Part 18

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.