Shell-shock and other neuropsychiatric problems

by Elmer Ernest Southard

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.