the lungs. Clinically the case resembles a case of 
multiple neuritis, and not one of acute ascending paralysis, 
in that the legs were the seat of sharp pains during many 
weeks and were almost absolutely anaesthetic, and the arms 
moderately so; the neuritis of both the anterior and pos- 
terior nerve roots thus producing characteristic symptoms 
in the domain both of motility and sensibility. There was 
no difficulty in swallowing, in breathing, or in speaking, 
there were no other bulbar symptoms, and the motor 
paralysis was showing decided improvement when the 
patient died in collapse. The fact that the patient died in 
collapse, apparently due to cardiac rather than to respira- 
tory failure, can not be taken as sufficient proof of bulbar 
paralysis in the absence of an.y previous symptom of such 
paralysis. It is quite as reasonable to suppose, consider- 
ing the weak condition of the patient resulting from 
the long-continued pulmonary tuberculosis and paralysis, 
that the collapse was due to the haemorrhage found after 
death in the lumen and in the walls of the small intes- 
tine, or even if the autopsy revealed no cause for the col- 
lapse, it does not follow that bulbar paralysis was the cause 
of it. This case, then, occurring in a tuberculous patient 
and presenting severe disturbances both of motion and sen- 
sation without' bulbar symptoms, running a chronic course 
and showing improvement in the paralysis previous to the 
sudden death, may be indeed a peculiar form of multiple 
neuritis, but can not be regarded as a typical case of acute 
ascending paralysis, and does not justify the conclusion of 
the authors " that Landry's paralysis is to be regarded as 
an infectio-toxic multiple neuritis." 
Finally, Klebs* attempts to refer the symptoms of Lan- 
dry's paralysis to a hyaline thrombosis of the branches of 
the central artery of the spinal cord, because in one case he 
found such a hyaline thrombosis which was exclusively 
limited to those branches of the central artery lying on 
each side of the central canal and supplying the anterior 
horns of gray matter. This thrombosis had apparently 
* Deutsch, med. Wochensckrift, Jan. 15, 1891. ACUTE ASCENDING PARALYSIS. 
19 
produced a dilatation of the circumcellular spaces about the 
motor cells, which dilated circumcellular spaces contained 
small round cells and a network of coagulated material. 
This lesion would explain the symptoms of the disease 
fairly well, but it is certainly of a very indeterminate nature. 
It has been found in only one case, and was not present in 
the case reported in this paper, and Hlaval * did not find, 
this hyaline thrombosis in a case reported by him under 
the title of Landry's paralysis, but which is evidently a case 
of myelitis of the anterior horns. 
In conclusion, it appears from this somewhat hasty and 
imperfect review of the subject that no conclusive evidence 
has as yet been brought forward which justifies us in 
abandoning the term acute ascending or Landry's paralysis, 
for neither has it been shown that those cases of the dis- 
ease in which no lesion has been discovered depend on 
faulty methods of examination, nor has any case been re- 
ported which was clinically a typical case of Landry's pa- 
ralysis in which, after death, characteristic lesions were 
found either in the central nervous organs or in the pe- 
ripheral nerves. Acute ascending paralysis (defined so as 
to exclude ail cases in which the sensory symptoms are 
prominent, or in which well-marked bulbar symptoms are 
not present) must therefore be regarded as a clinical entity 
for which no corresponding lesion has as yet been discov- 
ered. That there is some change in the nervous system 
causing the severe symptoms can not be doubted, but this 
change is probably of a chemical rather than of an anatomi- 
cal character. From the many points of resemblance which 
acute ascending paralysis bears both to myelitis of the an- 
terior horns and to multiple neuritis, this chemical change 
must affect either the motor cells of the spinal cord and 
medulla or the fibers springing from them ; and, although 
this chemical change is so great as to cause an entire arrest 
of the function of those cells or fibers, yet it leaves no trace 
in any altered character of cell or fiber, no more than does 
morphine or strychnine leave any trace in the structure of 
the nervous system of their fatal action. 
In regard to the nature of this supposed chemical poison 
we know nothing. The general tendency of the present 
* Archives bohbmes de medecine, vol. iv, No. 2, p. 270. 20 
ACUTE ASCENDING PARALYSIS. 
day is to consider i,t to be a ptomaine, and indeed the acnte 
course, the fact that it often follows an infectious disease, 
and that it is associated with an enlargement of the spleen, 
make it not improbable that Landry's paralysis is a germ 
disease. In further support of this view is the fact that the 
paralytic form of rabies closely resembles Landry's paralysis, 
■and that Baumgarten * found the anthrax bacillus in the 
spinal cord, and Curschmann f found the typhoid bacillus in 
the spinal cord in cases bearing some resemblance to, but 
evidently not true cases of, Landry's paralysis; and in two 
similar cases of so-called Landry's paralysis in which the 
diagnosis was, to say the least, extremely doubtful, Cen- 
tannij and Eisenlohr* have each found bacteria in the 
central nervous organs. In neither case were the bacteria 
cultivated, and in a second case observed by Eisenlohr no 
bacteria were found. In a number of cases bacteria were 
looked for, as was done in the case which I report, but were 
not found. So that the hypothesis that Landry's paralysis 
is due to bacterial agency, attractive as it seems, is far from 
being proved, and the pathology of the disease still remains 
to be discovered. 
* Arch. d. Heilk., 1876. 
f Verhandl. des v. Congress f. innere Medicin, 1886. 
£ Ziegler's Beitrdge zur path. Anatomie, etc., Bd. viii, Hft. 3. 
* Deutsch, med. Wochenschrift, No. 38, Sept. 18, 1890.