MYELITIS FOLLOWING ACUTE ARSENICAL 
POISONING (BY PARIS OR SCHWEIN- 
FORTH GREEN.) 
BY 
E. C. SEGUIN, M.D. 
CORRESPONDING MEMBER OF THE VEREINS FUR INHERE MEDICIN OF BERLIN, ETC. 
[Reprinted from the Journal of Nervous and Mental Disease, Vol. ix, No. 4 
October, 1882.] MYELITIS FOLLOWING ACUTE ARSENICAL 
POISONING (BY PARIS OR SCHWEIN- 
.FURTH GREEN.)* 
E. C. SEGUIN, M.D., 
CORRESPONDING MEMBER OF THE VEREINS FUR INHERE MEDICIN OF BERLIN, ETC. 
THE physician who, meeting with a case of arsenical 
paralysis, would seek for information on the sub- 
ject in the accessible and contemporary treatises upon 
disease of the nervous system, would be grievously disap- 
pointed. Such writers as Grasset, Ross, Wilks, Bauduy, 
Hamilton, do not mention the affection at all ; the illus- 
trious Romberg, and Erb merely give it a passing reference. 
Prof. Hammond (1881), in the last edition of his treatise, 
says nothing of paralysis following acute arsenical poison- 
ing, and refers to paralysis and anaesthesia as results of 
slow poisoning. Apparently, he has seen no cases of arseni- 
cal paralysis. Rosenthal (1875) devotes only a short para- 
graph to arsenical nervous symptoms ; refers to paralysis in 
the course of chronic poisoning. In a case which he saw 
there were paralysis, partial anaesthesia, and diminished elec- 
* Read at the meeting of the Medical Section of the New York Academy 
of Medicine, October 17, 1882. ( The original cases alone had already been 
read before the American Neurological Association, at its Eighth Annual Meet- 
ing, June 21, 1882.) 
Reprinted from the Journal of Nervous and Mental Disease, Vol. ix. 
No. 4, October, 1882, 2 
E. C. SEGUIN. 
tro-muscular contractility. Leyden (1875), in his classical 
work on diseases of the spinal cord,1 gives a resume chiefly 
after Leroy D’ Etiolles. He does not appear to have had 
cases of his own, and considers the disease a neuritis. 
A little more extended research in older books, and in 
periodicals brings to light numerous observations and some 
valuable experimental studies upon the subject. 
Indeed, arsenical paralysis seems to have been very early 
noticed, and to have attracted considerable attention until 
within the last twenty years. As early as the thirteenth 
century, P. Abano2 refers to paralysis and contractures after 
arsenical poisoning. These symptoms are also mentioned 
by Forestus3 (about 1560-70); and Zacchias4 (1630) men- 
tions paralysis, spasms, contractures, and anaesthesia as fol- 
lowing poisoning. From that time arsenical paralysis is 
frequently mentioned by medical writers. Hahnemann,5 in 
one of his earlier works (1786), relates several cases. 
In 1812, Sir Benjamin Brodie, in an interesting communi- 
cation to the London Royal Society, entitled “ Observations 
and experiments on the actions of poisons on the animal sys- 
tem,” devotes a section to the effects of arsenic, and relates 
how in several of his animals (rabbits and dogs) the hinder 
extremities became paralyzed. He considered the brain to 
be affected in these cases. 
The following interesting case was published, in 1809, by 
Dr. G. Thilenius.6 
A young lady having observed a hard lump in her left breast, 
neglected it until the ensuing spring, when it became very painful. 
A miserably ignorant barber who was consulted, applied a prepa- 
1 Klinik der Riickenmarks-Krankheiten, Bd. ii, p. 296. 
3 De venenis eorumque remediis, cited by Imbert-Gourbeyre, I. c. 
3 Cited by Imbert-Gourbeyre, I. c. 
4 Quaestiones medico-legales, Romae, 1621-50, cited by Imbert-Gourbeyre. 
6 Ueber das Arsenik-Vergiftung, Leipzig, 1786, cited by Imbert-Gourbeyre. 
8 Medic.-chirurgiscbe Bemerkungen, Frankfurt, 1809, in Leroy D’ Etiolles, 
P- 63. MYELITIS FOLLO WING ACUTE ARSENICAL POISONING. 
3 
ration of arsenic. This was followed by ulceration and increased 
pain, and, according to the father’s statement, three days later her 
arms and legs became insensible, and so much paralyzed that 
she could neither walk nor feed herself. The limbs were also 
cold. In the course of two months the arms recovered, and the 
legs improved steadily. Electricity was used ; the tumor removed 
by the knife. At various times there occurred prickling and jerk- 
ing in the legs. Anaesthesia and atrophy not mentioned. 
In about a year after the attack the patient was able to walk 
without a cane ; her limbs were warm, and the wound in the 
breast well healed. 
In 1793 (three years after the attack) patient was perfectly well, 
married, and had a child.—(Obs. No. 80 of Leroy D’ Etiolles.) 
Orfila,1 the great French chemist and toxicologist,, in 
experiments upon dogs, made prior to 1840, noticed pa- 
ralysis of the hinder extremities in dogs which survived ar- 
senical poisoning (also in fatal experiments). 
Prof. Christison,2 of Edinburgh, in his classical work on 
poisons, treats of symptoms of arsenical poisoning in a 
masterly way. He makes three categories of cases of ar- 
senical poisoning. In a first class of cases, in which, with 
symptoms of violent inflammation of the gastro-intestinal 
tract, death results in from twenty-four hours to three days ; 
nervous symptoms not present. In a second class of cases, 
with little evidence of inflammation, extreme prostration 
and syncope are the chief symptoms, death occurring within 
six hours; no paralysis observed. Convulsions may close 
the scene. In the third category, that of subacute cases, there 
is moderate gastro-intestinal inflammation; symptoms are 
same as in other classes, but milder. In the later stage these 
cases are apt to show marked nervous symptoms : coma, epi- 
leptoid attacks, mania, tetanus, hysterical seizures, partial 
paralysis resembling lead paralysis in affecting the extremi- 
ties ; contractures may exist. In speaking of symptoms con- 
1 Traite de Toxicologie, Paris, 1852. 
2 A Treatise on Poisons, Phila., 1845, p. 244, et seq. 4 
E C. SEGUIN. 
nected with irritation of the primes vivez, Christison makes 
this shrewd remark, which applies critically to many of the 
older cases of arsenical paralysis: “Cramps in the legs and 
arms (occur in arsenical poisoning), a possible concomitant 
of every kind of diarrhoea.” 
The father of modern clinical medicine, Graves1 (1842), 
after speaking of paraplegia from inflammation of the 
bowels, refers to Orfila’s experiments in which all (?) the 
dogs which survived arsenical poisoning were paralyzed in 
their hinder limbs, and states that in his opinion in cases of 
arsenical as well as of lead poisoning, the poison acts 
directly on the central nervous system (spinal cord), and 
that the palsy is not due to the intestinal irritation. 
H uss,a of Stockholm, in his work on alcoholism (1852), 
mentions several cases of arsenical poisoning with severe 
nervous symptoms. He gives one which is instructive as 
regards its etiology. 
For the cure of intermittent fever, a large teaspoonful of 
Fowler’s solution was given at one dose (equivalent to grain, 
or .035 gramme, of arsenious acid). After the usual symptoms 
of acute intoxication, there gradually ensued an almost complete 
paralysis of the extremities, with anaesthesia of the hands and 
feet, severe pains and cramps in the lumbar region and lower ex- 
tremities. 
In 1857 we meet with quite an important contribution to 
this subject. Leroy D’ Etiolles,3 in his work on paralysis 
of the lower limbs, devotes a chapter to arsenical paralysis, 
and relates the following three cases (in addition to the 
case of Thilenius already quoted). 
Obs. 79.—Poisoning from external application of arsenious 
acid ; general paralysis ; recovery of upper extremities first. 
1 Clinical Lectures, Gerhard’s edition, Phila., 1842, p. 94. 
* Cited by Imbert-Gourbeyre. 
3 Des paralysies des membres inferieurs, deuxieme partie, p. 28, et seq., 
Paris, 1857. MYELITIS FOLLO WING ACUTE ARSENICAL POISONING. 
5 
Male patient . . . age. Dr. Trochon, of the hospital at Pornic, 
amputated his leg for cancer. In the cicatrix cancerous buds ap- 
peared. Arsenical paste, made one hundred times too strong by 
druggist’s error, was applied, and very soon symptoms of acute 
intoxication appeared ; life saved with difficulty. At the end of 
ten days patient convalescent, but with well-marked paraplegia 
and paresis of the arms. 
Seen five months later by Leroy ; Arms weak and not adroit ; 
tendency to drop-wrist. Marked paralysis in remaining lower 
extremity, with emaciation, but not positive atrophy of muscles ; 
contracture in semi-flexion ; foot hyperextended (pes equinus) ; 
toes flexed. Sensibility to touch and pain much impaired on 
limbs. Electrical tests not used. 
Gradual improvement of paralysis in spite of progressive can- 
cerous infection. 
This case bears a certain resemblance to my own cases. 
Although it is stated that the muscles were not atrophied 
as in lead paralysis, yet from the contractures and the de- 
gree of emaciation present, it seems to me highly probable 
that there was atrophy, widely distributed, as in mild cases 
of poliomyelitis. It is a pity that electricity was not used, 
although at the time when this observation was recorded, 
1855, only the bare fact of diminution or loss of faradic 
contractility could have been determined. 
The contracture in flexion with pes equinus is strikingly 
like what existed in my own Case 3. 
Obs. 81.—Poisoning by the ingestion of arsenious acid : paresis 
of arms; paraplegia lasting fourteen months. 
A female patient aged thirty-seven years, was admitted to the 
service of Dr. Bouvier, Hospital Beaujon, January 22, 1850, suf- 
fering from severe toxic symptoms produced by eating cakes 
charged with arsenious acid. 
As soon as the urgent symptoms had subsided (time not noted), 
it was discovered that the patient was paralyzed in her lower 
limbs, and that they were the seat of painful jerking (reflex move- 
ments ?) Her arms were weak. On 18th February, on leaving 
the hospital, she was unable to stand, and said that she could not 
feel the floor under her feet. In September of the same year she 6 
E. C. SEGUIN. 
was readmitted with pleurisy; and it was noted that while her arms 
had recovered, her legs were just as weak, and as insensible to 
touch. At no time was there interference with the functions of 
the rectum or bladder. Later some improvement took place, but 
the patient finally died of exhaustion caused by a profuse diar- 
rhoea. No autopsy. 
Obs. 82.—Case of Aran in Union Mddicale, July 6, 1852. On 
June 9, M. Aran presented to the Societe Mddicale des Hopi- 
taux, one of two young men who had, two months previously, 
been poisoned by arseniate of sodium. The victims had swal- 
lowed this salt, supposing it to be tartrate of sodium. One died 
in twenty-four hours ; and a lady to whom they had given some 
of the poison, is not yet perfectly well. 
In the surviving male patient interesting nervous symptoms 
have appeared. In about fifteen days after the ingestion of the 
drug, symptoms of paralysis appeared in the lower limbs, more 
marked in the right leg. The upper extremities have also been 
weak. The paralysis has remained very much in statu quo. The 
paralyzed parts are somewhat anaesthetic. The lower limbs are 
the seat of tingling below the knees ; and the upper extremities 
in the finger-tips. At one time the paretic extremities showed 
diminished calorification. General health good. 
M. Duchenne examined the young man and found slight dimi- 
nution of electrical irritability, and the skin showed diminished 
sensibility to the current. 
Later, on Bth September, M. Aran reported to the Society that 
the patient had recovered, apparently in consequence of forty-six 
baths and forty-six douches at Bagneres de Luchon (hot sulphur 
springs).' Improvement showed itself distinctly after the thirty- 
sixth bath. 1 
Leroy makes these general statements : In lead paralysis 
the forearms are usually affected (sometimes only one) ; ar- 
senical paralysis tends to involve all the limbs ; the lower 
limbs are more affected ; often there is well marked para- 
plegia ; the action of the bladder remains normal. Sensi- 
bility is usually much impaired (nearly as much as motility). 
He refers to wasting of muscles, but states that it contrasts 
with the positive atrophy of lead paralysis. Electro-muscu- 
lar contractility persists, but Js_ diminished. Treatment is M YELITIS FOLLO WING A CUTE ARSENICAL POISONING. 
7 
efficacious, and the duration of the paralysis is usually less 
than one year. 
Shortly after the appearance of Leroy D’ Etiolles’ work, 
a learned French physician, Imbert-Gourbeyre,1 professor at 
the medical school of Clermont-Ferrand, published a series 
of articles in the Gazette Mtdicale (1858), in which he gave 
an elaborate account of our previous knowledge of arsenical 
paralysis. lam indebted to this essay for bibliographical 
data. The articles contain nothing original. In 1863, 
Smoler2 published a case of paralysis after acute arsenical 
paralysis, which referred to by Rosenthal (1875). 
Jaccoud 3 (1864) devotes several paragraphs to arsenical 
paralysis (paraplegia), and expresses his belief that the palsy 
is caused by the direct action of the metal or its compounds 
upon the tissue of the spinal cord. He does not, however, 
appear to have seen a case. 
In 1881, Seeligmiiller4 placed on record four cases; two 
after acute poisoning, and two after chronic intoxication. 
In his acute cases he noted paralysis, numbness, and anaes- 
thesia (in toes), contractures, wasting of the extensors es- 
pecially. The paretic and wasted muscles showed fibrillary 
contractions ; the nails were gradually lost. Electro-mus- 
cular contractility was diminished or even lost. 
He gives the following points for differential diagnosis 
from lead palsy : the acute origin of the paralysis, disorder 
of sensation as well as of motion, rapid muscular wasting, 
absence of blue line on the gums, and of cachexia. 
In the same year appeared the essay of Popow,5 of St. 
1 Etudes sur la paralysie arsenicale. Gazette Mddicale, 1858, pp. 5, ig, 
59, 94- 
2 Lahmung nach Arsenikvergiftung. CEslerreich Zeitschr. fur pract. Heil- 
kunde, 1863. 
3 Les paraplegics et 1’ ataxic du mouvement, Paris, 1864, p. 323, et seq. 
4 Ueber Arseniklahmung. Deutsche med. Wochenschrift, 1881, No. 14, 
et seq. 
6 Ueber die Veranderungen im Ruckenmarke nach Vergiftung mit Arsen und 
Blei. St. Petersburger 7ned. Wochenschrift, 1881, No. 36. 8 
E. C. SEGUIN. 
Petersburg, upon the pathological anatomy of arsenical 
paralysis as produced artificially in animals. Popow carried 
on his experiments under the guidance of Prof. Mierze- 
jewski; giving arsenious acid to dogs in doses ranging from 
to 2 grains at a dose, producing acute and chronic intoxi- 
cation. 
In cases where death ensued in four to five hours after 
ingestion of the poison, the spinal cord showed both macro- 
scopic and microscopic lesions. The gray matter appeared 
swollen, intensely red, more especially in its two enlarge- 
ments. Microscopic examination revealed enlargement and 
congestion of the small blood-vessels, and accumulations of 
lymph corpuscles in the lymph-spaces. 
There were also abundant extravasations of blood-cor- 
puscles and plasma around the vessels, especially in the 
central portions of the gray matter, The walls of the blood- 
vessels were in a state of fatty degeneration. 
The ganglion cells exhibited three degrees of change. A 
first degree of alteration showed cells well stained by 
carmine, and containing vacuoles of variable sizes, some of 
which could be traced into the cell-processes. A second 
form of cells had no processes, were feebly colored by carmine 
and exhibited a punctate granular infiltration. Lastly, here 
and there were cells in a third state of change, consisting 
only of a nucleus surrounded by dark brick-red pigment. 
The white substance only showed pigment masses here and 
there, more especially about the blood-vessels. 
In cases of acute intoxication in which a fatal result en- 
sued in the course of three, five, or six days, the spinal 
cord presented very much the same appearances. The 
distinction between the white and gray substances was less 
defined. The vascular injection and the exudation of 
plasma were less marked, but on the other hand the 
changes in the ganglion cells were more distinct, the MYELITIS FOLLO WING A CUTE ARSENICAL POISONING. 
9 
vacuoles larger, and the granular state more pronounced. 
There were more cells, or properly remains of cells, of the 
third category above described. The white substance was 
normal, except some enlargement of blood-vessels, and 
considerable accumulations of pigment. 
In the chronic cases, those in which death occurred in 
the course of three months (one animal had paresis of the 
hind legs not long before death), the spinal cord appeared 
less firm, and the microscopic appearances differed notice- 
ably from those observed in the acute cases. 
The walls of the blood-vessels were much thickened, and 
showed a distinct fibrillary structure, with diminution of 
the calibre of the vessels, and exudation of blood in the 
perivascular spaces. In the meshes of the perivascular 
spaces were extensive hyaloid masses. The number of 
ganglion cells was much diminished ; those remaining 
showed large vacuoles, and belonged to the first group 
described. In these cases the white substance was much 
more affected, especially in the postero-lateral columns. 
The cylinder-axes exhibited points of swelling here and 
there; they were granular; in many preparations they 
were merely represented by groups of fine granulations. 
The septa of the white substance likewise exhibited a 
granular change ; and the periphery of the white and gray 
substances was thickly strewn with small masses of black 
pigment. 
The spinal nerves, carefully examined at their origin, 
and at various points of their course and distribution, pre- 
sented no pathological alterations. 
From these post-mortem observations Dr. Popow con- 
cludes that; 
I. Arsenic, even in a few hours after its ingestion, may 
cause distinct lesions of the spinal cord, of the type known 
as acute central myelitis, or acute poliomyelitis. E. C. SEGUIN. 
2. In the more chronic cases the pathological changes 
are found in the white as well as in the gray substance, 
constituting a diffused myelitis. 
3. The peripheral nerves remain normal, even three 
months after intoxication. 
4. The paralysis of arsenical poisoning is of central 
origin. 
It might be added that in three guinea-pigs poisoned 
by lead, and dying on the sixth, seventh, and tenth 
days, similar lesions were found, i. e., evidences of more 
or less diffused myelitis, and no lesions of peripheral 
nerves. 
This essay, issued under the supervision of so dis- 
tinguished a neurologist and microscopist as Prof. Mierze- 
jewski, is in many respects the most important contribution 
to the subject. Connecting its conclusions with inductions 
which can be legitimately drawn from the cases of Leroy, 
Seeligmuller, Smoler, and Rosenthal, and my own, we are 
able, I think, to form a definite conception of the true 
nature and relations of arsenical paralysis. 
In last year’s Philadelphia Medical Times Prof. J. M. Da 
Costa1 relates a case of subacute myelitis which occurred in 
a man who had been taking “small pinches ” of arsenic (ar- 
senious acid ?) for three months. The general features of 
this case and the paralytic phenomena are so unlike what 
has been observed in the other cases referred to in this pa- 
per, that I entertain a doubt as to its having been an 
“ arsenical paralysis.” The rapid improvement under very 
large doses of iodide of potassium, and the history of a 
venereal sore one year before admission, would seem to 
furnish a better clue to the nature of the myelitis. 
The cases which have fallen under my own observation 
are three in number. The subjects were all would-be 
1 Clinical Lecture on Arsenical Paralysis, Phila. Med dimes, March, 1881. MYELITIS FOLLOWING ACUTE ARSENICAL POISONING. 
suicides with Paris green,1 and they presented remarkably 
similar symptoms. In many respects the cases resembled 
those already related. 
Case i.—Samuel L., hostler, seen March 21, 1879, in consulta- 
tion with Dr. M. Burke. 
At the end of January, while in good health, swallowed a large 
quantity of pulverized Paris green. Had much difficulty in swal- 
lowing it, and very soon was led to a drug store, where emetics 
were given ; and later he was taken to Bellevue Hospital, where 
the stomach-pump was thoroughly used. Vomiting, gastric pain 
and irritation, extreme prostration, lasted four or five days. 
Soon after he began to go about his room, he noticed numbness 
in his fingers and hands, followed in two or three days by similar 
sensations in his feet. Paresis appeared about the same time in 
all the extremities, and had steadily progressed to extreme paraly- 
sis below the knees, with wasting of the muscles there. Has had 
much burning, gnawing pain in soles and insteps ; a little in the 
hands. Ten days ago became unable to stand. No cerebral 
symptoms, or palsy of bladder, or jerking of legs. 
Examination.—Hands and forearms only weak ; no positive 
paralysis or atrophy ; no anaesthesia. 
Legs completely paralyzed below the knees ; cannot move feet 
or toes. Thigh muscles are weak. Marked atrophy of calves and 
of anterior tibial muscles. No anaesthesia of soles, unless it be a 
slight tactile dulness. 
Test with faradic current ; no reaction in right leg, nerves, or 
muscles. In left leg no reaction in anterior tibial muscles or 
nerves, but a feeble contraction can be produced in the calf. 
Patient is at times hysterical. 
At fifteen had a chancre, not followed by secondary symptoms. 
I have no further notes of the case ; but some sort of galvanic 
treatment was carried out. A few months afterward I learned 
that the patient was well, and some time in the winter of 1880-81 
he came to my office and exhibited a vigorous pair of legs. He 
1 Paris or Schweinfurth preen is a compound substance which is best desig- 
nated as aceto-arsenite of copper. 
In looking up this point I was astonished to find that such a popular and so 
constantly used a term as Paris green, was not to be found in the indexes of any 
of our dispensatories, treatises on materia medica, and, stranger still, not in 
works on toxicology. 
Prof. Chas. F. Chandler, in reply to a note, very kindly gave me all neces- 
sary chemical information on the subject. 12 
E. C. SEGUIN. 
had completely recovered and was at work again as a hostler at 
Jerome Park. 
Case 2.— Mary N., aged sixteen years, was admitted to the New 
York Hospital on December 11, 1878, in the service of Dr. Wool- 
sey Johnson. To Dr. R, W. Amidon, then house physician of the 
hospital, I am indebted for notes of the case and for the oppor- 
tunity of studying the case in its later stages. Dr. Johnson has 
kindly given me permission to use the case. 
The patient was a strong, rosy-cheeked girl of German parent- 
age. She had never suffered from rheumatism or malaria. Thir- 
teen days before admission she swallowed five cents’ worth of 
Paris green. In five minutes she vomited, and after an emetic 
had been given she vomited again, rejecting all (?) that had been 
swallowed. Probably had some gastro-enteritis, as she vomited 
and was purged for two or three days. 
It is reported (by patient and her friends) that on the first night 
she had fever. Second day, no fever or pain. Third day, at 3 
P.M., had fever for one hour and a half; burning pain in toes ; 
hands felt stiff. On the fifth day, at 9 a.m., fever returned, with 
slight headache, but no chill. The burning pain extended up to 
the knees. One week after taking the poison her legs became 
stiff, and she lost power in her arms; had “cramps” in her 
hands. These symptoms continued, but the headache ceased ; 
tried to walk, but found that she was partially paralyzed in her 
legs ; needed help to walk, and suffered pain in her knees (in the 
attempt). Three days later (tenth day) loss of power increased ; 
had cramps in hands; had tightening sensations in hands and 
feet, and they began to peel and showed a mottled red and white 
appearance. Bowels and bladder normal. 
Has not been unwell for twelve weeks ; previously regular. 
Condition on admission, thirteen days after taking poison : Pa- 
tient complains only of headache, and of inability to walk, be- 
cause “cords of knees are stiff.” Appetite, bowels, bladder, and 
eyes normal. 
Hands are cold and moist. The extensor muscles of both 
hands are weak, those of right hand weaker. Some twitching of 
long flexors and of interossei. 
The skin is lax. The small muscles of the region of the right 
little finger are completely paralyzed and wasted. The right 
thenar eminence is smaller than it should be. The hypothenar 
group on the left side is in the same condition. Grasp very weak. 
On dynamometer each hand shows about 20° (on outer circle). M YE LITIS FOLLO WING A CUTE ARSENICAL POISONING. 
13 
There is hyperidrosis. No anaesthesia is present, but she com- 
plains of a burning pain when pricked with a pin. 
The legs are semi-flexed, showing mostly palsy of the exten- 
sors of both feet. The left foot is more inverted than the right. 
Legs and thighs smaller and colder than normal. Toes are 
red ; the circulation is sluggish. The muscles of the legs are not 
flabby, but the anterior tibial regions are flattened. Hamstrings 
rigid on both sides. 
Circumference of right thigh, 30.5 ; right leg, 23.5. 
“ “ left “ 30-5 ; left “ 24.5. 
There is complete paralysis of the anterior tibial muscles. The 
peroneal and posterior tibial groups are somewhat atrophied and 
paretic. Great toes are motionless. Flexion of thighs is moder- 
ately good ; extension complete. No increased reflex actions. Is 
rather hypersesthetic (in legs). 
Dec. 14th. A tendency to retention of urine is noted (but is 
not again referred to). Examination with the faradic current 
showed good contractions in left thenar and hypothenar eminences, 
but none in the right. In the right leg there is slight reaction 
in the anterior tibial muscles ; none in the peronei. 
Dec. 26th. It is noted that there is no faradic reaction in the 
anterior tibials and peronei. Sensibility is good. Hamstrings 
less rigid. Patient has plaster apparatus for legs, and the appli- 
cation of the faradic current. 
Jan. 11, 1879. Walks with some support, and has done so for 
a week. Left leg nearly straight. 
Jan. 15th. Circumference of right thigh, 34.0 ; right leg, 24. 
“ left “ 34.5 ; left “ 26. 
Toes always cold and moist; tender to slight pressure. Less 
contraction of hamstrings. No reflex actions in legs. Interossei 
of hands do not improve, and remain as flaccid, atrophied, and 
weak as on admission (faradism not used on upper extremities). 
Jan. 24th. Galvanism tried for first time ; ten cells cause con- 
traction of tibialis and peronei; eight cells (Stohrer battery) 
cause contraction of quadriceps, sartorius, and muscles of calf. 
Some atrophy of extensors of the right forearm and hand ; good 
reactions (current not stated) in ulnar distribution, but not in 
wasted extensors. On the left side good reaction in forearm and 
hand, except abductor pollicis, to both galvanism and faradism. 
Jan. 27th. Menses appeared with great pain. 14 
E. C. SEGUIN. 
Feb. 4th. Electrical applications omitted because of malaise. 
Patient doing nicely ; muscles react with small amounts of elec- 
tricity. 
Feb. 9th. Some trophic changes in feet ; nail of big toe coming 
off. The skin is rough, and there is vaso-motor disturbance. Re- 
actions improving (in legs). 
March 10th. Walks quite well. Some remaining weakness of 
anterior tibial muscles. 
Discharged improved. 
This patient at once began to be treated as an out-patient at 
the Manhattan Hospital, and after several weeks of treatment by 
galvanism mostly was completely cured. 
The notes taken at this time have been misplaced, but our 
recollection is clear that her upper extremities were about well, 
though perspiring, and that the lower limbs exhibited paresis, a 
sluggish circulation, and a peculiar sensitiveness and tenderness. 
She was able to walk alone, but lame. Her general health was 
quite good. 
It seems certain that this was a case of subacute polio-mye- 
litis chiefly. The inflammatory action must have extended 
to deeper parts of the gray matter, as shown by con- 
tinued hyperalgesia and by the contractures. 
Case 3.—Ellen R., aged twenty-six years, admitted to Manhat- 
tan Hospital May 10, 1881. In September, 1880, took a large 
dose of Paris green. Was exceedingly ill; vomiting and diarrhoea. 
In a week nearly complete paralysis developed. Legs completely 
paralyzed ; forearms the same. 
A gradual recovery began in the course of a few weeks (no 
treatment). 
Three weeks before admission to the hospital, Dr. J. B. Emer- 
son, who visited her in the country, found her fingers and the 
soles of her feet nearly insensible to pricking. I examined the 
patient May 9, 1881, and the following notes were taken. Can 
walk with a little aid, impeded by moderate contracture of right 
knee, and tenderness of feet. No voluntary power (motion) be- 
low ankles. Complete ansesthesia to contact on soles of feet and 
on finger-tips. Feels cold and heat, however, and pricking quite 
well. The upper extremities simply present a slight paresis with 
moderate wasting of the hand muscles, some interossei quite MYELITIS FOLLO WING A CUTE ARSENICAL POISONING. 
15 
wasted, and some large fibrillary movements in the same. No 
cutaneous trophic changes. Thighs moderately wasted, with 
some contracture of right hamstrings. No patellar tendon reflex. 
Calves and anterior tibial muscles are much wasted ; legs and feet 
bluish and cold ; slight tactile anaesthesia of feet. 
Patient is thin and in poor health ; has been using an unknown 
quantity of morphia. 
She was ordered a mixture containing diminishing amounts of 
morphia ; and Dr. Adam, assistant physician of the hospital, ap- 
plied galvanism and faradism very faithfully to her for weeks. He 
also gave her passive movements and massage. The improvement 
was steady, and in a few weeks patient left the hospital almost per- 
fectly cured as regards paralysis, and in good general health. She 
was forty-eight days in the hospital. The day after admission 
Dr. Adam made a thorough testing of the affected muscles with 
the galvanic and faradic currents, which may be summed up by 
saying that most of the paralyzed parts exhibited the degenera- 
tion reactions, viz. : i, diminished or wholly lost faradic reaction 
in muscles and nerves ; 2, sluggish contractions to galvanism, 
with ancc = cacc in many muscles, and ancc > cacc in some. For 
example, in the muscles of the legs below knees a very strong faradic 
current caused no reaction. In the right gastrocnemius ancc > 
cacc. In other muscles cacc = ancc. In some interossei of hands 
ancc > cacc. 
This patient is again under my care at the Manhattan Eye 
and Ear Hospital (October, 1882,), for the cure of the only re- 
maining weakness, viz. : paralysis of both anterior tibial muscles 
causing pes valgus. This is the only muscle which does not res- 
pond to the will, but all the muscles of the legs show a most as- 
tonishing quantitative reduction in electrical reactions : no reac- 
tion in muscles or nerves to full strength of faradic secondary cur- 
rent, and few small reactions in nerves and muscles to fifty good 
Leclanche elements. Reactions obtained are of normal quality. 
In this case, besides the contracture of the hamstrings, as 
in Case 2, we have distinct though slight anaesthesia to in- 
dicate a certain extension backward of the lesion, in the 
spinal gray matter. 
To sum up, these three cases presented evidences of 
slight subacute, diffused myelitis, more distributed in the E. C. SEGUIN. 
anterior cornua. In Case I the symptoms were more purely 
those of poliomyelitis. 
In all cases the symptoms of myelitis followed within a 
week after the ingestion of the poison. 
If we compare the symptoms present in the various 
human cases related and quoted, and the pathological 
appearances found by Popow in his animals, it is, it seems 
to me, legitimate to reach the following conclusions : 
1. Arsenical paralysis is the expression of a myelitis. 
2. This myelitis approximates the type known as polio- 
myelitis in so far as the symptoms are chiefly motor; that 
the paralyzed muscles undergo some atrophy, and exhibit 
the degeneration reactions to electrical currents ; that the 
bladder is never palsied ; and that in animals the ganglion 
cells of the anterior horns are extensively diseased. 
3. There is usually more than poliomyelitis, as shown 
by Popow’s post-mortem findings, and by the presence in 
living human subjects of pains in the nerves and muscles of 
the affected limbs, and by the occurrence of actual anaes- 
thesia. 
4. Consequently it might be better to speak of arsenical 
paralysis as due to diffused central myelitis with special 
involvement of the anterior gray matter. 
5. Whether this myelitis is strictly arsenical, i. e., caused 
by the direct effect of the arsenic on the tissue of the spinal 
cord, or whether it is produced (as are many forms of 
myelitis) by the irritation of peripheral nerves (cutaneous, 
intestinal and gastric nerve-endings), is a question which 
cannot at present be definitely solved, but which presents an 
interesting field for future research and speculation. THE JOURNAL OF 
NERVOUS AND MENTAL DISEASE 
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