Shell-shock and other neuropsychiatric problems

by Elmer Ernest Southard

The first symptoms of his left brachial plexus neuritis had begun six months before, after 9 months’ work in the factory, and showed themselves in an increase of the deltoid paresis, with pains in the hand and forearm, and cramps of the hand, interfering with work, formication in the right hand and in the feet, diminution of visual peculiarity (objects forgotten and reading difficult). It was only in November that he got perturbed about these difficulties, which had begun in May. There was a paralysis of the levators and rotators of the left shoulder, with a slight atrophy of the deltoid and of the supra- and infraspinatus muscles. The arm could be extended almost to the horizontal with difficulty. There was one centimeter atrophy. The forearm and hand were not atrophic but slightly weak. There was an anesthesia of the shoulder-joint region, and of the outer surface of the arm; a hypesthesia of the posterior surface of the forearm and dorsal surface of the hand and fingers; tendon and periosteal reflexes normal. Sometimes the hand would contract firmly and could be opened only by the aid of the other hand. The nerve trunks of the axilla, upper arm, and forearm, were painful on pressure, especially on the left side, and the ulnar nerve was thickened and rolled under the finger. The knee-jerk and Achilles jerk were abolished on the right; plantar reflex diminished; right posterior tibial nerve painful on pressure, and its territory was hypesthetic. There were cramps in the feet.

Gymnastics and electrotherapy and rest reduced these phenomena. The eye grounds were normal; there was a paresis of accommodation, and an absolute blindness to green, with retraction of fields to 15 degrees in the right eye, and 20 on the left. There later developed a slight edematous neuritis of the nerve, corresponding to the evolution of a chronic retrobulbar neuritis of toxic origin.

It is the chronic retrobulbar neuritis which is typical of the so-called nitrophenol neuritis, developing in soldiers employed in making explosives. The above case is accordingly exceptional in its association of a severe peripheral neuritis with the optic neuritis. Typically, after six months to a year in the factory, the cramps and formication of the legs are felt, and the gradual diminution of vision with transient blindness, finally leading to inability to read, sets in. The green blindness, the accommodative paresis, and diminution of central vision, the concentric contraction of the visual fields, are the usual story. At first the eye grounds are normal; there is then an edematous neuritis, and finally a white atrophy. According to Sollier, the accommodative paresis is like that in post-diphtheritic paralysis—a disease due to cerebral cortex intoxication. In fact, the photomotor reflex is normal, and what we have is an inversion of the Argyll-Robertson sign. These symptoms are those of retrobulbar neuritis, of nicotino-ethylic origin, and it may be thought that the melinite was simply acting by creating a soil for alcoholic intoxication, but none of the patients examined has been alcoholic, nor has any been permitted to smoke in the factory. The injurious agent is probably a body in the nitrophenol series, perhaps dinitrochlorobenzol, but whether this substance is absorbed through the skin, inhaled, ingested from the hands, or by all three routes, is doubtful. These workers are often cyanotic while at work because the nitre products produce vasodilatation. Possibly this dilatation of vessels has something to do with the neuritis. The workmen will not use the spectacles and antitoxic masks given them, and even do not use the rubber gloves constantly. In some factories only, a liter of milk is given as counterpoison, every day.

Slight wound of occiput: Ophthalmoplegia externa, influencible, however, by tests and replaced by spasmodic convergence of globes with myosis; hysterical stigmata and convulsions.

Case 435. (Westphal, September, 1915.)

A German volunteer, 20, was slightly wounded in the occiput by revolver-shot at Ypres. Then followed headaches, vertigo, and complaints of pains in the eyes such that he could not open them or see sidewise. May 5, 1915, he showed a picture of an ophthalmoplegia externa: complete immobility of the two bulbi, lively blepharoclonus, rapidly passing into blepharospasm, photophobia. The visual field for white was practically limited to the fixation point. Central scotoma for all colors. Otherwise normal.

On further examination, the apparently immobile bulbi were found to pass into convergence upon request to look to the right or left. Thereafter, this position of convergence was assumed if any test made by a strong light, such as that of a pocket flash, was used. The pupils contracted to the maximum during this assumption of the convergent position of the globes, and no further light reaction could be observed. The convergence gradually passed off when the light was removed. The appearance of bilateral external ophthalmoplegia had disappeared.

If the patient was requested to follow a finger moved to one side, the globe of that side to which the finger was being moved, stood unmoved in its central position, but the other globe followed the eye and placed itself in the convergent position. The patient complained of diplopia. Even after the closure of one eye a double vision appeared (monocular diplopia). There was achromatopsia. The cornea failed to react to stimulation.

There was an analgesia of the skin of the whole body, with a hypesthesia for tactile stimuli on the left side. Smell and taste absent. The convergent position of the globes with myosis was preserved in the midst of convulsive seizures, which could be produced by exciting the patient. When it was attempted to dissolve the eye troubles by hypnosis, convulsive attacks occurred. The patient was pronouncedly hysterical.