Alcoholic Paralysis. 
BY 
HENRY HUN, M. D., 
Lecturer on Nervous Diseases in the Albany Medical College. 
FROM 
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES. 
April, 1885. Extracted from the 
American Journal of the Medical Sciences for April, 1885. 
ALCOHOLIC PARALYSIS. 
HENRY HUN, M.D., 
Lecturer on Nervous Diseases in the Albany Medical College. 
The immediate and transient effects of an excessive quantity of alcohol 
upon the human nervous system, whether they are manifested in the form 
of drunkenness, or of delirium tremens, or of an acute attack of insanity, 
are well known. Scarcely less evident are the effects produced upon the 
nervous system by a less excessive, but a more prolonged abuse of alcoholic 
drinks. These effects may be manifested either in a general failure of 
physical and mental power, or in a form of disease closely resembling 
progressive paralytic dementia, or in various forms of chronic insanity, or 
in epilepsy, or in neuralgia, or in paralysis. In the acute form of alcoholic 
poisoning, no change in the structure of the nervous system has been 
found, except that the meninges in common with the internal organs and 
the mucous membranes are the seat of a very decided injection and of a 
slight exudation. In the chronic form of alcoholism, a number of patho- 
logical changes have been discovered in the nervous system, which, how- 
ever, vary greatly in different cases. The pathological conditions most 
commonly found are, pachymeningitis interna haemorrhagica, thickening 
and opacity of the pia mater, serous exudation in the sub-arachnoid space, 
dryness and toughness of the cerebral substance, atrophy of the cerebral 
convolutions, fatty degeneration of the nerve-cells,1 and degenerative 
changes in the peripheral nerves.2 
Of late years the paralysis which results from the abuse of alcohol has 
been accurately described by numerous observers, and the attempt has been 
made to discover the lesion of the nervous system which is associated 
with this form of paralysis. The two cases here reported seem to be 
1 Wilks, Journal of Medical Sciences, 1864. 
2 Dejerine, Archiv. de physiol, norm, et Pathol., 1884, No. 2, p. 231. Lancereaux, 
Gazette Hebdom., 1881, Nos. 45 and 118. 
1 2 
typical examples of this disease, and may contribute somewhat to a better 
understanding of it. 
Case IA male, set. 28, single, entered St. Peter's Hospital September 
13, 1884, and gave the following history :- 
Family history good. Patient has always worked hard, and has enjoyed 
good health until a year ago. Has never had any venereal disease, but has 
always been a hard drinker, although he has never had delirium tremens. 
During many years he has drunk steadily and excessively, and during the 
year previous to this sickness he has drunk more than half a pint of undi- 
luted bad whiskey daily. He had no settled home, but slept about wherever 
he could find a place. Last winter he " caught cold," and on endeavoring 
to get out of bed the next morning he could not do so on account of 
general weakness, pains in legs and arms, and inability to walk. He was 
obliged to stay in bed for a week, during which period there were a numb- 
ness and tingling in his feet and legs. On getting out of bed, and on en- 
deavoring to walk, he was obliged to run forward to prevent himself from 
falling. He continued in the same condition for about two months, during 
which time improvement slowly continued, and after a time he could 
walk about as well as ever. About a month ago, the patient began to 
feel the disease returning, and in the course of a few days the same 
symptoms that he had last winter came on again, so that he was unable to 
walk. From this time until he entered the hospital he suffered from pain, 
numbness, and tingling sensations in his legs and arms on both sides, and 
from great loss of strength in his legs, and in a less degree in his arms. 
He also was troubled by frequent micturition, and by a sensation of sore- 
ness over the abdomen, but no girdle sensation. Appetite poor, and fre- 
quent vomiting. 
An examination at the time of entrance gave the following result: 
Patient is of strong frame, and well nourished. He seems to be somewhat 
under the effects of liquor; he talks and acts in a foolish manner, and is 
tremulous ; his stomach is irritable; the end of his nose is much enlarged 
and congested, and an acne eruption covers his face. Slight paresis of left 
side of face, but not of tongue nor of ocular muscles. Pupils equal, and 
react sluggishly to light and to efforts of accommodation. No absolute 
paralysis, but general paresis of muscles, of arms, and hands. Grasp of 
hands registered with Mathieu's dynamometer is, left 45, right 75. 
Patient cannot perfectly extend the last two fingers of each hand. Decided 
tremor of hands during voluntary movements. Considerable degree of 
ataxia in movements of left hand, a somewhat less degree of ataxia in 
movements of right hand. Patient has not the violent ataxic movements 
of locomotor ataxia, but rather the tremulous uncertain movements of the 
drunkard. No decided atrophy of muscles of arms. Sensibility to tactile 
impressions over hands, arms, and legs normal, except for small patches 
of anaesthesia to slight tactile impressions over feet. Decided hyperaes- 
thesia of skin, and great tenderness of muscles on pressure. No decided 
atrophy of muscles of legs. Patient walks with great difficulty. In walk- 
ing lie flexes his thigh strongly on his body, and then brings his foot down 
with a stamp in the manner described by Westphal.1 His movements are 
very rapid and uncertain, and he constantly appears to be just on the point 
of falling. His walk exhibits a mixture of weakness and ataxia. Patient 
1 Charite Annalen, iv. Jahrg. 1879, p. 395. 3 
cannot stand with his feet close together, unless he is given some little 
support. When slightly supported he apparently stands as well when his 
eyes are shut as when they are open, although he says that he feels more 
dizzy in the former case. When he attempts to stand his whole body is 
thrown into a tremor. When in bed he can move legs freely in all direc- 
tions, and such movements show a slight degree of ataxia. Plantar, cre- 
masteric, and umbilical reflexes normal; no patellar reflex; no ankle 
clonus ; no paradoxical contraction ; no rigidity, nor deformity of spine ; 
no tenderness over spinous processes ; slight tenderness in lumbar region 
on each side of the spinous processes over the muscle. Abdominal and 
thoracic examination negative, except that a short faint systolic murmur 
is heard over aortic valves and in subclavian arteries. No enlargement of 
the area of cardiac dulness. R. Blisters along spinous processes. R. Pot. 
iodide grs. xv, t. i. d. 
Oct. 7. Patient has slowly grown worse. The legs are very weak in 
all their movements, and exhibit a decided degree of ataxia. Small 
patches of anresthesia to tactile impressions scattered not only over feet, but 
also over legs. Sensibility to painful and thermic impressions normal; 
muscles painful on pressure; can neither walk nor stand. Patellar reflex 
absent. Plantar reflex exaggerated, and cutaneous reflexes of any part of 
skin of legs greatly increased, which seems to be due to a hypermsthesia 
of skin of legs ; cremasteric reflex normal; umbilical reflex slight; pupil 
reflex normal. Slight degree of ataxia of hands. Grasp of right hand 
equals 60 as registered by Mathieu's dynamometer. No tenderness along 
back. Slight paresis of left side of face, but this is less than on entrance. 
The congestion of the nose is very much less, and there is only a slight 
degree of tremor remaining. Patient sometimes loses his legs in bed, so 
that he cannot tell in what position they are. R. Pot. iodide grs. 
xxv, t. i. d. 
14z/z. The large doses of iodide cause much discomfort, producing an 
intense coryza, and a severe conjunctivitis. Paresis of left side of face 
has almost entirely disappeared. Muscles of legs flabby and atrophied. 
Muscles of legs decidedly tender on pressure. No pain on passive motion. 
Patient is quite unable to walk. Circumference of thigh two inches, above 
knee is 12 inches. Greatest circumference of calf of leg 11| inches. 
Nov. 10. No decided change ; patient is rather stronger. The coryza 
and conjunctivitis disappeared after about ten days, but he now has an 
extensive eruption of acne. Omit the iodide. R. Faradic current to 
arms and legs. R. Strychnim sulph. gr. glj-, t. i. d. 
Dec. 1. Decidedly better. Can walk a little once more. 
Patient is decidedly better. Can walk and stand for a short time. 
His walk is still very unsteady, and stamping as at time of entrance. Can 
button his clothes once more, which for a long time he was unable to do. 
No facial paresis. Ataxic movements are very slight. Grasp of hands 
strong. Sensibility to tactile impressions over both arms and legs normal. 
Localization of tactile impressions normal, except as regards the toes; the 
patient not being able to tell always which toe is touched. Sensibility to 
painful and thermic impressions normal. No retardation of conduction of 
painful nor tactile impressions. Patellar reflex and ankle clonus absent. 
Cutaneous reflex exaggerated. Circumference of thigh three inches above 
knee-joint, right inches, left 12 inches. Greatest circumference of 
calf of leg, right 11 inches, left 10| inches. 
Electric examination made with the Macintosh combined battery. 4 
The positive pole on upper part of sternum, the negative pole on point 
to be tested. 
Faradic current. 
Peroneus nerve, 
right, cylinder withdrawn If inches. 
u u 
left, 
" " If " 
Tibialis anticus muscle, 
left, 
" " 3 " 
but the contraction becomes much stronger as the electrode is slowly 
moved outwards towards the head of the fibula and the peroneus nerve. 
No contraction can be obtained from the right tibialis anticus muscle 
when the electrode is over the muscle itself, but when the electrode is held 
midway between the motor point for the muscle and the head of the fibula 
a sluggish contraction is obtained when the cylinder is withdrawn 
inches; when the cylinder is withdrawn more the contraction of the mus- 
cle loses its sluggish character and appears normal. A sluggish contraction 
of vastus internus muscle on both sides when cylinder is withdrawn 2% 
inches. 
Nerves of arms and muscles on anterior surface of forearm respond 
when cylinder is entirely in. Extensor muscles of forearm and muscles 
of base of thumb respond, quick contraction, when cylinder is withdrawn 
inches. 
Galvanic current measured in milliamperes by a Gaiffe galvanometer. 
Right peroneus nerve, 
negative closin 
g, 5^-; positive 
closing, 13 
Left " " 
u u 
" 12 
Right tibialis anticus muscle, 
U it 
14 " 
" 11 
Left " " " 
u cc 
10 " 
Right vastus interims, 
<< u 
20| . « 
" 17 
The extensor longus muscle gave no response to currents even stronger 
than those given above. 
22th. Is up and out of bed ; can walk easily, though rather awkwardly 
and unsteadily. Can stand with feet together and eyes shut without 
wavering, although he complains then of feeling a little dizzy. Very 
slight tenderness of muscles still remains. Grasp of left hand 90, right 
hand 100, as registered with Mathieu's dynamometer. A careful oph- 
thalmoscopic examination revealed nothing abnormal. 
Jan. 26, 1885. Galvanic current measured in milliamperes by a Gaiffe 
galvanometer. 
Right peroneus nerve, 
Left " " 
negative closing, ; 
" " 7 
positive closing, 12 
" " " 13 
Right tibialis anticus muscle, 
, " " 15 
" opening, 20 
" closing, 11 
Left 
" " 13 
" " 18 
Faradic current. 
All the muscles and nerves of arms and thumb respond readily when 
the cylinder is entirely in ; the muscles of the right arm responding more 
actively than those of the left. 
Peroneus nerve, left, cylinder fully in ; right, cylinder withdrawn 1 inch. 
Tibialis anticus muscle, left, " withdrawn 2 inch: right, ~ " " 
Extensor longus muscle, left, " " 3% " right, " 
" 3% " 
Vastus internus muscle, left, " " 1% " right, " 
" 1% "i 
1 In making the electrical examinations in this and the following case the 18 cell 
combined Macintosh battery was employed. A large sponge electrode was placed 5 
Patient can now walk without difficulty ; can stand on either leg alone, 
and feels strong. Grasp of hands measured with Mathieu's dynamometer 
is, right 115, left 100. There is no ataxia. Patellar reflex present in 
both legs; plantar reflexes increased; cremasteric and umbilical reflexes 
normal. No hyperaesthesia of skin of legs, nor tenderness on pressure over 
the muscles. Sensibility to tactile, painful, and thermic impressions nor- 
mal. Slight failure of localization on toes. No fibrillary contraction of 
muscles ; circumference of thigh three inches above knee-joint where the 
thigh is smallest is, left inches, right inches. Greatest circum- 
ference of calf of leg is inches, and is the same on each side. 
The cardiac murmur has disappeared. Slight murmur in carotids on 
deep pressure. 
Case II A male, set. 28, single; by occupation a barber; ex- 
amined Oct. 23d, 1882. Until the past year patient has always enjoyed 
good health, and denies ever having had any venereal disease. He has for 
a long time indulged too freely in alcoholic drinks, and for six months 
previous to his present illness he had been continuously under the influ- 
ence of liquor, although he did not have any attack of delirium tremens. 
As long as a year ago it was noticed that he seemed to be lazy, and it is 
only recently that his family have seen that his laziness is due to weak- 
ness. During the past year he has frequently said and done very foolish 
things, and during the months of last August and September he stayed 
away from his home and could not be induced to return to it, because he 
imagined that his family were not treating him as they ought. 
During the past six months he has been gradually but evidently losing 
strength in his legs, and during the past month or two he has also been 
losing strength in his arms. His memory has also failed greatly, and at 
times he talks in a foolish manner. During the past two weeks he has 
been confined to his bed by weakness, and during the past week he has 
been unable to sit up in bed without assistance. About a week ago he 
slipped otf his chair and was unconscious for a quarter of an hour, during 
which time he had general convulsive movements, but did not bite his 
tongue. 
Complains now of general weakness, of numbness of hands and feet, 
and of severe pricking pain under his nails. No other abnormal sensa- 
tions in legs or arms. Says that left arm and leg are weaker, more tender, 
and more painful than the right. Some time ago had a slight pain in his 
back, but not lately. Has not had any headache, no noises in ears or 
head, but is dizzy at times. Insomnia. No cough nor pain in chest. 
Appetite has been good, but is poor now ; digestion good. Bowels slightly 
constipated. No delusions, but patient is very hopeful, and treats his 
sickness very lightly. 
No facial nor oculai' paralysis. Tongue protruded straight. Pupils 
equal, and react normally. Speech is at times normal, at other times 
indistinct and explosive. General hyperesthesia of arms, legs, and body, 
especially of abdomen and calves of legs. He shrinks away in a nervous 
over the upper part of the sternum, and a small electrode (a metallic knob % inch in 
diameter and covered with a sponge) was placed over the motor point to be tested. 
The strength of the faradic current required to produce a minimal contraction was 
measured by the distance to which the metallic cylinder had to be withdrawn ; while 
the strength of the galvanic current was measured in milliamperes by a Gaiffe galva- 
nometer, and the strength of the current was regulated by a rheostat. 6 
manner from the slightest touch on the abdomen. With the exception 
of the hyperaesthesia the conduction of tactile, painful, and thermic im- 
pressions is normal. No retardation of the conduction of pain. No 
absolute paralysis of any muscle, but a very extreme degree of paresis of 
all muscles. Can scarcely walk when supported on both sides. Grasp 
of hand weak. All movements are painful-legs greatly emaciated. 
Arms scarcely at all so. Very slight ataxia of legs. Movements of 
fingers awkward. Patellar reflex absent. Cutaneous reflexes well marked. 
Neither tenderness nor rigidity nor deformity of head or spinal column. 
Left arm and leg seem weaker than the right. 
At this time the patient was taking several grains of opium daily to 
procure sleep. This was ordered to be gradually diminished. He was 
also chewing tobacco freely, and this he would not entirely stop, but con- 
sented to reduce the quantity. 
The galvanic current was applied daily for ten minutes, the positive 
pole on the nape of the neck,.and the negative pole rubbed over the arms 
and legs, and liq. potass, arsenitis npiij was given three times a day, and 
a laxative pill at night. 
November 25. Has steadily lost strength. Can move his left leg but 
little, and cannot raise the right foot from the bed. Cannot raise himself 
up in bed. Movements of the arms are also weaker, and he cannot exe- 
cute any delicate movements. All the muscles of the body have rapidly 
atrophied, so that the patient is much emaciated. 
Complains greatly of neuralgic pains and of cramps in his legs, and 
he always feels cold. General hyperassthesia of the skin, and pain on 
compressing the muscles still continues. Bladder and rectum act normally 
but sluggishly. Eats very little, and does not sleep well, although he 
takes a couple of grains of opium at bedtime. Mental condition is very 
variable ; at one minute he talks sensibly and the next minute is very 
delirious. The application of the electricity causes him much pain. The 
liq. potass, arsenitis was omitted, and in its place a pill composed of ferri 
redacti grs. ij, and strychnias sulph. gr. was given t. i. d. 
December 10. The general muscular atrophy continues to increase. 
There is no fibrillar contraction of the muscles even when they are 
mechanically irritated, except in the case of the right gastrocnemius after 
the application of electricity ; this muscle manifesting fibrillar contrac- 
tion for an hour or more after the application of electricity. In all other 
respects, except the muscular atrophy, he has improved. He cannot stand, 
but he can raise himself up and sit on the edge of the bed and get into bed 
again without assistance. He can raise his right foot easily from the bed. 
The patellar reflex is still absent. His movements are slow, stiff, awkward, 
and painful. The hyperaesthesia of skin and muscles is much less marked, 
and he complains less of pain and cramps in legs and numbness of hands. 
Is less sensitive to the electricity. His appetite is better, and he sleeps 
better, although he takes only gr. of opium at bedtime, now. 
All the muscles of the arms and legs respond readily to the faradic 
current when a strong current is employed. (The instrument made by 
the Galvano-Faradic Manufacturing Co., New York, two cells being in 
operation, and the metallic cylinder withdrawn 4 inches.) The extensor 
longus digitorum of left leg, however, will not respond to any force of the 
current; and in general the muscles of the left leg respond less readily 
than those of the right leg. 
The electro-motor excitability, as shown by the galvanic current, was 
measured in milliamperes by a Gaiffe galvanometer. 7 
-o ,. , . (right, 6 milliamperes. 
Feroneus nerve, negative closing, -t, 9 
° 1 left, 6 " 
Tibialis anticus muscle, " " '? 
(left, 5 
u 
Ct 
( pi or J i f 2 - 
Ulnaris nerve at elbow, " " (]eft ' 
Ct 
cc 
Median nerve at elbow, " " 2® 
Ct 
Flexor sublimis digitorum, 2d & 3d fingers, ( right, 3 
tc 
negative closing, 4 
tc 
Flexor subliinis digitorum, 1st & 4th fingers, ( right, 
tt 
negative closing, (left, 3| 
u 
January 5, 1883. Great and general diminution of the excitability of 
the muscles to the faradic current. The flexors of the index fingers con- 
tract but very slightly to the strongest faradic current. The extensor 
longus digitorum of left leg does not respond at all to the faradic current, 
and the corresponding muscle of the right leg responds but very slightly. 
After this date there was no examination of the muscles made with the 
faradic current. 
Excitability of the muscles to the galvanic current expressed in 
milliamperes is as follows :- 
-r, (right, negative 
Jreroneus nerve, j ' °u 
closing, 
U 
u 
2f 
; positive closing 
G| 
Tibialis anticus muscle, « 
U 
U 
3; 
3; 
u 
C6 
a 
u 
6 
8 
Extensor longus digito- ( right, " 
u 
5 ; 
U 
u 
7 
rum, j left, no reaction could be obtained. 
txt t . n f right, negative 
Median nerve at elbow, ° u 
closing, 
u 
2; 
5; 
positive closing, 
U it 
6 
8 
Ulnar nerve at elbow, u 
u 
u 
3f 
3f 
. u 
u 
u 
3 
3 
Flexor sublimis digito- ( right, " 
u 
4; 
u 
u 
7 
rum, 2d & 3d fingers, (left, " 
u 
4; 
u 
u 
7 
Flexor sublimis digito- ( right, " 
a 
3; 
u 
u 
5 
rum, 1st & 4th fingers, (left, " 
u 
3; 
u 
u 
5 
On the right side the index finger moves more than the little finger, 
while on the left side the little finger moves more than the index finger. 
All the muscles respond even to a very strong galvanic current only by 
very slight contraction. The electrical examination is rendered very 
difficult by the great irritability of the patient. 
The general atrophy of the muscles of the arms, legs, face, and body 
has steadily increased, and he is approaching the condition of a living 
skeleton. There is no fibrillar contraction of the rapidly atrophying 
muscles. He can move himself about in bed much better than when I 
first saw him, but not so well as he could a month ago. 
He is very averse to getting out of bed. Grasp of hands is weak. His 
feet are drawn down and held rigidly in a condition of plantar flexion. 
Toes also held in position of plantar flexion. Sensibility to tactile, pain- 
ful, and thermic impressions intact. The hyperesthesia of skin and 
muscles has almost entirely disappeared; and the hyperesthesia of the 
abdomen is very slight. He is still a little nervous about having his 8 
abdomen touched, although he himself can make firm pressure upon it. 
His appetite is rather better. For a long time his mind was quite clear, 
but for the last day or two he has again been a little delirious. 
All medicine was omitted except a laxative and a hypnotic pill at night. 
R. Iodide of potassium, grs. vi, was given t. i. d. 
February 5. No decided change, except that he is eating better, and 
requires no hypnotic. Indeed, he sleeps the greater part of the day and 
night. Iodide of potassium was increased to grs. x, t. i. d. 
Circumference of knee-joint, 
12 
inches. 
Circumference a little below knee, 
7i 
44 
Greatest circumference of calf of leg, 
7 
44 
Greatest circumference of thigh, 
71 
1 2 
44 
Measurements are the same on both legs. 
Patient refuses any further application of electricity on account of the 
pain it causes. 
March 5. Has eaten almost nothing lately. Will not even take milk. 
Is very weak. Has emaciated so much that he is almost nothing but 
skin and bone. Muscles of face partake in the general atrophy. Can 
move his hands and arms pretty well. Grasp of hand as measured by 
Mathieu's dynamometer shows left 25, right 38. Slight voluntary motion 
of muscles of thigh is still retained. Complete paralysis of muscles 
below the knee. Slight dulling of sensibility of skin of feet and lower 
leg to tactile, but not to painful impressions. Well-marked retardation 
(about two seconds) of conduction of painful impressions from feet. Skin 
of legs is still somewhat hyperaesthetic, and passive .motion of leg causes 
much pain. No tendon reflexes. Cutaneous reflexes well marked. 
Patient will not permit an electrical examination to be made. Bowels 
regular. Pulse rapid, weak, dichrotic. 
13</z. Yesterday a decided change appeared in patient. Lies in a 
semi-comatose condition, from which he is easily aroused to answer ques- 
tions. Answers are rational. Bowels are regular. Urine free, and he 
asks for bed-pan and urinal when he needs them. During the past three 
days the left arm has become paralyzed. The paralysis appeared first in 
the deltoid, then extended to biceps and triceps, and then to muscles of 
forearm, very slight motion of fingers and hand alone remaining. Motion 
of right arm is almost as good as it was a week ago. The muscles of the 
legs are completely paralyzed. Cannot raise his voice above a whisper. 
Will drink only a little wine. 
15M. Consciousness clear. Voice growing gradually weaker. Has an 
occasional dejection in bed. 
Died quietly last night. 
17<7z. Autopsy thirty-six hours after deathExtreme emaciation of 
whole body. Several spots of purpura htemorrhagica over anterior aspect 
of left uppei' arm. No hypostasis. Post-mortem rigidity not present. 
Muscular tissue very slight in amount. No decided replacing of muscular 
fibres by connective tissue could be seen by the naked eye. 
No decided abnormality about thoracic or abdominal organs except 
general atrophy and dryness. 
Brain-Veins of pia mater full of blood. Unusually large quantity 
of sub-arachnoid fluid over the surface of the hemispheres. No enlarge- 
ment of the ventricles, and very slight atrophy of the cerebral convolu- 
tions. Sections through the hemispheres, the ganglia at the base, and the 
cerebellum, appear normal to the naked eye. 9 
Spinal CordSlight adherence of the dura and the pia mater in the 
cervical region of the cord, but no marked congestion of the membranes 
nor other sign of meningitis. On section, the spinal cord appears normal 
to the naked eye. 
Microscopic Examination-A number of sections of several parts of 
the cortex, especially of the central convolutions, show a decided degen- 
eration of the nerve-cells in the cortex. Although the brain is well 
hardened the nerve-cells are so granular that their nucleus can scarcely 
be made out, and the cells themselves are rounded and contracted so that, 
instead of being surrounded by a small lymph space, they seem to be 
lying in large cavities. There is also a slight increase in the number of 
small round cells in the cortex and in the adjoining parts of the white 
matter. A large number of sections of the medulla oblongata and spinal 
cord, especially of the cervical and lumbar enlargements, show these 
organs to be entirely normal, and in particular the nerve-cells in the 
anterior horns are unusually well stained and sharply defined. 
Unfortunately, pieces of the peripheral nerves and muscles were not 
preserved. 
If we review in a general way the symptoms of these two cases, we 
find: First. Sensory disturbances in tlie form of neuralgic pains and 
paraesthesiae, pain on pressure over the muscles and on passive motions, 
a mixture of cutaneous hypermsthesia and anaesthesia, and retardation of 
the conduction of pain. Second. Motor disturbances in the form of mus- 
cular weakness, which rapidly increases in intensity and is accompanied 
by muscular atrophy without fibrillar contraction and by the electrical 
reaction of degeneration, or at least an approach to this reaction. And, 
third. Ataxic disturbances which are associated with a loss of the tendon 
reflexes, whi e the cutaneous reflexes, especially the plantar reflex, are 
increased. All these disturbances are symmetrically distributed. They 
appear first and most decidedly in the legs and then extend to the arms, 
where they are less severe. Associated with these symptoms is a greater 
or less degree of mental weakness and derangement. 
Such a combination of sensory disturbances, absence of patellar reflex, 
ataxia, muscular paralysis and muscular atrophy, is very uncommon, and 
there can be but little doubt that these two cases which possess these and 
other characters in common are due to the same lesion. There is, however, 
a great difference in the severity of the symptoms in the two cases. In the 
first case the initial sensory disturbances and the cutaneous and muscular 
byperaesthesia were only slightly marked, the pain on passive motion was 
entirely absent, and there was only a slight degree of muscular atrophy. 
In the second case, not only were all these symptoms extremely well 
marked, but in addition there was retardation of the conduction of pain, 
and the disease terminated fatally after the muscular atrophy had become 
so extreme that the patient was reduced to the condition of the so-called 
" living skeletons." 
In regard to the anatomical lesion associated with these symptoms, it is 
evident that it must be situated somewhere in the cerebro-spinal nervous 10 
system ; that is, either in the brain, or spinal cord, or in the peripheral 
nerves, or simultaneously in one or more of these divisions. The lesion 
cannot be in the brain alone, for no lesion of the brain can cause absence 
of tendon reflex, rapid muscular atrophy, reaction of degeneration, etc. 
All the symptoms in the case, except the mental disturbance, might be 
explained by a lesion of the spinal cord, provided that the lesion was 
situated in the anterior horns of gray matter and in the posterior columns 
of white matter; so that a combination of the symptoms of poliomyelitis 
anterior and of locomotor ataxia would result, although in these cases 
several symptoms of locomotor ataxia are absent. Not only is it very 
improbable that two portions of the spinal cord so widely separated from 
each other, both by space and by function, as the posterior columns and 
the anterior horns, should be simultaneously attacked by disease, while the 
rest of the spinal cord remained healthy, but a careful examination of the 
spinal cord in the second case revealed no trace of disease. By a process 
of elimination then it becomes altogether probable that the lesion is 
situated in the peripheral nerves. At first sight it may seem improbable 
that such a general, wide-spread, primary inflammation of the peripheral 
nerves should occur, but it is now well known that many cases, formerly 
called myelitis of the anterior horns, are really due to a general neuritis 
of the smaller branches of the peripheral nerves, the larger trunks 
being only slightly or not at all affected. Leyden1 described the disease 
very accurately, and gave it the name of multiple neuritis, and since that 
time it has been called by that name. The symptoms of multiple neuritis 
resemble, in respect to muscular paralysis and atrophy, very closely those 
of myelitis of the anterior horns, but in addition to these motor symp- 
toms there are many symptoms of sensory disturbance, viz., neuralgic 
pains, para3sthesia3, hyperaesthesiae, muscular tenderness, anaesthesia, 
retardation of the conduction of pain, absence of tendon reflexes, etc. ; 
these sensory symptoms being absent in myelitis of anterior horns; and 
the prominence of these sensory disturbances often enables us to decide 
whether a case is one of multiple neuritis or of myelitis of the anterior 
horns. The symptoms, therefore, of multiple neuritis are very similar to 
those of the two cases above reported, and in the absence of any change 
in the spinal cord of our second case, it is very probable that the lesion 
was in the peripheral nerves, and especially so since, in some cases of 
alcoholic paralysis reported by Lancereaux,2 Dejerine,3 and others, degen- 
erative processes were found in the peripheral nerves, while the spinal 
cord was healthy. 
The supposition of a general neuritis would explain the symptoms of 
these cases very well. The inflammation of the nerves would account for 
1 Zeitschrift fur klinische mediein, vol. i. p. 387. 
2 Gazette des Hdpitaux, 1883, No. 46 ; Gazette Hebdom., 1881, Nos. 45 aud 118. 
3 Archiv. de Physiol, norm, et pathol., 1884, No. 2, p. 231. 11 
the neuralgic pains and the paraesthesiae which are met with in the com- 
mencement of the disease. Along the inflamed nerves the conduction of 
nervous impulses would be both difficult and painful, and would thus give 
rise to muscular weakness and hyperaesthesia, and perhaps, also, to the 
retardation of the conduction of pain. The inflamed and degenerated 
nerves would naturally give rise to the reaction of degeneration, and 
would cause, also, the rapid muscular atrophy ; and when the nerves 
become destroyed by the inflammation muscular paralysis and cutaneous 
and muscular anaesthesia would result. The destruction of the nerve- 
fibres of muscular sense would explain the loss of the tendon reflex, the 
ignorance of the patient as to what position his legs were in, and the 
ataxia in part at least. Of course the mental symptoms could not be due 
to any disease of the peripheral nerves, but must be due to a change in 
the cerebral cortex, and this change in the second case was found to be a 
degeneration and shrinking up of the nerve-cells in the cortex, and a 
congestion of the pia mater and effusion of serum in the subarachnoid 
space. The ataxia might also be due, in part at least, to cerebral distur- 
bance, for it was associated with tremor, and in its appearance resembled 
the uncertain movements made by a drunken man, which form of inco- 
ordination is probably of cerebral origin. It seems probable, then, that 
the lesion of the nervous tissue occurring in alcoholic paralysis is a degene- 
ration of the nerve-cells in the cerebral cortex, and of the nerve-fibres in the 
smaller peripheral nerves, while the spinal cord is normal, and the nerve- 
cells lying in the anterior horns exhibit not the slightest degeneration nor 
change. 
That the disease attacks especially the small nerve branches and not 
the nerve trunks, is indicated in the first case by the action of the right 
tibialis anticus muscle to electricity. The muscular fibres respond 
readily to the galvanic current with a reversal of the formula, that is, the 
positive pole becomes the most active, but the nerve filaments are so 
degenerated that they cannot be directly excited by the faradic current, 
although they will still transmit strong impulses from the nerve trunk which 
remains excitable to the faradic and galvanic current. The left tibialis 
anticus muscle shows the same thing, but less decidedly. Indications of 
the same thing are furnished, though less clearly, by the electrical exami- 
nation of the second case. The electrical examination of the second case 
was, however, much less satisfactory, and is less reliable than that of the 
first case, partly because of the want of a suitable place and of proper 
appliances for the testing, and chiefly because of the great irritability of 
the patient. 
In regard to the treatment of these cases : iodide of potassium was in the 
beginning given freely to the first case. Under this treatment there was 
only very slight improvement, and this might well be due to the con- 
tinued rest in bed. Later strychnia was substituted for the iodide of 12 
potassium, and the faradic current was daily applied to the arms and legs, 
and under this treatment the improvement was very rapid. The patient's 
back was cauterized once or twice without any apparent result. In the 
second case the galvanic current,was employed on the arms and legs, and 
iron and strychnia were given <Xternally. For a short time after he com- 
menced taking the strychnia the patient improved decidedly, but he soon 
fell back again and ultimately died. 
In regard to the cause of the disease, there is in each case a history of 
excessive drinking. In the first case, when the patient entered the 
hospital he had every appearance of chronic alcoholism, general tremor, 
confusion of mind and speech, irritable stomach, and very well-marked 
acne rosacea ; and he did not hesitate to confess that he had for many 
years drunk a very excessive quantity of whiskey, etc. In the second case 
the family of the patient gave an account of very excessive drinking. 
The fact that many other cases closely resembling these two, and all 
following excessive use of alcohol, have been reported, confirms the view 
that we have to do with cases of disease which are due to the action on 
the nervous system of the long-continued abuse of alcohol. 
The whole subject of alcoholic paralysis is of comparatively recent 
date, and it is yet an open question whether or not it should be regarded 
as a special form of disease. A brief statement, therefore, of the cases of 
this disease which have been hitherto reported may lead to a better 
understanding of the subject. 
In his great work on chronic alcoholism, published in 1852, Magnus 
Huss divides the nervous symptoms occurring in chronic alcoholism into 
a paralytic, an anaesthetic, a convulsive, an epileptic, and a hyperaesthetic 
form according to the symptom which is most prominent, for in any one 
case a number of the above symptoms may occur in a greater or less 
degree, and the different forms cannot always be sharply separated from 
each other. He attributes these symptoms to a disease of the spinal cord 
and medulla oblongata, although he was unable actually to demonstrate 
this. ? 
CThe prognosis is rather J'avorable when the alcohol can be stopped In 
1864 Lancereaux described the forms of paralysis due to alcohol more 
systematically in the Dictionnaire Encyclopedique des Sciences medi- 
cales, and Leudet added a note to the effect that these were cases of 
painful paralysis. In 1867, Leudet published some cases of the hyper- 
aesthetic form of chronic alcoholism, and considered that it was of more 
frequent occurrence than Magnus Huss supposed. In these cases there 
was not only great hyperesthesia of the skin, muscles, and bones, but also 
neuralgic pains, muscular weakness, ataxia, anaesthesia, increase of cuta- 
neous reflexes, and in one case retardation of the conduction of pain. 
Cerebral symptoms were present in some cases and absent in others. 13 
Leudet, like Huss, considers these symptoms as of spinal origin. In 1868, 
Dr. Reginald Thompson read before the Royal Medical and Chirurgical 
Society of England the report of a case of paralysis of the extensors due, 
in part at least, to alcoholic excesses. 
In the Lancet, of 1872, Dr. S. Wilks quotes from a lecture which he 
delivered in October, 1867, to the effect that he has seen many cases of 
paraplegia in ladies who were addicted to alcoholic excesses, and says 
that since 1867 he has seen a number of similar cases. The symptoms of 
the disease, according to Wilks, are severe pains in all the limbs, especi- 
ally the lower ones which are much wasted, together with numbness and 
considerable anaesthesia, and at the same time only slight power of move- 
ment or total inability to stand. With the addition of the akinesia, the 
symptoms are not unlike those of ataxia. In one case there was hyper- 
aesthesia. Wilks considers the disease to be due to a change in the struc- 
ture of the spinal cord, similar to that which takes place in the brain in 
chronic alcoholism (viz., degeneration of the nervous tissue and thickening 
of the membranes), but he offers no proof of any such change. In such 
cases the prognos s is hopeful, and the most important thing in the treat- 
ment is the immediate and complete stopping of all alcoholic drinks. 
In the same year and journal {Lancet, 1872), J. Lockhart Clarke 
published some cases similar to those of Dr. Wilks, and endorsed Dr. 
Wilks's views as to the cause and nature of the disease. 
In 1879, Westphal1 described a peculiar form of walking in cases of 
chronic alcoholism which presented a certain resemblance to locomotor 
ataxia. The peculiarity of this kind of walking consists in lifting the leg 
very high so that the thigh is flexed strongly on the body, and then 
bringing the leg strongly down to the ground with a stamp. 
In 1881, Lancereaux2 published a number of cases of alcoholic paralysis 
in which the disease commenced with sharp pains in the legs, followed by 
a combination of anaesthesia and hypermsthesia, and a motor paresis. 
The symptoms are frequently confined to the legs, and when the arms are 
involved, the symptoms occur especially in the distribution of the radial 
nerves. The disease is more common in women than in men (12 women 
out of 15 cases), and the patients are affected by other symptoms of 
alcoholism. There are no contractures. The faradic electro-motor excita- 
bility is diminished or abolished. On careful microscopic examination of 
several cases, no change was found in any part of the nervous system 
except that the nerves of the affected extremities showed evident changes. 
The myelin was segmented and run into drops, and some sheaths were 
empty and collapsed, and the nuclei of Schwann were somewhat nearer 
together than normal. These changes did not however affect the whole of 
1 Charite Annalen, iv. Jarhgang, 1879, p. 395. 
2 Gazette Hebdom., Noe. 45 and 188. 14 
the nerve. In 1883, Lancereaux1 describes alcoholic paralysis as being 
symmetrical, attacking either the upper or lower extremities, and gradu- 
ally extending towards the body. The lower extremities are always more 
affected than the upper, and the extensor than the flexor muscles. The 
electrical excitability is greatly diminished, and extensive anaesthesia is 
often present. In such cases the brain and spinal cord were found to be 
normal, while the muscles and the peripheral nerves showed extensive 
degenerative changes. 
In August, 1882, Dr. Myrtle published in the British Medical Journal 
a rather imperfectly observed case of alcoholic paralysis, and in the same 
year Dr. G. Fisher2 reported two cases of alcoholic paralysis, which were 
very accurately examined and described, and of which he gives the follow- 
ing summary:- 
" Two men of a very low order of intelligence, almost imbeciles, who had no 
hereditary nor syphilitic taint, in consequence probably of the habitual abuse 
of alcohol, of excessive smoking, and of an indolent life, presented a complex of 
very severe disturbances of innervation, together with decided symptoms of mental 
derangement. The symptoms were paresis of all the muscles connected with the 
spinal cord, muscular atrophy with diminution of absence of the electric excita- 
bility, a remarkable hardness and remarkable sensitiveness on pressure of the 
paretic muscles, loss of mechanical excitability and of the patellar reflex, evident 
ataxia, slight initial parsesthesiae, dulling of tactile sensibility, retardation of the 
conduction of pain, peculiar, but sharply defined abnormalities of the perception 
of pain. Remq/ks double perception, retardation of the cutaneous reflexes. In 
addition to the above symptoms there were slight febrile and gastric disturbances, 
rapid pulse, and signs of diminished heart force. No strong subjective symptoms 
in the domain of sensibility; no lancinating pains ; no girdle sensation, neither 
rigidity nor pain, nor sensitiveness of spinal column. The vegetative functions 
and sphincters intact. The functions of the cranial nerves normal, except for 
slight abnormality of the pupil, probably due to other causes. In the first case 
recovery, in the second decided and permanent improvement." 
From a consideration of the symptoms in these cases Fischer concludes 
that the lesion is a subacute inflammation of the gray matter, the pos- 
terior columns, and the inner portion of the lateral columns of the spinal 
cord, and admits the possibility also of a lesion of the peripheral nerves. 
In July, 1883, Dr. R. Glynn reported several cases of alcoholic para- 
plegia in the Liverpool Medico-Chirurgical Journal. 
At a meeting of the Royal Medical and Chirurgical Society, held on 
February 12, 1884, Dr. Broadbent reported a case of alcoholic paralysis 
in which the paralysis came on insidiously, and attacked especially the 
extensors; the patellar reflex was absent, and there was no disturbance of 
the sphincters nor of sensation. No pain, but there was hyperaesthesia. 
The hands and feet were pale, puffy, and purplish. (This condition of 
cedema was noticed in a number of cases which had been previously re- 
ported.) The case of Dr. Broadbent quickly terminated fatally, and a 
careful microscopic examination revealed nothing abnormal. In the dis- 
1 Gazette des Hopitaux, No. 46, 1883. 
2 Archiv. fur Psychiatrie und Nervenkrankheiten, vol. xiii. p. 1. 15 
cussion following this case, Dr. Wilks reiterated his views as to this dis- 
ease which he had published in the Lancet twelve years before. He was 
constantly meeting with such cases, which recovered when the alcohol was 
withdrawn. Alcohol, in his opinion, acted on the whole cerebro-spinal 
system, though the spinal cord might be more affected in many cases. No 
change had hitherto been found in the true neural substance of the brain 
or cord, though these organs might be wasted and their meninges thick- 
ened. 
Dr. Buzzard spoke of a number of cases which he had seen, and called 
attention to the lancinating pains and the muscular atrophy which were 
often present. He said that in alcoholic paraplegia there was a diminu- 
tion or loss of response to the faradic current, with exaggerated response 
to the galvanic current. These facts showed the disease to be of spinal 
order. In alluding to the fact that Lancereaux bad found degenerative 
processes in the peripheral nerves, Dr. Buzzard stated that, in 1880, 
Mr. de Watteville had suggested that a dynamic change in the cells of the 
anterior horns of a temporary character might be sufficient to cause de- 
generative changes in the peripheral parts of the nerve-fibres. 
In the summer of 1884, Dr. Lbwenfeld1 reported two cases, the first of 
which was due to alcoholic excesses and was almost identical with the 
cases reported by Fischer mentioned above. The second case was not due 
to alcoholic excess, and differed in many respects from the first case, although 
it presented a combination of weakness, ataxia, and disturbances of sensa- 
tion. From a consideration of his cases Dr. Lbwenfeld regarded the 
lesion as being situated in the spinal cord. In an appendix to his article, 
however, written after he had read Dejerine's article, he is led to consider 
that the symptoms in his first case depended on a disease of the peripheral 
nerves, while he continued to regard his second case as due to a disease of 
the spinal cord. 
In February, 1884, J. Dejerine2 published two cases similar to the first 
two of Fischer's, although there was less muscular atrophy and paralysis, 
and the first one of Lbwenfeld's. Both cases terminated fatally, and at 
the autopsy a neuritis of the peripheral nerve was discovered with integ- 
rity of the nerve-roots, the spinal ganglion, and the spinal cord. By 
Dejerine these cases are considered as a variety of locomotor ataxia. 
In Sept. 1884, Dr. Kriiche3 published an article on the pseudo-tabes 
of drunkards, and pointed out the great similarity of this form of disease to 
locomotor ataxia. He bases his remarks on seventeen patients that he 
had had in his asylum, and he points out that in the false locomotor 
ataxia of drunkards there is great hyperaesthesia to the electric brush, 
and the girdle sensation is absent. On an ophthalmoscopic examination 
1 Archiv f. Psychiatrie u. Nervenkrankheiten, vol. xv. p. 438. 
2 Archiv. de Physiologic norm, et pathol., No. 2,1884, p. 231. 
3 Deutsche Medizinal Zeitung, Sept. 8, 1884. 16 
of these cases he found in three cases the papilla white and in nine cases 
a venous fulness of the retina. 
Indeed in 1884 the literature of this disease is quite abundant, for in 
addition to that above given Drs. Moeli1 and Dreschfield2 have each 
published cases of alcoholic paralysis in which degenerative processes were 
found in the peripheral nerves, and Charcot3 and Fere4 have each pub- 
lished reviews of the disease; and in the Lancet of August, 1884 (Ameri- 
can reprint), is an editorial on alcoholic paralysis. Charcot and Fei£ 
state that the muscles of the face are never involved. 
From the considerable number of cases which have been reported we 
are justified in regarding alcoholic paralysis as a special form of disease 
with the following symptoms: After a number of cerebral and gastric 
disturbances due to the alcoholic poisoning the symptoms of the disease 
proper commence with neuralgic pains and parsesthesire in the legs, which 
gradually extend to the upper extremity, and which are accompanied at 
first by hyperaesthesia, later by anaesthesia, and in severe cases by re- 
tardation of the conduction of pain. Along with these symptoms appears 
a muscular weakness, which steadily increases to an extreme degree of 
paralysis, and is accompanied by rapid atrophy and by great sensitiveness 
of the muscles to pressure and to passive motion. Both the sensory and 
the motor disturbances are symmetrically distributed, and the paralysis 
attacks especially the extensor muscles. In addition to these motor and 
sensory symptoms there is also a decided degree of ataxia. The tendon 
reflexes are abolished, and vaso-motor symptoms, such as oedema, conges- 
tion, etc., are usually present. Symptoms of mental disturbance are 
always present in the form of loss of memory, and in transient delirium. 
These symptoms, with the exception of the mental derangement, and 
perhaps the ataxia also, are very similar to those of multiple neuritis not 
dependent upon alcoholic poisoning. 
In regard to the lesion associated with these symptoms, the spinal cord 
has been found entirely normal in all the cases in which a post-mortem 
examination has been made. On the other hand, during the past four 
years, degenerative processes have been found in the peripheral nerves in 
a number of cases of alcoholic paralysis. Lancereaux has reported three 
cases in which such changes were found, Dejerine and Moeli have each 
reported two such cases, and Dreschfeld one; eight cases in all. 
It therefore seems altogether probable that drunkards are especially sub- 
ject to multiple neuritis, and that alcoholic paralysis is simply multiple 
neuritis complicated by other' symptoms of alcoholic poisoning, such as men- 
1 Charite Annalen, 1884, and Berl. Klin. Woehenschrift, No. 14, 1884. 
2 Brain, July, 1884. 
3 Gazette des HOpitaux, Aug. 28,1884. 
4 Prog res Medical, June 14, 1884. 17 
tai derangement, tremor, and ataxia. These latter symptoms seem to be 
due to changes in the cerebral cortex, for in the second case reported in this 
article there was found a degeneration and atrophy of the nerve-cells in 
the cerebral cortex, a congestion of the pia mater, and an effusion of serum 
in the sub-arachnoid space. Very little attention appears to have been 
given to the study of the pathological histology of the cerebral cortex, 
either in cases of alcoholic paralysis or in other forms of chronic alcoholism, 
but a degeneration of the nerve-cells in the cerebral cortex similar to that 
found in the second case has been described by Dr. Wilks1 as occurring 
in cases of chronic alcoholism. An effusion of serum in the sub-arachnoid 
space, and a chronic congestion or inflammation of the pia mater are very 
commonly found in cases of chronic alcoholism. 
The lesion, then, in alcoholic paralysis, is in all probability a degenera- 
tion of the peripheral nerve-fibres and of the nerve-cells in the cerebral 
cortex, together with a chronic congestion or inflammation of the pia 
mater. This lesion explains well the symptoms, although it is certainly 
curious that alcohol should not attack the spinal cord, but only the highest 
and the lowest part of the nervous system if one may so call the cortex of 
the brain and the terminal branches of the peripheral nerves. 
1 Journal of Mental Sciences, 1864.