Part 49

Another case was wounded in the right arm by a shell fragment September 7, 1914, and showed two scars above the epitrochlea and along the internal border of the triceps. Examination December 30 showed a normal elbow movement, pronation and supination, with slight flexion in repose of the palm of the hand and the fingers. Active flexion movements of the fingers could be performed only imperfectly, and the finger pad could only be brought within three fingers breadths of the palm, despite the greatest effort on the part of the patient. Minute passive movements were entirely possible. The fifth finger could not be abducted and both abduction and adduction of the third and fourth finger could not be made on account of the nerve lesion. The thumb was in a condition of contracture which placed it in abduction in front of the index finger, and the thumb could not oppose. Passive movements, on the other hand, were entirely possible. The hand was flexed upon the forearm through hypertonia of the flexors, which could be easily overcome with slight but distinct resistance. The hand was in the position of a radial paralysis. There was a slight degree of muscular atrophy. Tendon reflexes were normal. Electric examination showed that stimulation of the ulnar nerve at the elbow was unable to produce flexion of the last two fingers or any movement in the hypothenar eminence, of which the muscles were also not excitable. The interossei could, however, be made to contract. The median and radial nerves were normal electrically. The above examinations were with the faradic current.

With the galvanic current the ulnar nerve proved unexcitable at the elbow, and the muscles of the hypothenar eminence contracted more slowly. The median and radial nerves and their muscles were electrically normal.

In short, there was a complete R. D. of the hypothenar and partial R. D. of the interossei as a result of the lesion of the ulnar nerve. There was nothing abnormal in the other nerves or muscles of the arm. The attitude of radial pseudoparalysis is due to the contracture of the muscles of the thenar eminence.

As to therapy, the general movements of flexion of the fingers, thumb and hand yielded a marked improvement, but such results cannot be expected in like cases unless a physician or experienced masseur treats the case. Babinski and Froment have tried thermotherapy and diathermy in these cases, finding that the paralysis diminishes and becomes partial if the limb is warm, although it is important that it should not become too warm. Sometimes a few treatments with diathermy will produce movements in a case of long standing paralysis. Babinski and Froment counsel not only diathermy, but a general motor reëducation. The idea of the diathermy is that the deeply penetrating heat affects blood vessels and muscles, bringing about a vasodilatation or even a direct addition of needed calories. In like manner, galvanism, light baths, or simple baths in combination, and with diathermy, especially with the diathermy, act favorably. Casts and apparatus have also proved without avail, as well as faradic or galvanic reëducation.

The above two cases show how in one instance there may be no electrical change and in another instance a slight one. In these cases, reflex hypertonic contracture, hypotonic paralysis, vasomotor disorder, decalcification of the skeleton (X-ray), mechanical overexcitability of muscles, unmodified tendon reflexes (except elective exaggeration of reflex under anesthesia, _e.g._, a persistent unilateral patellar clonus when all other reflexes have been abolished), and disorders of electrical excitation are enumerated by Babinski and Froment.

Delherm sums up the electrical disorders as follows: Muscle faradized:

(_a_) No change.

(_b_) Subexcitability.

(_c_) Overexcitability.

(_d_) Diminished contractility to faradism, associated with increased contractility by galvanism (Charpentier).

(_e_) Anticipated fusion of shocks (Babinski and Froment).

(_f_) Slow contraction and decontraction on faradism (Charpentier).

(_g_) Rapid exhaustion of rhythmic faradic contraction with metronome.

Muscle galvanized:

(_a_) No change.

(_b_) Subexcitability.

(_c_) Overexcitability.

(_d_) Suddenness of galvanic contraction with subexcitability.

_Re_ decalcification and osteo-articular changes, Babinski points out that the reflex or physiopathic phenomena run historically back to John Hunter, Charcot, and Vulpian. Charcot and Vulpian called especial attention to the peculiar amyotrophy and paralysis which occurred in joint disease, and upon the lack of parallelism betwixt the intensity of the joint disease and the severity of the paralysis or atrophy. The atrophy was without R. D.

Shell-shock: Functional blindness (monosymptomatic).

=Case 433.= (CROUZON, January, 1915.)

A shell burst above the head of a sergeant in a battle near Neuf château, August 22, 1914. The man was kneeling at the time; felt a terrible shock, slipped prone, lost consciousness and woke in the evening blind. Next day he could hardly distinguish light from dark. Yet the light reflexes were normal; the fundus was normal.

This Crouzon calls the symptomatic triad for functional nerve blindness of Dieulafoy. There have been similar cases following eclipse of the sun and nervous shock. The eclipse cases suggest that the bright flash might have something to do with the sudden blindness (yet blindness has appeared in cases in which the shell burst behind the patient).

The diagnosis of temporary blindness, with a prognosis of early recovery, was made. The neurological examination was normal.

For its suggestive effect, glycerophosphate injections and progressive reëducative measures were adopted. The patient was shown that he could see, first, the contour of objects, then details and colors, then large letters and later small letters. In a month the blindness was almost well. Five months afterwards there was still a certain haze over the field of vision and a slight difficulty in distinguishing certain colors.

Jousset states that aside from visual alterations as the result of cranial trauma, and aside from various transitory amblyopias such as scintillating scotoma, the main varieties of amblyopia are:

_First_, Congenital amblyopia.

_Second_, Amblyopia due to cerebral intoxication.

_Third_, Retrobulbar neuritis and toxic amblyopia.

_Fourth_, Amblyopia ex anopsia.

_Fifth_, Hysterical amblyopia.

The most frequent amblyopias among the soldiers are exanopsia. Aside from a few amblyopias caused by prolonged occlusion of the eyelids, ptosis, or blepharospasm, the most frequent are due to opacities, ametropia, and strabismus. The hysterical amblyopias are, as a rule, associated with blepharospasm due to intense photophobia, and are sometimes associated with constant lacrimation. Vision at a distance is poor. The patient succeeds in reading but shows an asthenopia of fatigue. The cornea and the conjunctiva are anesthetic, and sometimes the eyelids also,--the so-called anesthesia _en lunettes_. The pupils are large but react properly. The patient complains of many species of disorder; loss of the sense of the third proportion, micropsia, megalopsia, diplopia, erythropsia, diplopia in two colors, inverted image, hemierythropsia, rotatory amblyopia. There is concentrated limitation of visual fields, exaggerated by fatigue and by intense light; reduced in dim light or when the patient is provided with smoked glasses; enlarged upon the instillation of atropin or with convex glasses. As a rule, with unilateral amblyopia, the functional disorders start in binocular vision. Practically the most important diagnostic feature is the anesthesia, since this cannot be readily simulated. Sometimes corneal anesthesia is found in non-hysterical persons, who may perhaps be regarded as potential hysterics.

Retrobulbar neuritis (nitrophenol).

=Case 434.= (SOLLIER AND JOUSSET, April, 1917.)

A soldier of the 54th Artillery entered hospital 45, November 4, 1916. He had had a slight paralysis of the left brachial plexus in 1913, following a shoulder dislocation, but the only relic of this when the war began was a deltoid paresis. He had been working from August 13, 1915, at the factory in Saint-Fons, and was as yellow as the majority of the workers there. He had never shown xanthopsia.

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.

The case is beyond question hysterical,--the phenomena consisting of an ophthalmoplegia externa, alternating with spasmodic contracture of the internal recti, associated with myosis and loss of light reaction. The influencibility of this situation during the process of tests, to say nothing of the other stigmata, clinches the diagnosis--an important one, since the development of an external ophthalmoplegia after occipital trauma might possibly be regarded as an organic disease due to hemorrhage in the region of the eye-muscle nuclei.

Sandbag drops on head: Internal strabismus and diplopia. Various diagnoses. Cure by lenses.

=Case 436.= (HARWOOD, September, 1916.)

A four-pound wet sandbag fell eight feet on the head of a sergeant-major, 28, lying in a Gallipoli dug-out, November 24, 1915. The sergeant-major was removed to Lemnos with headache and giddiness, and a week later developed bilateral internal strabismus with double vision and head noises. The diagnosis was “brain tumor” or “syphilitic meningitis of the base.” On the voyage home, the diagnosis was altered to “multiple neuritis or neurasthenia.”

He was admitted to the King George Hospital, January 1, 1916, unable to move the eyes outwards; they moved rather poorly up and down. There was a slight lateral nystagmus. The patient had been unable to read or stand since the accident. The visual acuity of each eye was less than 6/60, but with an arrangement of lenses he could get 6/5 with either eye. He had perfect binocular vision and could read ordinary type comfortably. In a week’s time he was able to stand without support and walk with a stick. Whenever he took off the glasses, the strabismus and diplopia immediately returned. Other combinations were tried but failed to relieve symptoms. The lenses given were +0.375 c. Vert. and L. +0.25 S. +0.25 C. 75 do.

Hemianopsia: organic or functional?

=Case 437.= (STEINER, October, 1915.)

A 19-year old volunteer, never ill (no nervous disease in the family), after a period of training went into the field, October 3, 1914. November 5, a shell struck the trench nearby but failed to explode. Up to that time everything had been quiet. The soldier had been looking out of the loophole, surveying the terrain. He felt a great fear, got a blow in the neck, fell down unconscious, remained unconscious for an unknown time, and later walked back with his comrades. About an hour later, this volunteer,--who was a very intelligent young man, possessing much knowledge of biology, including the nature of visual fields,--noticed a black spot in the field of vision, which came and went, but after a few hours remained continually without disappearing. Otherwise, there was no complaint except a feeling of dizziness when stooping.

Upon examination there could be found no disorder of the internal organs. Neurologically there was blinking, vasomotor excitability, slight reddening of the face, and dermatographia. An expert in ophthalmology confirmed the existence of a homonymous defect in the fields of vision. This defect could not be influenced by suggestion or by any other treatment, nor did any other change whatever occur in the condition.

Steiner inquires whether this hemianopsia is to be taken as organic or functional. The air-pressure of the shell hissing past might have produced a concussion, or the falling unconscious might have produced a commotio cerebri or a slight hemorrhage. The tic-like blinking and vasomotor excitability, however, suggest functionality.

Hysterical pseudoptosis.

=Case 438.= (LAIGNEL-LAVASTINE and BALLET, January, 1916.)

Laignel-Lavastine and Ballet present a case of what they term hysterical pseudoptosis in a patient who showed no signs of organic disease of the nervous system, and moreover no special mental disorder. This soldier, 30 years of age, working in the auxiliary service, suffered from a troublesome lowering of his left upper eyelid. He went to the front in February, 1915. Aside from suffering a few mild and temporary blindnesses (_éblouissements_), he was entirely well up to the time of being wounded, March 18, 1915, by a bullet in the arm, and a bullet occasioning a superficial and slight wound 2½ centimeters above the middle of the left eyebrow. About three years later, a shell burst near him and made a large contusion about the right eye, without hurting the globus. He was then evacuated to Châlons-sur-Marne, and there remained for 48 hours, totally blind, probably on account of spasmodic closure of his eyelids. He then began to be able to use the left eye, which remained, however, very photophobic. A fortnight later, the wounds were healed, but the patient found himself unable to open his right eye. Three months later he returned to his dépôt, and left for the front October 24.

He was reëvacuated November 4, as unsuitable for service. He was then examined by an ophthalmologist at Chartres, who found a very mobile right pupil and a slightly atrophic right papilla; vision ½; left eye normal; vision ⅔; total paralysis of right levator palpebrae superioris without contracture of orbicularis. There was also paresis of the left upper lid, which ceased when the right eye was closed. The right half of the face was anesthetic, but there was no corneal anesthesia.

November 15: Right eyebrow lower than left; if the head was moved backward, the right eyelid followed the movements, and in this position there was no ptosis.

November 16: Analgesia in the super- and sub-orbicular region. November 17: frontalis and orbicularis functions normal.

At time of examination, patient complained of not being able to open his right eye, and that he could only partly open the left eye. To catch a view of his examiner, he had to throw his head back and to the right. He could not open his eyelids, and in the effort to do so, the forehead muscles contracted; and whereas the left eyebrow was properly elevated, the right eyebrow was only partially elevated. Associated movements could be noted in the musculature of the lower part of the face. In looking to the right, the eyelids, especially the left, were elevated slightly. The patient complained of photophobia. From time to time, he felt completely blind, and at the end of these spells of blindness, he had a severe headache. His head felt heavy. Sometimes on looking to the left, he saw objects double, although this diplopia had grown less marked of late. All the muscles of both eyes appeared to work normally. Upon pressure on the right globus, especially pressure directed from above and behind on the internal part, the patient would raise his left eyelid, but the paresis reappeared the moment the pressure was released; a fact which the patient himself noted while a tampon was being placed upon his eye.

It seems there had been a wound at the external angle of the eye, some nine or ten years before, as a consequence of which the eyelid of this side could never be parted as well as before. The accident in question had happened in 1905, and there had been a slight suppuration of a wound 2½ centimeters from the external angle of the palpable fissure.

The patient then went through a period of reëducation. It seemed that when he was trying to raise his eyelids, there was a mental inhibition which could be overcome only by effort. An attempt may be made to resolve the phenomena into three groups:

First, enophthalmia of the right side (post-traumatic, antebellum, a predisposing cause).

Secondly, a situation corresponding to so-called hysterical pseudoptosis of Charcot and Parinaud (eyelid falling without wrinkles, head thrown back, frontalis contraction on effort to open eyes, eyelid lowered). The diagnosis of hysteria was supported by the transient opening of both eyelids when a sudden sharp order was given to move the eye-_balls_, and further supported by synergic automatic lid-movements when the patient voluntarily raised his eyes. He could not raise his eyelids to order.

Thirdly, functional ocular palpable synergy (left eye opening upon compressing the right eye).

Shell-shock Rombergism.

=Case 439.= (BECK, June, 1915.)

A soldier, 24, had sundry signs of traumatic neurosis. A curious and unexplained feature is the fact that in the course of testing for Rombergism he would fall forward like a log if his head were held in the vertical position, but if it were turned to the right he fell to the right; if it were turned to the left, he fell backward. Tests showed that he had no disease of the vestibular apparatus and no sign either of cerebral or of cerebellar disease.

The question is raised whether shell-shock can produce a differential Rombergism such as hitherto would have been explained on the basis of some organic vestibular disease.

_Re_ Rombergism, see especially Bourgeois and Sourdille’s (edited by Dundas Grant) remarks on disturbances of balance which, if of labyrinthine origin, obey Romberg’s law, namely, are greatly increased with the eyes closed. Upon test, however, normal equilibrium, tottering, or a tendency to fall will be usually found. The tendency to fall is, as a rule, toward the side of the affected labyrinth, yet it varies according to the position of the head; that is to say, actually upon the position of the labyrinth with relation to the body. If there is a lesion of the right labyrinth, for example, and the head is turned to the right, falling is to the right; but if the head is turned 90 degrees toward the right, the patient tends to fall backward because in fact the injured right labyrinth has now become posterior in position. But if the head with the injured right labyrinth is displaced 90 degrees to the left, the tendency would be to fall forwards.