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.