Chapter X: Section D: Shell-Shock Treatment and Results (6)

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.)