large in Lépine’s account of military delinquency. Fugue subjects are
not infrequently alcoholic. Minor disobedience is also often alcoholic.
Acts of violence are characteristically alcoholic, or executed by
subjects with hereditary alcoholic taint. (Such acts were in France
especially common before the anti-absinthe law in 1915.) Alcoholic
episodes and impulses often culminate in arson. No doubt, espionage
employs alcoholism for a portion of its technique, though delusional
mystics and subnormal hypersuggestibles are more often the purveyors
of information to the enemy. The theft list, also, shows its share of
alcoholics. Alcoholics are less common amongst those who, contrary
to rules, assume shoulder-straps or other decorations. Here the
sub-normals and victims of imbalance, as well as the drug cases, are
more likely to figure if the matter is psychiatric at all.
Remarks upon an atrocity.
=Case 94.= (KASTAN, January, 1916.)
April 15, 1915, a German soldier went with three comrades to a farm, to
select a sheep for slaughter; they were obliged to go to three farms.
The man carried a revolver and cartridges in his pocket. He threatened
the farmer that he met with this revolver, and desired to rape the
farmer’s daughter. He was very drunk, and said to the non-commissioned
officer who was called in at the time, “You have served only a year
longer than I have.” He staggered, struck violently with his hand at
the sergeant, and gave insolent replies.
He had already choked the peasant’s daughter, scratched her face, and
bitten her fingers, hand and arm. She could not run away as she was
lame. The soldier held the revolver to her face and shot it off several
times, offered sex assault, scratched her feet with his spurs, and
tried to twist her neck. The non-commissioned officer threatened to
shoot him, and he then became still. He said to the first-lieutenant
before whom he was taken, that he would do anything but allow himself
to be beaten, and at this moment moved his arms about in the air, and
bloody foam came from his mouth. The first-lieutenant previously had
always thought him to be normal except for a strange flicker and unrest
of the eyes. There was a history that he had already once attacked a
servant girl. The man had amnesia for the affair, only remembering how
the non-commissioned officer had come on a white horse. He remembered
nothing about the peasant and the girl. He said that he had been given
to earache on the right side in winter. There was a history of his
having fallen from a tree in childhood, becoming unconscious. He had
been a sufficiently good scholar up to the second class in school. He
had been an excellent soldier.
Alcoholism: Atrocity.
=Case 95.= (KASTAN, January, 1916.)
September 15, 1914, a German soldier was missed. He had said that
he wanted to get to the enemy quickly, and that he was going to
march alone against the Russians. A shot was fired that night by
this soldier, on the ground that he had been insulted by a civilian,
although no civilian was present.
September 21, a farmer in a wagon reached a farm, where he found the
soldier aiming at a woman. He fired, wounded the woman severely, and
jumped on the farmer’s wagon and rode off with him. It seems that
the soldier had come to the farm at noontime and accused the woman
of treachery, ordering her to come with her husband to a certain
farmhouse, where she should be placed against the wall and be shot. The
soldier had shot her and wounded her husband also. According to the
woman, the idea was to take revenge because she had denounced certain
persons as spies.
He was arrested during the night, and told how he had left his troop
because he could not get at the enemy. He had been informed that there
were spies who ought to be shot; there had been talk in a certain inn
about it. He did not know he had wounded the husband, and he only
wanted to give that dangerous woman a piece of his mind.
After wounding the woman, he had given himself no further thought about
her, but had gone to partake of the holy sacrament at the pastor’s. He
then had drunk another glass of beer and gone to bed. He was, in fact,
still drunk at the time of arrest. He had not been aware that he would
be punished for the crime of going alone against the Russians.
Some days later, he wrote that he did not intend to kill the woman,
that he had been drunk at the time and was always a bad man when drunk;
that he had other times when he absented himself from home for days
when drunk. He had had, he said, a number of attacks of delirium, in
which he had seen animals. At one time, he had fallen on his head.
On the day in question, he had drunk 1½ litres of liquor. He was
remorseful for his deed.
A disciplinary case: Alcoholism; amnesia.
=Case 96.= (KASTAN, January, 1916.)
A German soldier, New Year’s Eve, 1915, got away from his company,
drank whiskey, and came back drunk. He bothered his comrades so that
the non-commissioned officer had to call for help; whereupon the
soldier said, “A man who comes on late and hasn’t been in much, hasn’t
much to say. If it is a non-commissioned officer, I shall hit him
in the snout.” The officer kept talking to him kindly but he cried
“_Halt’s Maul_, you crooked …!” He staggered up to the lieutenant
without saluting, but at a slight push fell prone into the straw.
It transpired that the man had not been intoxicated enough to lose all
control of himself. He did not remember anything about what he had
done; he had drunk a half-bottle of rum during the evening. There was a
demonstrable lack of memory. He did not know the German provinces, and
thought that Bismarck had once been war minister. There was a tremor,
hypalgesia of the left leg and analgesia of the left arm and left
shoulder.
It was found that he came from a strongly tainted family, with
two insane sisters and three insane cousins. He had been a good
soldier during his service, but had accused his father of alcoholism
baselessly. He had always been difficult to manage when drunk and had
been convicted nine times: five for dangerous assault and battery. He
drank up to 1⅓ litres of whiskey a day if he got time, and also took
ether. For some ten years he had been amnestic for what he did while
drunk; nor, according to his wife, had he been able recently to stand
so much alcohol. He said that he had had a fall from a wagon in 1911 or
’12, after which he had been unconscious.
Antebellum, run over by an automobile; intolerance of alcohol; episodes
of amnesia after moderate alcohol.
=Case 97.= (KASTAN, January, 1916.)
A German soldier was advanced in rank February 26, 1915, and in honor
thereof drank six or seven glasses of beer. On his way home, he met a
captain and failed to salute him. When called to account, he said he
could not see, and made remarks about regrettable behavior. He refused
to go along with the officer. Afterwards he remembered that he had been
stopped by an officer but had forgotten subsequent happenings.
March 24, he was riding in an electric car with a lieutenant. He said
to the lieutenant who had unbuckled his sabre, “It is a piece of
insolence and improper to unbuckle the sabre.” He repeated the phrase
on questioning. He was then asked to give his name, and replied, “I
know my name but what is your name, Mr. Lieutenant?” He looked drunk at
the time but afterwards remembered nothing.
Physically he was tremulous and showed blepharospasm. His face grew red
on bending over.
This man had been run over by an automobile in 1910, after which he had
become excitable, slow-thinking and forgetful. The spinous processes
were painful on pressure, as was also the hip joint. The history
showed that he had been convicted six times of various crimes, such as
disturbing the peace, embezzlement, and the like. Since this accident
he had not been able to work effectively. He had gone into the army in
a spirit of enthusiasm.
Adventure with a stranger in Paris.
=Case 98.= (BRIAND and HAURY, 1916.)
A soldier had seven days’ leave in Paris, beginning December 27, 1915,
and the first day drank a good deal of wine with another man on leave.
They met, in some place that the patient had forgotten, a well-dressed
man whom they did not know, and all three fell to drinking. The
stranger told them he knew a trick to prolong the leave to 3 or 4
weeks. “All I have got to do is to prick you, and it will cost only 100
sous.” The operation was done at the café after payment in advance.
The operation was a puncture with a needle between the middle and ring
fingers of the left hand. Next day there was a phlegmon of the dorsal
surface of the hand, and he was put into hospital saying that he had
gotten a barbed wire prick in the trenches. The surgeon who opened the
phlegmon was surprised at its gummy appearance, gangrenous odor, and
greenish tint. In point of fact, petrol had been injected.
Morphinism: Tetanus.
=Case 99.= (BRIAND, 1914.)
Mdm. L. was a morphinist. After the outbreak of the war, she went to a
general hospital to recover from morphinism, but was too excited to be
kept there. Accordingly, she had to be sent to Sainte-Anne, but upon
arrival she developed distinct signs of tetanus.
It seems that Mdm. L. was the widow of a Colonial who had given her the
first injections ten years before, for dysentery. She tried several
times to stop. Daily dose 1.5 grams.
She was in a cachectic state, and according to her mother, took no care
of her syringe, trailing it about everywhere. Her thighs, arms, and
anterior aspect of the body were covered with scars. There were small
phlegmons in places. Did she inoculate herself with bacillus tetani
from an infected needle? In any case, she died of tetanus.
Medicolegal question concerning a morphinist.
=Case 100.= (BRIAND, 1914.)
A man worked in Paris on the ’Change, where there are a number of
syringe victims. He had been brought up in Paris but was not a
Frenchman. Enthused by his friends and the prey of deep emotion, he
enlisted. He was of an introspective nature and himself wondered
whether the morphine did not have something to do with his enlisting.
He said, “I had been unnerved for a number of days by reading the
papers, and after a number of heavy injections, I went to a recruiting
station and signed on.” In his regiment, he continued the injections,
but shortly found that he would be unable to replenish his diminishing
stock of drug. He explained his unhappy fate to the corps physician,
and was sent to Val-de-Grâce. He asked to be retired, alleging that
he was under the influence of a poison when he went to the recruiting
office and had therefore committed an illegal act.
Social effects of the war on two drug addicts.
=Cases 101 and 102.= (BRIAND, 1914.)
Fernand and Emilienne were two recidivists in morphinism. Although
neither was over 22 years of age, both had been several times convicted
of shop-lifting. They stole only if they had no money for morphine.
Prostitution served to care for Emilienne, while Fernand was at times a
cocaine seller, and at times made money in devious ways at Montmartre.
Emilienne’s patronage scattered with the war, and it was the same with
Fernand’s. Accordingly, there was no money for either morphine or
cocaine. Moreover, the shops being not crowded were easier to watch. As
Emilienne did not care to be arrested and sent off as an undesirable,
she presented herself at the hospital for the insane at Sainte-Anne.
Fernand shortly joined her there.
V. ENCEPHALOPSYCHOSES
(THE FOCAL BRAIN DISEASE GROUP.)
Left-sided hemiplegia and aphasia: Contrecoup and local lesions.
=Case 103.= (LHERMITTE, June, 1916.)
A soldier of 23 was wounded in the left parietal region and showed a
_left_-sided hemiplegia with aphasia. The speech difficulty, although
very marked, retrograded almost completely, but the hemiplegia remained
severe. This hemiplegia was a spastic one, of a classical nature, with
Babinski sign and exaggeration of tendon reflexes. Lhermitte thinks
that the left hemisphere was directly affected by the contusion, as
in point of fact there was an actual loss of bony tissue, but that it
would not be necessary to suppose the ipsilateral hemiplegia was due to
an absence of pyramidal decussation. The transient aphasia was probably
due to direct affection of the tissues on the left side of the brain;
the permanent hemiplegia was doubtless due to a lesion of the opposite
hemisphere produced by contrecoup. It appears that sometimes a surgeon
may be led to superfluous surgical intervention in a case of such
paradoxical hemiplegia, since the surgeon may believe that a bullet
or shell fragment has traversed the brain substance to the opposite
side of the skull, when as a matter of fact the brain parts have been
injured merely by contrecoup.
_Re_ such amnesia, it is of note that many head cases, even if they do
not show amnesia, show a conspicuous euphoria and lack of understanding
of the seriousness of the injury in question and of the necessary
treatment. According to E. Meyer, there are constantly to be found
in head cases disturbances of perception and lack of coördination
(especially for time), perseveration, difficulty in thinking and
calculating.
CHART 5
COMMOTIO CEREBRI
I. SENSES: Asymmetrical hyp- or anesthesia (with hyperalgesia
and osseous hyperesthesia).
II. MOTILITY: Disorder, muscular or reflex. General or
unilateral hyperexcitability.
III. VASOMOTOR CONTROL: Dermatographia. Cardiac, splanchnic
disorder; also, Headaches, Vertigo.
IV. EMOTIONS: Disorder.
V. INTAKE OF IDEAS: Disorder. Persistent lacunae of memory.
VI. INTELLIGENCE: Disorder of recollective memory.
Speech-disorder. Intellectual inertia. Overimagination
(hallucinations, tremors).
Mairet, Piéron, Bouzansky.
Gunshot wound of head; alcoholism: Amnesia.
=Case 104.= (KASTAN, January, 1916.)
A German soldier had a bullet pass through his right eye and lower
jaw, leaving a fistulous opening from the mouth. He said that he was
completely blind, but ophthalmological examination cast doubt upon the
blindness. There had been immediately after the injury a number of
severe attacks of dizziness, which lasted several hours; and another
attack developed after he had come back from hospital, to which he had
gone by reason of his pains.
He was to be arrested on account of a disciplinary crime and had
ostensibly gone to his mother’s house, there to await arrest. The
non-commissioned officer found him in a saloon. As soon as the phrase,
“You are my prisoner!” was said, the soldier lost track of his
surroundings. He had drunk a few glasses of beer but did not himself
think he was drunk at the time. He was insulting and violent when asked
to proceed with the officer, and a policeman was called in to take
charge. He then lay down in the street and had to be put upon a wagon,
still firing abusive phrases at his captors.
Upon examination, aside from the effects of the gunshot, excessive
knee-jerks and tremors of the body were found. The eyebrows met but
there was no other sign of bodily stigmata. There seems to have been no
hereditary disease, or any history of severe alcoholism, though the man
had been convicted previously of violence and theft. The amnesia is to
be ascribed to effects of the head injury.
Bullet in brain: Crises; cortical blindness; vertigo; hallucinations.
=Case 105.= (LEREBOULLET AND MOUZON, July, 1917.)
An invalided soldier, 40, was sent to be observed, Oct. 23, 1916,
because he wanted his pension renewed. He had been retired a year
before for diminution of binocular vision with impaired perspective
of objects in the right half of the visual field. He had now become
completely blind.
He had been wounded, March 12, 1915, in the Argonne, without losing
consciousness. He was wounded at ten o’clock at night and waited until
the next day to walk to the ambulance and was at this time able to see
perfectly. Arriving at the ambulance he lost consciousness. He was
trephined but remembers nothing about the trephining.
His memory grew better from his arrival at a hospital in the rear in
April. An attempt was made to remove the bullet in May, 1915. Though
the surgeon’s finger was pushed as far as the tentorium the patient
did not lose consciousness or sight, but on leaving the operating
room he fainted and, after a few days of restlessness and delirium,
he became completely blind. There was a cerebral hernia difficult to
reduce. Vision became a little better and light and persons could
be distinguished at the time when he was retired. A month after the
operation there was a convulsive crisis beginning in the left arm,
affecting the legs and ending in unconsciousness. Several similar
crises occurred in August, sometimes with and sometimes without loss
of consciousness. Later these crises began to be limited to the left
side and then to be ushered in by visual hallucinations. At home he
was unable to care for, clothe or feed himself. The crises became more
frequent. The visual hallucinations began to dominate.
This situation lasted to February, 1916, when the blindness which had
been increasing since the onset of the hallucinations became complete.
The crises now became less frequent and intense. Headaches not severe
were exaggerated after seizures. The patient acted like a totally
blind person and said that he had before him a uniform and constant
gray without any light or dark spots or any color. Upon this background
bizarre pictures, caricatures, disguised persons, animals or nameless
things appeared colorless without relief, in silhouette, but highly
suggestive of reality to such a degree that at first, according to the
patient, he had made gestures to reach, or push aside these pictures.
The crises were Jacksonian.
Pallor, perspiration, shivering, irresponsiveness, clonic spasms of
left arm followed. The patient always had a premonition permitting him
to get into bed if he was sitting, for example, in his chair. Sometimes
there was a dizzy sensation as if the body were being rotated to the
left. This sensation did not occur at the beginning of the seizure and
the patient fought against it, turning to the right. Sometimes he felt
as if he were sliding at great speed down an inclined plane. Headaches
and sleepiness followed, but there was never any complete loss of
consciousness of memory.
The eye grounds proved normal and all the photomotor reflexes were
normal, though there was no pupil reflex to pain. The patient could
write readily to dictation printed letters. It would seem that these
printed letters mean that he had visual memories, as he traced the
characters as if from a design. Speech was monotonous with some
stuttering; but his speech had always been of this sort according to
information. He walked with difficulty, not merely on account of his
visual but on account of his equilibration disorders. Outside of his
seizures he always turned to the right and if left to himself standing
he turned to the right. If asked to walk straight ahead, he always
turned to the right. Silent and uncommunicative, he was amiable and
sometimes even gay. He often had troublous dreams, sometimes seeing
his relatives. He said he could bring up in his mind the faces of his
relatives and even the appearance of the Salpêtrière. Reflexes and
sensations were normal. There was a traumatic rupture of the tympanum.
Lumbar puncture showed a slight excess of albumin and 1.8 lymphocytes
to the cubic millimeter. The Mauser bullet was found by X-ray in the
left calcarine region with its base touching the median line, and
applied to the inner table of the skull about a centimeter above the
internal occipital protuberance pointing forward, outward, and upward.
He was treated on a salt free diet with bromides. The seizures grew
fewer and at the time of report two months had elapsed with nothing
but a slight vertigo and frequent nightmares. Intellectually also the
patient had improved.
The case is one of cortical blindness. The seizures are explained by
the vicinity of the right Rolandic region to the lesion. The rotatory
vertigo is to be explained by the contact of the Mauser bullet with
the tentorium and vermis of the cerebellum, which may also explain
the difficulties in orientation that occurred between the crises. The
visual hallucinations are doubtless due to lesion of the calcarine
region.
Tunisian theopath with mystical hallucinations; gun-shot wound
of occiput (bullet extracted): After the trauma, Lilliputian
hallucinations and micro-megalopsia.
=Case 106.= (LAIGNEL-LAVASTINE AND COURBON, 1917.)
A. ben S. was sent to Villejuif with the diagnosis: “depression,
feeling of impotence, discouragement,” having been found on the public
street. He was indifferent, almost completely mute, and was at first
considered not to understand French. In a fortnight, however, he was
talking freely and was then found to be afflicted with hallucinations,
melancholia, and delusions, apparently following trauma to the skull.
A. ben S. might have been about thirty years old, and was of a rich
family, indigenous in Tunis, well educated in the Koran and Arabic
literature.
Upon examination, this Tunisian gunner showed contraction of visual
fields, poor color vision, and general hypalgesia. During examination,
the man seized the needle and plunged it deeply under his skin,
exclaiming that a prophet felt nothing and that he could be cut into
bits without feeling pain.
It seems that he had had divine visions from early childhood. In his
youth he had once gone to a mountain near his home and talked with
Mohammed and Allah. Of course, Allah did not appear in human form, but
he appeared like a ball or a wheel of fire, slowly turning. Mohammed
was a tall man, with a long white beard, his eyes darting rays of
fire, and his forehead bearing a gleaming bright body. Allah was heard
talking to Mohammed. Orders were given concerning the sun and stars.
Subterranean treasures were displayed, as well as Paradise full of
yellow, blue, and green houris, transparent, such that, when food was
taken, it could be seen going down their throats. Hell too was visible,
and the devil very tall and black, an eye behind and another on top.
There were also many genii--little men who climbed over the Tunisian’s
body. Sometimes in dreams, Allah carried him to all countries of the
earth. It was hard to tell whether these effects were hallucinations
or vivid imaginings. The Tunisian had been wounded after several months
of service by two bullets in one day: the one causing an insignificant
lip-wound; the other entering the skull behind. After several months
the bullet had been extracted by trephining.
His further history was obscured by the fact that he wove delusional
elements into his story. He said, for example, that he had been
court-martialed, though there was no evidence that this was a fact. It
is probable that after his wound the patient in a delirium felt that he
was going to be shot. The visual hallucinations were very interesting,
being Lilliputian. He would see three or four hundred Tunisian gunners
walking along, knee-high or taller. Sometimes they all would stop and
aim at him. He also showed micromegalopsia, real objects changing their
height under his eyes. Both the Lilliputian hallucinations and the
micromegalopsia dated from the trauma to the skull. There was no change
whatever in the mystical delusions concerning Allah and Mohammed. These
he had before the trauma.
Meningococcus meningitis with apparent recovery: Dementing psychosis.
=Case 107.= (MAIXANDEAU, 1915.)
A soldier in the Heavy Artillery, 42, developed occipital headaches and
Kernig’s sign, December 27, 1915.
December 31, at the Hôtel-Dieu, he showed myosis, slight photophobia,
meningitic tâche, temperature 39.6, pulse 84, heart sounds dull. Lumbar
puncture: hemorrhagic fluid.
January 1, the headache was intense, neck stiffness increased, Kernig’s
sign less marked; morning and afternoon temperature 39.2. Lumbar
puncture yielded hypertensive cloudy fluid and 30 cubic centimeters of
serum were administered.
This dose was repeated January 2 and January 3, on which date there was
no headache.
January 4, Kernig’s sign and neck stiffness were diminished; fine râles
at the bases without dulness. 30 cubic centimeters of electragol were
injected intravenously.
January 5, Kernig and neck stiffness slight. Meningitic tâche;
exaggerated knee-jerks; unequal pupils; temp. 36.6 morning, 39.4
afternoon; respiration 36; pulse 120; no râles; splenic enlargement.
6, no headache or photophobia; constipation; fine râles, right base;
spartein; meningococci found in hypertensive spinal fluid. 30 cc. serum.
7, more râles; exaggerated heart sounds; intestinal worms in stools.
8, temperature fell to 37; pulse to 90.
9, patient worse; involuntary stools; Kernig’s sign; stiff neck; fever.
30 cc. serum injected.
10, 20 cc. injected.
11, delirious all night; tetaniform stiffness of neck; more râles.
12, delirious, incoherent words, Cheyne-Stokes breathing.
13, less stiffness, Kernig almost absent; pupils normal; Romberg sign
slightly developed; pulse 120.
14, a few râles at right base.
15, pains in elbows, knees and hands with joint swelling; moist râles;
temp. 38.4; pulse 140. Digitalon.
16 and 17, serum erythema of thorax; edema of left knee; pulse 150;
spartein 16.
17, ice pack over heart.
18, edema of knee diminished; no headache, delirium or pupillary sign.
19, improvement. Temperature normal thereafter.
20 and 21, fine râles. Then all symptoms disappeared.
Recovery was predicted, but on January 28 it was observed that the
patient was untidy, made mistakes in dressing, such as trying to put
his legs into the armholes of his shirt, and denied the most evident
facts: His _képi_ on his head, he said it was not. Face drawn; skin
yellow. Appearance of asthenia. Deep depression and hebetude. At this
time the knee-jerks were exaggerated, pupils unequal, vermicular tremor
of tongue; the patient walked on a broad base with tremulous legs
suggesting contracture and weakness.
February 8, in a similar state the patient wandered about his room,
moving his bed and chairs about, answering questions with an absent
air. He had now been taught to be less untidy.
March 5, stiff neck and Kernig’s sign were distinct. He made believe he
was on his farm. Ecchymosis of right upper eyelid: he had fallen (his
sheep had pushed him over!). The improbability of this idea did not
persuade him to think it had not happened. He walked after the manner
of a tabetic.
In April he became bedridden, unable to walk, with marked stiffness and
Kernig’s sign. He had at this time periods of excitement in which he
would tear the bedclothes. He was invalided as demented.
Meningococcus meningitis.
=Case 108.= (ESCHBACH AND LACAZE, November, 1915.)
During his eleven months captivity at Grafenwöhr, Eschbach and Lacaze
had the opportunity of observing the case of a soldier, 24, who
sustained a shell-wound in the left lung and was made prisoner August
20, 1914, at Chateau Salins. He got well of his wound, but February
16, 1915, began to cry out and was restless in the night. He was found
on the straw muttering words among which only the word, “Head, head,”
could be distinguished. He was irresponsive, possibly deaf. Suddenly he
had a convulsive crisis and whenever touched he would have jactitations
and cry out. Otherwise, he was calm and stuporous. The pupils were
widely dilated. In short, he showed a mental confusion associated with
paroxysmal excitement due to cerebral and cutaneous hyperesthesia. The
first symptoms had occurred the morning before, when he leaned his head
against a wall and complained.
Lumbar puncture yielded intra- and extracellular meningococci. The
patient was isolated. In the afternoon he became less agitated,
kept his eyes closed, mumbled, repeated gestures, would spit in his
hands, rub his hands together, rub his neck, shoulders and body, or
else he would pass his hands over his forehead and through his hair.
Occasionally he would seize the straw and draw it to him with all his
strength. Once when asked, “What is your name?” he said, “Not true. Not
true.” Hallucinations appeared to have been added to the situation. The
neck was a little stiff to forced flexion. Temperature 37.8. Lumbar
puncture under chloroform anesthesia; antimeningococcus serum was
injected. Next day quieter; able to get up and walk. Slept, mumbled
less, was able to answer simple questions, desired to urinate and
finally succeeded.
February 19, no mental disorder. Headache and lassitude. Neck stiff,
Kernig’s sign marked. Lumbar puncture yielded a fluid now puriform;
antimeningococcus serum injected. February 20, lifting the head
produced opisthotonos. Labial herpes. The fluid yielded, besides
meningococci, also endothelial cells. Serum injected. February 21,
fibrin in fluid; serum injected. February 22, no head symptoms. Herpes
more intense, involving also arms. Tongue coated. Temperature 37.5,
evening 38.3. February 23, meningococci and lymphocytes in fluid.
February 24, left knee swollen. Serum injected; puncture fluid showed
meningococci and polynucleosis. Fluid from knee showed polynuclear
cells without organisms. February 25, patient reached evening
temperature of 39.5; serum injected. A few meningococci, altered
polynuclear leucocytes. February 26, patient rigid, tongue coated,
serum injection. Rare meningococci, degenerated polynuclear leucocytes.
February 27, rigidity decreased, evening temperature 37.7. February
28, Kernig’s sign absent. Herpes dry. Serum injection. Fluid clear;
lymphocytes and polynuclear cells; no meningococci. March 6, painful
inguinal gland on the left side. March 7, epididymitis left (mumps two
years before, with headache two weeks and double orchitis). March 9,
serum eruption. March 17, epididymitis practically absent. Lymph node
painful. Later data impossible to get, except that there was apparently
an arthritis of the hip and a sacral decubitus with eventual recovery.
Shell-explosion: Meningitic syndrome, fourteen months.
=Case 109.= (PITRES AND MARCHAND, November, 1916.)
A soldier sustained shell-shock at the distance of a meter at
Saint-Hilaire, September 26, 1915. He lost consciousness and blood
flowed from his ears. He arrived, September 28, at the neurological
center in Bordeaux in a semistupor, knowing that he had been shocked
and had lost consciousness. He groaned, cried out, and kept stroking
his head with his right hand; lay on the right side; showed Kernig’s
sign right, ptosis, and stiff neck. Headache was increased on moving
and noises. Patient constantly asked for food, but refused to drink.
Lumbar puncture yielded a yellowish fluid, due to laked blood. October
3, headache, ptosis, left internal strabismus, temperature 38.5.
October 4, lumbar puncture, slightly blood-tinted fluid. October 5,
improvement; gap in memory for period since shock. No strabismus,
ptosis diminished, temperature normal, improvement continued. Kernig’s
sign and headache persisted. He lay doubled up on the right side, eyes
closed, right hand on pillow. Defense movements on touching the neck
or occipital region. The condition of semistupor often passed off in
the afternoon, when he could talk, write or play cards. He had always
smoked, even at the beginning of his disease. Lumbar puncture yielded
a normal fluid December 12, 1915. He was sent February 23, 1916, to a
hospital in the country, but came back May 9.
It seems that several days after transfer he had had an attack of
delirium in the night, having lost consciousness, and tried continually
to get up out of bed, saying that he wanted to go to Verdun to fight.
This spell lasted several hours and on the days following came mutism,
refusal of food, and a state of stupor. Nutritive enemata were given.
As he grew better he sometimes ate a great deal, sometimes nothing,
even wanted poison from his family, and wrote to a comrade that he
wanted to commit suicide.
May 9, he was clearer, told of seeing the shell, which he said he had
not heard, nor did he know how he had gotten to a hospital. His head
and spine had hurt him ever since the shock. He had had difficulty
in urination for two days after the shock. He could not remember
the delirious attack in the country hospital. He gave various data
about his life, but not fully. He refused to lie on the left side,
or to walk, because of pain. He could lift either leg from the
bed, but hardly both. There was an irregular coarse tremor of the
extremities. The right hand was weaker than the left; there were no
reflex disorders; no change in the eye grounds. There was a patchy
analgesia. May 26, stupor reappeared as before, with semimutism. June,
the patient presented the appearance of a dementia praecox in stupor,
with stereotyped gestures and attitudes, without catatonia. The patient
was sent to a hospital for the insane at Cadillac. November 9, 1916, he
returned to the neurological center, as mental and cerebral disorder
had disappeared. There still persisted a difficulty in remembering
facts since the shock and there was still a functional paresis of the
legs.
We here deal with a case of a meningitic syndrome following shell-shock
and lasting fourteen months.
Brain abscess in a syphilitic: Matutinal loss of knee-jerks.
=Case 110.= (DUMOLARD, REBIERRE, QUELLIEN, 1916.)
An unmarried subaltern officer, 30, entered an army neuropsychiatric
center, April 8, 1915, looking exhausted and bearing a ticket “nervous
asthenia, evacuated for neurological examination.” He said he had had
scarlet fever at ten; strongly denied syphilis, of which he presented
no trace; had not been excessively alcoholic and had had no nervous
seizures. Detailed information showed that he had been a normal child.
He left his two years’ military service with promotion and was a man of
above the ordinary intelligence.
He was wounded in the right buttock with a shrapnel bullet about the
end of September, 1914. He went back to his regiment two months later
and had shared in a number of actions up to the time of his evacuation.
He said he had been very tired for several weeks, and had finally been
sent to the physician. There were pains in the kidney region and in
the head, especially on the right side. The head felt empty. He could
not sleep, but did not dream. Ideas were not distinct. Memory had
become impaired. He could not keep his accounts right, and was afraid
something might go wrong.
There was no pain or nervous or reflex disorder of any sort except for
the knee-jerks and Achilles jerks (see below). A special examination
proved complete normality of eyes. There was a slight hesitation in
words, but no dysarthria. There was a slight tremor of the tongue and
fingers.
As to the tendon reflexes, April 9, on waking, the knee-jerks were
absent, but later in the day gradually came in evidence again. The
Achilles jerks were also absent at first, but could be obtained after
a prolonged examination and after percussion of the calf. In the
afternoon, after exercise, the knee-jerks and Achilles jerks were
easily demonstrable. The left Achilles jerk was always a little weaker
than the right. Massage brought these jerks out to virtual normality.
April 10 and thereafter, similar findings; percussion of the muscular
masses of the thighs and calves always brought out the reflexes.
Lumbar puncture yielded a clear fluid with hyperalbuminosis, 20 cells
per c.mm. (lymphocytes and mononuclear cells 95 per cent) and a
positive W. R. Iodide of mercury treatment was given April 18.
April 23, the patient went into a coma, with trismus, stiff neck,
Kernig’s sign, sluggish pupils, incontinence. He was transferred
to a special hospital, showed on lumbar puncture, April 23, 85 per
cent polynuclear leucocytes, and died April 27. The autopsy showed a
yellowish, quasidiffluent softening of the size of a small egg in the
first occipital gyrus on the right side. The authors comment on the
fact that the only objective sign in this case was the variable tendon
reflexes of the lower extremities, “_l’unique cri de souffrance des
centres nerveux_.”
Early recovery from a spinal cord lesion.
=Case 111.= (MENDELSSOHN, January, 1916.)
Mendelssohn reports a soldier, who was sent to a Russian hospital,
April 12, 1915, with a diagnosis of chronic appendicitis. Operated
on next day, the patient appeared to be passing through a normal
convalescence, when ten days later, he had an intense headache and some
trouble in vision, which disappeared the next day, only to be followed,
two days later, by the patient’s complaint that he could no longer
urinate or rise from bed.
In fact, Mendelssohn found a complete flaccid paraplegia with urinary
retention, without fever or pain. Knee-jerks and Achilles jerks were
absent, and there was a slight extension of the great toe on plantar
stimulation. There was disorder of sensation, with heat sensibility
abolished, painful points poorly localized, and position sense poor.
Electric reactions normal. Pain on pressure in and about the lumbar
vertebral region. Cerebrospinal fluid showed lymphocytosis and an
excessive albuminosis.
This paraplegia lasted six weeks. At the end of May, the patient began
to be able to move his toes and to lift his heel. Improvement was
gradual and progressive. Early in June he could walk if supported.
The weak knee-jerk then began to reappear and the urinary retention
gradually disappeared.
This patient was not hysterical, although a bit emotional. Perhaps,
according to Mendelssohn, an organic lesion was grafted on a neurosis.
Perhaps the spinal lesion was infectious. At any rate, a presumably
organic paraplegia had recovered in two months and a half.
Shell-explosion: Meningeal hemorrhage: Pneumococcus meningitis.
=Case 112.= (GUILLAIN AND BARRÉ, August, 1917.)
An infantryman, 20, came to the Sixth Army Neurological Center, October
13, 1916, as a case of “choluria, due to shell explosion; epistaxis
needs watching.” He was somnolent, had waked vomiting, pulse 108.
Kernig’s sign, defensive movements of the legs on stimulation, with
flexion of leg on thigh and of thigh on pelvis, plantar reflexes
flexor. Puncture showed typical meningeal hemorrhage. Two days later,
temperature 40, pulse 70, that is to say, a bradycardia in proportion
to the fever. Vomiting, pulse persisted. Next day the patient was
moaning and semi-delirious and showed stiff neck, Kernig’s sign,
accentuation of vasomotor disorder, plantar response flexor with leg
retracted, thigh flexion both homolateral and contralateral. The
spinal fluid upon the next day, that is, four days after his arrival
at the clinic, showed a purulent fluid in which there was an excess of
albumin, no sugar, diplococci extracellular (proving on culture to be
pneumococci and able to kill a mouse in twenty-four hours).
As a rule such hemorrhages remain aseptic, and in fact meningeal
hemorrhage is said by Guillain and Barré to have, as a rule, a
favorable prognosis. The above described case was the only one of
infected meningeal hemorrhage that had occurred in the Sixth Army
Neurological Center.
ANTEBELLUM cortex lesion: right hemiplegia; recovery. Struck by
shrapnel on right shoulder: Athetosis.
=Case 113.= (BATTEN, January, 1916.)
A British soldier, aged 27, showed a somewhat remarkable phenomenon.
It appears that at five years of age, this man had had poliomyelitis,
affecting the left leg. At 20 years of age, he had had pneumonia, and
this had been followed by a paralysis of the right arm and leg with a
loss of speech. The man recovered from this illness, although he never
quite regained full control of the right hand. It is evident that
this lack of control was not marked, else the man would not have been
enlisted, and it is Dr. Batten’s opinion that at all events he could
not have shown pathological movements of the right hand at the time of
enlistment.
However this may be, in October, 1914, the soldier was struck on the
right shoulder with shrapnel. Apparently he was not wounded, but
thereafter he was not able to use the right arm well, and in two
months’ time he had become unable to manipulate his rifle. On January
13, 1915, he was sent home. The remnants of the old poliomyelitis of
the left leg were shown in a general weakness of that leg as compared
with the right. _The movements of the right hand were those seen in
athetosis._ The movements were independent of volition. The patient
had difficulty in releasing his grasp. He improved rapidly during the
six weeks he was in hospital, although the movements of the right hand
never became entirely normal.
In this case, according to Batten, “the stress was sufficient to bring
into prominence the symptoms due to an old cerebral lesion.”
Hysterical versus thalamic hemianesthesia.
=Case 114.= (LÉRI, October, 1916.)
A soldier, 40, had been suffering for a number of months with pains in
the left side of the trunk and feelings of weakness in the left arm and
leg. In the summer of 1915 he was on leave and while walking, fell,
lay down, and found he could hardly move his left arm and leg. Two or
three weeks later he got up, walking with a stick. After some time in
hospital, he was sent back to the trenches, a little weak.
He had shortly, however, to be examined neurologically again. He could
hardly raise the left leg and his passive resistance was poor on this
side. The left side was almost completely anesthetic to all forms
of stimulus, although an intense faradic current yielded a feeling
like that of a fly. Nor was the tactile sensation absolutely nil,
as it could be got with a flat finger on the upper arm and thigh.
Cold and heat sensations not well localized. The hemianesthesia was
sharply limited at the median line and affected the buccal, lingual
and nasal mucosa. Deep sensibility was almost abolished on the left
side. Stereognostic sense was lost and the sense of position was lost
absolutely for hand and foot.
The patient said that he heard less well on the left side. There was
also a slight contraction of the left visual field. The reflexes
were lively, but equal on both sides. A diagnosis of hysterical
hemianesthesia was apparently called for, but psychoelectric treatment
failed. The plantar reflex was, in fact, completely absent on the left
side, as well as the corneal reflex. The faradic current failed to
produce as marked a dilatation of the pupil on the left side as on the
right. The forehead wrinkles were less marked on the left side. The
mouth deviated slightly to the right. The left nasolabial fold was a
little less marked. The tongue did not deviate, but was a little narrow
on the left side. The palate deviated a little to the left. The left
side of the trunk seemed a little less developed than the right, and
the scapula stuck a little less closely to the body on the left side,
when the arms were raised. The left buttock was a little narrower than
the right and the left gluteal fold was less marked. In combined
flexion of thigh and trunk the left foot readily left the floor. There
was a left-sided hypotonia in forced flexion of the forearm. There were
no tremors of the limbs in repose, except a few contractions of the
left lower extremity. In movement, however, there was a marked tremor
and in coördination the finger to nose test could not be performed.
Speech was slow and hesitant, sometimes stuttering. Food was sometimes
taken into the air passages. Headaches were localized on the right
side. They had begun when the first symptoms began. There was mental
disorder, with gaps in memory. In short, the case is probably one of
thalamic disease, though there were no pains except a few in the left
side of the trunk at the beginning of the disease. The diagnosis of
hysteria was at first made in this case, but the rule that hysterical
hemianesthesia is never found without auto- or hetero-suggestion caused
the alteration of diagnosis to thalamic.
Shell-explosion: Syndrome suggesting multiple sclerosis.
=Case 115.= (PITRES AND MARCHAND, November, 1916.)
A soldier, 40, carriage painter, underwent shell-shock at Voquois,
May 2, 1915, following ten hours’ bombardment. At the time he felt
tinglings. The bombardment had just ceased when he fainted suddenly
while repairing a telegraph line. There was no loss of consciousness.
He could not move his arms or legs, was able to spit, and did not
suffer at all except for the tingling. He was evacuated to the
interior, where the diagnosis of psychopathic double paraplegia,
Kernig’s sign, zones of anesthesia in the legs, was made. He
was immediately treated with gray oil, and got an injection of
neosalvarsan, and iodides. He grew slowly better. He could lift a
leg from the bed, but then both legs began to tremble. The arms had
recovered their movement, before the legs, but always trembled in
movement.
November, 1915, he was able to get up; two months later, he walked
alone.
At the neurological center, which he entered December 17, his gaze
was fixed and there was a slight exophthalmos. The folds of the face
were smoothed out. The nose was deep set (as a result of a fall at the
age of eight). In the upright position he could not remain still, but
trembled markedly on the left side, so that he had to make a few steps
to keep his balance. He was unable to stand on his left leg. He walked
on a broad base, in little steps, and rather unsteadily on account
of tremors augmenting upon movement. General muscular weakness; left
hand slightly weaker than right. He could not lift both legs more than
20 cm. from the bed and in the process they both trembled, trembling
together. There was also intention-tremor of the arms, a little less
marked than that of the legs, of an irregular rhythm. The arms trembled
as a whole. In a state of rest there was no tremor. There was a slight
muscular stiffness and the patient himself felt difficulty in relaxing.
Patellar reflexes absent, even on reinforcement; Achilles jerks
absent. Speech monotonous and tremulous, but not scanning; syllable
doubling observed by the patient. Manuscript tremulous and, on account
of tremors, illegible. Hypalgesia of legs, more marked distally.
Deep sensibility of tendo Achillis and patellar reflexes lost. Pain
on compression of eyes diminished. Formication in arms. W. R. of
blood negative. Slow improvement followed and the patient left the
neurological service May 4, 1916, able to walk more easily and without
tremor. The knee-jerks and Achilles jerks were still absent.
We here deal with a syndrome in part that of a multiple sclerosis, that
is, the intention-tremor, gait disturbance, muscular rigidity, and
weakness.
_Re_ multiple sclerosis, Lépine remarks that there are numerous army
cases of pseudo multiple sclerosis which are actually hysterical or
hystero-traumatic cases of hypertonus and tremor. The true cases of
multiple sclerosis, according to Lépine, are of interest inasmuch as
they are usually found in officers. These men have apparently at first
but a slight motor disorder, quite compatible with desk work. We have
usually under-rated the cortical element in multiple sclerosis. Spells
of confusion, delusional ideas, sometimes grandiose, start up without
warning in these cases. To be sure, alcohol and syphilis sometimes also
enter these cases etiologically. Any case of localized tremor ought to
be carefully examined psychically, and such cases in general ought not
to be given responsibility.
Coexistence of hysterical and organic symptoms in two cases of mine
explosion.
=Cases 116 and 117.= (SMYLY, April, 1917.)
A soldier was blown up by a mine and rendered unconscious. Upon
recovery of consciousness, he was dumb, unable to work, very nervous,
paralyzed as to left arm and leg. The paralysis improved so that in
the hospital at home the patient became able to get about. However, he
threw his legs about in an unusual fashion. Several months later, the
patient was much improved.
Shortly, however, there was a relapse. Transferred to a hospital for
chronic cases, the patient was unable to walk without assistance on
account of complete paralysis of the leg. Insomnia, general tremor, and
a bad stuttering developed, with a habit of starting in terror at the
slightest noise.
Hypnotic treatment was followed by almost complete disappearance
of the tremor. The patient began to sleep six or seven hours a
night; nervousness diminished, and the stuttering slowly improved;
but neither the paralysis nor the anesthesia of the left leg was
affected by suggestion. The leg remained cold, livid, anesthetic, and
flaccidly paralyzed to the hip. Though a slight improvement has since
been produced by faradization, the patient still can walk only with
assistance.
A man was injured in 1906 by the fall of a heavy weight on his back. In
1914 he went to France as a soldier, and eight months later was hurled
into a shell hole so that his back struck the edge. He was rendered
unconscious. Upon recovery of consciousness, the right leg was found to
be swollen, and there were severe pains in the legs and back.
Since return home the patient had gone from one hospital to another,
for the most part unable to walk, suffering from agonizing pain in the
head and eyes, unable to sleep, and in the night subject to horrible
waking dreams.
CHART 6
MINOR SIGNS OF ORGANIC HEMIPLEGIA (LHERMITTE)
I. Hyperextension of forearm (hypotonia).
II. Platysma sign: Contraction absent on paralyzed side.
III. Babinski’s flexion of thigh on pelvis (spontaneous, upon
suddenly throwing seated subject into dorsal decubitus).
IV. Hoover’s sign: Complementary opposition (on request to
raise paralyzed arm, presses _opposite_ arm strongly
against mattress).
V. Heilbronner’s sign of the broad thigh (hypotonia).
VI. Rossolimo’s sign: flexion of toes on slight percussion of
sole.
VII. Mendel-Bechterew sign: flexion of small toes on percussion
with hammer of dorsal surface of cuboid bone.
VIII. Oppenheim’s sign (extension of great toe on deep friction
of calf muscles); or Schaefer, or Gordon (on pinching tendo
Achillis).
IX. Marie-Foix sign: withdrawal of lower leg on transverse
pressure of tarsus or forced flexion of toes, even when leg
is incapable of voluntary movement.
At first able only to bring himself to an upright position and to rush
a few steps, he later acquired considerable control of his feet and
legs through crutches. The insomnia persisted.
Smyly regards this case, like Case 116, as more neurological than
mental.
_Re_ organic neurology, much of great value has been reported.
Sargent and Holmes say that, contrary to expectation, there have been
few war cases of bad sequelae of cerebral injuries, such as insanity
and epilepsy. During early stages, after infection of the head wounds,
there is dulness and amnesia, irritability and childishness,--symptoms
which disappear during and after repair of the wounds. Mental disorder
requiring internment is surprisingly rare. During 12 months only eight
cases were transferred from the head hospital in a year to the Napsbury
war hospital, where cases of insanity attributable to the service are
sent; and in but two of these could the persisting mental symptoms be
attributed to head injury.
Col. F. W. Mott confirms the opinion of Col. Sargent and Col. Holmes,
remarking that from all the London County Council Asylums, only one
case of insanity associated with gunshot head wound had been admitted,
and that this was one of a Belgian who died from septic infection
of the cerebral ventricles. Yet all cases of insanity in invalided
soldiers belonging to the London County Council area (about one-seventh
of the population of the United Kingdom) are transferred to these
asylums.
Again Sargent and Holmes point out that both generalized and Jacksonian
epileptiform seizures are comparatively rare in patients suffering from
recent head wounds; even convulsions in later stages have been as yet
less common than was feared. Thus, after evacuation to England, fits
occurred in 37 (6 per cent) of 610 cases with complete notes, and in
only eleven of these 37 cases were the convulsions frequent. Sargent
and Holmes remark, however, that the practice of giving bromides
regularly to all serious cranial injuries until the wound is healed,
and for some months afterwards, seems advisable. In 33 of the 37
convulsive cases there have been severe compound fractures of the
skull, and in four of these a missile was still present in the brain.
Five secondary operations were performed with good results, after
drainage of small abscesses in two and removal of spicules of bone in
three. The In-patient and Out-patient records of the National Hospital
for the Paralyzed and Epileptic were searched for epileptics already
discharged from the army, but notes of but two patients attending this
hospital for epilepsy were found.
As for other neurological complications aside from septic infection
and hernia formation, there are a few subjective symptoms that may
necessitate the invaliding of soldiers. The most common of these is
headache, usually in the form of a feeling of weight, pressure, or
throbbing in the head, which headache is increased by noise, fatigue,
exertion, or emotion. Attacks of dizziness also occur, and nervousness
or deficient control over emotions and feelings. Changes of temperament
are found in some soldiers, who become depressed, moody, irritable, or
emotional, and unable to concentrate attention.
Foix, under the direction of P. Marie, worked upon aphasia in 100
cases, reporting results at a surgical and neurological meeting, May
24, 1916, in Paris. Only lesions on the left side of the brain have
produced important and lasting speech disorder, although lesions on the
left side may leave behind them a little dysarthria or difficulty in
finding words in conversation. It is, of course, hard to tell speech
disorder from stupor or clouding of consciousness. Foix notes certain
specialties in speech defect according to which region of the left
brain is affected.
First: Prefrontal lesions produce a transient dysarthria, lasting but
a few weeks, and right-sided prefrontal lesions produce just as much
disorder.
Occipital lesions produce no speech disorder.
Second: Patients with right-sided hemianopsia due to lesions of
occipital regions were not aphasic and could read or write perfectly.
Lesions of the left visual centers certainly do not affect reading.
If, however, the injury is not to the visual centers, but is upon the
lateral part of the occipital lobe, then alexic phenomena appear, and
these the more the lesion approaches the temporal-parietal region.
Third: Central convolutional lesion produces a variety of disorders
according to the site and extent of the lesion. There is no aphasia
with the crural monoplegia due to superior paracentral disorder. But
slight aphasic disorder accompanies the brachial monoplegia of middle
central lesion, though writing, reading, and calculation are slightly
affected, and the more so the more the lesion extends posteriorly to
the stereognostic regions. The lower down in the precentral region the
lesion appears, the more likely is the Broca syndrome to be observed.
But if the hemiplegia is chiefly a brachial monoplegia, the aphasic
disorder may remain slight, involving reading, writing, understanding
of words, the spoken word, articulation, and calculation.
Fourth: Lesions of the lateral-frontal region produce more or less
marked aphasic disorder, just as do those of the inferior part of the
precentral gyrus. This aphasia is more apt to occur when the wound is
deep. However, no case of permanent aphasia has been observed in cases
of lesion of the lateral-frontal region (termed in Foix’s nomenclature,
the precentral region, but referring to the tissues in front of
the precentral (or ascending frontal) gyrus of the more familiar
nomenclature). Almost absolute, or absolute, anarthria follows the
wound, and the patient is hemiplegic. This hemiplegia may last from ten
days to two or three months. After a time there is no longer more than
a slight dysarthria, and writing becomes good again; reading remains,
perhaps, a little difficult. A complete or almost complete cure is the
rule.
Fifth: When the retrocentral region is injured, various aphasic
syndromes appear. The retrocentral region is the parietal-temporal lobe
except the superior part of the parietal lobe and the anterior part
of the temporal lobe, which latter two regions when injured do not
allow any marked aphasic disorder. Lesions of the middle or posterior
temporal region are particularly important for speech, and produce more
marked disorder than lesions of the angular gyrus or the supramarginal
gyrus. At first, words cannot be spoken, for a period of a fortnight
to three months. Speech returns progressively, with an increased power
of comprehension. At the same time, the patients begin to read and
write. But there is no further spontaneous progress after a period of
six or eight months, and then special reëducation must be started.
These speech disorders of retrocentral (parietal-temporal) origin are
either aphasic syndromes or slight remains of psychical disorders,
or again, a disorder practically limited to alexia. The true aphasic
syndromes concern the spoken word, understanding the words, writing,
and calculation. The disorder is not especially dysarthric and consists
particularly in loss of vocabulary. It might be called an amnestic
aphasia (Pitres). These cases have well-marked intellectual disorder
and their power of calculation is especially poor. As to the aphasic
traces, which are more important to understand than they are extensive
in point of fact, they relate particularly to calculating power, to
vocabulary (slowness in finding words), and to reading (reading without
comprehension). As to the cases of alexia, these are cases of lesions
of the posterior part of the parietal-temporal lobe, and are usually
accompanied by a hemi- or a quadrantanopsia.
To sum up, cases with central lesions (precentral and postcentral
gyrus) have hemiplegia and a Broca aphasia without much tendency to
cure. Cases with lesions anterior to the central convolutions have a
transient anarthria and their recovery is ordinarily complete. Cases
with retrocentral lesions have an aphasia suggestive of Wernicke’s
aphasia, and ordinarily leave behind them extensive defects in
intelligence and language. These cases should be taken account of
from the standpoint of compensation, since they are much worse off
for work than many cases with amputations; and though their disorder
looks slight, it quite interferes with working at a trade. From the
point of view of military effectiveness, the retrocentral cases are not
very good soldiers, and especially not good officers, as they do not
understand commands completely.
Neuropsychiatric phenomena in rabies.
=Case 118.= (GRENIER DE CARDENAL, LEGRAND, BENOIT, September, 1917.)
A farmer, 34, mobilized in veterinary work, fell sick at a station
for sick horses, April 25, 1917. He breakfasted well, drank coffee,
and went to the _abreuvoir_ at eleven o’clock. He told his mates that
he felt bad in his head. He fainted over a table at the eating house,
refused to eat or drink. At noon he went out into the court, vomited
and went to lie down. A physician thought he was suffering from angina
because of the pronounced dysphagia. He entered the hospital at eleven
o’clock at night on the 25th. He was found next morning on his back,
with a fixed and haggard look, crimson face, masseter and phalangeal
spasm at times. Respiration irregular, interrupted by moans. The pulse
would go up to 120 during agitation and then go down to 50 as soon as
the patient lay down again. Pupils slightly dilated and unequal. As
the patient came from a sick horse dépôt, the first question was that
of tetanus, suggested somewhat by the jactitation of the limbs and
the trismus. A violent headache began and the patient cried out, “My
head! My head!” Painful vomiting movements, with very slight bilious
material. Convulsive movements increased. The pulse was slow. The
diagnosis “meningitis” was suggested, despite the absence of fever
and the absence of Kernig’s sign. Lumbar puncture gave limpid fluid
with a normal lymphocytosis, without increase of albumin or reducing
substance. The bacteriological smear and culture were negative.
Soon another sort of symptoms appeared. The patient would rise, cry
out, threaten his neighbors. He was calmed with morphine. There were
periods of excitement alternating with periods of calmness, during
which he would reply sharply but accurately, being somewhat vexed by
the questions, and would walk up and down without offering a word. When
a glass of water was offered to him, as soon as his glance met the
glass his eyes expressed fear. He drew back in repulsion and cried out
in terror. When the liquid was out of his sight the hydrophobic spasm
ceased. This hyperesthesia of the sensorium was so intense that the
mere sight of the shining glassware of the laboratory brought out a
sharp crisis.
He was sent that evening to the neuropsychiatry center, walking jerkily
and as if slightly drunk, with a number of small gesticulations and
murmurings. He was immediately isolated, undressed himself and went
to bed. He did not move in his bed, and seemed to sleep. The next day
he got up, dressed and had a small spell of excitement, but was quiet
enough on the medical visit, though the floor was soiled with urine
and vomitus and the clothing was in disorder. He now had a pronounced
phase, deep sunk eyes, drawn features and anxious look; dilated pupils
and an expression of mixed fear and anger. His breathing was hard and
he kept his hand on his heart. He was oriented. He suddenly rose and
said, “I am thirsty.” A glass of milk was given him. He hesitated a
moment, plunged his mouth and hands into it and aspirated the drink
without making any swallowing movements. He pushed away the glass, spat
a little, and vomited a small quantity of a black liquid. Then followed
an anxious crisis, and he fell upon his side, absolutely immobile,
without breathing for a few seconds. Again in the sitting posture, he
was taken with contractions of the limbs and face. The tendon reflexes
were at this time normal.
A quarter of an hour later the attendant found him dead, in the sitting
posture, leaning against the wall, mouth open, arms dependent, hands
extended, pupils dilated--a death in syncope. The brain was found
congested. There was a slight effusion of blood over the posterior
aspect of the brain. There were no hemorrhages or softenings in the
brain substance. The muscles were of a dark red to black. The adherent
lungs were very slightly congested at the base. The stomach contained
a quarter of a liter of black, inodorous fluid in which there was
much bile and little blood. There were numerous small hemorrhages of
the mucosa near the great curvature. The spleen was large, the liver
congested. The Pasteur Institute confirmed the diagnosis of rabies.
There is no history of the man’s having been bitten by a dog.
Tetanus: Psychosis.
=Case 119.= (LUMIÈRE AND ASTIER, 1917.)
A soldier wounded May 18, 1916, was given antitetanic serum May 26th.
The wounds healed, but on June 16, that is, 29 days after the trauma,
contractures began, at first localized. There had been numerous wounds
of legs and scrotum by shell fragments and the contractures were
limited to the right leg and scrotum. There was no trismus or any
lumbar symptom.
During the next few days the contractures became general, the
temperature rose, a shell fragment was found by X-ray at the root
of the thigh and was surgically extracted. B. tetani was found upon
inoculation of media with material from the shell fragment. Persulphide
of soda and antitetanic serum 90 cc. in three days were given
intravenously. The temperature fell and the general health was greatly
improved. July 6, hallucinations and terrors, worse at night, set in.
The man believed himself surrounded by flames, that daggers were being
plunged into his old wounds, that his hair was being pulled. These
symptoms lasted a fortnight only, whereupon the patient recovered.
This case and six others accompanied by cerebral disturbances all
recovered, and all the patients retained a perfect memory of their
delirium and of their hallucinations.
The chronological distribution of these cases was odd. One case was
found early in the war; then no other cases of cerebral disorder
presented themselves until the group observed at the end of 1916.
Besides flames and daggers, zoöpsia was several times observed. One of
the cases showed these symptoms without having been given antitetanic
serum.
_Re_ tetanus in the war, see in the _Collection Horizon_ a book by
Courtois-Suffit and Giroux on _Les formes anormales du tétanos_.
Tetanus fruste versus hysteria.
=Case 120.= (CLAUDE AND LHERMITTE, 1915.)
Claude and Lhermitte describe a condition of _tetanos fruste_. The neck
was absolutely rigid. The patient had not been wounded in any way and,
being regarded as a pure neuropath, was sent to the Centre Neurologique
at Bourges.
The differential diagnosis lay between true tetanus and the hysterical
pseudotetanus or pseudomeningitis. In pseudotetanus there is a
contracture of the superficial and deep neck muscles, especially the
trapezii, sternomastoid, and deep muscles. The condition somewhat
suggests that of acute meningitis or tetanus, and especially suggests
tetanus because it is often associated with masseter contracture
(hysterical trismus). The head is immobile, stiff, and inclined
backward; eyes directed above, throat slightly prominent. Upon attempts
to move the head, intense pain occurs. The pain and contracture
sometimes even suggest a suboccipital Pott’s disease. This form of
hysterical pseudotetanus is of sudden onset, as a rule following burial
in a trench or else contusion, or a slight wound in the cervical
region. Pressure on the spinous processes produces no pain, nor does a
blow upon the head; and an X-ray examination will definitely eliminate
the hypothesis of Pott’s disease.
To return to the Claude-Lhermitte case of limited true tetanus:
It showed marked modifications in the tendon and bone reflexes.
Upon percussion of the zygoma, of the occiput, or of the clavicle,
there was a marked further contraction in the contractured muscles.
Although there was no apparent spasticity in the legs, there was an
ankle clonus and a bilateral patella clonus, combined with a distinct
exaggeration of all bone and tendon reflexes. In such cases also there
is hyperexcitability of the nerves and muscles to faradic and galvanic
currents.
An officer’s letter concerning local tetanus.
=Case 121.= (TURRELL, January, 1917.)
The following letter from an officer who had had local tetanus and was
treated by Turrell by ionization Dec. 6 and 7, 1915, by diathermia Dec.
7 to 22, and occasionally by static breeze ionization and chlorine
ion to relieve contractions from Dec. 29, 1915, to Feb. 4, 1916. The
tetanus was in the muscles of the legs. Of course diathermia is a
purely symptomatic treatment and does not replace antitoxin serum or
other specific treatment; thus its effect in relieving the contractions
of local tetanus is precisely like its effect in the treatment of
sciatic neuritis or lumbago.
November 15, 1916.
“Dear Major Turrell,
“I have been meaning to write to you for some time, as I knew
you would be interested to hear how I was getting on. Your
letter has just been received, and I am only too happy to give
you any information I can with regard to my leg. I was wounded
in the left leg on October 13, 1915, by high explosive shell,
and arrived at Oxford on October 22. There was no operation as
the surgeon in charge did not consider it advisable to remove
the pieces of shell: my leg seemed to be getting better, and
after about a month I was able to hobble round with sticks. My
foot at this time used to swell a great deal towards night,
and the foot seemed then to gradually stiffen up with violent
pains at intervals, this gradually spread up the whole leg to
about the knee, and I was compelled to take to my bed again.
The pain at times was very bad, similar to a very bad attack of
cramps, and then my leg became rigid and stiff, and at other
times used to get horrible jumps and it was impossible to keep
it still, and whenever the doctor or nurse looked at it it
used to stiffen up at once. The night seemed to be the worst,
and consequently I got very little sleep. I often had to get
up in the middle of the night on crutches to try and obtain
relief, my leg was so cramped and sore. It was about this time
that you first visited me and prescribed a course of electric
treatment for my leg, and I shall never be able to thank you
enough for the relief it gave me. I cannot remember the names
of the different treatments, but the first one--diathermy, or
heat pads--certainly relieved the pain, and after the first
two or three visits to you I got immense relief. I never
looked back after this, and, although the progress was slow, I
gradually lost all pain and was able to get sleep at night. The
nervous jumps slowly disappeared and my leg became gradually
normal except for contraction of the tendons. I was unable to
straighten my ankle or knee, and it was thought at one time
that my tendo Achillis would have to be severed. Gradually
the knee straightened and I was able to get my heel to the
ground. I was for some time on crutches, and was able to leave
the hospital on February 5, 1916, walking with sticks.… I am
now able to walk comfortably, but am unable to flex the ankle
more than at right angle to my leg. The circulation is not
very good, and I feel anything tight round my calf. I am still
getting Boards, and have not been passed fit for overseas yet.”
VI. SOMATOPSYCHOSES
(THE SYMPTOMATIC, NON-NERVOUS, GROUP)
Dysentery: Psychosis.
=Case 122.= (LOEWY, November, 1915.)
Out of a large number of dysentery patients, many of whom had very
serious symptoms, but one of Loewy’s patients became psychotic.
Loewy in fact had discharged this one as normal, and he had been put
on the wagon train (no opium or alcohol) to go to a sanatorium. As
the fighting shifted, the sanatorium site changed and could not be
reached with the wagon. Finally, the wagon train met the battalion
once more and Loewy was told that the man was “dying.” At this time he
was afebrile, without collapse symptoms, with a strong and normally
frequent pulse, and with few signs of exhaustion. Yet the guard had
thought that he looked moribund. Both upper eyelids were drawn rigidly
up but conveyed a different impression from that in maniacal or
anxious conditions. The expression was that of staring astonishment,
helplessness, and apathetic lack of orientation. The patient recognized
Loewy, spoke to him as “Herr Doctor,” said he was doing quite well;
he was found to be well oriented. There was no fabricating tendency
even as to the number of stools (although Loewy had noted such in
bad dysenteries of the _Shiga-Kruse_ type). He was apparently hard
of hearing, as if at the beginning of a typhoid fever. He showed a
retardation in his intake of ideas, and his voice in answering sounded
absent-minded. There was an expression of absent-mindedness, and the
patient seemed markedly unconcerned about his health, the direction of
the journey, the terrible rain, etc. These phenomena are attributed by
Loewy to attention disorder.
The patient had been out of reach of fire for days. Loewy reports the
case as one of beginning amentia or as an exhausted state resembling a
Korsakow condition, recalling one of emotional hyperesthetic weakness
(Bonhoeffer).
Typhoid fever: Hysteria.
=Case 123.= (STERZ, December, 1914.)
A soldier entering hospital for typhoid fever, October 2, 1914, was
discharged to another hospital and again, November 10, to a hospital
for nervous disease. The typhoid was serious and complicated by
delirium. After defervescence, the patient was weak and could not stand
or walk, especially on account of pains and weakness in the left leg.
Sometimes he had had pains in the sacrum and left hip. He complained
of tinnitus, deafness, dizziness, headache. He said he had fallen from
a cart, had been sick for three months, since which time he had been
under medical treatment for his present condition. He had, he said,
been given a small pension.
The gait disorder sometimes amounted to a real astasia-abasia. The
left leg became stiff and was dragged behind. There was a paresis
demonstrable in dorsal decubitus, of the left side, especially of the
leg, without atrophy. There was a hypesthesia of the whole left side
of the body, with the exception of the head. Hyperesthesia of the left
leg, hip and upper sacrum. The left corneal reflex was diminished.
Moody, hypochondriacal, lachrymose. The general attitude of the patient
was affected and theatrical. Paradoxical innervations were frequently
found on test. There was no neurological disorder except for the
absence of the right Achilles jerk.
The absence of this Achilles jerk may be regarded as a residuum of the
previous accident. The localization of the pains points to a neurotic
lumbosacral plexus disorder on the left side. Superimposed upon this
picture are the hysterical phenomena. The typhoid fever and its
attendant neuritis are therefore to be interpreted as the liberating
factor for a severe hysteria in a subject already disposed to such
symptoms through previous accident.
Dementia praecox versus post-typhoidal encephalitis.
=Case 124.= (NORDMAN, June, 1916.)
A butcher, 29 (aunt insane, sister melancholy, one child stillborn,
deformed), had had several days convulsions at eight; went through
military service without incident; was at the Marne and was evacuated
October 19, 1914, with typhoid fever,--a severe fever with a delirium
prolonged into the last weeks. Three months convalescent leave was
given, passed at Paris with the man’s aunt, but he had become strange.
One day he wanted to strangle neighbors of German origin; another day
departed for Dunkirk and then returned, having lost all his documents.
February, 1915, he went back to the front, did strange things and was
soon evacuated to Tarascon. In April he went back to his dépôt; May 18,
to the hospital at Rennes for erythema. June 15, he was given 15 days
in prison for setting off a cannon too quickly and then running off
through the fields. August 11, he was interned at Rennes for stealing
a priest’s cap. September 12, two months convalescence. December 10,
headaches. Back to Rennes January 14, February 18, Val-de-Grâce, then
Maison Blanche.
Here he was found sometimes sad, immobile; at other times laughing and
singing. He was very irritable on small occasion. Once on leave he
had a fugue with complete amnesia, though alcohol may account for the
latter. His memory was vague, especially for his crimes and for recent
events. He was emotional, indifferent even in the presence of his wife
or aunt. Sexual indifference. He often complained of his head, saying
that he felt it blocked and that he could not think. The headache was
frontal and would last several hours. The man would, however, not
complain spontaneously. He was physically, in general, negative.
This case might possibly be due to a post-typhoidal encephalitis, but
Nordman believes rather that it is a case of dementia praecox. Perhaps
the convulsions at eight produced a slight brain lesion, brought to an
issue by the typhoid fever.
Paratyphoid fever: Psychosis outlasting fever.
=Case 125.= (MERKLEN, December, 1915.)
A Breton farmer, 34, had paratyphoid alpha. Admitted to hospital
September 3, 1915, he had headache, anorexia, asthenia, coated tongue
and tense abdomen, algosuria; later, abdominal swelling, borborygmi in
the right iliac fossa, rose spots, dicrotism, albuminuria, bronchitic
rales. The disease was severe, and was complicated by sacral decubitus
and ran a month.
At first somnolent, September 8th the patient went into a state of
mental excitement with agitation and delirium. He got out of bed, cried
out, sang, talked to his neighbors, complained that his papers (colis)
had been stolen, as well as his watch and tobacco; that his horses’
hoofs had been injured, and the like.
He grew calmer in a few days, and now no longer tried to get up,
remaining inert in his bed. The occupation delirium persisted--he was
not being paid what he owed, and the like. He had hallucinations;
looked for scissors, and one day said, “Here they are!” At intervals he
appeared lucid and responded appropriately to questions.
The fever dropped and the paratyphoid disease appeared past, but the
mental state remained for three weeks without change, having the same
periods of lucidity when he would be regarded as cured, but falling
again forthwith into his post oniric ideas. He was soon sent to a
convalescent hospital and was not wholly well for another month.
Psychopathic taint brought out by paratyphoid fever.
=Case 126.= (MERKLEN, December, 1915.)
A soldier, 31, was a victim of paratyphoid alpha, entering hospital
October 21, 1915, with the usual symptomatology: fever, asthenia,
headache, abdominal swelling, tongue coated and red along its edges,
diarrhoea. After admission he passed into a deep toxic state.
He woke up in the night with a cry, got up afraid, and refused to go
back into his own bed. He was mute, except for curses addressed to the
nurses. After two hours he went to bed and to sleep. Next day he sat
quietly with a depressed look, occasionally groaning deeply, talking in
brief phrases about his anxiety, wanting his wife telephoned to, saying
that he would not see his children, was going into the four planks, and
the like.
This situation lasted about a week. He became afraid of medicines and
thought he had been poisoned, saying that he would rather be shot
than poisoned and complaining that, though he had served France for
fourteen months, they now wanted to kill him. In the night time he
was agitated. He gave vent to cries, and threats, but this delirious
state rapidly decreased and he became calm the night of September 27th.
The upper extremities showed a tendency to catatonia. From this time
forth, during the remaining month, the patient was immobile, mute,
fearful, and mistrusting, depressed and always wore a cunning look. His
disorientation decreased and he passed good nights. He would answer
questions by groaning. He would say, “They think I am a Tartar.” The
end of the mental disorder coincided with the cure of the paratyphoid
fever. According to Merklen, the paratyphoid bacillus in these cases
serves to bring out a psychopathic taint. This particular patient had
always been of a sad demeanor, uncommunicative, very impressionable and
emotional. Two other cases had always been somewhat below normal.
Diphtheria: Post-diphtheritic symptoms.
=Case 127.= (MARCHAND, 1917.)
A farmer, 37, was evacuated March 20, 1916, for diphtheria. April 1,
paralysis of tongue and uvula, impairment of vision. These symptoms
rapidly improved, but paralysis of the legs appeared and then of the
arms. This paralysis lasted until he was sent to the neurological
center June 28 for post-diphtheritic paralysis, wherein it was found
that voluntary movements of the legs could be performed, though
painfully and of slight extent, that walking was impossible, that there
was a considerable atrophy of legs and arms, that the knee-jerks,
Achilles jerks and plantar reflexes were absent. There was complaint of
pains in the legs and over nerve trunks.
Improvement followed, the atrophy gradually passed away, and the
voluntary movements of the legs became more extensive; but by October
the reflexes had not yet reappeared. Yet the patient had begun to
walk on crutches and soon was able to get on with canes only. The
improvement did not continue. He did not raise his heels and dragged
his toes. There was now a clonic tremor of the legs as soon as the
weight of the body was put on them. During movements of legs carried
on in dorsal decubitus there was found an irregular tremor of the legs
with twisting of the trunk. The muscular strength was well preserved.
There was a slight muscular atrophy. The tendon reflexes had now come
back, though the right Achilles jerk was weak and the plantar reflexes
were absent. There was a hypalgesia of the legs which ceased sharply
at the middle of the thighs. There was a slight hypoacusia on the left
side. Visual fields normal. The patient complained of feelings in the
inside of his bones. Electrical reactions normal.
Diphtheria: Hysterical paraparesis.
=Case 128.= (MARCHAND, 1917.)
A soldier, 24, was evacuated June 24, 1915, from Roussy for diphtheria
and was treated by serum, receiving 80 cc. in 8 injections. A few
days later there was a paralysis of the uvula with regurgitation of
liquids from the nose; but patient was able to go on convalescence July
21. A few days later, however, he noticed that his legs were weak.
Vertigo, vomiting and painful walking followed, and his convalescence
was increased a month. The paralysis got progressively worse.
September 10, he went by automobile to Libourne where he stayed two
months. He arrived at the Neurological Center at Bordeaux November 9
with diagnosis “polyneuritis of legs.” He could not walk and could
hardly flex thighs on pelvis or legs on thighs. Voluntary movements
of extension and flexion of feet and toes were limited. There was
neither atrophy, pain nor reflex disorder. Both legs were analgesic,
as was also the abdomen up to the umbilicus. There was complaint of
dorsolumbar pains and of stomach trouble and lack of appetite; vomiting
after meals frequent, pulse 120.
January 3, the patient was able to lift his legs a few centimeters
above the bed but not together. There was now a slight muscular atrophy
especially on the left side. Knee-jerks lively, analgesia limited to
legs, no vomiting, pulse rapid.
The patient was sent to a hospital in the country May 8 to July 8. He
was now much better. His legs were able to support his body but he
could not walk. Slight atrophy of left leg. There was hypalgesia now in
the feet and legs below the knee. There was no pain on pressure over
the nerve trunks. The electric reactions normal. The patient could now
walk on crutches. He was invalided on the temporary basis, December 12,
1916.
It does not appear that in this case the hysterical paralysis was
preceded by polyneuritis.
Malaria: Amnesia.
=Case 129.= (DE BRUN, November, 1917.)
A soldier lost all memory of his hospital stay in Salonica and the
voyage home. He could only remember a little about the hospital at
Bandol. There is a period of transition to full memory in malarial
cases characterized by sure memory, vague on certain points,
alternating with phases of almost complete amnesia. The soldier
in question had very inexact memories of the Bandol Hospital, and
could only remember about his fevers, that they began about noon and
terminated about four o’clock. Twice he had been found in his shirt,
walking, unconscious, in the passageway of the hospital. Having
obtained leave for convalescence, three months after his memory gap
began, he went to Paris, and probably had attacks at home. He vaguely
remembered afterward being carried by automobile to the Pasteur
Hospital, December 1. There he remained to the end of March, 1917,
without preserving anything but the vaguest memories of an intermediary
period of more than six months. The memory in these malarial cases
often remains permanently altered and there may even be a retrograde
amnesia, carrying back to facts prior to the gap and an anterograde
amnesia relative to facts after the main gap.
Thus, there is in the febrile period a retrograde amnesia and in the
post-febrile period a retrograde or anterograde amnesia. One group of
subjects are severe cerebral cases, and the memory gap appears to run
back to a period of true mental confusion. But there is another group
of patients who preserve throughout the febrile period an absolute
consciousness of all acts, and yet the memory gap is just as sharp and
definite as in the confusional cases.
Malaria: Korsakow syndrome.
=Case 130.= (CARLILL, April, 1917.)
A stoker, 45, was admitted to the Royal Naval Hospital, Haslar,
November 6, 1916, from the Fifteenth General Hospital in Alexandria, to
which he had come from a hospital in Bombay about three weeks before.
At Alexandria he was anemic and showed an edema of legs which had been
present for six weeks. Cylindruria; no albuminuria. At Haslar there was
no cylindruria and no edema, and nothing but weakness, gouty arthritis
of left wrist, right ear and left great toe. Red cells 4,650,000,
leucocytes 10,000 (52 per cent polymorphonuclear, 46 per cent
lymphocytes). He was rather dull mentally. December 10th, Dr. Fildes
found malarial organisms in the blood on the occasion of a hyperpyrexia
(104°). Quinine was given. December 14th, he was transferred
neurological. According to the patient’s own story, he was born June
10, 1868, lived in Fulham, had a daughter aged 12 years, had recently
seen his wife at the hospital: all this seemed plausible enough.
Later, however, he said that the year was 1899, that King Edward was
king, that the war was between England and some field forces, etc. This
well-nourished, pale, simple-looking stoker spoke quietly and politely;
told about intermittent fever; about being eight years on the active
list, becoming a reservist and being called up for the war. He read
intelligently, could do sums, but did not know the name of the hospital
and was confused about the war. He recognized that his memory was not
as it should be; constantly stroked his moustache and chin. He was
happy and contented.
The gait was normal, systolic blood pressure 140 mm.; no evidence of
alcoholism. Blood, January 15, 1917, contained 5,050,000 reds, 10,300
leucocytes (63 per cent polymorphonuclear, 37 per cent lymphocytes).
There was a bilateral absence of the ankle-jerks, repeatedly confirmed
at subsequent examinations. Wassermann reaction was negative. Puncture
fluid contained no cells.
Instead of living at Fulham, this stoker lived at Portsmouth, and had
not been seen by his wife for four years. He had done 18 years’ active
service and had last sent his wife a letter from the Sailors’ Home
at Bombay, November, 1916. They had been married 21 years. He caused
astonishment with his wife and friends by announcing that Lord Roberts
and General Buller were in command at the battle of the Falklands.
He continued to say that he lived at Fulham. He was discharged home,
January 22. It seems as if he were living through the period of the
Boer war.
Carlill considers that alcoholism may be ruled out, and there is no
likelihood that the gout was the cause of the neuritis. He believes
that the neuritis was probably malarial. Possibly the illness suffered
in Bombay may have been beriberi or it may have been malarial
nephritis.
A complication of malaria.
=Case 131.= (BLIN, August, 1916.)
A Senegalese corporal of machine gunners, 21 (early life normal save
for sore throats and coughing), was a robust, well-developed man of 75
kilos when he entered the hospital at Konakry, February 15, 1916. He
was given the diagnosis: malarial anterior spinal paralysis.
It seems that he had joined a Colonial regiment, April 8, 1915,
attended classes as a recruit, left Bordeaux November 1 for Dakar,
arriving there November 11. He stayed there some sixteen days, during
which time he slept without mosquito-netting. November 16, he left for
Konakry, and had his first febrile symptoms November 27, with vomiting,
headache, and prostration. His temperature ran as high as 41, but by
December had fallen to normal, after quinine.
The corporal was sent away, cured, to his company at Kouronesa,
December 6. There was more fever, headache, and vomiting during the
railway trip. Quinine again relieved the fever, but a bloody diarrhoea
set in so that it was only at the end of January that he could go on
service.
February 6, another attack of fever, with shivering and perspiration,
lasted for some three hours. He could hardly stand by himself and had
to be helped in walking. Next day, another spell of three hours of
fever; definite paralysis set in, affecting both legs. February 8 the
arms were attacked by paralysis which, unlike that of the legs, was a
progressive one, attacking first the shoulders, then the elbows, the
wrists, and finally the hands. All the body muscles were in a state
of flaccid paralysis, as well as the muscles of the face. The patient
was now afebrile. February 9 there was a slight speech defect; the
tongue was slightly paralyzed, and swallowing became painful. The jaw
movements remained normal. The muscles of the face were intact and the
patient could whistle, move his lips, and move his eyeballs normally.
Vision normal. The pupils were fixed in dilatation, more widely on the
left side. There was a slight contracture of the vesical sphincter,
necessitating the catheter. The tendon and cutaneous reflexes were lost.
By February 14, when the patient was sent to the Bellay Hospital,
muscular atrophy had made its appearance. No plasmodia could now be
found in the blood, which showed 71 per cent polynuclear leukocytes, 20
per cent mononuclears, 9 per cent lymphocytes.
This state lasted til February 25. Despite the fact that the patient
ate well, emaciation rapidly progressed. The buttock showed a very
few signs of decubitus. Upon this date there was pain from a marked
orchitis of the left side, the cause for which remains unknown (no
history of gonorrhœa; catheter used for the last time, February 15).
The temperature which attended the orchitis came down in three days;
the patient’s appetite was singularly good, but the muscular atrophy
increased. The speech defect meantime disappeared, and the patient
swallowed more readily.
March 7 a slight and hardly perceptible movement could be noted in the
fingers of the left hand. Two days later, similar movements appeared in
the right. March 11 he could spread his fingers in a kind of creeping
movement. Next day slight movements were possible with the legs, and
March 13 the knees were movable. March 14 the patient could lift his
head from the pillow. The range of movement now increased all over the
body. According to the patient, those parts were the first to regain
power that had been attacked last. This certainly seemed to be the case
with respect to the left upper limb, in which first the hand and wrist,
then the elbow and shoulder, successively recovered power. The legs
regained their power in the same way proximad. March 17 the patient
could sit up and grasp objects with the left hand. The cremaster and
plantar reflexes appeared,--the former, more on the right; the latter,
more on the left. The left pupil remained in wider dilatation than the
right.
The treatment was by quinin and potassium iodide, with massage. The
patient was apparently on the highroad to complete recovery, and left
for France March 21, weighing 63 kilos.
Trench-foot: Acroparesthesia.
=Case 132.= (COTTET, September, 1917.)
A fantassin, 36, carpenter by trade, went into the trenches October,
1914, and had two attacks of trench-foot, first in January, 1915, when
there was a painful swelling of the foot and secondly in July, 1916,
when there were some bullae on the dorsal aspect of the feet. These
were not serious and the fantassin did not report sick.
He was wounded, August 27, 1916, by shell fragment on the right elbow,
was evacuated to the ambulance where the fragment was extracted and
then to a hospital which he left cured with a seven days’ leave.
Although he had not suffered in any way from his feet while in
hospital, and had not been exposed to cold, the bullae reappeared on
the feet just as they had been in July. They in fact now formed a sort
of exanthem occupying symmetrically the dorsal surfaces of the toes.
The bullae contained serum. They were confluent, varying from pin head
to a nut in size, were as a rule round, but sometimes irregular. The
eruption went on to a cure rapidly and on the twelfth day the bullae
had dried up. This patient had hypesthesia up to the knees, hypesthesia
of the dorsal surfaces of the feet, hyperesthesia of the plantar
surfaces and ankles, hypesthesia of the forearm and the elbow and of
the dorsal surfaces of the hands with possibly exaggerated sensibility
of the palma surfaces. Hypesthesia of the face was limited to a small
part of the right ear. The reflexes were normal and there was no
atrophy. The name “paresthetic trench acrotrophodynia” was given to it.
In a service of eighty beds Cottet found within two months fifteen
instances of these acroparesthetic disorders regarded as neuritic
changes in trench-foot of a latent and lasting character which would
have remained unobserved unless there were disorders of sensibility. In
fact similar disorders of sensibility may be found without any history
of _gelure des pieds_, forming a latent type of neuritic alteration
hardly noticed by the patient himself. In twenty-six cases Cottet found
sixteen with hypesthesia of the ears and of the nose.
Bullet injury of spine; bronchopneumonia: état criblé of spinal cord.
=Case 133.= (ROUSSY, June, 1916.)
As to the development of eschars, Roussy reports the case of a
lieutenant wounded September 25, 1915. There was a penetrating wound
of the interscapular region. The bullet had entered on the posterior
aspect of the right scapular region and had emerged at the level of the
first dorsal vertebra. October 1, a neurological examination showed
flaccid paraplegia, knee-jerks normal, Achilles jerk weak on the right,
plantar reflexes flexor, cremasteric reflex absent on the right, and
both abdominal reflexes absent. There were pains in the legs and arms.
There was retention of urine with overflow. A slight dulness on the
right; temperature from 38 to 39 degrees.
Four weeks later the knee-jerks had become very weak, and the Achilles
jerks were now absent. There was an extensive diffuse atrophy of the
lower leg and thigh muscles, and a hypesthesia of pronounced degree had
developed throughout the legs, over the buttocks, and in the lumbar
region. Anal and vesical sphincters relaxed; dejections voluminous;
sacral decubitus as well as healed eschars. December 5, the patient was
transferred to the Army neurological center; temperature rose; there
was much expectoration; paracentesis yielded no fluid; pneumococcus
in the sputum. Cystitis had developed despite extreme care. Extensive
edema of the legs developed. There was increased dulness on the right
side, coughing and dyspnea. Death, January 17.
The autopsy showed a bronchial pneumonia of the right lower lobe,
confluent, imitating a lobar pneumonia. The left lung also showed
extensive confluent bronchopneumonia at the base as well as
disseminated areas and edema of the middle and apical portions.
Infectious splenitis, large fatty liver, swollen kidneys, no
pyonephritis.
The spinous processes of the 6th and 7th cervical vertebrae were
injured. There was no obvious gross disease within the theca except
that there was a slight adhesion between the dura mater and the
anterior surface of the spinal cord at the level of the 7th cervical
and highest dorsal vertebrae. There was, however, a depression on
the anterior surface of the spinal cord at a lower level, namely, at
the level of the 4th dorsal vertebra. Microscopic examination showed
myelomalacia with small cavities in the 1st and 4th dorsal segments,
suggesting the _état criblé_.
According to Roussy, these patients injured in the spinal region are
particularly sensitive to cold and support transfer badly even when the
disease is short. Such patients should be evacuated to the interior
after the shortest delay possible. Sometimes these patients show rib
fractures; these are in the posterior portions of the ribs and are due
to the fall of the man when struck. It might be possible even that the
spinal lesions should through the action of the sympathetic nervous
system favor lung infection.
Shell-explosion: Hystero-organic symptoms; decubitus; radicular sensory
disorder.
=Case 134.= (HEITZ, May, 1915.)
A soldier, 32, was bowled over in a first-line trench by the bursting
of a shell that he did not see coming, September 14, 1914. He regained
consciousness only in the middle of the night, finding himself half
covered with water. He was taken up by the stretcher-bearers at
eleven in the morning. Paralysis in the legs was then absolute. There
were pains in the legs and in the back, but there was no evident
lesion. Knee-jerks, plantar reflexes, and abdominal reflexes absent;
cremasteric reflex absent on the left, weak on the right. Tactile
sensations, on the contrary, were almost intact except for a slight
diminution over the feet and the external aspects of the lower legs.
Sensitiveness to pin-prick, however, was abolished throughout both
lower extremities, and diminished in the abdomen and back up to two or
three centimeters above the level of the umbilicus; that is, including
the territory of the first lumbar and the last three dorsal roots.
Sensibility to heat was abolished in the feet, the external aspect
of the lower legs, and the posterior aspect of the thighs, but was
preserved in the second and third lumbar territory, in the anterior
aspect of the thighs, as well as in the region below the umbilicus.
Micturition was impossible. Constipation the first few days yielded
spontaneously September 20. There were signs in the bases of both
lungs, corresponding with a suffocating feeling. September 22, he was
evacuated, almost well, without signs of pulmonary congestion, having
regained the power of urination and some capacity to move the legs
sidewise. February, 1915, after evacuation to a hospital at Vic, he
showed sacral decubitus, soon reaching the size of a hand, as well as
trochanteric decubitus; traces of albumin in the urine, sacral and
sciatic pains (recalcitrant to morphine).
He began to improve December 25. Camphorated oil and the sitting
posture relieved the pulmonary congestion; the temperature, which had
oscillated round 38 degrees, fell; the decubitus scarred over; the
knee-jerks reappeared to some extent, and movements began. February 5,
the patient had become able to walk without crutches. There was still a
two-franc sized area of decubitus over the sacrum, and still a little
spinal pain in walking.
It is difficult to consider this case only functional in view of the
decubitus, to say nothing of the radicular distribution of the sensory
disorder. Heitz brings this and the previously given case (No. 1) into
relation with Elliot’s case of transient paraplegia (see Case 210) and
Ravaut (see Case 201).
Shell-shock (windage?); typhoid fever; “neuritis” actually hysterical.
=Case 135.= (ROUSSY, April, 1915.)
A Colonial soldier was sent back from the front, September 12, 1914,
for nervous disorder due to the shock of the windage of a bullet.
He had not lost consciousness. Under observation at his station, he
got typhoid fever, and was cared for at Paris from the beginning of
October. About October 15 he began to feel pains in his left shoulder,
neck, and arm. The diagnosis, neuritis, was made and was strongly borne
in upon the patient, so that upon the cure of his typhoid, he went out
on two months’ leave with a complete impotence and much pain of the
left arm. At the end of his relief, he was evacuated to Villejuif.
January 24, it was found that he had no somatic phenomena whatever,
despite the fact that the left arm and a part of the forearm was
powerless, and so painful that the patient cried out when his arm was
moved. There were a few cracklings in the scapulo-humeral joint.
Hot air and reëducation cured the man in less than two months (March
20), though the disorder had lasted for four months. The patient had
been retired for hysteria before the war and had re-enlisted.
Bullet wound of pleura: Reflex hemiplegia and double ulnar syndrome.
=Case 136.= (PHOCAS AND GUTMANN, May, 1915.)
A soldier, 26, was wounded in the enfilading of an Argonne trench
December 17, 1914. He felt the bullet like an electrical shock, and
fell. He had been leaning forward at the time and suddenly felt the
left half of his body go paralyzed and his mouth pulled to one side.
He did not lose consciousness, and spat up a good deal of blood five
minutes after falling. He lay in the trench all night, unable to move
his left leg except by the aid of his right. He was evacuated next
day. There was a five-franc piece wound at the upper border of the
left scapula, four finger-breadths from the median line. There were a
few lung signs which rapidly cleared up. December 28, the hemiplegia
was better, although neurological examination showed weakness of left
upper extremity, abolition of deep reflexes, and certain skin changes
of the left hand with edema (_main succulent_), decreased resistance of
muscles of lower extremity to passive motion, especially of adductors
and flexors, exaggerated polykinetic left knee-jerk, ankle clonus,
Babinski reflex, abdominal and cremasteric reflexes absent on left,
platysma paralysis left, with complete paralysis in the inferior
distribution of the facialis; whistling impossible. Also the left eye
could not be closed singly. Synergic movements of the lower part of the
paralyzed face when the right hand of the patient was grasped.
There were also sensorimotor disorders in the ulnar distribution on
both sides, with complete anesthesia to pin prick. There was also an
area of hyperesthesia of the anterior and postero-internal aspect
of the right forearm from below the elbow to the wrist. The tendon
reflexes were weak but distinct on the right side. The left arm had
feelings of pain, with _élancements_ and formication from the shoulder
to the fingers on the ulnar distribution. There was, of course, also,
local hyperesthesia due to the wound of the thorax.
Lumbar puncture showed a fluid normal in all respects. We deal with
a hemiplegia of organic nature, associated with the bilateral ulnar
syndrome. The hemiplegia followed the trauma immediately. When the
ulnar phenomena appeared is unknown.
The lung complications cleared. The pains disappeared; motion returned
up to the level of the facialis. The patient got up and three months
later went on convalescence, still presenting Babinski, exaggerated
knee-jerk and weak arm reflexes on the left side. The bilateral
ulnar syndrome had disappeared six weeks after the patient entered
hospital. Phocas and Gutmann cite a considerable literature on
nerve complications of pleural trauma, among them syncopes of grave
prognosis; a relatively frequent pleural epilepsy (forty-five per cent
fatal) or epileptic status (seventy per cent fatal); and the rare
hemiplegia. Accidents and death have followed exploratory puncture of
the pleura. Air embolism is probably not the cause. Phocas and Gutmann
prefer the theory of a reflex disorder starting from the pleura.
Hysterical tachypnoea.
=Case 137.= (GAILLARD, December, 1915.)
A man, 23, came to the Lariboisière November 29, 1915, in a hurry
to show evidence that he had been invalided for valvular lesion of
the heart. In point of fact, the interne found a murmur at the base.
Yet there were things in the military papers suggesting caution. The
patient next morning showed no malaise, dyspnoea, or any evidence of
serious disorder. The contractions of the thorax beat in time with
contractions of the alae of the nose, about 112 per minute. Here, then,
was a cardiopulmonary patient. The heart impulse was exaggerated; the
patient could not or would not stop breathing to aid the auscultation,
but almost absolutely normal sounds could be heard at the apex and the
base. A valvular lesion could be excluded. The lungs were perfectly
normal. The patient was requested to stop his gymnastics, which might
have succeeded elsewhere but could not at the Lariboisière!
How could the man have established the synchronism of pulse and
respiration and synchronous tachypnoea and tachycardia? Why should he
persist in this form of sport, since he had already been invalided?
The family history was not especially suggestive (father albuminuric,
died at 59; mother well, probably tuberculous). Scarlet fever at eight;
occupation, tourneur. After four months of service there was gastric
disorder followed by typhoid fever (despite vaccination, according to
the patient). Convalescent leave at Paris, during which leave he had
swollen legs and albuminuria. May, 1915, gastric difficulty; valvular
lesion determined; examination; invalided. At home, a variety of
complaints, for which treatment was unsuccessful.
During further examination it was noted that in auscultation the head
of the examiner was lifted, as if there were hypertrophy of the heart
or an aortic aneurysm. The synchronism was less exact on December 2;
112 beats to 128 respiration. Was this man a simulator? Had he become
the victim of his own enterprise? There was no evidence of simulation.
It was a question of a monosymptomatic hysteria. Gaillard discontinued
the _manière forte_ and undertook a softer treatment, but the _manière
forte_ had caused the family to want to take him away. Perhaps they
feared a too efficacious treatment. He then escaped observation. It is
probable that the tachypnoea ceased during sleep. It was not so marked
after the medical visit was over.
Soldier’s heart.
=Case 138.= (PARKINSON, July, 1916.)
A corporal, 21, who had been a miner and entirely well up to enlistment
in August, 1914, went to France in 1915. In June, came shortness of
breath and palpitation on exertion; later, precordial pain (fifth
space, between nipple and median line) and giddiness on walking. Like
all cases of true so-called “soldier’s heart,” this soldier had no
physical signs indicative of heart disease, yet reported sick for
cardiac symptoms on exertion. In this particular case, as in about half
of forty cases reported by Parkinson, there had been no disability in
civil life.
August, 1915, the soldier was admitted to the casualty clearing
station, where the apex beat was found in fifth intercostal space
internal to the left nipple line. The first sound was duplicated in all
areas. The second sound was duplicated, though not loudly, at the base.
After nine months’ treatment, this man went back to light duty with
slight symptoms.
According to Parkinson, the absence of abnormal physical signs in
the heart of a soldier should not prevent his discharge from the
army if under training or on active service he shows breathlessness
and precordial pain whenever he undergoes exertion well borne by his
fellows. A simple exertion test, such as climbing 25 to 50 steps,
reproduces the symptoms in such a patient. The rate of the heart at
rest is a little higher than that of normal men, though the increase on
exertion is greater. Nevertheless, it has been proved that the increase
of rate on exertion bears no relation to the symptoms elicited and is
therefore without value in judging the functional efficiency of the
heart.
Soldier’s heart?
=Case 139.= (PARKINSON, July, 1916.)
A sergeant, 36, had been in the army from 17 to 29, but in 1908 he
had acute rheumatism and was discharged from the army. He then became
a furnace man and had shortness of breath and palpitation on severe
exertion with syncope three times.
He re-enlisted in August, 1914, and had an attack of orthopnea and
edema after exposure at a review. However, he improved and went to
France in May, 1915, where he again had symptoms; namely, precordial
pain and breathlessness on severe exertion. One day while carrying
telephone wire under fire, the sergeant felt a sudden pain in the
region of the apex beat, shooting down the right arm. “I thought I
was shot.” He fell down, very short of breath. His left arm remained
sore and weak. Two days later came a similar attack, this time with
unconsciousness, and the left arm was now useless. Two days later he
was admitted to hospital, where slight breathlessness but no pain and
no enlargement of cardiac dulness could be found. No further details
are available but it seems clear that this man is unfit for duty.
According to Parkinson, it is probable that the infection indicates the
presence of some degree of myocardial disease.
Strain and shell-shock: Acceleration of diabetes mellitus.
=Case 140.= (KARPLUS, February, 1915.)
An infantryman, aged 22, previously healthy and from a healthy family,
was struck by a shell fragment in the forehead and lay for several
hours unconscious. He did not vomit. He had a number of furuncles on
his body and his urine, upon examination, showed a severe diabetes
mellitus which increased despite treatment. Upon an attempt to withdraw
carbohydrate, the sugar suddenly sank from six to four per cent.
Acetone at the same time increased. An abrasion had been noticed by the
patient a few days before the shell explosion on the spot rubbed by the
_tornister_. The patient said that since his accident he had had to
urinate every night several times and was often very thirsty, neither
of which tendencies had he had before. A month before he became _merod_
he had had an injury of the hand produced by a shell fragment. He had
undergone tremendous strain.
The chances are that the excitement and the strain had more to do with
the diabetes mellitus than the shell explosion.
Dercum’s disease.
=Case 141.= (HOLLANDE and MARCHAND, March, 1917.)
An adjutant in a chasseur battalion was buried by a shell explosion,
which killed his lieutenant beside him, January 5, 1915, at
Hartmannsweilerkopf. Hematuria followed; ten days later, fever with
anorexia, and the appearance of two or three lipomata on the anterior
surface of the thighs. Remaining at his post, the adjutant took part
in an attack, March 5; was evacuated on the 8th; “lipomatosis with
febrile reactions.” He spent eight days at Bussang, and thence went to
the hospital at Pont-de-Claix. Here marked albuminuria was noted; the
lipomata increased in volume; others appeared in the arms. The patient
was transferred to the Des-Genettes, where the diagnosis nephritis
was added to the previous diagnosis, and a milk diet was prescribed.
Convalescence of five months was proposed. The lipomata increased in
volume and in number. The patient was then hospitalized at Avenue
Berthelot, placed in the auxiliaries, and stationed eight months at his
dépôt.
When he was observed by Hollande and Marchand, four nut-sized tumors
were found on the anterior surface of the left thigh; two smaller
tumors: one of them painful to pressure, lay on the inner aspect,
another the size of a small egg lay in the right thigh, and there
were two others on the internal aspect and two on the external aspect
of the thigh. A nut-sized tumor was found on the inner border of the
right forearm, and below it another lenticular tumor. A nut-sized
tumor was found on the left forearm below the elbow on the internal
border. Small tumors were found on the buttocks. There were no tumors
below the knees, in the upper arms, or on the thorax. There were 14
tumors in all. The smaller the tumor the more sensitive, and there
was more pain when the tumor had just appeared and during the first
days of its growth. There was no spontaneous pain; pain only upon a
blow or pressure. Diminished knee-jerks, especially the right; no
other neurological disorder, although the patient complained of often
having something before his eyes. There was a marked diminution in
the memory. Heart was in the 5th space on the nipple line, pulse 110;
Wassermann reaction negative; red blood cells, 3,520,000, white cells,
6500; albuminuria, hematuria, leucocytes, and urethral cells in the
urine. The temperature had now become normal. The lateral lobes of
the thyroid were slightly larger than normal, but not painful. Sella
turcica was unchanged upon X-ray. Exploratory puncture of a tumor
showed much free fat, without fatty acid crystals and with some fat
cells. The cells could not be cultivated in test tube. The authors
believe it doubtful whether this instance of Dercum’s disease is
related with the shell explosion.
Hyperthyroidism.
=Case 142.= (TOMBLESON, September, 1917.)
A private, 22, was selected by Col. Garrod for hypnotic treatment by
Tombleson from among the hyperthyroid cases. He was admitted April 3,
1916, with a typical hyperthyroidism, with manual tremor, enlarged
thyroid, pulse 120, blood pressure 136-40, and hemic murmur. Tombleson
induced deep somnambulism at the first hypnotic sitting and suggested
an increase of nerve strength and steadiness. The suggestions under
somnambulism were repeated for ten days. An occasional added suggestion
was given as to lessening of the thyroid. At the end of the ten days
the patient declared himself quite well.
Eight of twenty consecutive functional cases treated by hypnotism by
Tombleson were cases of hyperthyroidism and in virtually all of these
an effect like the above was registered.
Shell-shock; thrown against wall, stunned, emotional: Paroxysmal heart
crises six days later, observed for two months. Neurasthenia? Mild
Graves’ disease?
=Case 143.= (DEJERINE AND GASCUEL, December, 1914.)
An infantryman, 29, was sent to auxiliary hospital No. 274, for heart
trouble, a little thin but looking vigorous enough (typhoid fever at
13 and some diseases of unknown nature and of brief duration while in
military service).
September 24, a large calibre German shell burst and threw him against
a wall, producing no wound or contusion. He was momentarily stunned,
emotionally much affected, and noted at the time extreme palpitation.
He was evacuated to Paris September 30, six days after the shock. His
pulse was 130-134, regular, and the heart seemed not to be anomalous in
any respect.
But there were paroxysmal crises in which the pulse rose to 180 and
in which the patient fell into a state of great anxiety. The mouth
temperature in the midst of such crises would always rise to 38°,
and this temperature would outlast the rest of the seizure. The man
was mentally depressed and apparently indifferent, preoccupied with
his heart and his insomnia, but at the same time emotionally easily
affected. In short, he was a neurasthenic. There was no change in
mental state, tachycardia, or paroxysmal seizures in two months, except
that he gained weight. Walking and climbing stairs produced dyspnoea.
Urine was negative. According to Dejerine, such a case should be
treated by psychotherapy.
Alquier, in discussion, called attention to the slight but distinct
tremor in this case, dermographia, and spells of perspiration. He
suggested that the case might be one of mild Graves’ disease.
Hyperthyroidism three months, following ten months’ service, at times
under protracted shell fire.
=Case 144.= (ROTHACKER, January, 1916.)
A man in service ten months, under strong excitement and at times under
protracted shell fire, complained of palpitation, insomnia, dizziness,
and dyspnoea. Hospital notes showed that the left lobe of the thyroid
was somewhat enlarged. Before the war his neck could not have been
very thick; he had served his year out without difficulty. His mother
is said to have suffered at one time from thick neck. According to the
patient, he had never suffered with heart trouble. Heart not enlarged;
blowing first sound over the apex. Graefe, Stellwag and Möbius signs
negative. Heart rapid, not irregular; pulse strong. There was fine
tremor of the hands, as well as a tremor of the tongue. Knee-jerks
increased.
The patient was at first sleepless and excited, but after three weeks
in bed the heart murmur had disappeared. After three months, he was
ordered to _Ersatz_ with the left side of the neck measuring 20 as
against 18 cm. on the right. There was a soft pulsating swelling of the
thyroid. First sound over apex still impure; heart action now regular;
pulse 64; blood pressure 120 Riva-Rocci; after test exercises, slight
dyspnoea. No cyanosis. The outstretched hands were no longer very
tremulous. The knee-jerks were still increased. The man had begun to
sleep well. His neck was apparently much diminished in girth.
Here then was a case of Graves’ disease of acute development, brought
out by nervous stress and excitement as well as by 10 months of war
work and exposure to shell fire,--with approximate recovery after three
months of rest.
Graves’ disease, forme fruste.
=Case 145.= (BABONNEIX AND CÉLOS, June, 1917.)
A farmer, 31, entered the Rosendael Hospital, Jan. 25, 1917. He had
been two years in active service. The family history was negative
except that one of his sisters had had dyspepsia. The patient denied
venereal disease and alcoholism and had always been well. At the Battle
of the Marne he was slightly wounded in the left knee. January, 1915,
he was exposed to gas bombs and explosive shells. He was several days
in the hospital spitting, or perhaps vomiting blood and was sent on a
long convalescence. On returning to the front, he had to be sent back
to hospital with a note, “not fit for service, nervous troubles and
paroxysmal tachycardia.” In point of view he now showed a number of
symptoms suggestive of Graves’ disease, such as a definite exophthalmia
which, according to the patient, started up a short time after the
shock and a tachycardia (110-120) with circulatory excitement, a
tumultuous heart, neck arteries contracting, almost dancing in their
contractions, together with a systolic murmur maximal in the pulmonary
area, not retaining, variable,--in short, suggestive of an inorganic
murmur. There was also a generalized rapid tremor and a variety of
vasomotor disorders, such as blushing and paling, perspiration,
exaggerated reflexes, emotionality, logorrhea, jactitation. There were
also digestive troubles, regurgitation after meals and the patient had
become thin and weak.
There was, however, no swelling of the thyroid gland nor any eye signs
other than the exophthalmia. In short this case is doubtless one of
the _forme fruste_ of Graves’ disease. It seems to show that Graves’
disease may have a traumatic origin.
Somatic complication in a shell-shock hysteria (Trauma).
=Case 146.= (OPPENHEIM, February, 1915.)
Musketeer. No faulty heredity, but was always somewhat nervous. On
October 26, a shell burst one meter in front of him, burying him under
the anterior wall of the trench. He was dug out and taken to the field
hospital, where he remained unconscious until the next morning. On
October 29, he was taken to the reserve hospital. Severe pain in the
head, entire scalp tender on pressure, especially in the left frontal
region, left side upper lip swollen, bluish and discolored. Left tenth
and sixth ribs broken. Fracture of skull(?). November 10, at eight
o’clock at night, sudden attack of vomiting, and the patient was found
in a faint in the water closet. Almost complete paralysis of speech
and all of the four extremities. Consciousness obscured; no sensory
disturbances. November 11, severe headache and vertigo. Speech somewhat
more intelligible. Pulse, 60 to 68. “Evidently secondary hemorrhage in
the brain.” November 12, to Augusta Hospital. November 20, admission
to nerve hospital. Typical aphonia. Limitation of motion in all four
extremities, but no paralysis--anergy. Reflexes normal. Unable to
stand and walk. Sensibility preserved. Under suggestive treatment,
curative gymnastics, as well as electrotherapeutics, the aphonia
and abasia disappeared in a few days, but the patient continued to
complain of headache and insomnia. December 16, an attack of nausea,
headache, vomiting, loss of consciousness, followed by epistaxis,
marked tachycardia. January 4, in his sleep he felt a prick in his left
upper arm, as if he had pushed a sewing needle into the arm. X-ray
examination showed a needle in the arm. This was extracted under local
anesthesia.
VIII.[5] SCHIZOPHRENOSES
(DEMENTIA PRAECOX GROUP)
[5] VII. Geriopsychoses (senile-senescent group) not
represented in war cases (see page).
The Sister’s ear boxed for blow to a German soldier’s pride: Diagnosis
PSYCHOPATHIC CONSTITUTION! A true psychosis develops: hate of Prussia
and the Junkertum: Diagnosis, DEMENTIA PRAECOX!!
=Case 147.= (BONHOEFFER.)