C. THE DIAGNOSIS OF SHELL-SHOCK (continued 2)

Re pathological movements such as tremors, tics, and choreiform movements, Roussy and Lhermitte divide the tremors (see also under Case 337) into typical and atypical.

The atypical ones are either limited, or more usually generalized when they are merely parts of the Shell-shock syndrome. Sometimes the tremors are paroxysmal, aggravated by noises. Now and then, a condition of tremophobia appears (see Case 225). As for the typical tremors, see classifications under Case 337.

Re tics, the tonic or postural tic is, according to Roussy and Lhermitte, much less common than clonic or spasmodic movements, which are Shell-shock phenomena like tremors and usually yield to psychotherapy if treated early. These tics are usually observed in and about the head, involving the sternomastoid, trapezius, and platysma muscles to produce clonic contractions of the neck. Other tics involve coarser head movements, nodding, eyelid and facial spasms, bilateral or unilateral, and shoulder movements. Babinski has suggested that some of the tremors are possibly due to organic disease, in view of the fact that they are not readily influenced by psychotherapy. Meige has suggested that some of the tics may also be in some sense organic. As for the differential diagnosis of tremor and tic, according to Roussy and Lhermitte, the Shell-shock onset may be an indicator. The non-rhythmic and irregular nature of the tic movements, and their exaggeration on voluntary movement, may be of some importance. Most of the tremors appear to be attended by a certain degree of permanent contraction of the muscle groups concerned. Tremors cease when these contractions disappear.

A point in treatment is that complete muscular relaxation should be obtained by having the patient open his mouth and breathe deeply.

Re diagnosis of neurasthenia in this case, it may be inquired whether the term is properly used, and whether there is not some confusion here betwixt neurasthenia and hysteria.

Re hyperalgesia, Myers states that about 25 per cent of his Shell-shock cases have shown a variety of disorders of the skin sense. Hyperesthesia and over-reaction is one phenomenon in the list, but is far less common than hyperesthesia. According to Myers, the hyperesthesia was more relative than absolute, and was probably due to increased affective response.

Shell-shock; unconsciousness: Tremors, anesthesias. Recovery by suggestion.

Case 414. (Mott, January, 1916.)

August, 1915, between Ypres and Flamentières, a Jack Johnson exploded one day about three o’clock in the morning near an experienced gunner, who had been on service in the R. F. A. for 15 years, and in France during the present war 10 months. He came to in the military hospital at Chatham, two weeks later, and was told he was lucky to be there at all as the shell had killed many comrades. He was transferred to Colchester, and thence to the Fourth London General Hospital.

Sitting in a chair, the man showed continuous rhythmic movements of legs, hands, and jaw, exaggerated when he was spoken to. The tremor was almost a clonic spasm. Every now and then, the patient would start and look sidewise and upwards, as if a shell were about to drop. Hyperacusis was such that the firing of the guns as far off as Woolwich alarmed him. In telling his story, he would repeat the same words over and over. He dreamt of shells bursting. His sleep was disturbed with groaning and moaning. The face was flushed, and the palms sweating. Because of the constant tremor, he could not stand or walk without assistance, and it was difficult to test reflexes. The tremor somewhat resembled the intention tremor of multiple sclerosis. He was unable to feel the prick of the needle on legs, left arm, or hand. He could not feel vibrations of the tuning-fork on feet, legs, or hands, though he could on the forehead. The fork was heard quite well six inches from the ears. There was some difficulty in recognizing colors. Bitter fluids could be tasted, but vinegar, salt, and various fluids, could not be recognized. He could not recognize tincture of assafetida, attar of roses, or oil of cloves, though nitrite of amyl, ammonia and glacial acetic acid were recognized.

Major Mott felt that, though this prolonged severe disease in a long-service man might possibly be related to some organic change in the brain, he might well treat him by suggestion. Major Mott told him that the careful examination just made showed that there was no organic disease, and made it certain that he would recover. In a fortnight, he sat in a chair without tremors and with a profound belief in Major Mott.

Hysteria as appendix to traumata.

Case 415. (MacCurdy, July, 1917.)

A private, 25, something of a liar and of rather a low personality, had enlisted in the regular army in 1911, but deserted to become a football player. He reënlisted, and went to France in September, 1914, enjoying the first six months. He broke his ankles by falling into a deep dug-out, and got frost-bite. After three or four months in England, he found that he did not wish to go back to France. He was two months in barracks, and then went up the line in a good deal of a panic. Soon after, he was wounded in the thigh and was able to remain in hospital a fortnight, exposed, however, to shell-fire and given to starting at noise and occasional war dreams. Sent to his base, he remained jumpy and was now permanently afraid of the line. After three weeks in the trenches, he again got wounds, spent five months in England, came back to France in May, and fought till September, 1916. He tried to convince the medical officer that he had appendicitis and trench fever.

About the middle of September he saw with horror a man crushed by a tank, and thereafter was markedly affected by the sight of blood. Another slight wound sent him to a rest camp for two weeks, whence he was again thrown into the line, suffering acutely from fear and horror of blood. In three days he fractured his left collarbone and wrist. He gave a pint and a half of blood for transfusion purposes, and in turn was shipped to England. On removal of the splint, he found “probably not without satisfaction” that the arm was paralyzed. It remained paralyzed for five months, until treatment in a special hospital eventually cured the arm; but upon cure of the arm, nightmares developed,—an indication, according to MacCurdy, of the strong resistance he felt to the idea of returning to the front.

Neurasthenic hyperalgesia after peripheral nerve injury.

Case 416. (Weygandt, January, 1915.)

A German volunteer, a sportsman, was under heavy shell fire after the middle of October, 1914, and was wounded in the upper arm in November, with an injury to the median nerve that occasioned severe pain. These strictly localized pains increased upon any sort of physical or mental strain. If he walked down steps he kept thinking he might have an accident, and then the pains set in with greater force. He became apathetic so that he did not eat, drink or urinate. If his head were touched he felt pain as if from an electric shock. He also felt the pain when he saw anybody approaching a door to close it, through apprehension of the noise. Meantime, the wound was well healed. The pulse was accelerated. The visual fields were only slightly contracted. The patient wanted to get well and go back to the service.

Weygandt regards this hyperalgesia after peripheral nerve injuries as neurasthenic.

Military training: Peripheral neuritis in lead workers.

Case 417. (Shufflebotham, April, 1915.)

Among fourteen cases of lead poisoning, members of the territorial forces, largely from North Staffordshire, was a patient suffering from peripheral neuritis. He had been in the dipping-house. Two years before going into the service he had been suspended for lead poisoning by the factory surgeon. Giving up his work at the pottery, he became a general laborer in a non-lead process factory.

Three weeks after enlistment, the man began to complain of pains, tenderness in the arms, weakness of the wrists, headache, giddiness, nausea, and constipation. The bowels were opened by a large dose of epsom salts. On blood examination the hemoglobin was found diminished 40 per cent; cells with basophilic granules were found to the number of 500 per cu. mm. The face was characteristically pasty. There was albuminuria. Alcohol could be excluded. The man had to be discharged.

All Shufflebotham’s cases occurred from three to seven weeks after mobilization, nor have any cases ever been reported in territorials after their annual training. Constipation was invariable. In two cases returned to service, there was a recurrent attack. An epidemic could be excluded. Shufflebotham suggests that the altered conditions of life, especially the marching and drilling, caused increased metabolism, setting free lead compounds from the muscles and organs of the body. It is true that a glost placer always works very hard with his muscles, but not with the muscles used by the soldier.

“Peripheral neuritis” cured by faradism.

Case 418. (Cargill, February, 1916.)

A Naval Service man, 20, was thought to have peripheral neuritis. A long history of pain and numbness in arms and legs, a well-marked analgesia and anesthesia over the anterior aspects of forearms and legs, and an anesthetic band across the front of the chest, seemed consistent with the diagnosis. The calf muscles tightly squeezed yielded no pain. Pins could be thrust without pain into the anesthetic areas. When told to say yes when the pin was felt, and no when it was not felt, the man persistently said no when the areas noted above were touched. The deep reflexes were normal. Faradism by wire brush at two sittings yielded a complete cure. It seems that once this man, after seeing his sister fall in a fit on returning from a funeral, retired to the garden and had a similar fit himself.

Cargill found in 1052 sailors fifteen cases of total absence of one or both ankle-jerks; seven of the fifteen were probably cases of tabes.

Re peripheral neuritis and hysteria (see under Case 387).

Re differential diagnosis between peripheral neuritis and reflex (physiopathic) paralysis, Babinski and Froment offer the following table:

Peripheral Neuritis.Reflex Paralysis and Contracture.

1. Motor disorder, degenerative amyotrophy, and sensory disorder corresponding topographically to anatomical distribution of nerve (neuritic) topography. 1. More or less segmentary topography.

2. Amyotrophy very pronounced, regardless of localization. 2. Amyotrophy variable; ordinarily well-marked but not so severe as that of neuritis.

3. Reaction of degeneration, especially weakening or abolition of faradic excitability of muscles. 3. Reaction of degeneration absent, never marked weakening of faradic excitability, which is often normal and may even be exaggerated.

4. Tendon reflexes, corresponding to the muscular territory of the nerve, weakened or abolished. 4. If reflexes are altered, they are as a rule exaggerated and never abolished.

Multiple wounds; signs of late tetanus 7-8 weeks later: Pain and contracture of neck, tetanic, 14 weeks after trauma. Dysentery. Recovery.

Case 419. (Bouquet, 1916.)

A soldier invalided for endocarditis July 8, 1908, went back to the colors on his own request August 8, 1914. He was wounded at noon September 6, 1914, in the attack at Abbaye Woods. He lay in the woods, with several comrades as badly wounded as himself, until September 10, eating berries and drinking rain water. He had five wounds in all; in left lower leg, thigh, left external malleolus, right calf, and left forearm. Moreover, he had dysentery.

He was picked up by the Germans September 10 and carried by them to the ambulance at Saint André, where he was given belated first dressing. When the enemy retreated September 12 he was left behind and finally carried back September 13 into the French lines by a French physician who had been a prisoner likewise. A second dressing was given September 14 at Rambluzin. He was then carried in a sanitary train to Bar-sur-Aube, where, September 15, injection of antitetanic serum was given. He left Bar-sur-Aube on December 18, 1914, practically cured, though one of the wounds still needed care. The dysentery was still present and walking was difficult. He was then cared for at Auxiliary Hospital No. 102 in Paris.

It seems that about six weeks after his entrance in the hospital at Bar-sur-Aube he had had some difficulty in opening his jaws, with acute pains at the temporomaxillary joint. Similar pains appeared a few days later in the neck, with a sensation of stiffening. The jaws still opened easily enough December 18, yet the man got pains in his jaws as soon as he began to speak. The pain and contracture in the neck region were sharp and permanent. Sometimes the contracture got more marked, and the board-like muscles could be felt stiffening under the examining finger. During such crises the patient had to lie or sit down. Sometimes the pains descended below the shoulders along the vertebral column. The crises occurred more often in the night, in bed.

The diagnosis of late tetanus was made, and alcohol rubs were given. The phenomena gradually disappeared. The dysentery also had not yielded to therapeutics until eight or ten days before the patient left the hospital. There was still, at the time of report, a certain difficulty in walking, with a tendency to use the external border of the left foot rather than the sole.

Shell-shock: Spasmodic neurosis and neurasthenia. Treatment without great success.

Case 420. (Oppenheim, July, 1915.)

August 19, 1914, a shell exploded very close to a soldier, whose bread bag, cartridge container, and field flask were pulled away from him, but who was not himself wounded. He fell down. Shortly developed headache, vertigo, palpitation. In running he fell down repeatedly. Spasms soon appeared in the legs. He had previously suffered from gastric disturbances, and heavy food did not agree with him.

At the time of admission to hospital he complained of great irritability, nervous twitching, formication in his limbs, war dreams, tachycardia. The heart boundaries were normal. The muscles of lower extremities were attacked by tonic spasms, and felt board-like. This tonic spasm occurred on each attempt at motion, very gradually disappearing when at rest. Passive movements also had the same effect. Fibrillary tremor affected the left quadriceps. On each attempt at motion, pains were felt in the legs. At first the cramps were so severe that all locomotion or even standing was impossible.

Treatment: Cold-water pack (Priessnitz), hyoscin injections, magnesium sulphate injections (5 to 10 c.c. of ten per cent solution), perineural injections, lumbar spinal analgesia,—all without success. Fibrillary tremors persisted in the quadriceps and in the extensors of the toes. The tonic spasms on increased attempts at motion became combined with clonic twitchings. From the end of November on the patient made attempts to walk with straddling legs, and under considerable vibratory tremor. Picture of severe crampus-neurosis, combined with neurasthenia gravis.

Chart 13

SHELL CONCUSSION

Cause physical from explosives—amnesia for shell episode and for a subsequent period—followed by traumatic neurosis

SHELL HYSTERIA

Shell heard—victims already unstable—rum issue preparatory?—overemotionalism—sensory and motor disorder

SHELL NEURASTHENIA

Headache, dizziness, insomnia, anorexia, visceral pain—victims, older men

After H. P. Wright

(a) Bullet-wound of forearm: Combination of hysterical (brachial) monoplegia, and reflex (physiopathic) disorders. (b) Refrigeration: Combination of hysterical paraplegia and reflex (physiopathic) disorders.

Case 421. (Babinski, 1916.)

The forearm of a soldier was pierced in its lower part by a bullet, which produced no lesion of large nerve trunks or blood vessels. A complete brachial monoplegia followed. Every movement of the different segments of the arm was abolished. The hand and forearm were slightly atrophied, and were of a reddish salmon color. The temperature of the affected hand and forearm was about three or four degrees lower than that on the other side. The sphygmometric oscillations of the forearm were twice as small in the paralyzed limb as in the healthy limb, but the systolic blood pressure was normal. There was a mechanical over-excitability of the muscles, and a slight exaggeration of the bone and tendon reflexes. The paralysis was in part of reflex (physiopathic) nature. On account however, of the completeness of the monoplegia, and the fact that the reflex paralyses as a rule affect only the distal portion of the limb, the diagnosis of hysteria had to be made in addition to the diagnosis of reflex disorder.

As a result of freezing, this patient had also a complete crural paraplegia. He showed vasomotor disorders and hypothermia of both feet, together with mechanical over-excitability of the muscles; and these latter disorders appeared to be of a reflex nature. The paraplegia, however, was of a hysterical nature.

Re refrigeration, see Case 309 (Binswanger) of glossolabial spasm.

Differential diagnosis of organic (central) monoplegia and reflex (physiopathic) contracture and paralysis. (Babinski-Froment.)

Organic Monoplegia Reflex Contracture and Paralysis

1. Paralysis often affects the whole extremity, either arm or leg. 1. Paralysis almost always partial. In arm paralysis, affects as a rule fingers and hand. The leg is often affected at its origin, and then only partially.

2. After several weeks of flaccid paralysis, as a rule contracture occurs. 2. Paralysis may remain flaccid for a long time, and frequently coexists with contracture, hypertonicity and hypotonicity of different muscular groups.

3. The upper extremity shows flexion with clawhand. The lower extremity shows contracture of extensors. The patient walks throwing his leg sidewise (Démarche helicopode). 3. The upper extremity in hypertonic cases often shows the main d’accoucheur, the main en bénitier (holy-water vessel hand), the doigts en tuile (crowded fingers). The lower extremity does not exhibit the sidewise movements.

4. Tendon reflexes, a few weeks after paralysis begins, exaggerated. 4. Reflex status variable. Hyperreflexia often absent even in hypertonic forms.

5. Babinski sign in crural monoplegia. 5. Babinski sign absent. The skin reflex may be abolished but may be reproduced on warming the foot.

Slight bullet wound of hand: Flaccid paralysis with vasomotor and thermic disorder. A case “non-organic” in the ordinary sense and non-hysterical, i.e., reflex or physiopathic.

Case 422. (Babinski and Froment, 1917.)

Struck by his observations upon the persistence of tendon reflexes in narcosis in a wounded soldier, Babinski continued observations in the same general direction in a case which may be termed briefly one of hypotonia of the extensors of the hand following the passage of a bullet through the arm without nerve trunk lesion.

This patient had flaccid paralysis of hand and fingers following wound in second dorsal interosseous space and vasomotor disorder and local hypothermia in the hand. There was a slight diffuse atrophy of the muscles of the hand, forearm, and arm; but this atrophy was not systematized, and there was no R. D. The tendon reflexes of the extremity were preserved. There were no signs of organic disease of the central or peripheral nervous system; that is, in the ordinary sense of these terms.

Was it a question of hysteria or of simulation?

Babinski was struck by the following symptoms:

First, the remarkably intense hypotonia, especially noteworthy in the thumb, a hypotonia quite equal if not superior to that observed in paralysis following marked nerve lesions;

Second, mechanical over-excitability of high degree in the muscles of the hand and forearm, with retardation of the muscular response; and

Third, electric over-excitability of the muscles, with what Babinski calls “anticipated fusion” of the faradic reactions.

It appears that this patient had been wounded in September, 1914, and that the paralysis had developed five months later. Before the development of this paralysis, there had been simply a meiopragic state.

Without perforating the hand, the bullet had remained in the wound, being excised therefrom three months after the trauma.

In January, 1916,—that is, some sixteen months after the injury and eleven months after the recovery of the paralysis,—the vasomotor disorder and the hypothermia, and the faradic, voltaic and mechanical over-excitability of the hand and forearm muscles, were in evidence. Hypotonia was marked, permitting an overflexion of the hand upon the forearm. If the patient moved his forearm, the affected hand would hang and oscillate inertly; likewise in walking, seeming to obey only the laws of physics.

In May, 1916, the patient was invalided and found to be still in possession of the above-mentioned signs. Similar phenomena have been found in the main figée acrocontracture, and main d’accoucheur, and belong, in the opinion of Babinski, to a group which is neither hysterical nor organic in the ordinary sense of the terms. Vasomotor and thermic phenomena are in the foreground of the picture, and are, in fact, practically constant, though they vary somewhat in degree. They react abnormally to the temperature of the surrounding medium; there is undoubtedly a local perturbation of the vasomotor and heat-regulating mechanism. There is also certain evidence of vascular spasm. The vasomotor and thermic disorders run parallel with the mechanical over-excitability of the muscles and the slowness of the response.

Chloroform to demonstrate asymmetry of reflexes.

Case 423. (Babinski and Froment, 1917.)

A soldier, 26, sustained, September 22, 1914, a bullet injury of the right calf. There was no fracture, as X-ray showed, but healing was slow, taking no less than three months. The right knee-jerk was a little stronger and a little sharper than the left, but the difference was controversial; and the difference between the two Achilles reflexes was still more doubtful.

Chloroformed October 10, 1915: As the patient was going to sleep, even before the phase of excitation and motor agitation had passed, the two knee-jerks and left Achilles jerk had disappeared. They grew rapidly less marked before disappearing, and none of the tendon reflexes presented any phase of exaggeration while the patient was going under. At this point anesthesia was arrested. The right Achilles reflex, which had not disappeared, was sharply defined. It was even stronger than in the normal state and polykinetic. During the whole phase of awaking from the chloroform, the right Achilles reflex remained strong and polykinetic, without, however, any ankle clonus. Thus, the difference between the two Achilles reflexes became indisputable; also the right knee-jerk reappeared before the left, and became stronger without any patellar clonus. At this time, the difference between the two knee-jerks was sharp and beyond cavil. This status, in which the knee-jerk and Achilles reflexes were asymmetrical, lasted about ten minutes after anesthesia ceased and lasted a little longer for the knee-jerks than for the Achilles jerks.

Reflexes under chloroform.

Case 424. (Babinski and Froment, October, 1915.)

A soldier sustained a clean-cut wound of the supero-external aspect of the right thigh without much destruction of tissue or any adherent scar. He showed marked lameness, September 15, 1915, walking with his right leg extended and the foot in external rotation. There was a slight limitation of the movements of the hip joint in respect to internal rotation and flexion of thigh. The right knee-jerk was a little stronger than the left, and this condition persisted several days. After a few tests, the knee-jerk became even slightly polykinetic. The Achilles jerks were normal and equal. There was no epileptoid trepidation of the foot, and no patella clonus. There was a slight hypothermia of right leg, with ill-defined muscular atrophy. Walking caused pain.

Chloroform anesthesia, September 20, 1915, yielded an exaggeration of the knee-jerks with a suggestion of patella clonus even before the phase in anesthesia of motor excitation had set in. As anesthesia proceeded the exaggeration was rapidly lost on the left side but progressively increased on the right. In the phase of complete muscular resolution, when all the other tendon reflexes (such as the knee-jerk, Achilles jerk on the left side, the radial and olecranon reflexes on the left side) were abolished, the patella clonus on the right side was perfectly distinct and could be elicited either by the usual method or by raising the thigh and letting it fall. On percussion of the patella tendon, a strong polykinetic reflex was obtained; right Achilles jerk preserved; right leg in external rotation. Internal rotation could be passively performed better than in the waking state, but this movement was still limited. As the man was waking from anesthesia, when reflexes were reappearing, there was a suggestion of left patella clonus—right clonus as strong as before. At no time any trepidation of the foot. The patella clonus on the right side lasted an hour after waking, at which time all the reflexes returned to their previous state.

Reflexes under chloroform.

Case 425. (Babinski and Froment, October, 1915.)

A soldier sustained a bullet wound, September 22, 1914, in the right calf. There was no fracture, as X-ray showed. Cicatrization was slow and took at least three months. He was examined October 2, 1915, at the Pitié,—not complaining of pains, but lame. There were no pains, limitation of movement, or joint sounds in the hip joint, and X-ray was negative. There was a slight atrophy of the limb, 1.5 c.m. less in circumference on the right. There was a sharply defined local hypothermia of the right leg up to the knee. The right knee-jerk was a little stronger and brisker than the left, yet it was difficult to be sure of this, and there was a still more doubtful difference between the Achilles reflexes.

The man was anesthetized with chloroform, October 10. As he was going to sleep, before the phase of excitement and agitation had ceased, the two knee-jerks had disappeared. At the same time, the left Achilles jerk vanished, followed by the plantar cutaneous reflexes. Anesthesia was then stopped. The right Achilles jerk, which had not disappeared at any time, remained distinct. It was stronger than in the waking state, and polykinetic. During the waking phase, this reflex remained strong and polykinetic, but there was no epileptoid trepidation of the foot. Accordingly, under chloroform, the difference of the two Achilles reflexes had become very sharp. The right knee-jerk reappeared before the left and became stronger, though without patella clonus. This difference was much more striking than in the waking state. This asymmetry of the patella and Achilles reflexes lasted about 10 minutes after anesthesia was stopped, and lasted a little longer for the patella reflexes than for the Achilles reflexes.

Shrapnel wound above clavicle: Brachial monoplegia, partly hysterical, partly organic.

Case 426. (Babinski and Froment, 1916.)

Babinski speaks of certain symptomatic incompatibilities which emerged in the study of cases of combinations of hysteria, organic nervous disease, and the so-called physiopathic disorders. An example of such an incompatibility might be that of a patient who should, three months after a sudden hemiplegia, show complete or almost complete flaccid paralysis and but slight exaggeration of tendon reflexes—yet the Babinski reflex. Of course, the Babinski reflex would permit a diagnosis of pyramidal tract disease. Yet a sudden intense hemiplegia lasting three months, if it were merely a matter of pyramidal tract disorder, ought to show hyperreflexia of a pronounced degree as well as contracture. An example from the arm is as follows:

A soldier got a shrapnel wound in the left supraclavicular region, and had a complete paralysis of the arm, which had lasted more than a month. Electrical examination showed marked reaction of degeneration in the muscles controlled by the musculo-cutaneous nerve, as well as a diminution of electrical excitability in the muscles innervated by radial branches. On the contrary, in the circumflex territory, ulnar and median, electrical excitability was normal. There were no vasomotor disorders. The diagnosis of an association of hysteria and organic disease was made. Babinski affirmed that electrification would effect a partial cure; and in point of fact, the patient, after having submitted to the current for several minutes, was able to use all the muscles whose faradic contractility was normal or almost normal. Thus, he could raise his arm, flex the thumb, flex the fingers, close the hand, and extend the hand and fingers. Flexion of the forearm on the arm was still difficult, since there was, in fact, a reaction of degeneration in the muscles of the anterior region of the arm. The fact that the movements could be partially executed was dependent upon action of the supinator longus.

Gunshot fracture of upper arm; recovery with motor power in five weeks: Six weeks later, Erb’s palsy (plus). Hypothesis: “Reflex paralysis” preferred.

Case 427. (Oppenheim, January, 1915.)

A reservist, 26, was shot through the middle of the left upper arm, sustaining an oblique fracture of the humerus, August 26. The external wounds healed in a month; the fracture somewhat later. The left arm was at first stiff and motionless, but in five weeks it could again be moved. Pains disappeared with return of motility.

About the middle of November the arm began to lose power to move again, especially the muscles of the upper arm. November 20, the patient showed atrophic paralysis (left deltoid, biceps, brachialis internus, and supinator longus) suggesting at first glance the appearance of an Erb’s palsy; but the triceps and the adductor of the upper arm were also unable to move and there was a slight paresis in the distal muscles of the extremity. There were no pains or other objective disorders.

The diagnosis of subacute poliomyelitis was considered. Electric excitability, however, was found to be normal, both faradically and galvanically.

When patient walked, the left arm swung helpless without sign of innervation or any tonus. Abduction of the shoulder could also not be performed, though a slight flexion of the forearm shortly began to be demonstrable. If the patient inclined his head to the right, extended his hand at the wrist, and flexed the fingers forcibly, he could then flex the forearm somewhat, and a slight tension of the biceps and supinator longus developed. Sometimes fibrillary tremors developed in deltoid and biceps.

Of course a transient peripheral palsy can be produced by pressure of the radial nerve without any change of electrical excitability, but such a change is not associated with atrophy.

Neuritis and poliomyelitis producing an Erb’s palsy without any effect upon the electrical reactions is an hypothesis not to be entertained.

Accordingly, the hypothesis of psychogenic or hysterical palsy may be set up. Yet an atonic atrophic palsy with loss of tendon reflexes (supinator) is inappropriate. According to Oppenheim, this case falls into the category of the arthrogenic atrophies. A simple muscular atrophy may follow disease of joints and bones. However, such cases have rarely shown a complete palsy, as in Oppenheim’s case.

In short, we return to the old doctrine of reflex paralysis, conceiving that a stimulus passing from the periphery influences the gray matter in its trophic functions.

How much effect had the psyche upon this condition? The patient had stuttered from childhood and had sustained a fracture of the skull at 9, following which his school work, especially mental arithmetic, had been poor. The lack of psychic inhibitions may play some part in the situation, but on the whole, the reflex hypothesis is preferred by Oppenheim, the nerve conceived to be dynamically affected, the muscles organically.

Paralysis: Hysterical? organic?

Case 428. (Gougerot and Charpentier, May, 1916.)

A soldier, 20, was wounded May 15, 1915, by a large number of shell fragments, 15 of which struck the right leg, two producing serious injuries,—the one, a penetrating wound of the popliteal space followed by stiffness of the knee, later cured by extraction of the fragments; the other, causing a deep wound at the internal malleolus. The fragment was extracted June 3, but osteomyelitis persisted and a fistulous contraction was developed in January, 1916. There was a slight equinism.

By contrast with these deep bony lesions of the right leg, on the left side a fragment had struck the dorsum of the left foot at about its middle point, along the extensors of the fourth and fifth toes. The fragment was removed toward the end of June, 1915. The wound closed in a fortnight, leaving a loose 20 mm. scar. The man complained of pains, which he called electrical, in the third and fourth toes, if one bore down on this scar, a symptom suggesting that the dorsal nerves had been injured. Immediately after the wound both legs had been paralyzed, according to the soldier. He had been able only to drag himself along on his shoulders. This indeterminate paralysis lasted three days. It may have been hystero-traumatic, or it may have been a sort of diffuse inhibition. Just after the injury, the left foot was in contracture, which gave place a month later to paralysis. Only the great toe was still able to move a little. In December, 1915, the patient still could extend and flex the toes on the left side very badly, though he could execute movements easily on the right side. There was no stiffness of joints; there were no tendon reflex disorders. There were no trophic vasomotor or secretory disturbances.

The diagnosis of hysterical paresis seemed warranted, but electrical examination showed that the troubles were organic. There was an increase in the faradic and galvanic excitability of the external popliteal nerve. The response was more sudden than normal, and there was an increase in faradic and galvanic excitability in the tibialis anticus. There was a decrease of faradic and galvanic excitability in the extensor communis of the toes and in the external peroneus.

Thus, this patient after being wounded in both feet May 15, 1915, paralyzed in both feet for a period of three days, undergoing a contracture of the left foot for a month, giving place to paralysis of foot and toes, with slow improvement from the end of July, 1915, was still in this latter state in March, 1916; though without trophic disorder, he showed faradic and galvanic over-excitability of the external popliteal nerve and of the tibialis anticus, pari passu with diminished electrical excitability for other muscles.

Paralysis: Hysterical? organic?

Case 429. (Gougerot and Charpentier, May, 1916.)

A man was wounded Oct. 11, 1914, on the back of the right hand. Two hours later, he was attended at the relief post. At this time, his hand was straight, with fingers extended. He said that he could not move his fingers, although there was no pain in them. Three hours after the wound, the hands swelled and the edema spread as far as the middle of the forearm. There was a long suppuration, complicated by lymphangitis. All of the fragments were removed October 26, 1914; healing was complete in three months. The swelling, however, persisted to June, 1915, and when the swelling disappeared, the hand began to show drop-wrist. The wound was sutured between the second and third metacarpals, and the X-ray showed that the bones had not been injured, nor had the nerves of the forearm muscles been touched. The situation was such that the case was catalogued “functional paralysis.”

October 5, 1915, the hand was still drooping, fingers extended, and middle finger and ring finger trembling. A slight stiffness of wrist and fingers did not interfere with movements. Extension of the wrist could be made very slightly above horizontal. Flexion was not quite complete, nor were adduction or abduction. Extension of the fingers could be performed normally, as well as that of the thumb, but flexion was not quite complete. There was a slight palmar retraction. Such were the movements that could be produced electrically. Voluntarily, flexion of the wrist was good, abduction and adduction incomplete; extension could not be executed to the horizontal position. There was a tendency to flexion of the ring finger. When the patient tried to flex the middle and index fingers, these fingers trembled but did not flex. Weak extension and abduction of the thumb but without opposition could be voluntarily performed; adduction good; flexion of the first phalanx, weak; of second phalanx, better. Slight muscular atrophy of the forearm, which was one centimeter less in circumference than the left. The hand was subject to a general atrophy; the skin reddish and moist. The X-ray showed a decalcification of all the bones of the hand and wrist; trophic disturbance of the small carpal bones although the trauma had affected only the second interosseous space. No joint lesions or periosteal thicknesses were found by X-ray. There was a slight hypesthesia of the palmar surface of the middle finger and of the index finger. The patient complained of sharp transient pains in hand and fingers.

In this case, therefore, a wound of the back of the hand produced an immediate inhibition of muscular action in the forearm, a rapid edema of the hand and arm, lasting for eight months and followed by reflex disorders.

There was a considerable diminution in faradic excitability of the flexor brevis of the thumb, the anterior cubital, the flexor brevis minimi digiti, and of the dorsal interossei, and slighter evidence of diminution of galvanic excitability in some of the muscles.

Sollier is said to have been the first to remark trophic bone disorders in cases of neuropathic contracture.

Re bone changes, Babinski enumerates trophic changes in the tissue of bones and joints amongst objective signs that permit us to distinguish the reflex or physiopathic disorders from the hysterical or pithiatic disorders. Objective signs of this group (indicators of reflex or physiopathic disorders) are: (a) Well-marked and persistent vasomotor and thermic disorder; (b) alterations of muscular tone (either hypotonus, hypertonus, or a combination of the two); (c) increase in the mechanical excitability of the muscles and sometimes nerves; (d) quantitative changes in the electrical excitability of the muscles, but without R. D.; (e) muscular atrophy and atrophy of skin, bones, and joints. For cases of this nature, see especially Cases 431 and 432 of Delherm.

Paralysis: Hysterical? organic?

Case 430. (Gougerot and Charpentier, May, 1916.)

A man, 22, was wounded September 17, 1914, in the left hand, the bullet passing from the lower part of the fourth interosseous space out through the palmar face. The bones were not injured, and it was evident that only a few nerve filaments could have been injured; but he had a paralysis extending far beyond this region, which increased little by little from November, 1914, to August, 1915. Babinski, examining him in November, 1914, had made the diagnosis of psychic paresis of the extensors with diminution of electric excitability, with a very slight slowing of the contraction of the last two interossei and the hypothenar eminence, connected with lesion of the branches of the ulnar nerve. The disorder spread to the flexors of the fingers and the thumb muscles. The fifth finger was flexed at rest; there was no stiffness of joint or tendon retraction. The extensors and flexors of all the fingers and the thumb, and the abductor of the thumb showed paresis. The thumb was able to oppose; the hands were cyanotic. Augmentation of these phenomena in a period of months, their bizarre distribution, and the preservation of the opposing power of the thumb suggested a hystero-organic disease, and Babinski’s notes read, “Partial and incomplete paralysis of the ulnar nerve, attacking slightly the hypothenar eminence and the last two interossei; psychic paresis of the extensors and flexors of the fingers and thumb and of the abductors of the thumb.” Electrical examination showed, however, that there was not only electrical disorder of the common extensors of the fingers, the extensor proprius of the index and of the ring fingers, of the long and short extensors of the thumb, but also there was a considerable diminution to faradic and galvanic reaction in extensor ossis metacarpi pollicis, the radials, the supinator longus, the pronator teres, the large and small palmar, the common and superficial flexors of the fingers, the muscles of the thenar eminence, the anterior ulnar, and the anterior biceps and brachial. In short, there was an irradiation of seemingly organic phenomena in the domain of the radial, median, and the non-injured part of the cubital distribution, as well as in the distribution of the musculo-cutaneous. Apparently, organic paralytic disorder had spread even to the biceps and had increased over a period of many months after the wound had healed.

Re what he terms organo-hysterical association, Babinski proposes to distinguish it from hystero-organic association. In Babinski’s organo-hysterical association, the organic symptoms are preceded by hysterical symptoms. These cases of organo-hysterical association,—e.g., a case in which a hysterical monoplegia is followed by a musculospiral crutch paralysis,—are one of the mainstays of the proof that hysteria and simulation cannot be confounded. Babinski concedes that he has sometimes said that hysteria was a sort of semi-simulation; yet a semi-simulation is not a simulation.

As for Babinski’s hystero-organic association, we here deal with cases of organic paralysis or contracture in which the fundamental disorder is organic, and the psychic disorder is grafted upon it. Both the fundamentally organic and the fundamentally hysterical associations are instances, according to Babinski’s phrase, of symptomatic incompatibilities. In such instances, the hysterical part of the disorder, whether grafted or original, is dissolved by psychotherapy. There is a third group of symptomatic incompatibilities, namely, the hystero-reflex associations, in which, e.g., a hysterical gait is combined with vasomotor and thermal disturbances. There may even be combinations of all three types of disease, namely, the type of structural disease, of vasomotor disorder, and of hysteria, in what would then be termed a hystero-reflex-organic association.

Wound of toes—Wound of arm: Reflex or physiopathic paralyses, diagnosis and treatment.

Cases 431 and 432. (Delherm, September, 1916.)

A soldier was wounded in the soft parts of the last two toes and in the furrow between toes on the left side, September 15, 1914, arriving in the Central Physiotherapeutic Service of the 17th Army Region, December 27, 1915, left foot in varus, with marked contracture of tibialis anticus, though passive movements of flexion, extension, adduction and abduction were well performed. There was a slight atrophy of the leg (33 cm. left to 34 cm. right). The scar was a little painful, and there was a slight degree of hypesthesia of foot and lower leg. The foot was cold and cyanotic; the reflexes were normal. An electric examination in the region of the external popliteal branch of the sciatic nerve showed that there was no electrical disorder either faradic or voltaic.

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.

According to Beck, there was in his case of Shell-shock Rombergism no ear disease or any evidence of cerebellar or cerebral disease.

Walking with the eyes open yields in marked instances a sidewise bending or even the classical staggering called the duck’s walk and drunken gait upon a broad base. The most delicate test, according to Bourgeois and Sourdille, is the Babinski-Weil test of walking with the eyes shut. A man with labyrinthine disease deviates from the straight path (he is made to walk forwards and backwards ten times in a clear space); bends pretty constantly to one side when walking forward, and pretty constantly to the other side when walking backwards. Spontaneous and Babinski’s induced nystagmus (rotation; caloric) and Babinski’s voltaic vertigo test are the other tests commonly employed in equilibrium investigation.

Otology and neuropsychiatry should go hand in hand.

Case 440. (Roussy and Boisseau, May, 1917.)

A soldier in the engineers, 29, entered the neuropsychiatric center at Scey-sur-Saône, August 23, 1916. His diagnosis was: organic shock syndrome with right-side deafness and tremors. He carried a ticket showing an otological examination: tympanum normal; Rombergism absent; walks with eyes closed swerving to right; tends to fall, eyes closed, on standing on one foot; vertigo produced by rotation in either direction; no nystagmus either spontaneous or by test; deafness especially on the right side; equilibrium function insufficient.

The patient had undergone shock in April, 1915, being buried and then losing consciousness for twenty-four hours. The tremors appeared next day, and also deafness but without speech disorder. Nine comrades are said to have been killed beside him. The hospital ticket, April 13, said: deafness and multiple contusions from shell explosion. The patient was evacuated to Clarmont-Ferrand and went back to service with the same tremor and auditory disorder. He was shortly sent back to the interior for six months and returned improved to the front August, 1915. But he heard the cannon in the distance, and, under the influence of emotion and the fatigue of the journey, the tremors and deafness reappeared.

The tremor was generalized, involving both arms and legs and a slight lateral movement of negation of the head every ten or twelve seconds. Occasionally tonic contracture of the face, lips, cheeks, forehead; tremors of tongue; winking. The tremors were somewhat suggestive of toxic tremors.

The deafness was evidently exaggerated. Voltaic vertigo tested normal. Reflexes normal.

The diagnosis psychoneurosis was made and the patient was rigorously isolated, given a long psychotherapeutic talk concerning the nonreality of his deafness and his vertigo and the possibility of cure by means of a very disagreeable electrical treatment. He made improvement upon psycho-electrical treatment and the next day both tremors and deafness had greatly diminished. September 4, the patient was considered completely well. There was a slight diminution of hearing in the right ear, the whispered voice was heard at 50 centimeters on the right side, the watch at 25 centimeters on the right and 60 on the left.

October 5 the patient was sent back to his corps. On the evening of his departure, angry at not having received leave, he boasted to his comrades of having passed but three days at the front since his injury.

It is remarkable, according to Roussy and Boisseau that this patient had passed sixteen months without ever having been taken for a neuropath or treated as one. The otologists gave the diagnosis of labyrinthine shock, but did not attend to the tremors. The pseudo-symptoms disappeared in six days at the neurological center and the cure had lasted six weeks at the time of report.

Re otology in these cases, see Bourgeois and Sourdille’s book mentioned under Case No. 439, particularly Chapter III, upon the functional examination of hearing. In the present instance, it will be noted that voltaic vertigo tested out normal. According to Bourgeois and Sourdille, the Babinski electrical test is the most convenient one to begin with, to learn in a few moments whether the vestibular system is working normally or not. These authors found amongst twelve patients, three normal reactions and one instance of hypo-excitability amongst four subjects who, by other tests, failed to show vestibular disturbance. Inexcitability as to voltaic vertigo was found in one man with a destroyed labyrinth. There were four instances of hyperexcitability in Babinski’s cases with marked equilibrium disorder. A case of Ménière’s disease yielded the same results. According to the intensity of the current, the following phenomena (in addition to the pricking sensation) are noted; (a) salty taste; (b) sidewise swaying with slight vertigo; (c) nystagmus with more pronounced vertigo; (d) sensations of sound. In short, nerve branches that go through the petrous bone, namely, the chorda tympani, the vestibular nerve, and the cochlear nerve, have been successively stimulated. Babinski’s test was published before the Barany work on induced nystagmus, but Barany’s rotation test for the physiological excitation of the semi-circular canals, and his caloric test for the investigation of the ears and canals separately are to be utilized in addition to the Babinski voltaic test. Babinski’s law of voltaic vertigo is that a normal subject inclines to the side of the positive pole; a pathologic subject falls to the side to which he tends to incline spontaneously. If the labyrinth has been destroyed, there has been no reaction.

Re Case 440, Roussy and Boisseau in their capacity as neuropsychiatrists, point out the inadequacy of an otological examination taken by itself. They insist that neuropsychiatrists should be called in. It is probably equally true that neuropsychiatric work upon deaf cases is often inadequate on account of the lack of otological examinations. According to Bourgeois and Sourdille, the expert otologist’s problems are as follows: (a) Deafmutism; here Gault’s cochleopalpebral reflex is of value. The hearing of a sudden noise causes contraction of the orbicularis palpebrarum on the side upon which the noise is suddenly and unexpectedly made. Eyelash tips are particularly watched.

(b) Complete bilateral deafness. This is practically never organic; complete bilateral deafness is a phenomenon either of traumatic hysteria or of simulation. Sundry methods of surprising the patient into hearing have been adopted. The practice of teaching lip-reading to simulators and hysterics has led to some difficulties in diagnosis, but tests have been produced by Gosset (of one sound with the lips set to form another, and the like) which are of service.

(c) Extreme bilateral dulness of hearing.

(d) Total unilateral deafness. For the minutiae of tests for these types of hearing disorder and their simulation and exaggeration, see the War Manual of Bourgeois and Sourdille.

Jacksonian syndrome: Hysterical.

Case 441. (Jeanselme and Huet, July, 1915.)

A Lieutenant of Infantry, 32, was struck by a bullet September 6, 1914, in the upper part of the left temporal fossa 4 cm. above the external auditory meatus. He did not lose consciousness, but had the sensation as if his head had been shot off, and about three minutes later he turned about, fell down, and lost consciousness. However, he regained consciousness a few minutes later and walked with support for about an hour. At the ambulance, he lost consciousness again, for half an hour. He was then carried to Amalie-les-Bains. The trip lasted 108 hours. The left side of the face was now swollen so that he could not open the eye nor could he chew from swollen mucosa folded between the jaws. The bullet was removed Sept. 12, from just below the scalp outside the bone, the point being slightly bent back. The bone had been depressed slightly for an area the size of a franc piece, and pressure at this point yielded a feeling of pain and discomfort. There was no suppuration. After a week, the man got up. He returned to his dépôt October 3 or 4 and was about to rejoin his corps when he had a sensation of pressure in the head and fell. When he came to himself he found that there was a frothy saliva at the left side of the mouth and that the whole left side of the body felt weak. The tongue had not been bitten nor had urine been passed, and twenty minutes later he felt as well as ever. He returned to the front in the Argonne, having from time to time similar crises,—at least once a week. Ordered to take a trench the night of January 17, he failed the first time, about midnight, but succeeded at four in the morning,—just afterward falling exhausted in another crisis, with unconsciousness. The stretcher bearers took him back and he was evacuated to Perpignan. He had two convulsions.

While with his family the crises grew in number to three or four a week, and sometimes twice a day. Upon request, he was sent to hospital in the Pantheon May 5.

There was always a sensory aura, consisting in a violent shock felt in the left side of the cranium like a blow of a club. There immediately followed a crawling sensation in the fingers and hand of the left side, running up the arm, with loss of consciousness coming on before the crawling reached the elbow. The seizure would last two or three minutes. There was no initial cry. The face grew pale. There was apnea, and frothy fluid running out of the left side of the mouth. There was no jerking of face or limbs; at the end of the seizure there were no deep inspirations. The extremities of the left side were rather flaccid during the attack.

A hemianesthesia was found affecting both skin and mucosae of the left side, and a slight retraction of the visual field on the left side was found. There were no other sensory disorders; the knee-jerks were lively on both sides but not actually exaggerated. Plantar stimulation was not perceived on the left side. The toes, except the great toe, were slightly extended. The fascia lata reflex failed to demonstrate itself. On the right side the great toe went into flexion on forcibly stimulating the sole. Sometimes the abdominal reflex on the left side was weak or even absent. The patient, who had never been nervous, had now become so since his attacks. He had had nocturia up to 12. There was no evidence of neurosis or psychosis in the family. Bromides diminished the crises a little in number. Static electricity was given from January 8,—no attacks for 8 to 10 days.

According to Jeanselme and Huet, this is a case of Jacksonian syndrome of an hysterical nature, about which it may be noted that the bullet struck the left side of the skull and the hemianesthesia and muscular resolution appeared on the same side as the injury.

Leg tic: Phobia against crabs.

Case 442. (Duprat, October, 1917.)

A man, shell-shocked in 1916 (with loss of consciousness, disorientation and confusion followed by nightmares, memory disorder, attention disorder, irritability, mental instability and over-emotionalism) later still showed a choreiform tic. He had a knife-grinding movement of the left leg which made standing and walking difficult. There were no signs in the reflexes or reactions of organic disease. The man himself said that he felt a sensation like little electric shocks when his foot touched the ground, a sensation like pinching. He also had certain hysteriform crises. He was able to remember nightmares in which he felt as if he had fallen into a hole where there were crabs. In point of fact, he had a true phobia against crabs, crayfish, lobsters and the like; if he saw one, he always felt as if he were going to have a new crisis. The defense movement of the leg and foot was against a supposed pinch of the crab. At rest, there was no trace of the choreiform movement. The tic was especially marked when the man was suddenly asked to get up and walk. In a few days, when he had become more clearly conscious of his phobia and had slept better, the tic grew appreciably less.

Convulsions reminiscent of fright.

Case 443. (Duprat, October, 1917.)

A soldier, 28, was blown up February 8, 1915, by a shell burst. He sustained no contusions but became completely mute. On July 3, he began to speak in a low voice. The torpillage treatment was unsuccessful because the man felt a morbid apprehension that the vibration of a loud voice or even of a rapid walk would resound in his brain. He had a sort of noise phobia, probably maintained by nightmares which frequently woke him up with a jerk though he could not remember their content. On the way back to his dépôt this man got off the train at the first station and went to a hospital complaining that the vibration of the train was going to be transmitted to his brain. Hysteriform crises developed in a few days.

According to Duprat these crises are nothing but a psychomotor development of the initial complex. The clonic and tonic convulsions are reminders of his states of extreme fright, a phenomenon of revival of the ideo-affective process, aggravated however by the oniric or post-oniric images.

Re diagnosis of hysterical fits, the absence of facial cyanosis, sub-conjunctival hemorrhages, petechiae of skin, and the Babinski reflex are suggestive for hysteria. Babinski points out that the initial cry, the fall, the loss of consciousness, the tongue-biting, the bloody frothing at the mouth, the urinary incontinence, and the post-convulsive prostration can all be consciously or unconsciously imitated. Hysterical convulsive movements are apt to be of wide range, gesticulatory, and opisthotonic.

Babinski announces to the supposed hysteric that he is going to reproduce the attack, as he is perfectly able to do by electricity. A mild current or mere electrode application suggests a fit in a hysteric, often very quickly. Babinski now announces that he can arrest the fit; carries out some selected procedure, and stops the fit. During the hysterical fit, the patient of course hears what is being said and during this time wrong suggestions must not be offered.

Fugue in a motor cyclist, with prodromal fatigue and subsequent delusions—recovery in six weeks.

Case 444. (Mallet, July, 1917.)

A motor-cyclist, 36, with the colors from the outbreak of the war, about April, 1916, grew very weary, suffering from headache and seizures without loss of consciousness. Finally there was a voice: “Sleep, you must sleep.” Then other voices; then ideas of thought transference with people around him.

Observed in the psychiatric center, May 12, 1916, he had the same ideas of thought transference, and he made as if to talk with the attendants by responsive-looking gestures. Sometimes, he said, fluid struck his forehead, calling on his thought. Whereupon he listened. The man made no complaints about his plight, was not astonished in any wise at what was happening, nor did he seek to explain it. There was nothing in his history to suggest psychopathy except perhaps that his father was unknown.

The diagnosis of a chronic hallucinatory psychosis was made, but the outcome promptly overset the diagnosis. The man talked with ward-mates, and particularly with another patient who also talked about thought transference. This shook the man in his convictions, and he decided that it was but imagination and delirium.

He now told his story: How it seemed that he had in his thoughts the phrase, “Sleep, you must sleep;” how he had gotten up, saying, “No;” had noticed the others paying no attention to him; had gone back to his work and from that moment had begun to go into delirium. During this delirium or delusional state, his whole life from birth up, came back to him, as if some one were telling him. The headaches, which he at first felt due to Hertzian waves, suddenly ceased.

Shortly, however, a new phase had set in, in which he felt himself surrounded by spies and that others had control of his thoughts and were reading them. In fact, he grew a little proud of the fact that people reading newspapers all around him were actually reading his own thoughts. The letters he wrote were being dictated. May 9, he spent a night with a succession of nightmares, and woke up with the firm purpose of going back to Paris by motor cycle to find the spies. He described his fugue and the thousand ideas he had on the way, his arrest, his imprisonment in a cell of Hertzian waves with a smell of sulphur and poisoned bread—a necessary fate on account of the spies.

On arrival at hospital, he had not known what was going forward. The nurses were giving him milk to destroy the taste of sulphur; the delirium then grew less and less. The room-mates were neutrals, war-weary; he seemed to be reading the newspapers before his mates, and they seemed to be talking of thought transference. May 20, the ward was changed. The new ward-mates did not believe in thought transference and laughed, causing the man to doubt.

June 2, the cure was in full process, and the ward was changed again; but in the new ward was a patient who had the same ideas of thought transference as the patient. At this time, the man’s autocritique saw through the delusion. He talked with his telepathic comrade and pretended to engage in a fake conversation about it. The delusions shortly disappeared, having lasted about six weeks.

Ordinary gunner’s life; a few days’ feeling of moral and physical discomfort: Obsession leading to fugue.

Case 445. (Mallet, July, 1917.)

An artilleryman, 32, gave himself up a few kilometers back of the lines, three days after deserting his post. The man was a very good gunner and had never been punished once. Moreover, the battery was not under any special bombardment, and he had been in the same place a number of weeks.

He explained that he had gotten tired during the last few days. Everything was well at home and in the regiment, but he felt sad, his head felt bad, and he couldn’t sleep. Something drew him to leave, but then “sang froid came back to me, and I gave myself up.” He had lived the three days without eating and without sleeping. He was very emotional over what he had done, but he began to work and asked that he be sent back.

His mother had been very nervous. There was a marked facial asymmetry and faulty arrangement of teeth. The man was not alcoholic.

According to Mallet, in these cases of fugue, and in other cases of absolute delirium of apparently sudden onset, there is a feeling of moral and physical discomfort for some days before the outbreak. The outbreak itself is sudden on the occasion of some idea, either an obsession or a hallucination. Of all the prodromal signs, headache is the most striking. According to Mallet, such fugues are the expression of a mental imbalance allied to the onirism of Régis.

Aprosexia and bird-like movements.

Case 446. (Chavigny, October, 1915.)

A soldier of the dragoons, 25, entered Chavigny’s service May 30, 1915. He acted like a mechanical figure, requiring guidance. The face was without expression except for the mobile eyes, and sudden bird-like movements of the head, continually attracted to new noises and objects. An interlocutor was glanced at but not responded to. If an intense electrical shock was passed through his abdomen, for example, the man would look for a moment in that direction, but only the most fugitive defence reaction would be made, and the stimulus could be repeated with the same result, a moment later.

After three days, this aprosexia began to clear, and in four or five days, answers to questions and ordinary associations set in. Memory reappeared. It seems that he had been in concealment in the loft of a barn, when he saw his commanding officer carried by, having lost an arm and a leg. He lost consciousness and fell three meters, through the trapdoor of the loft. There was thus a combination of trauma and emotional shock. No external lesion was produced in the fall. His memory showed a very sharply defined gap for the period of his aprosexia with the bird-like movements, of eight days, and his memory was perfectly good up to the time of the fall. This is one of five cases observed by Chavigny, who remarks that there is something in the attitude of the young child which recalls the aprosexia of these patients. (Perhaps the phrase of James, “buzzing, blooming confusion” might be used.) One must go back to a period in the child’s development when he is not yet able to smile or keep his glance fixed on a shining object. On the whole, the resemblance is closer to the attitude of certain caged birds.

Re aprosexia and bird-like movements, see discussion under Case 353. See also Case 334.

Shell-shock; unconsciousness (45 days): Mutism (monosymptomatic).

Case 447. (Liébault, 1916.)

A soldier, 32, had a large caliber shell burst one meter from him September 26, 1915, lost consciousness and remained comatose 45 days. He then got progressively better but did not recover speech. He was neither blind nor deaf. He was examined at the neurological center at Nantes and there Mirallié called him a case of hysterical mutism, finding no paralytic disorder of any sort and finding the patient able to write his story, to read and to understand what he read, but without much power of retention. He was placed in the phonetic reëducation service March 30, but made no progress. In the effort to speak the patient made strong generalized contractions, including contractions of his face and winking of his eyes, contractions of the jaw, and movements of the neck muscles. In fact, he seemed to be agitated by a sort of cervico-facial tic, and sometimes, although not always, he succeeded in getting out a loud voice sound, in which one could imagine the syllable that he was trying to utter.

In this case the mutism was evidently secondary to motor disorder. It is an example of functional dyskinesia (Benon). As long as this functional dyskinesia remains, the patient will not speak. The respiratory muscles are disordered, since the respiratory capacity does not go over 3 liters. This approaches the normal, however, and if the subject cannot speak it is because his diaphragm is subject to jerky or cramplike movements and because the lips and tongue do not execute the proper movements either for sounds, syllables or words. Such a patient cannot protrude the tongue or even bring it beyond the teeth.

Shell-explosion: Recurrent amnesia.

Case 448. (Mairet and Piéron, April, 1917.)

A shock case of Mairet and Piéron had a disorder of memory. Association paths were open one day and closed the next. Subjected to shell-shock, September 18, 1915, he was found wandering in the woods a few days later, having completely lost his memory, even for his name. In November he recovered his surname but not his given name. On stimulation he was gotten to remember his city, his father, the street, and the like. Shortly he could get back his memories more quickly; after a week it took only 35 seconds to remember that he was born at Paris. However, his recollection of the Trocadero and of the Eiffel Tower, which had come back to him in November, 1915, was lost again in April, 1916, to return once more in August. December, 1915, he could not write to dictation, but copied writing as he would a design. He suddenly felt himself able to write in the Morse code (he was a telegrapher); then ordinary writing returned. February, 1916, however, he had forgotten what the Morse code was. In April, he was taught numbers. One day he would know left from right, but had forgotten it by evening.

Shell-explosion: Comrade killed: Amnesia.

Case 449. (Gaupp, April, 1915.)

F. K., a 23-year old soldier, in civil life a turner, of Polish descent, and of a somewhat nervous and easily excitable disposition, early in August went from Strassburg into the Vosges and Lorraine. On the 26th a number of shells exploded near him. The troop was excited and took refuge in a cellar. K.’s best friend was torn to pieces by a shell. When his body was removed, K. felt sick and lost consciousness. He arrived at the clinic in Tübingen in a stuporous condition, by hospital train, on August 31, 1914. He walked weakly to his bed, supported by two men, and lay in the bed, apathetic and reacting to questions only with a stare. Things put in his mouth were swallowed. He remained motionless.

Next evening he answered a low Yes to a nurse’s question about eating. A little afterwards he said he supposed he was a prisoner in the enemy’s country. A little later he got properly oriented but still did not know how he had come. September 2, however, he was much clearer and said he had awakened out of a long dream. There was a complete amnesia, however, from the moment when he went to help remove the torn body of his friend up to September 1. Memories became clearer for the period before the shell explosion. The patient became very lively, talking vividly of war experiences, imitating shell hissing with an expression of intense anxiety, getting accustomed to battle scenes, saying that he was now seeing everything again as if real. He remained anxious for some days, complaining of weight on his chest and of feelings of internal restlessness and tension.

Amnesia for the period of August 26 to September 1 remained; all that K. could add to the story of those days was that he had been thrown sidewise for some distance by the air pressure of the shell.

From September 6 onwards, he grew calmer but he was still very labile, given to lively imaginings and emotion. By the middle of September he was well and discharged for garrison duty.

Shell-explosion: Recurrent amnesia.

Case 450. (Mairet and Piéron, July, 1915.)

A man, 33, had suffered shell-shock early in December, 1914. His intervening history is not reported, but he showed on admission to the service of Mairet and Piéron, May 5, 1915, a remarkable amnesia. There was a complete cutaneous anesthesia, anosmia, and ageusia, and he was mute. He lived only in the specious present. His previous life was completely abolished for him. He could dress himself, eat, use a fork and spoon, and a glass. He understood ordinary words; such words as man, woman, day and night, however had no meaning. He was observed for 15 months and presented four phases.

In phase one, there was a measure of success in reëducation, such that he grew able to recognize a few persons, to find his bed, and name objects. He was got to copy writing, to learn the alphabet, and to say a few words. He could not write from dictation, however. Less than two seconds after looking at an A, he had forgotten how it looked and could not trace it. This first phase lasted about two months.

The second phase began with fatigue, headaches, and the rather quick effacement of all he had relearned. If an errand was given him to do, he would run to do it before he should forget it; but if the trip required more than 4 or 5 seconds, he had to stop, not knowing what to do with the thing in his hands. He was still able to recognize 4 or 5 persons, but could add no more to his repertoire; and when one of them had been absent for a fortnight, he did not recognize him on his return. He could not remember the time for his meals.

The third phase was ushered in by improvement after vomiting; his speech came back in a feeble voice, November 16, 11 months after the shock. Reëducation could now be undertaken again. He easily relearned a number of things, feeling the greatest astonishment at his new acquirements as to the sun and the moon, the trees and the flowers, and the like. He expressed a curiosity to see his own home, but when he went thither, he could recognize nothing. He wanted to get back home, namely to the hospital where he had lived all his life; where, in fact, he had been born from the psychic point of view.

At this time began the fourth phase, April, 1916—a phase of decline once more, in which a large portion of his acquisitions were again lost and he fell back to his condition in the second phase.

See discussion under Case 353 and under Case 367. Re confusional mental states, Roussy and Lhermitte, after distinguishing stuporous confusion from simple confusion, go on to differentiate what they call obtusion (see also discussion under Case 353). These authors say that Régis, in common with most psychiatrists, fails to distinguish the slow thinking and amnesia of true mental confusion from the temporal and the spatial disorientation that characterize the so-called obtusion. Of course, in all attacks of confusion, both attention and memory are affected, but there are special types in which attention defects and memory defects stand out in relief. The first of these types is the aprosexic type with birdlike movements, described by Chavigny (see for an example, Case 446). This aprosexia may be combined with mutism, deafness, or convulsions. The form of confusional disease in which amnesia is the out-standing feature is due to toxic or infectious disease, or is a Korsakow phenomenon, i.e., in the psychiatry of peace times; but the war has brought out amnestic confusion in other states than the toxic, infectious, and alcoholic states (Régis, Chavigny, Dumas, Roussy and Lhermitte). The amnesia may be incomplete, a sort of dysmnesia, or twilight memory, but as a rule, the amnesia is lacunar. The toxic and infectious amnestic confusions have a loss of memory for events following the onset, but these war cases of amnestic confusion have the loss of memory running back far into the patient’s past, slipping from the mind his name, his parentage, age, and vocation. Instead of being like the toxic confusional amnesia, an anterograde amnesia of fixation, the Shell-shock amnesia is apt to be antero-retrograde. These antero-retrograde amnesias, whether due to emotion or to strong physical shock, may sometimes leave in sharp relief the recollection of the shock or event itself which initiated the amnesia. Meanwhile the patient does not forget automatic actions of dressing, reading, writing, and the like. The amnesia may be very selective, imitating aphasia, word blindness, letter blindness, agraphia, and the like. All this is part of the hallucinatory form of mental confusion which Régis describes as oniric delirium (see for oniric delirium, discussion under Case 333).

Lépine distinguishes amongst the confusions, five forms as follows: Simple confusion, hallucinatory confusion, acute delirium, stuporous confusion (under which Lépine also considers the battle hypnosis of Milian, see Case 365, and Roussy’s narcolepsy), and amnestic confusion. All these phenomena from the clinical point of view are connected with an acute and fleeting insufficiency of the most delicate or, as it were, psychic portions of the cerebral cortex, the delirium, so to speak, being activity of the unconscious, whereas a confusion is due to a clouding of the centre O of Grasset’s polygon.