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.