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.”