VI. Somatopsychoses (the Symptomatic, Non-Nervous, Group)

Dysentery: Psychosis.

Case 122. (Loewy, November, 1915.)

Out of a large number of dysentery patients, many of whom had very serious symptoms, but one of Loewy’s patients became psychotic. Loewy in fact had discharged this one as normal, and he had been put on the wagon train (no opium or alcohol) to go to a sanatorium. As the fighting shifted, the sanatorium site changed and could not be reached with the wagon. Finally, the wagon train met the battalion once more and Loewy was told that the man was “dying.” At this time he was afebrile, without collapse symptoms, with a strong and normally frequent pulse, and with few signs of exhaustion. Yet the guard had thought that he looked moribund. Both upper eyelids were drawn rigidly up but conveyed a different impression from that in maniacal or anxious conditions. The expression was that of staring astonishment, helplessness, and apathetic lack of orientation. The patient recognized Loewy, spoke to him as “Herr Doctor,” said he was doing quite well; he was found to be well oriented. There was no fabricating tendency even as to the number of stools (although Loewy had noted such in bad dysenteries of the Shiga-Kruse type). He was apparently hard of hearing, as if at the beginning of a typhoid fever. He showed a retardation in his intake of ideas, and his voice in answering sounded absent-minded. There was an expression of absent-mindedness, and the patient seemed markedly unconcerned about his health, the direction of the journey, the terrible rain, etc. These phenomena are attributed by Loewy to attention disorder.

The patient had been out of reach of fire for days. Loewy reports the case as one of beginning amentia or as an exhausted state resembling a Korsakow condition, recalling one of emotional hyperesthetic weakness (Bonhoeffer).

Typhoid fever: Hysteria.

Case 123. (Sterz, December, 1914.)

A soldier entering hospital for typhoid fever, October 2, 1914, was discharged to another hospital and again, November 10, to a hospital for nervous disease. The typhoid was serious and complicated by delirium. After defervescence, the patient was weak and could not stand or walk, especially on account of pains and weakness in the left leg. Sometimes he had had pains in the sacrum and left hip. He complained of tinnitus, deafness, dizziness, headache. He said he had fallen from a cart, had been sick for three months, since which time he had been under medical treatment for his present condition. He had, he said, been given a small pension.

The gait disorder sometimes amounted to a real astasia-abasia. The left leg became stiff and was dragged behind. There was a paresis demonstrable in dorsal decubitus, of the left side, especially of the leg, without atrophy. There was a hypesthesia of the whole left side of the body, with the exception of the head. Hyperesthesia of the left leg, hip and upper sacrum. The left corneal reflex was diminished. Moody, hypochondriacal, lachrymose. The general attitude of the patient was affected and theatrical. Paradoxical innervations were frequently found on test. There was no neurological disorder except for the absence of the right Achilles jerk.

The absence of this Achilles jerk may be regarded as a residuum of the previous accident. The localization of the pains points to a neurotic lumbosacral plexus disorder on the left side. Superimposed upon this picture are the hysterical phenomena. The typhoid fever and its attendant neuritis are therefore to be interpreted as the liberating factor for a severe hysteria in a subject already disposed to such symptoms through previous accident.

Dementia praecox versus post-typhoidal encephalitis.

Case 124. (Nordman, June, 1916.)

A butcher, 29 (aunt insane, sister melancholy, one child stillborn, deformed), had had several days convulsions at eight; went through military service without incident; was at the Marne and was evacuated October 19, 1914, with typhoid fever,—a severe fever with a delirium prolonged into the last weeks. Three months convalescent leave was given, passed at Paris with the man’s aunt, but he had become strange. One day he wanted to strangle neighbors of German origin; another day departed for Dunkirk and then returned, having lost all his documents.

February, 1915, he went back to the front, did strange things and was soon evacuated to Tarascon. In April he went back to his dépôt; May 18, to the hospital at Rennes for erythema. June 15, he was given 15 days in prison for setting off a cannon too quickly and then running off through the fields. August 11, he was interned at Rennes for stealing a priest’s cap. September 12, two months convalescence. December 10, headaches. Back to Rennes January 14, February 18, Val-de-Grâce, then Maison Blanche.

Here he was found sometimes sad, immobile; at other times laughing and singing. He was very irritable on small occasion. Once on leave he had a fugue with complete amnesia, though alcohol may account for the latter. His memory was vague, especially for his crimes and for recent events. He was emotional, indifferent even in the presence of his wife or aunt. Sexual indifference. He often complained of his head, saying that he felt it blocked and that he could not think. The headache was frontal and would last several hours. The man would, however, not complain spontaneously. He was physically, in general, negative.

This case might possibly be due to a post-typhoidal encephalitis, but Nordman believes rather that it is a case of dementia praecox. Perhaps the convulsions at eight produced a slight brain lesion, brought to an issue by the typhoid fever.

Paratyphoid fever: Psychosis outlasting fever.

Case 125. (Merklen, December, 1915.)

A Breton farmer, 34, had paratyphoid alpha. Admitted to hospital September 3, 1915, he had headache, anorexia, asthenia, coated tongue and tense abdomen, algosuria; later, abdominal swelling, borborygmi in the right iliac fossa, rose spots, dicrotism, albuminuria, bronchitic rales. The disease was severe, and was complicated by sacral decubitus and ran a month.

At first somnolent, September 8th the patient went into a state of mental excitement with agitation and delirium. He got out of bed, cried out, sang, talked to his neighbors, complained that his papers (colis) had been stolen, as well as his watch and tobacco; that his horses’ hoofs had been injured, and the like.

He grew calmer in a few days, and now no longer tried to get up, remaining inert in his bed. The occupation delirium persisted—he was not being paid what he owed, and the like. He had hallucinations; looked for scissors, and one day said, “Here they are!” At intervals he appeared lucid and responded appropriately to questions.

The fever dropped and the paratyphoid disease appeared past, but the mental state remained for three weeks without change, having the same periods of lucidity when he would be regarded as cured, but falling again forthwith into his post oniric ideas. He was soon sent to a convalescent hospital and was not wholly well for another month.

Psychopathic taint brought out by paratyphoid fever.

Case 126. (Merklen, December, 1915.)

A soldier, 31, was a victim of paratyphoid alpha, entering hospital October 21, 1915, with the usual symptomatology: fever, asthenia, headache, abdominal swelling, tongue coated and red along its edges, diarrhoea. After admission he passed into a deep toxic state.

He woke up in the night with a cry, got up afraid, and refused to go back into his own bed. He was mute, except for curses addressed to the nurses. After two hours he went to bed and to sleep. Next day he sat quietly with a depressed look, occasionally groaning deeply, talking in brief phrases about his anxiety, wanting his wife telephoned to, saying that he would not see his children, was going into the four planks, and the like.

This situation lasted about a week. He became afraid of medicines and thought he had been poisoned, saying that he would rather be shot than poisoned and complaining that, though he had served France for fourteen months, they now wanted to kill him. In the night time he was agitated. He gave vent to cries, and threats, but this delirious state rapidly decreased and he became calm the night of September 27th. The upper extremities showed a tendency to catatonia. From this time forth, during the remaining month, the patient was immobile, mute, fearful, and mistrusting, depressed and always wore a cunning look. His disorientation decreased and he passed good nights. He would answer questions by groaning. He would say, “They think I am a Tartar.” The end of the mental disorder coincided with the cure of the paratyphoid fever. According to Merklen, the paratyphoid bacillus in these cases serves to bring out a psychopathic taint. This particular patient had always been of a sad demeanor, uncommunicative, very impressionable and emotional. Two other cases had always been somewhat below normal.

Diphtheria: Post-diphtheritic symptoms.

Case 127. (Marchand, 1917.)

A farmer, 37, was evacuated March 20, 1916, for diphtheria. April 1, paralysis of tongue and uvula, impairment of vision. These symptoms rapidly improved, but paralysis of the legs appeared and then of the arms. This paralysis lasted until he was sent to the neurological center June 28 for post-diphtheritic paralysis, wherein it was found that voluntary movements of the legs could be performed, though painfully and of slight extent, that walking was impossible, that there was a considerable atrophy of legs and arms, that the knee-jerks, Achilles jerks and plantar reflexes were absent. There was complaint of pains in the legs and over nerve trunks.

Improvement followed, the atrophy gradually passed away, and the voluntary movements of the legs became more extensive; but by October the reflexes had not yet reappeared. Yet the patient had begun to walk on crutches and soon was able to get on with canes only. The improvement did not continue. He did not raise his heels and dragged his toes. There was now a clonic tremor of the legs as soon as the weight of the body was put on them. During movements of legs carried on in dorsal decubitus there was found an irregular tremor of the legs with twisting of the trunk. The muscular strength was well preserved. There was a slight muscular atrophy. The tendon reflexes had now come back, though the right Achilles jerk was weak and the plantar reflexes were absent. There was a hypalgesia of the legs which ceased sharply at the middle of the thighs. There was a slight hypoacusia on the left side. Visual fields normal. The patient complained of feelings in the inside of his bones. Electrical reactions normal.

Diphtheria: Hysterical paraparesis.

Case 128. (Marchand, 1917.)

A soldier, 24, was evacuated June 24, 1915, from Roussy for diphtheria and was treated by serum, receiving 80 cc. in 8 injections. A few days later there was a paralysis of the uvula with regurgitation of liquids from the nose; but patient was able to go on convalescence July 21. A few days later, however, he noticed that his legs were weak. Vertigo, vomiting and painful walking followed, and his convalescence was increased a month. The paralysis got progressively worse. September 10, he went by automobile to Libourne where he stayed two months. He arrived at the Neurological Center at Bordeaux November 9 with diagnosis “polyneuritis of legs.” He could not walk and could hardly flex thighs on pelvis or legs on thighs. Voluntary movements of extension and flexion of feet and toes were limited. There was neither atrophy, pain nor reflex disorder. Both legs were analgesic, as was also the abdomen up to the umbilicus. There was complaint of dorsolumbar pains and of stomach trouble and lack of appetite; vomiting after meals frequent, pulse 120.

January 3, the patient was able to lift his legs a few centimeters above the bed but not together. There was now a slight muscular atrophy especially on the left side. Knee-jerks lively, analgesia limited to legs, no vomiting, pulse rapid.

The patient was sent to a hospital in the country May 8 to July 8. He was now much better. His legs were able to support his body but he could not walk. Slight atrophy of left leg. There was hypalgesia now in the feet and legs below the knee. There was no pain on pressure over the nerve trunks. The electric reactions normal. The patient could now walk on crutches. He was invalided on the temporary basis, December 12, 1916.

It does not appear that in this case the hysterical paralysis was preceded by polyneuritis.

Malaria: Amnesia.

Case 129. (De Brun, November, 1917.)

A soldier lost all memory of his hospital stay in Salonica and the voyage home. He could only remember a little about the hospital at Bandol. There is a period of transition to full memory in malarial cases characterized by sure memory, vague on certain points, alternating with phases of almost complete amnesia. The soldier in question had very inexact memories of the Bandol Hospital, and could only remember about his fevers, that they began about noon and terminated about four o’clock. Twice he had been found in his shirt, walking, unconscious, in the passageway of the hospital. Having obtained leave for convalescence, three months after his memory gap began, he went to Paris, and probably had attacks at home. He vaguely remembered afterward being carried by automobile to the Pasteur Hospital, December 1. There he remained to the end of March, 1917, without preserving anything but the vaguest memories of an intermediary period of more than six months. The memory in these malarial cases often remains permanently altered and there may even be a retrograde amnesia, carrying back to facts prior to the gap and an anterograde amnesia relative to facts after the main gap.

Thus, there is in the febrile period a retrograde amnesia and in the post-febrile period a retrograde or anterograde amnesia. One group of subjects are severe cerebral cases, and the memory gap appears to run back to a period of true mental confusion. But there is another group of patients who preserve throughout the febrile period an absolute consciousness of all acts, and yet the memory gap is just as sharp and definite as in the confusional cases.

Malaria: Korsakow syndrome.

Case 130. (Carlill, April, 1917.)

A stoker, 45, was admitted to the Royal Naval Hospital, Haslar, November 6, 1916, from the Fifteenth General Hospital in Alexandria, to which he had come from a hospital in Bombay about three weeks before. At Alexandria he was anemic and showed an edema of legs which had been present for six weeks. Cylindruria; no albuminuria. At Haslar there was no cylindruria and no edema, and nothing but weakness, gouty arthritis of left wrist, right ear and left great toe. Red cells 4,650,000, leucocytes 10,000 (52 per cent polymorphonuclear, 46 per cent lymphocytes). He was rather dull mentally. December 10th, Dr. Fildes found malarial organisms in the blood on the occasion of a hyperpyrexia (104°). Quinine was given. December 14th, he was transferred neurological. According to the patient’s own story, he was born June 10, 1868, lived in Fulham, had a daughter aged 12 years, had recently seen his wife at the hospital: all this seemed plausible enough.

Later, however, he said that the year was 1899, that King Edward was king, that the war was between England and some field forces, etc. This well-nourished, pale, simple-looking stoker spoke quietly and politely; told about intermittent fever; about being eight years on the active list, becoming a reservist and being called up for the war. He read intelligently, could do sums, but did not know the name of the hospital and was confused about the war. He recognized that his memory was not as it should be; constantly stroked his moustache and chin. He was happy and contented.

The gait was normal, systolic blood pressure 140 mm.; no evidence of alcoholism. Blood, January 15, 1917, contained 5,050,000 reds, 10,300 leucocytes (63 per cent polymorphonuclear, 37 per cent lymphocytes). There was a bilateral absence of the ankle-jerks, repeatedly confirmed at subsequent examinations. Wassermann reaction was negative. Puncture fluid contained no cells.

Instead of living at Fulham, this stoker lived at Portsmouth, and had not been seen by his wife for four years. He had done 18 years’ active service and had last sent his wife a letter from the Sailors’ Home at Bombay, November, 1916. They had been married 21 years. He caused astonishment with his wife and friends by announcing that Lord Roberts and General Buller were in command at the battle of the Falklands. He continued to say that he lived at Fulham. He was discharged home, January 22. It seems as if he were living through the period of the Boer war.

Carlill considers that alcoholism may be ruled out, and there is no likelihood that the gout was the cause of the neuritis. He believes that the neuritis was probably malarial. Possibly the illness suffered in Bombay may have been beriberi or it may have been malarial nephritis.

A complication of malaria.

Case 131. (Blin, August, 1916.)

A Senegalese corporal of machine gunners, 21 (early life normal save for sore throats and coughing), was a robust, well-developed man of 75 kilos when he entered the hospital at Konakry, February 15, 1916. He was given the diagnosis: malarial anterior spinal paralysis.

It seems that he had joined a Colonial regiment, April 8, 1915, attended classes as a recruit, left Bordeaux November 1 for Dakar, arriving there November 11. He stayed there some sixteen days, during which time he slept without mosquito-netting. November 16, he left for Konakry, and had his first febrile symptoms November 27, with vomiting, headache, and prostration. His temperature ran as high as 41, but by December had fallen to normal, after quinine.

The corporal was sent away, cured, to his company at Kouronesa, December 6. There was more fever, headache, and vomiting during the railway trip. Quinine again relieved the fever, but a bloody diarrhoea set in so that it was only at the end of January that he could go on service.

February 6, another attack of fever, with shivering and perspiration, lasted for some three hours. He could hardly stand by himself and had to be helped in walking. Next day, another spell of three hours of fever; definite paralysis set in, affecting both legs. February 8 the arms were attacked by paralysis which, unlike that of the legs, was a progressive one, attacking first the shoulders, then the elbows, the wrists, and finally the hands. All the body muscles were in a state of flaccid paralysis, as well as the muscles of the face. The patient was now afebrile. February 9 there was a slight speech defect; the tongue was slightly paralyzed, and swallowing became painful. The jaw movements remained normal. The muscles of the face were intact and the patient could whistle, move his lips, and move his eyeballs normally. Vision normal. The pupils were fixed in dilatation, more widely on the left side. There was a slight contracture of the vesical sphincter, necessitating the catheter. The tendon and cutaneous reflexes were lost.

By February 14, when the patient was sent to the Bellay Hospital, muscular atrophy had made its appearance. No plasmodia could now be found in the blood, which showed 71 per cent polynuclear leukocytes, 20 per cent mononuclears, 9 per cent lymphocytes.

This state lasted til February 25. Despite the fact that the patient ate well, emaciation rapidly progressed. The buttock showed a very few signs of decubitus. Upon this date there was pain from a marked orchitis of the left side, the cause for which remains unknown (no history of gonorrhœa; catheter used for the last time, February 15). The temperature which attended the orchitis came down in three days; the patient’s appetite was singularly good, but the muscular atrophy increased. The speech defect meantime disappeared, and the patient swallowed more readily.

March 7 a slight and hardly perceptible movement could be noted in the fingers of the left hand. Two days later, similar movements appeared in the right. March 11 he could spread his fingers in a kind of creeping movement. Next day slight movements were possible with the legs, and March 13 the knees were movable. March 14 the patient could lift his head from the pillow. The range of movement now increased all over the body. According to the patient, those parts were the first to regain power that had been attacked last. This certainly seemed to be the case with respect to the left upper limb, in which first the hand and wrist, then the elbow and shoulder, successively recovered power. The legs regained their power in the same way proximad. March 17 the patient could sit up and grasp objects with the left hand. The cremaster and plantar reflexes appeared,—the former, more on the right; the latter, more on the left. The left pupil remained in wider dilatation than the right.

The treatment was by quinin and potassium iodide, with massage. The patient was apparently on the highroad to complete recovery, and left for France March 21, weighing 63 kilos.

Trench-foot: Acroparesthesia.

Case 132. (Cottet, September, 1917.)

A fantassin, 36, carpenter by trade, went into the trenches October, 1914, and had two attacks of trench-foot, first in January, 1915, when there was a painful swelling of the foot and secondly in July, 1916, when there were some bullae on the dorsal aspect of the feet. These were not serious and the fantassin did not report sick.

He was wounded, August 27, 1916, by shell fragment on the right elbow, was evacuated to the ambulance where the fragment was extracted and then to a hospital which he left cured with a seven days’ leave. Although he had not suffered in any way from his feet while in hospital, and had not been exposed to cold, the bullae reappeared on the feet just as they had been in July. They in fact now formed a sort of exanthem occupying symmetrically the dorsal surfaces of the toes. The bullae contained serum. They were confluent, varying from pin head to a nut in size, were as a rule round, but sometimes irregular. The eruption went on to a cure rapidly and on the twelfth day the bullae had dried up. This patient had hypesthesia up to the knees, hypesthesia of the dorsal surfaces of the feet, hyperesthesia of the plantar surfaces and ankles, hypesthesia of the forearm and the elbow and of the dorsal surfaces of the hands with possibly exaggerated sensibility of the palma surfaces. Hypesthesia of the face was limited to a small part of the right ear. The reflexes were normal and there was no atrophy. The name “paresthetic trench acrotrophodynia” was given to it.

In a service of eighty beds Cottet found within two months fifteen instances of these acroparesthetic disorders regarded as neuritic changes in trench-foot of a latent and lasting character which would have remained unobserved unless there were disorders of sensibility. In fact similar disorders of sensibility may be found without any history of gelure des pieds, forming a latent type of neuritic alteration hardly noticed by the patient himself. In twenty-six cases Cottet found sixteen with hypesthesia of the ears and of the nose.

Bullet injury of spine; bronchopneumonia: état criblé of spinal cord.

Case 133. (Roussy, June, 1916.)

As to the development of eschars, Roussy reports the case of a lieutenant wounded September 25, 1915. There was a penetrating wound of the interscapular region. The bullet had entered on the posterior aspect of the right scapular region and had emerged at the level of the first dorsal vertebra. October 1, a neurological examination showed flaccid paraplegia, knee-jerks normal, Achilles jerk weak on the right, plantar reflexes flexor, cremasteric reflex absent on the right, and both abdominal reflexes absent. There were pains in the legs and arms. There was retention of urine with overflow. A slight dulness on the right; temperature from 38 to 39 degrees.

Four weeks later the knee-jerks had become very weak, and the Achilles jerks were now absent. There was an extensive diffuse atrophy of the lower leg and thigh muscles, and a hypesthesia of pronounced degree had developed throughout the legs, over the buttocks, and in the lumbar region. Anal and vesical sphincters relaxed; dejections voluminous; sacral decubitus as well as healed eschars. December 5, the patient was transferred to the Army neurological center; temperature rose; there was much expectoration; paracentesis yielded no fluid; pneumococcus in the sputum. Cystitis had developed despite extreme care. Extensive edema of the legs developed. There was increased dulness on the right side, coughing and dyspnea. Death, January 17.

The autopsy showed a bronchial pneumonia of the right lower lobe, confluent, imitating a lobar pneumonia. The left lung also showed extensive confluent bronchopneumonia at the base as well as disseminated areas and edema of the middle and apical portions. Infectious splenitis, large fatty liver, swollen kidneys, no pyonephritis.

The spinous processes of the 6th and 7th cervical vertebrae were injured. There was no obvious gross disease within the theca except that there was a slight adhesion between the dura mater and the anterior surface of the spinal cord at the level of the 7th cervical and highest dorsal vertebrae. There was, however, a depression on the anterior surface of the spinal cord at a lower level, namely, at the level of the 4th dorsal vertebra. Microscopic examination showed myelomalacia with small cavities in the 1st and 4th dorsal segments, suggesting the état criblé.

According to Roussy, these patients injured in the spinal region are particularly sensitive to cold and support transfer badly even when the disease is short. Such patients should be evacuated to the interior after the shortest delay possible. Sometimes these patients show rib fractures; these are in the posterior portions of the ribs and are due to the fall of the man when struck. It might be possible even that the spinal lesions should through the action of the sympathetic nervous system favor lung infection.

Shell-explosion: Hystero-organic symptoms; decubitus; radicular sensory disorder.

Case 134. (Heitz, May, 1915.)

A soldier, 32, was bowled over in a first-line trench by the bursting of a shell that he did not see coming, September 14, 1914. He regained consciousness only in the middle of the night, finding himself half covered with water. He was taken up by the stretcher-bearers at eleven in the morning. Paralysis in the legs was then absolute. There were pains in the legs and in the back, but there was no evident lesion. Knee-jerks, plantar reflexes, and abdominal reflexes absent; cremasteric reflex absent on the left, weak on the right. Tactile sensations, on the contrary, were almost intact except for a slight diminution over the feet and the external aspects of the lower legs. Sensitiveness to pin-prick, however, was abolished throughout both lower extremities, and diminished in the abdomen and back up to two or three centimeters above the level of the umbilicus; that is, including the territory of the first lumbar and the last three dorsal roots. Sensibility to heat was abolished in the feet, the external aspect of the lower legs, and the posterior aspect of the thighs, but was preserved in the second and third lumbar territory, in the anterior aspect of the thighs, as well as in the region below the umbilicus. Micturition was impossible. Constipation the first few days yielded spontaneously September 20. There were signs in the bases of both lungs, corresponding with a suffocating feeling. September 22, he was evacuated, almost well, without signs of pulmonary congestion, having regained the power of urination and some capacity to move the legs sidewise. February, 1915, after evacuation to a hospital at Vic, he showed sacral decubitus, soon reaching the size of a hand, as well as trochanteric decubitus; traces of albumin in the urine, sacral and sciatic pains (recalcitrant to morphine).

He began to improve December 25. Camphorated oil and the sitting posture relieved the pulmonary congestion; the temperature, which had oscillated round 38 degrees, fell; the decubitus scarred over; the knee-jerks reappeared to some extent, and movements began. February 5, the patient had become able to walk without crutches. There was still a two-franc sized area of decubitus over the sacrum, and still a little spinal pain in walking.

It is difficult to consider this case only functional in view of the decubitus, to say nothing of the radicular distribution of the sensory disorder. Heitz brings this and the previously given case (No. 1) into relation with Elliot’s case of transient paraplegia (see Case 210) and Ravaut (see Case 201).

Shell-shock (windage?); typhoid fever; “neuritis” actually hysterical.

Case 135. (Roussy, April, 1915.)

A Colonial soldier was sent back from the front, September 12, 1914, for nervous disorder due to the shock of the windage of a bullet. He had not lost consciousness. Under observation at his station, he got typhoid fever, and was cared for at Paris from the beginning of October. About October 15 he began to feel pains in his left shoulder, neck, and arm. The diagnosis, neuritis, was made and was strongly borne in upon the patient, so that upon the cure of his typhoid, he went out on two months’ leave with a complete impotence and much pain of the left arm. At the end of his relief, he was evacuated to Villejuif. January 24, it was found that he had no somatic phenomena whatever, despite the fact that the left arm and a part of the forearm was powerless, and so painful that the patient cried out when his arm was moved. There were a few cracklings in the scapulo-humeral joint.

Hot air and reëducation cured the man in less than two months (March 20), though the disorder had lasted for four months. The patient had been retired for hysteria before the war and had re-enlisted.

Bullet wound of pleura: Reflex hemiplegia and double ulnar syndrome.

Case 136. (Phocas and Gutmann, May, 1915.)

A soldier, 26, was wounded in the enfilading of an Argonne trench December 17, 1914. He felt the bullet like an electrical shock, and fell. He had been leaning forward at the time and suddenly felt the left half of his body go paralyzed and his mouth pulled to one side. He did not lose consciousness, and spat up a good deal of blood five minutes after falling. He lay in the trench all night, unable to move his left leg except by the aid of his right. He was evacuated next day. There was a five-franc piece wound at the upper border of the left scapula, four finger-breadths from the median line. There were a few lung signs which rapidly cleared up. December 28, the hemiplegia was better, although neurological examination showed weakness of left upper extremity, abolition of deep reflexes, and certain skin changes of the left hand with edema (main succulent), decreased resistance of muscles of lower extremity to passive motion, especially of adductors and flexors, exaggerated polykinetic left knee-jerk, ankle clonus, Babinski reflex, abdominal and cremasteric reflexes absent on left, platysma paralysis left, with complete paralysis in the inferior distribution of the facialis; whistling impossible. Also the left eye could not be closed singly. Synergic movements of the lower part of the paralyzed face when the right hand of the patient was grasped.

There were also sensorimotor disorders in the ulnar distribution on both sides, with complete anesthesia to pin prick. There was also an area of hyperesthesia of the anterior and postero-internal aspect of the right forearm from below the elbow to the wrist. The tendon reflexes were weak but distinct on the right side. The left arm had feelings of pain, with élancements and formication from the shoulder to the fingers on the ulnar distribution. There was, of course, also, local hyperesthesia due to the wound of the thorax.

Lumbar puncture showed a fluid normal in all respects. We deal with a hemiplegia of organic nature, associated with the bilateral ulnar syndrome. The hemiplegia followed the trauma immediately. When the ulnar phenomena appeared is unknown.

The lung complications cleared. The pains disappeared; motion returned up to the level of the facialis. The patient got up and three months later went on convalescence, still presenting Babinski, exaggerated knee-jerk and weak arm reflexes on the left side. The bilateral ulnar syndrome had disappeared six weeks after the patient entered hospital. Phocas and Gutmann cite a considerable literature on nerve complications of pleural trauma, among them syncopes of grave prognosis; a relatively frequent pleural epilepsy (forty-five per cent fatal) or epileptic status (seventy per cent fatal); and the rare hemiplegia. Accidents and death have followed exploratory puncture of the pleura. Air embolism is probably not the cause. Phocas and Gutmann prefer the theory of a reflex disorder starting from the pleura.

Hysterical tachypnoea.

Case 137. (Gaillard, December, 1915.)

A man, 23, came to the Lariboisière November 29, 1915, in a hurry to show evidence that he had been invalided for valvular lesion of the heart. In point of fact, the interne found a murmur at the base. Yet there were things in the military papers suggesting caution. The patient next morning showed no malaise, dyspnoea, or any evidence of serious disorder. The contractions of the thorax beat in time with contractions of the alae of the nose, about 112 per minute. Here, then, was a cardiopulmonary patient. The heart impulse was exaggerated; the patient could not or would not stop breathing to aid the auscultation, but almost absolutely normal sounds could be heard at the apex and the base. A valvular lesion could be excluded. The lungs were perfectly normal. The patient was requested to stop his gymnastics, which might have succeeded elsewhere but could not at the Lariboisière!

How could the man have established the synchronism of pulse and respiration and synchronous tachypnoea and tachycardia? Why should he persist in this form of sport, since he had already been invalided? The family history was not especially suggestive (father albuminuric, died at 59; mother well, probably tuberculous). Scarlet fever at eight; occupation, tourneur. After four months of service there was gastric disorder followed by typhoid fever (despite vaccination, according to the patient). Convalescent leave at Paris, during which leave he had swollen legs and albuminuria. May, 1915, gastric difficulty; valvular lesion determined; examination; invalided. At home, a variety of complaints, for which treatment was unsuccessful.

During further examination it was noted that in auscultation the head of the examiner was lifted, as if there were hypertrophy of the heart or an aortic aneurysm. The synchronism was less exact on December 2; 112 beats to 128 respiration. Was this man a simulator? Had he become the victim of his own enterprise? There was no evidence of simulation. It was a question of a monosymptomatic hysteria. Gaillard discontinued the manière forte and undertook a softer treatment, but the manière forte had caused the family to want to take him away. Perhaps they feared a too efficacious treatment. He then escaped observation. It is probable that the tachypnoea ceased during sleep. It was not so marked after the medical visit was over.

Soldier’s heart.

Case 138. (Parkinson, July, 1916.)

A corporal, 21, who had been a miner and entirely well up to enlistment in August, 1914, went to France in 1915. In June, came shortness of breath and palpitation on exertion; later, precordial pain (fifth space, between nipple and median line) and giddiness on walking. Like all cases of true so-called “soldier’s heart,” this soldier had no physical signs indicative of heart disease, yet reported sick for cardiac symptoms on exertion. In this particular case, as in about half of forty cases reported by Parkinson, there had been no disability in civil life.

August, 1915, the soldier was admitted to the casualty clearing station, where the apex beat was found in fifth intercostal space internal to the left nipple line. The first sound was duplicated in all areas. The second sound was duplicated, though not loudly, at the base. After nine months’ treatment, this man went back to light duty with slight symptoms.

According to Parkinson, the absence of abnormal physical signs in the heart of a soldier should not prevent his discharge from the army if under training or on active service he shows breathlessness and precordial pain whenever he undergoes exertion well borne by his fellows. A simple exertion test, such as climbing 25 to 50 steps, reproduces the symptoms in such a patient. The rate of the heart at rest is a little higher than that of normal men, though the increase on exertion is greater. Nevertheless, it has been proved that the increase of rate on exertion bears no relation to the symptoms elicited and is therefore without value in judging the functional efficiency of the heart.

Soldier’s heart?

Case 139. (Parkinson, July, 1916.)

A sergeant, 36, had been in the army from 17 to 29, but in 1908 he had acute rheumatism and was discharged from the army. He then became a furnace man and had shortness of breath and palpitation on severe exertion with syncope three times.

He re-enlisted in August, 1914, and had an attack of orthopnea and edema after exposure at a review. However, he improved and went to France in May, 1915, where he again had symptoms; namely, precordial pain and breathlessness on severe exertion. One day while carrying telephone wire under fire, the sergeant felt a sudden pain in the region of the apex beat, shooting down the right arm. “I thought I was shot.” He fell down, very short of breath. His left arm remained sore and weak. Two days later came a similar attack, this time with unconsciousness, and the left arm was now useless. Two days later he was admitted to hospital, where slight breathlessness but no pain and no enlargement of cardiac dulness could be found. No further details are available but it seems clear that this man is unfit for duty. According to Parkinson, it is probable that the infection indicates the presence of some degree of myocardial disease.

Strain and shell-shock: Acceleration of diabetes mellitus.

Case 140. (Karplus, February, 1915.)

An infantryman, aged 22, previously healthy and from a healthy family, was struck by a shell fragment in the forehead and lay for several hours unconscious. He did not vomit. He had a number of furuncles on his body and his urine, upon examination, showed a severe diabetes mellitus which increased despite treatment. Upon an attempt to withdraw carbohydrate, the sugar suddenly sank from six to four per cent. Acetone at the same time increased. An abrasion had been noticed by the patient a few days before the shell explosion on the spot rubbed by the tornister. The patient said that since his accident he had had to urinate every night several times and was often very thirsty, neither of which tendencies had he had before. A month before he became merod he had had an injury of the hand produced by a shell fragment. He had undergone tremendous strain.

The chances are that the excitement and the strain had more to do with the diabetes mellitus than the shell explosion.

Dercum’s disease.

Case 141. (Hollande and Marchand, March, 1917.)

An adjutant in a chasseur battalion was buried by a shell explosion, which killed his lieutenant beside him, January 5, 1915, at Hartmannsweilerkopf. Hematuria followed; ten days later, fever with anorexia, and the appearance of two or three lipomata on the anterior surface of the thighs. Remaining at his post, the adjutant took part in an attack, March 5; was evacuated on the 8th; “lipomatosis with febrile reactions.” He spent eight days at Bussang, and thence went to the hospital at Pont-de-Claix. Here marked albuminuria was noted; the lipomata increased in volume; others appeared in the arms. The patient was transferred to the Des-Genettes, where the diagnosis nephritis was added to the previous diagnosis, and a milk diet was prescribed. Convalescence of five months was proposed. The lipomata increased in volume and in number. The patient was then hospitalized at Avenue Berthelot, placed in the auxiliaries, and stationed eight months at his dépôt.

When he was observed by Hollande and Marchand, four nut-sized tumors were found on the anterior surface of the left thigh; two smaller tumors: one of them painful to pressure, lay on the inner aspect, another the size of a small egg lay in the right thigh, and there were two others on the internal aspect and two on the external aspect of the thigh. A nut-sized tumor was found on the inner border of the right forearm, and below it another lenticular tumor. A nut-sized tumor was found on the left forearm below the elbow on the internal border. Small tumors were found on the buttocks. There were no tumors below the knees, in the upper arms, or on the thorax. There were 14 tumors in all. The smaller the tumor the more sensitive, and there was more pain when the tumor had just appeared and during the first days of its growth. There was no spontaneous pain; pain only upon a blow or pressure. Diminished knee-jerks, especially the right; no other neurological disorder, although the patient complained of often having something before his eyes. There was a marked diminution in the memory. Heart was in the 5th space on the nipple line, pulse 110; Wassermann reaction negative; red blood cells, 3,520,000, white cells, 6500; albuminuria, hematuria, leucocytes, and urethral cells in the urine. The temperature had now become normal. The lateral lobes of the thyroid were slightly larger than normal, but not painful. Sella turcica was unchanged upon X-ray. Exploratory puncture of a tumor showed much free fat, without fatty acid crystals and with some fat cells. The cells could not be cultivated in test tube. The authors believe it doubtful whether this instance of Dercum’s disease is related with the shell explosion.

Hyperthyroidism.

Case 142. (Tombleson, September, 1917.)

A private, 22, was selected by Col. Garrod for hypnotic treatment by Tombleson from among the hyperthyroid cases. He was admitted April 3, 1916, with a typical hyperthyroidism, with manual tremor, enlarged thyroid, pulse 120, blood pressure 136-40, and hemic murmur. Tombleson induced deep somnambulism at the first hypnotic sitting and suggested an increase of nerve strength and steadiness. The suggestions under somnambulism were repeated for ten days. An occasional added suggestion was given as to lessening of the thyroid. At the end of the ten days the patient declared himself quite well.

Eight of twenty consecutive functional cases treated by hypnotism by Tombleson were cases of hyperthyroidism and in virtually all of these an effect like the above was registered.

Shell-shock; thrown against wall, stunned, emotional: Paroxysmal heart crises six days later, observed for two months. Neurasthenia? Mild Graves’ disease?

Case 143. (Dejerine and Gascuel, December, 1914.)

An infantryman, 29, was sent to auxiliary hospital No. 274, for heart trouble, a little thin but looking vigorous enough (typhoid fever at 13 and some diseases of unknown nature and of brief duration while in military service).

September 24, a large calibre German shell burst and threw him against a wall, producing no wound or contusion. He was momentarily stunned, emotionally much affected, and noted at the time extreme palpitation. He was evacuated to Paris September 30, six days after the shock. His pulse was 130-134, regular, and the heart seemed not to be anomalous in any respect.

But there were paroxysmal crises in which the pulse rose to 180 and in which the patient fell into a state of great anxiety. The mouth temperature in the midst of such crises would always rise to 38°, and this temperature would outlast the rest of the seizure. The man was mentally depressed and apparently indifferent, preoccupied with his heart and his insomnia, but at the same time emotionally easily affected. In short, he was a neurasthenic. There was no change in mental state, tachycardia, or paroxysmal seizures in two months, except that he gained weight. Walking and climbing stairs produced dyspnoea. Urine was negative. According to Dejerine, such a case should be treated by psychotherapy.

Alquier, in discussion, called attention to the slight but distinct tremor in this case, dermographia, and spells of perspiration. He suggested that the case might be one of mild Graves’ disease.

Hyperthyroidism three months, following ten months’ service, at times under protracted shell fire.

Case 144. (Rothacker, January, 1916.)

A man in service ten months, under strong excitement and at times under protracted shell fire, complained of palpitation, insomnia, dizziness, and dyspnoea. Hospital notes showed that the left lobe of the thyroid was somewhat enlarged. Before the war his neck could not have been very thick; he had served his year out without difficulty. His mother is said to have suffered at one time from thick neck. According to the patient, he had never suffered with heart trouble. Heart not enlarged; blowing first sound over the apex. Graefe, Stellwag and Möbius signs negative. Heart rapid, not irregular; pulse strong. There was fine tremor of the hands, as well as a tremor of the tongue. Knee-jerks increased.

The patient was at first sleepless and excited, but after three weeks in bed the heart murmur had disappeared. After three months, he was ordered to Ersatz with the left side of the neck measuring 20 as against 18 cm. on the right. There was a soft pulsating swelling of the thyroid. First sound over apex still impure; heart action now regular; pulse 64; blood pressure 120 Riva-Rocci; after test exercises, slight dyspnoea. No cyanosis. The outstretched hands were no longer very tremulous. The knee-jerks were still increased. The man had begun to sleep well. His neck was apparently much diminished in girth.

Here then was a case of Graves’ disease of acute development, brought out by nervous stress and excitement as well as by 10 months of war work and exposure to shell fire,—with approximate recovery after three months of rest.

Graves’ disease, forme fruste.

Case 145. (Babonneix and Célos, June, 1917.)

A farmer, 31, entered the Rosendael Hospital, Jan. 25, 1917. He had been two years in active service. The family history was negative except that one of his sisters had had dyspepsia. The patient denied venereal disease and alcoholism and had always been well. At the Battle of the Marne he was slightly wounded in the left knee. January, 1915, he was exposed to gas bombs and explosive shells. He was several days in the hospital spitting, or perhaps vomiting blood and was sent on a long convalescence. On returning to the front, he had to be sent back to hospital with a note, “not fit for service, nervous troubles and paroxysmal tachycardia.” In point of view he now showed a number of symptoms suggestive of Graves’ disease, such as a definite exophthalmia which, according to the patient, started up a short time after the shock and a tachycardia (110-120) with circulatory excitement, a tumultuous heart, neck arteries contracting, almost dancing in their contractions, together with a systolic murmur maximal in the pulmonary area, not retaining, variable,—in short, suggestive of an inorganic murmur. There was also a generalized rapid tremor and a variety of vasomotor disorders, such as blushing and paling, perspiration, exaggerated reflexes, emotionality, logorrhea, jactitation. There were also digestive troubles, regurgitation after meals and the patient had become thin and weak.

There was, however, no swelling of the thyroid gland nor any eye signs other than the exophthalmia. In short this case is doubtless one of the forme fruste of Graves’ disease. It seems to show that Graves’ disease may have a traumatic origin.

Somatic complication in a shell-shock hysteria (Trauma).

Case 146. (Oppenheim, February, 1915.)

Musketeer. No faulty heredity, but was always somewhat nervous. On October 26, a shell burst one meter in front of him, burying him under the anterior wall of the trench. He was dug out and taken to the field hospital, where he remained unconscious until the next morning. On October 29, he was taken to the reserve hospital. Severe pain in the head, entire scalp tender on pressure, especially in the left frontal region, left side upper lip swollen, bluish and discolored. Left tenth and sixth ribs broken. Fracture of skull(?). November 10, at eight o’clock at night, sudden attack of vomiting, and the patient was found in a faint in the water closet. Almost complete paralysis of speech and all of the four extremities. Consciousness obscured; no sensory disturbances. November 11, severe headache and vertigo. Speech somewhat more intelligible. Pulse, 60 to 68. “Evidently secondary hemorrhage in the brain.” November 12, to Augusta Hospital. November 20, admission to nerve hospital. Typical aphonia. Limitation of motion in all four extremities, but no paralysis—anergy. Reflexes normal. Unable to stand and walk. Sensibility preserved. Under suggestive treatment, curative gymnastics, as well as electrotherapeutics, the aphonia and abasia disappeared in a few days, but the patient continued to complain of headache and insomnia. December 16, an attack of nausea, headache, vomiting, loss of consciousness, followed by epistaxis, marked tachycardia. January 4, in his sleep he felt a prick in his left upper arm, as if he had pushed a sewing needle into the arm. X-ray examination showed a needle in the arm. This was extracted under local anesthesia.