Part 16

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.