B. Shell-Shock: Nature and Causes (part 1)

—la buia campagna
tremò sì forte, che dello spavento
la mente di sudore ancor mi bagna

La terra lagrimosa diede vento,
che balenò una luce vermiglia,
la qual mi vinse ciascun sentimento;

E caddi, come l’uom, cui sonno piglia.

—the dusky plain
trembled so violently, that the remembrance
of my terror bathes me still with sweat.

The tearful ground gave out wind
which flashed forth a crimson light
that conquered all my senses;

And I fell, like one who is seized with sleep.

Inferno, Canto III, 130-136.

Bombardment; shell explosion nearby: Mania; death in 24 hours. The AUTOPSY showed superficial punctate hemorrhages of brain and congestion of pia mater. CAUSE OF DEATH—small bulbar hemorrhage, congestion of veins, and nerve-cell changes of a local and differential nature (chromatolysis of vago-accessorius nucleus). SHELL-SHOCK SYMPTOMS due to capillary anemia and chromatolysis of various regions.

Case 197. (Mott, November, 1917.)

A soldier became rather nervous at the Somme, and later underwent intense bombardment for some four hours, February 22, 4 to 8 P.M. Although he said he “could not stand it much longer” he carried on for twelve hours more when perhaps six shells went over, February 23. One of the shells burst about ten feet away, just behind the dugout. The first day of the bombardment he was tremulous and depressed; later coarsely tremulous in the limbs. February 23 there was crying and inability to walk or do any sort of work. Questions were not answered. The pupils were dilated. The evening of February 23 the man was admitted to the field ambulance in acute mania, shouting: “Keep them back! Keep them back!” He was quieted with morphine and chloroform and slept well during the night. There were at least two hypodermic injections of morphine in the ambulance. He woke up the morning of February 24 apparently well, but suddenly died.

The autopsy showed small scratches on the anterior chest wall, but otherwise no sign of external violence. Both lungs were edematous; the left lower lobe showed a considerable hemorrhage. The heart was enlarged and the right side dilated. The liver was somewhat congested. The kidneys were small, but otherwise showed no gross change (urine without sugar or albumin).

Chart 7 Effects of High Explosive Shells

• EMOTIONAL
• COMMOTIONAL
• LESIONAL

After Vincent and others

Chart 8

The scalp showed a slight frontal bruise. The brain was extremely congested. On each side of every superficial vessel there was an ecchymosis. A number of minute punctate hemorrhages was found on the surface of the brain in connection with very small vessels. The brain substance was soft, but not markedly edematous. The cerebrospinal fluid was tinged with blood. On each side of the great sinuses of the skull there was considerable ecchymosis. This examination was made by Capt. A. Stokes, R.A.M.C., in the mobile laboratory. There were no areas of large hemorrhage anywhere in the brain substance and no smaller petechiae, except the superficial ones above noted.

Microscopically Mott confirmed the pial congestion and macroscopic subpial hemorrhages described in the gross. He found besides congestion also actual hemorrhage in the vascular sheaths of the corpus callosum, internal capsule, pons and bulb. Now and then blood corpuscles were found extravasated into the nervous tissue.

The microscopic examination showed a generalized early chromatolysis in the nerve cells of varying intensity, especially affecting the small cells. The Nissl granules of the larger cells were also somewhat abnormal, being smaller and packed rather loosely together.

The small cells of the bulb and pons were slightly swollen and their nuclei large and clear. As to the larger cells of the bulb and pons, there was less evidence of this swelling and nuclear change.

According to Mott, this chromatolysis may perhaps be regarded as a sign of loss of biochemical neuropotential. The chromatolysis indicates a relative degree of exhaustion of the kinetoplasm. Mott assumes that the cells of this victim of shell-shock are in a state of beginning nervous exhaustion. He remarks that the cells of the vago-accessorius nucleus show more signs of this nervous exhaustion than others. With respect to cerebellar findings Mott remarks that the changes found are very similar to those described by Crile in the case of an exhausted and wounded soldier. Mott correlates the mania shown on the evening of February 23 with the venous congestion of the cortex, the small subpial hemorrhages and evidence of scattered arterio-capillary collapse.

Mott suggests that the sudden death of the case may be due to a hemorrhage into a sheath of a fair-sized vessel in the median raphe of the bulb; the general venous congestion; and the almost complete chromatolysis of the vago-accessorius nucleus (adjacent hypoglossal nucleus normal).

According to Mott, also, many Shell-shock symptoms, e.g., headache, giddiness, amnesia (anterograde and retrograde), dizzy feelings, lack of power of attention, and fatigue, stupor, inertia, mental confusion, terrifying dreams, are to be explained on the basis of capillary anemia and chromatolytic changes.

Mine explosion. Ecchymoses; no bone or visceral consequences seen at AUTOPSY (third day after explosion) except SUBDURAL HEMORRHAGE and PUNCTATE HEMORRHAGES OF BRAIN.

Case 198. (Chavigny, January, 1916.)

A sergeant in a Chasseur Battalion was in a mine explosion and entered hospital June 19, 1915, so agitated that he had to be tied to the stretcher during transfer from the railway. There were remains of epistaxis and blood in the right ear, not proved to be due to otorrhagia; blue-black ecchymoses of both eyelids; and small ecchymoses of the bulbar conjunctiva of the right eye. No other sign of trauma or fracture. The explosion had probably taken place on June 17 or 18. Patient was but semiconscious and irresponsive; rolled upon the mattress, beating the air with arms and legs, assuming fighting postures and uttering cries. Urinary incontinence. No fever.

There was doubt as to the diagnosis, which lay between fracture and concussion. The persistent agitation and oniric delirium pointed rather to concussion. Without further sign, however, the patient died on the night of June 20.

The autopsy was extremely careful and showed no sign of cranial fracture of vault or base. The cerebrospinal fluid was strongly bloodstained. The inner surface of the dura mater had a thin sheet of hemorrhage, hardly 1 mm. thick, covering both hemispheres and the cerebellum and spreading over the bulb. There was no distension of the lateral ventricles. Serial sections of the brain showed no lesions of the substance, except for slight hemorrhagic points.

According to Chavigny, so slight a meningeal hemorrhage is incapable of producing a mechanical disturbance of the brain and the cause of death could not be said to be meningeal hemorrhage. Massive multiple gas embolism through sudden decompression is not a suitable explanation of a case with death delayed, as in this instance, even if Arnoux’s explanation is suitable for cases of immediate death.

Mine explosion: no skin, bone, or visceral consequences seen at AUTOPSY (death in seven days) except slight LOCALIZED MENINGEAL HEMORRHAGE.

Case 199. (Roussy and Boisseau, August, 1916.)

A soldier entered Val-de-Grâce February 27, 1915, in a state of confusion following mine explosion the night before. He was delirious, thought himself on leave, and had spells of excitement. Lumbar puncture, February 29, showed a slightly darkened fluid, with approximately normal amount of albumin, one or two lymphocytes and rare red blood cells.

A brief period of slight improvement followed, but the restlessness and delirium increased once more, became particularly severe March 3, and the patient died on the night of the third, seven days after the explosion.

The autopsy showed slightly congested lungs; no other lesion except a sharply defined hemorrhage in the cervical spinal meninges and over the meninges of the temporal and occipital lobes. Microscopic section of the brain failed to show any hemorrhages within the brain substance.

Here is a case of death following explosion without external wound. The meningeal hemorrhages are hardly enough to explain the death. The explanation of the death must probably be made after histological examination.

Concussion of spinal cord from shell burst—WITHOUT spinal fracture, WITHOUT penetration of splinters of shell or bone into canal or cord substance: Microscopic demonstration of intraspinal AREAS OF SOFTENING with classical secondary degenerations. Such a case forms a link in the argument that serious lesions of the nervous system may develop as a result of VIOLENCE directly TRANSMITTED through investing tissues EN BLOC.

Case 200. (Claude and Lhermitte, October, 1915.)

A man, 23, was struck in the left thorax and shoulder, in both thighs and the neck, by fragments from a bursting shell March 27, 1915. One fragment was imbedded near the vertebral column.

Twenty days later there was an absolute, flaccid paraplegia, yet the legs occasionally gave spontaneous, jerky movements. Tactile anesthesia reached the fourth dorsal root-level, except that the perineoscrotal region and the penis were somewhat sensitive. There was anesthesia to pain and heat, as well as in bones and joints, along with the tactile anesthesia. There was a hyperesthetic region on the right side, corresponding with the distribution of the fourth dorsal root. All the cutaneous reflexes up to the abdominals were gone; but defense reflexes could be brought out in foot and leg by skin, bone or joint stimulation. The deep reflexes of the legs were also lost, whereas those of the arms were increased. Retention of urine without incontinence; no retention of feces. Sacral, trochanteric and heel decubitus had developed in the course of the three weeks following injury. A lymphangitis ran all the way up the right thigh from one of the sores, with a corresponding hyperpyrexia.

Surgical intervention was indicated from the evidence of spinal compression at a definite level, but the lymphangitis grew worse. Oniric delirium, and finally a stuporous state, set in, with death May 6, forty days after the wound, a death due to septicemia, without special alteration in the paraplegia itself or in the sensory and reflex situation.

At autopsy the spine and dura mater proved normal; but microscopically serial sections through the fourth and fifth dorsal segments showed softening of the right anterior horn and posterior columns, with cavitation in the radicular zones, and the white matter of the fifth dorsal segment was in a state of acute degeneration. There were also ependymal changes, namely, at the fifth dorsal level a dilatation with deposit of albumin; in the lumbar region, breakage of the ependymal wall, with cellular gliosis. The dilated ependyma was surrounded by an area of fibrillary gliosis which had proliferated in the form of a septum in the interior of the canal. (According to Claude and Lhermitte, these data concerning hydromyelia, which they regard as secondary to trauma, are an argument in favor of the traumatic origin of certain syringomyelias. They regard the breakage of the ependymal wall as due to hypertension of the spinal fluid due to mechanical lesions.) Their interpretation of such acute degeneration as was found in the fifth segment is that this degeneration, as well as that of the posterior roots, is due to the direct impact of the cerebrospinal fluid upon the cord structure. As for the softenings with cavitation, they regard them as surely due to spinal concussion and as very possibly due to an ischemic necrosis, suggesting that older work by Duret and Michel on concussion of the brain indicates the possibility of a temporary ischemia of the spinal cord from the violent impact of the spinal fluid upon the cord due to shock of the spinal column. The transient hypertension of the spinal fluid might well induce, they believe, a vascular spasm with anemia, to which the gray matter is well known to be especially sensitive. In the present case, a period of somewhat less than six weeks had sufficed to produce secondary degenerations above and below the fifth dorsal segment, of a quite classical sort.

Accordingly, we here deal with a severe form of spinal concussion due to a shellburst, in which intraspinal lesions were produced without spinal fracture or penetration either of bone or of shell fragments into the spinal cord or the spinal fluid.

Shell explosion (1 meter distant) kills a soldier by bursting both lungs within the intact thoracic cage.

Case 201. (Sencert, January, 1915.)

A man of the 26th Regiment of Infantry was brought October 26, 1914, to Ambulance No. 6 of the Twentieth Army Corps at the Chateau d’Henu. Weakly and jerkily the man was able to tell how, as he was going forward, a large calibre shell fell less than a meter in front of him and exploded. He fell back and lost consciousness, was picked up in the evening and carried to the relief post and then to the ambulance, where he arrived ten hours after the fall. There were signs of a considerable shakeup, with pale and anxious face, nose pinched, hollow eyes, rapid superficial respiration, small pulse, 120, and a feeble voice. There were small skin wounds of the right arm, a finger, and ear, but there was otherwise no wound. The thorax and abdomen were somewhat painful all over, but there was no especial point of pain. The chest showed a slight dulness at the bases. Examination of the abdomen produced defensive movements and the man vomited blood during examination. He was put on his back, kept warm, given artificial serum, hypodermic injections of camphorated oil and caffeine, and carefully watched. In the night he had another bloody vomiting, his pulse became smaller and smaller, dyspnea became more and more intense, and he died late in the night.

The autopsy showed that the abdomen was free of lesions and that all the organs were of a normal appearance and color. There was no sign of perforation or of peritonitis. The stomach itself was filled with blood and there was a generalized ecchymotic appearance of the mucosa, with small, submucous hematomata and a number of tears in the pyloric portion.

The pleurae were found filled with blood, almost a quart in each cavity. The right lung showed a large tear at the level of the middle lobe, 15 cm. long. An orange-size, black bit of lung protruded through the tear. There was no sign of rib fracture opposite this tear, and no subpleural, intercostal or subcutaneous contusion. The thorax wall was perfectly normal.

The left lung showed, in the middle portion of the upper lobe, a somewhat analogous pleural tear, almost as big as that on the right, with another large hernia of black lung. Bits of the herniated lung sank in water. The thorax wall was intact. The pericardium was free from blood. There was nothing else abnormal about the body.

Re effects of an explosion upon structures with intervening objects left intact, Fauntleroy notes that a shell bursting three yards from an aneroid barometer may force its levers into an abnormal position. A further fact will indicate how permanent is the physical state into which the levers are forced; for when the barometer with its levers placed right was placed under a bell-jar and the pressure therein was reduced to 410 mm., the levers resumed the position into which the explosion of the big shell had thrown them.

Re windage and internal effects in the human body, Ravaut recalls the fact that the internal and intraneural hemorrhages of Caisson disease (“bends”) are well known. The external hemorrhages of aeronauts and mountain climbers belong in the same physical class. Dynamite exploded in a pond kills fish. Dynamite may break pillars inside a building without damaging its front. Cases like Chavigny’s , Roussy and Boisseau’s , Claude and Lhermitte’s , as well as Ravaut’s own case are in point.

Shell explosion near by: Paraplegia, interpreted as due to windage. Two foci of HEMORRHAGE (SPINAL CANAL, BLADDER) clinically proved to exist in a case without external sign of injury.

Case 202. (Ravaut, February, 1915.)

An infantry sergeant was brought to the ambulance, one day in November, 1914, with a paralysis which had set in immediately upon the explosion of a large shell a short distance away. Both legs were paralyzed and there was anesthesia to the navel. He could not urinate. It was early in the war, and Ravaut thought he would find an injury to the vertebral column, but on undressing the soldier there was no wound. The skin was intact, and there was not even an ecchymosis. The patient was suffering not at all, but said that after the shell exploded he felt a forcible shock, was stunned for a moment, and when he wanted to rise, found that his legs were inert. His state did not change during the day and he did not urinate. Catheterization showed a urine full of blood. This indicated a lumbar puncture, and a bloody fluid emerged under great pressure. Thus two foci of hemorrhage were proven to exist in this patient despite the fact that there was no external lesion.

Re windage effects, see suggestions of Ravaut under Case 201. Ravaut also suggests that certain cases of emotional jaundice may be similarly explained on the basis of internal lesion due to windage. Sundry cases of gastro-intestinal disorder and of hemoptysis fall into the same class; possibly the cases of death in a fixed posture belong there, too. Ravaut thinks, despite the look of hysteria about the shell-shock cases of paraplegia, deafness, mutism, and the like, that the cases are actually ones in which there has been at the beginning a slight or severe hemorrhage, clearing up in a few days. He states that there is a pretty definite parallelism between the course of the clinical symptoms and the chemical characteristics of the spinal fluid.

Shell-explosion in confined space; paraplegia after fifteen minutes; slight hemorrhage and LYMPHOCYTOSIS of spinal fluid; Hematomyelia.

Case 203. (Froment, July, 1915.)

A Sergeant lying down in a small dugout space, 2 × 1 m. high, had a 77 shell burst behind his head and between his head and the back of the dugout. The patient was not moved by the explosion, but was buried in a small amount of earth and stones to a depth of about 20 cm. He was not wounded and showed no ecchymoses either then or later. Aided by stretcher bearers, he was able to walk to the relief post about 400 meters from the trench. He did not lose consciousness, and got to the relief post about a quarter of an hour after the shell burst. Thereafter, however, he was unable to move his legs. The accident happened February 6 at 4 o’clock. He was examined 24 hours after the trauma. The accompanying diagrams show the variations in sensory disorder at intervals during six months.

A lumbar puncture, February 8, 1915, showed hypertensive clear fluid without macroscopic clot on centrifuging, but showing a number of red blood cells and lymphocytes—3 or 4 to the microscopic field. There was a slight hyperalbuminosis. The development of the muscular atrophy and hypo-excitability of the left lower extremity, the exaggeration of the left knee-jerk, together with the spinal fluid appearances, seemed to prove the organic nature of the paraplegia. There was an intense rhachialgia, with radiation along the sciatic nerve. This outlasted all other symptoms. Thermo-analgesia was the most prominent sensory disorder. There were no sphincter disorders.

During the first days, the anesthesia was of a pure segmentary type, with nothing about it to suggest that it was later to be supplanted by a radicular type of disorder. Hematomyelia was, years ago, thought—according to Froment—to tend to yield sensory disorders of a segmentary nature. At the outset this anesthesia was total, though there was a vague, poorly localized feeling on intense painful excitations,—as with energetic pricking or burning. Thus the protopathic sensibility of Head had remained, whereas the epicritic sensibility had disappeared.

Detailed examination of this case showed extreme errors in the position sense. For example, pricking the foot might be localized as pinching above the knee. The cremaster reflex was extremely marked and would appear upon even slight excitation of any part of the lower extremity, even at times when the patient declared he felt nothing. These phenomena at the beginning early gave place to a syringomyelic type of anesthesia.

At the time of report, July 29, 1915, Froment regarded this case as analogous to hematomyelias of divers, although there is not such a degree of decompression; the suddenness of the decompression is more marked in these Shell-shock cases than in divers.

Shell explosion; bowled over; loss of consciousness: Hemiplegia with reflex signs thought to be organic; hypertensive spinal fluid; LYMPHOCYTOSIS.

Case 204. (Guillain, August, 1915.)

A corporal in the engineers was going the night of June 7th to a creneau of mitrailleuses, when he was bowled over by a bursting shell. He lost consciousness and was carried to the cantonment by his comrades. Next morning he complained of headache and pain in the back; had a convulsion; and proved on examination to have a left-sided hemiplegia. He was given the diagnosis of hysterical hemiplegia.

He was sent to the 6th Army neurological center, and there showed a complete left-sided hemiplegia with tendency to contracture. The left knee-jerk and arm reflexes were exaggerated, and there was ankle and patella clonus with Babinski sign. There was a dysesthesia on the left side, with wrong interpretation and poor localization of painful stimuli, and non-recognition of cold and heat sensations. Muscle sense and stereognosis were impaired. There was a slight dysarthria. Lumbar puncture yielded a clear hypertensive fluid with a slight lymphocytosis.

The situation remained without change for a month, when the patient was evacuated to the rear. Thus, a shell-burst can produce destructive nerve lesions without evidence of external injury.

Re hypertensive spinal fluid, Sollier and Chartier cite Dejerine as having brought the proof of hypertension in the cerebrospinal fluid in Shell-shock cases. They also believe that the Shell-shock hysteria is built up on a physical basis, more or less after the model of Charcot’s hysterotraumatism. Shock, windage, and gas may bring about the same kind of result. They rely especially on the cases of Sencert and Ravaut for their argument (1915). They recall the fact that Charcot found a hysteria due to lightning stroke and to high tension electric accidents. They quote Lermoyez as attributing like results in ear cases to labyrinthine shock, tympanic rupture, and ear hemorrhages.

Shell-shock: Hemiparesis, amnesia. Lumbar punctures early (but here as late as one month after shock and after disappearance of hemiparesis) showed PLEOCYTOSIS and hyperalbuminosis.

Case 205. (Souques, Megevand and Donnet, October, 1915.)

A French sergeant, a machine gunner, was the victim of shell-burst September 25, 1915, was evacuated with a diagnosis of commotio cerebri, and, when examined at Paul-Brousse October 5, showed a right-sided hemiparesis, clouding of consciousness and somnolence, the hemiparesis involving the face, with deviation of tongue to right, Babinski reflex right, cremasteric and abdominal reflexes abolished on right. Normal respiration and pulse.

Lumbar puncture October 7, that is, thirteen days after the injury, yielded a clear fluid with an excess of albumin, 144 small lymphocytes (some degenerate) and a single endothelial cell.

October 12, the knee-jerk was a little less lively on the right side. The plantar reflex varied between extension and flexion on the right side. The cremasteric reflex had been weakly regained on the right side.

The patient was now less stupid and could tell how he jumped when the shell burst, and how he had been in the air ten minutes (!) and fell, getting up at once, with nothing wrong except nosebleed. After a half-hour he felt weaker and was ordered to leave the post, whereupon, on the road, his weakness increased and he tended to fall to the right, but reached the ambulance on foot.

October 23, there was no longer any evidence of hemiparesis, the Babinski reflex had entirely disappeared; there was no complaint except of dizziness and headaches. He got back his autocritique on the matter of remaining in the air ten minutes, but there was still an amnesia for the ten day period between the shock and his arrival at Paul-Brousse. He forgot that he had had a lumbar puncture October 7.

Another puncture, October 25, yielded some 14 or 15 lymphocytes to the cmm. There was still an excess of albumin. The lymphocytes decreased further according to a puncture November 2. Had this patient been examined some weeks after the shock there would have been no signs of an organic paresis, no special modification of the spinal fluid, and no reason for regarding the man as other than an hysteric. Early spinal puncture is, accordingly, important.

Of course, the question whether the lymphocytes and hyperalbuminosis of the fluid might not be syphilitic must be raised. At the Hospital Medical Society meeting, October 29, 1915, Souques states that Ravaut and Guillain believe that simple shell-shock often produces “syphilitic” chemical, physical or cytological changes in the spinal fluid. Roussy is cited as thinking such changes rare.

Shell-shock; burial: Coma and semicoma; BLOOD-STAINED SPINAL FLUID. Improvement on puncture. Persistent astasia abasia with spasticity.

Case 206. (Leriche, September, 1915.)

A man was buried March 15, 1915, following the bursting of a large calibre shell. He is said to have had hemoptysis and arrived at hospital March 17 in coma. He kept moaning while asleep. March 18, he was still stupid and as if stunned. He did not talk or understand what was said, but was able to write a few words. The knee-jerks were a little exaggerated. There was a slight spasticity of the limbs, which was exaggerated on emotion into a sort of spasmodic crisis.

Lumbar puncture gave a reddish fluid under strong tension. After lumbar puncture the man came out of coma and the next day, after another puncture (fluid slightly yellowish), there was further improvement and the patient spoke. The third puncture, March 20, yielded yellow fluid. The spastic phenomena still persisted, however. The patient could not walk or stand. Every time he touched the ground he had a clonic crisis. He was evacuated to a neurological center.

Re astasia-abasia, Nonne found these cases heading a group of 63 cases of war hysteria treated in a twelvemonth. Figures as follows:

Astasia-abasia 14

Generalized tremor 12

Brachial monoplegia 11

Isolated contracture 6

Crural paraplegia 5

Mutism 5

Isolated tic 4

Hemiplegia 3

Isolated respiratory convulsions 2

Isolated sensory disorder 1

Fifty-one of the 63 cases were freed by therapy from their main symptoms (twenty-eight cases cured in one or two hypnotic sittings).

Prolonged bombardment; shell explosion (nearby?): Depression; suicidal attempt; hypertensive spinal fluid.

Case 207. (Leriche, September, 1915.)

A patient entered an evacuation hospital June 27, having come from an ambulance with a ticket reading, “Melancholic depression, with stupor—attempt at suicide (threw himself into a pond)—sprained ankle—to be evacuated, lying down, on a milk diet.” The patient was depressed, indifferent to surroundings, irresponsive, and did not even look at an interlocutor. There was no other somatic sign except a pulse of 62. He did not eat, and remained lying down, without movement. Lumbar puncture in a sitting posture yielded a clear liquid under pressure of 34. June 30, another lumbar puncture yielded clear fluid of a dichroic appearance when looked at from above. 25 c.c. were removed. July 1, there had been a good deal of improvement. The patient said he was better and began to take a little milk. July 2, there was still some improvement. Pulse 60. He said that his condition had lasted a month and that it followed a violent and prolonged bombardment for ten days in his sector. July 3, he was much better, began to look about, talk, and eat a little. July 4, lumbar puncture yielded a clear fluid with a pressure of 30, reduced to 22 after withdrawal of 20 c.c.

According to Leriche, explosion of large calibre shells or of a mine can produce cerebral or spinal symptoms, some of which are removed by lumbar puncture. The fluid is red shortly after the explosion and under hypertension for some days. Such hypertension may be found even in shell cases that have no other sign of cerebral condition. This particular melancholy patient had a relapse and another depression with fugue.

Example of HEMATOMYELIA, indirect result of bullet wound. Partial recovery.

Case 208. (Mendelssohn, January, 1916.)

An infantry subaltern, 23 years old, was injured September 24, 1914, by a rifle bullet, which entered above the left clavicle and emerged between the right scapula and the vertebral column. The patient leaped into the air when he was struck, but fell at once and found that his legs were paralyzed. A feeling of cold crept up from the feet to the region of the umbilicus. Consciousness was preserved. There was hemoptysis because of the bullet’s passing through the left lung. The wounds all healed quickly. There was retention, followed by incontinence, of urine and feces; and the situation was complicated by eschars in the gluteal and trochanteric region.

For three months there was no change in the paraplegia, except that at the beginning of the third month the patient could move his fingers a little and raise his knees slightly. He was transferred back through three hospital units, with a diagnosis of spinal cord lesion or fracture due to a vertebral column lesion at the second and third dorsal vertebrae.

Seven months after injury, he reached a Russian hospital for a laminectomy, incapable of standing or walking without support, although able to sit and rise with extreme difficulty. He could now very slightly flex and extend the knees, and very slightly flex and rotate the ankle, and weakly move the toes. Passive movements could be carried out without much difficulty, though there was a slight joint and muscle stiffness. Both quadriceps muscles were markedly atrophied. There was slight amyotrophy of the lower legs. Tendon reflexes were exaggerated, and there was a marked ankle clonus, a Babinski reflex, and an abolition of the abdominal and cremasteric reflexes.

There was a sensory disorder of an incomplete syringomyelic pattern, with diminished sensibility to heat and complete abolition of pain sensibility. Touch and electric sensations were somewhat delayed. There was a diminution in the faradic and galvanic excitability of the legs and feet; vasomotor disturbance (slight hyperidrosis) of the paralyzed limbs. Two of the eschars had not yet cicatrized. The sphincteric disturbances had diminished. For the rest the patient was normal. The second and third vertebrae showed deformity and were painful to pressure and percussion of spinous processes.

The patient was treated by galvanization of the spine, with a current descending at first and then ascending, and by faradization of the paralyzed muscles. There was progressive improvement, irregular but constant. At the time of report, July 1, 1915, he was perfectly well, able to take long walks, and without sphincter or sensory disturbance. The tendon reflexes were still exaggerated, and there was still a slight ankle clonus and Babinski. The abdominal and cremasteric reflexes were still abolished. The last of the seven eschars had not yet healed over.

For the organic nature of this lesion, the numerous early eschars, the persistent sphincter disturbances, the limited paresis of the legs, the reflex disorders, and the dissociation of sensations seem abundant evidence. It is probable that there was no fracture of the vertebrae (X-ray confirmation), and it is probable that there was a meningeal hemorrhage, together with some hemorrhagic foci in the spinal cord substance, especially in the gray matter. A good deal remains doubtful: Mendelssohn remarks that the sphincter disturbances ought to be related to disorder of the fourth and fifth sacral segments, and the knee-jerk and Achilles jerk absence with disorder of the lower lumbar, and sacral region; the abdominal reflex disorder with the low thoracic lesion; the distribution of the anesthesia ought to indicate a lesion in the lower part of the spinal cord. Was not the hemorrhage therefore lower down than the spot where the vertebrae were displaced? It is surely of prognostic note that the eschars did not necessarily foretell a fatal outcome; in fact, the patient had become functionally well before the seventh eschar was healed over.

Shell explosion with subject lying down applied to machine-gun; no contusion: HEMATOMYELIA. Partial recovery.

Case 209. (Babinski, June, 1915.)

A veterinary student, six months captive in Germany, wrote out for Babinski the following:

“September 1, 1914, I was about to operate a machine gun when a shrapnel shell exploded very near me,—probably about two or three metres overhead. I base this estimate on comparisons made with shells I saw exploded beside me before this one.

“Just after the explosion, which deafened me and at the same time took my breath away a little, from the powder, I felt a rather severe pain in the kidney region,—a pain which then persisted without interruption. I moved my left arm, to find the effect produced by a bullet which I heard whistle by my ear and which struck the upper part of the left shoulder without entering. At the same time, I tried to turn to see what had become of my legs, and had a feeling that they had vanished. Almost immediately I felt little prickings, not very painful, in the lumbar region and in the upper part of the thighs. Just then, seeing my comrades going away I tried to imitate them, but could not. All these feelings passed very rapidly.

“A comrade then came near to tell me to go back. I told him that I could not move and that I must have been wounded in the lumbar region. He looked at my kit and my coat and said there was no trace of shot or tear. Not wanting to leave me, he lifted me by the armpits and knees. I could not help him get me up, and my legs hung flexed and inert. After a few steps he had to put me down, and tried to stand me up. I immediately crumpled. I had no sensation of my feet touching the ground. I sent my comrade back, asking him to tell my brother, who was in my squad. I did not lose consciousness or any feeling of my situation, or of the danger being run by my comrade.”

The man remained four days on the battle field without food. He was on the edge of a stream. He did not defecate, nor for two days did he urinate. Eventually the bladder and rectal functions were re-established, though they remained irregular. Catheterization was never resorted to. The lumbar pains were diffuse, fixing themselves a few days after the accident in the region below the umbilicus. There were pains at the waist predominating on the left side. The paralysis of the lower extremities grew rapidly better. Movements in the right leg reappeared, and 27 days after the accident the man was able to stand and walk around his bed. Still further movement followed (left leg weaker).

At the time of the report, May 28, 1915, the patient could walk without a cane, but he could get about only slowly. The left toes would rub against the ground, and he could not support himself for any length of time on his legs. The knee-jerks were exaggerated, especially the left. The Achilles jerks were increased. There was a Babinski reflex on the left side and an abduction of the fifth toe on plantar stimulation. The same reflexes were found on the right side, but less marked. Abdominal reflexes absent, except the right superior reflex, which was distinctly present. Cremasteric reflexes absent. Anal reflexes preserved. The defense reflexes were exaggerated, but more markedly on the left side. The zone from which the defense reflexes could be elicited on the left side included the whole lower extremity and rose as far as 2 or 3 cm. above the nipple. Stimulation of the lateral parts of the left lower extremity would even produce defense reflex movements on both sides of the body. On the right side, however, the defense reflex movements could only be tried out by scratching the anterior surface of the ankle, which was then followed by a flexion of the foot.

Sensibility to touch and deep sensibility were preserved; but sensibility to temperature and pain, normal on the left,—i.e., paralyzed—side, was weak in the right leg. There was a marked sudation on the left side, limited by the white line, the inguinal fold, the iliac spines, and a horizontal line passing through the umbilicus.

Here, then, paralysis followed a shell explosion while the subject was lying down. No contusion therefore was possible. According to Babinski, we are dealing probably with a hematomyelia, the result of shell explosion.

Struck by missile in back; unconsciousness; no wound: Hysterical paraplegia? HERPES and SEGMENTARY Hyperalgesia suggest radicular and spinal injury. Recovery.

Case 210. (Elliot, December, 1914.)

November 1, 1914, a sergeant in the 20th Hussars, with other dismounted cavalrymen, was chasing Germans with a bayonet, over turnip fields pitted by shells. Several hours later, he found himself in a house in a nearby village, to which he had been carried unconscious. Probably he had been struck by some missile in the back, as the bottom of his haversack had been torn off. His face was blackened with smoke, and his clothes were muddy. He had no wound. His left arm was weak and his legs powerless and numb. The passing of water was painful, but there was no blood in the water and no hemoptysis.

Five days later, he was examined at a base hospital and found to be paralyzed and numb in the legs. The knee-jerk and ankle-jerk were retained upon the right side only. Pain occurred on passive movements of the legs, which were flaccid; there was a hyperalgesia about Poupart’s ligament, more marked on the left side. Lower abdominal reflexes were weak on the left side; pain in lower abdomen with bladder full and at outset of micturition. Pain and paresis also affected the left arm, but there was no numbness. Pain on pressure over lumbar and cervical vertebral spines. There was no evidence of bruising.

The physicians were inclined to regard the phenomena as hysterical. Three days later, the arm movements became much freer, and after another three days, the arm movements were fairly powerful, and the legs much stronger, although the patient could not yet stand or walk. He still had pain if his bladder was full.

Chart 9 Causes of Shell-Shock

• HEAD INJURY
• ATMOSPHERIC CONCUSSION
• MENTAL STRAIN
• NON-NERVOUS TRAUMA
• NEUROPATHIC HEREDITY

After Ballard

As against the diagnosis of hysteria, three herpetic clusters appeared on the skin of the left thigh, from three to six inches above the knee. Elliot regards it as certain that the posterior root ganglia were injured. He regards the case as one of injury to the spinal nerve roots. The hyperalgesia about the body of course suggested damage to the spinal cord. According to Elliot, therefore, this case is one of organic disease; whether of the roots or of the cord was uncertain. At any rate the cases of this type, though not functional, recovered.

Mine-explosion; burial; labyrinthine lesions and head bruises, more marked on left side: Focal canities (WHITE HAIR developing OVERNIGHT) on left side.

Case 211. (Lebar, June, 1915.)

A soldier, 23, in the Argonne was blown up by a mine in a trench, fell, and was covered by a mass of earth, from which he extricated himself. He immediately became deaf from what was medically determined to be a double hemorrhagic labyrinthitis. There were also superficial powder burns of the face, as well as several bruises on the head, especially on the left side.

The next day, at the English hospital at Arc-en-Barrois, the patient noticed tufts of white hair on the left side of the head. There were four islets of gray hair in the left fronto-parieto-occipital region, separated from one another by normal hairs. The gray hairs were gray completely from the roots to the ends of the hair. The longest hairs were as white as the shortest. There was not a brown hair amongst them. The gray hairs were solidly implanted, and could be pulled out only by strong traction. There was a discoloration also of the bulbar swelling of the hair. The rest of the head hair was dark brown. His hair was described in the military description: “deep chestnut brown.” There was no other symptom aside from an incessant twitching of the left eyelids. The place of whitening was apparently determined by the region of the scalp injured. Not only were the bruises on the left side of the head and face, but the labyrinthine lesions were more marked on this side and the twitching of the eye-lids was confined to the left side.

Shrapnel wound of skull; focal canities over wound; shell-shock and shrapnel wound of right leg. Head tremors and contractions, changing in relation to posture; glove anesthesia and local anesthesia of trunk.

Case 212. (Arinstein, September, 1915.)

A Russian private, 24, was wounded twice: once in the head by a bullet, and at another time by a bit of shrapnel that imbedded itself in the skull. The hair over the injured spot became gray.

Later, September 16, 1915, the soldier was subjected to shell-shock, and at the same time wounded by shrapnel fragment in the right leg (operated next day).

Upon examination at Petrograd, the hearing was found diminished and the eardrum was pulled in. At first the patient could not speak or open his eyes, and made incessant lateral movements of the head, jerking backwards and to the right. The right half of the face gave convulsive movements, which began at the lip and spread upwards. During sleep, there was an entire cessation of these head shakings and jerks. In the lying posture, the head shook at a rate of 100 to 120 per minute. The jerking movements became more marked when the patient sat up or walked. He carried his head bent toward the right shoulder. When he sat down, the side-shaking movements disappeared, only to reappear when he lay down. The swallowing reflexes were absent. The sensitiveness to touch, pain, and temperature was lost in the upper part of the trunk including the neck, to the level of the tenth dorsal vertebra. There was anesthesia of the arms as far as the elbow on the right, and as far as the shoulder on the left. The mucosae of the mouth were anesthetic. Dermatographia was strongly marked.

Shell explosion; burial: Hemiplegia, probably organic.

Case 213. (Marie and Levy, January, 1917.)

A soldier was blown up by a shell and then buried at Vaux, March 29, 1916, and entered the Salpêtrière, July, 1916, with a right-sided hemiplegia and contracture without evidence of wound. He remembered nothing for the first fortnight after the trauma. When he came to himself, he was paralyzed and was unable to say more than a few words, but at the end of a month his aphasia ceased and he began to walk.

The hemiplegia was spastic. There was pronounced contracture. The arm was extended, hand open, fingers stretched. Finger movements were diminished, as well as extension of the wrist, but the arm was otherwise normal. The leg was not so stiff. The great toe was in a state of continuous extension. The toes could not be moved, and the foot scarcely; but the leg could be strongly flexed and extended on the thigh. The tendon reflexes of the right side were more lively than on the left. Cloniform movements followed tapping the patellar tendon on the right side, and a patellar clonus and ankle clonus could also be demonstrated. Plantar reflex, flexor on the right. Distinct adduction of the foot. Slight disturbance of tactile sensibility in the paralyzed limbs; marked disorder of position sense and gross disturbance of stereognostic sense. Moderate dysarthria.

Ten months after the traumatism, the hemiplegia and spastic walk remained. The upper limb was now carried in extension back of the body, with hand supinated, fingers sometimes in extension, sometimes in flexion, index finger separately from the others. Finger movements difficult and shoulder movements limited. The leg, however, was almost normal except that the toes could not be moved. The tendon reflexes were more lively and cloniform on the right, but there was no longer patellar or ankle clonus. Stereognosis slow, but finger movements were naturally difficult. W. R. of blood, negative. Probably this is an organic case.

Blown up by a shell; no skin or bone lesion: Mixture of organic (e.g., lost knee-jerks) and functional (e.g., urinary retention) disorders.

Case 214. (Claude and Lhermitte, October, 1915.)

A man, 38, was blown up in a trench without sustaining skin or skeletal lesions, April 5, 1915. He lost consciousness for a half hour and, coming to, found a crural paraplegia and urinary retention. Examined July 24, in addition to the paraplegia were found tactile and algesic hypesthesia of the legs with preservation of deep sensibility. Pains were felt in the legs, especially in the hips. The knee-jerks were abolished; the Achilles jerks were preserved, as well as the flexor plantar reflexes and somewhat weakened cremasteric and abdominal reflexes. Micturition was difficult. Constipation. Slight paresis of left arm. Lumbar puncture, July 28, yielded a clear fluid of normal tension without chemical or cytological changes.

The sphincter disorders gradually disappeared. The knee-jerks reappeared in a weakened form August 31. The legs could, at the time of report, be moved somewhat, though not above the level of the bed.

We here deal, presumably, with a mild form of concussion of the spinal cord, in which, however, some of the transient symptoms are very possibly merely functional in origin.

Re complicated pictures of organic and functional nature, some experimental work has been carried out. Mairet and Durante set off explosives, such as melinite, at a distance of 1 to 1.5 metres, near rabbits. Some died at intervals from an hour to thirteen days; others lived. Pulmonary apoplexy was found in the cases dying early. Spinal cord and root hemorrhages, hemorrhages in the cortical and bulbar gray, perivascular and ependymal hemorrhages were found, always small and without diffusion, suggesting rupture by rapid decompression following the first wave of aerial compression. The functional effects are thought to be brought about through the anemia of the areas supplied by the ruptured vessels. Russca of Berne got similar results and notes direct and contrecoup brain lesions, tympanic perforations, intra- and extra-ocular hemorrhages, thoracic, cardiac, and splenic hemorrhages, ruptures of kidney, stomach, intestine, and diaphragm. As in the work of Mairet and Durante, the lung proved the most sensitive organ. (Compare also the human case of Sencert [Case 201].) Some experiments with fishes yielded lesions of the swimming bladder. Persalite and other explosives were used.

GASSING: Organic-looking picture.

Case 215. (Neiding, May, 1917.)

A German soldier, 21, was a serious case of gassing. He was unconscious two days (venesection twice). When he came to, he could not walk and felt as if he were drunk. October 22, 1916, he was incoördinate in walking and tended to fall forward when standing with eyes closed. The ataxia of the legs was demonstrable in the position of dorsal decubitus, and there was also a slight ataxia of the arms. The pupils were dilated and reacted poorly to light.

December 12, all symptoms had disappeared. The clinical picture in this case was somewhat like that of a multiple sclerosis. According to Neiding, the disorder is not a functional one but an organic cerebellar disorder.

Re the neurology of gas poisoning, Neiding regards the condition as a new nosological unit. We do not know what the ultimate results of apparently cured cases will be. Court questions of importance will doubtless arise with reference to their compensation. Ninety-six of Neiding’s 274 cases failed to show any nerve symptoms whatever; forty-six cases showed one symptom only, such as headache, dizziness, abnormality of reflexes, or abnormality in sensation. One hundred and thirty-two cases presented a fairly full picture. The picture of a complete traumatic neurosis not infrequently appears, aided perhaps by the psychic features of the gas attacks; and possibly some cases are entirely psychogenic from the beginning. Such symptoms, for example, as dermatographia, rapid and irregular heart, hyperidrosis, blepharospasm, mental perturbation, hypochondria, etc., do not necessarily point to any directly toxic effect of the gases. Thirty-seven of Neiding’s cases showed pupillary changes, hyperreflexia, and analgesia. Thirty-one showed analgesia and absence of laryngeal and corneal reflexes. Twenty-six showed pupillary changes and hyperreflexia, four of these latter showing also an absence of laryngeal and corneal reflexes. One case yielded hyperalgesia alone; ten yielded headache, dizziness, and analgesia.

GASSING: Mutism, tremors, depression, battle dreams.

Case 216. (Wiltshire, June, 1916.)

An infantryman, aged 27, had been at the front for three months. He was wounded a month before coming to hospital; but when the wound healed he went back to the front, quite mute but intelligent and able to write the following:

“We were on our way to the trenches, and as we were going through the railway cutting they started to shell us, with gas shells mostly, and we had not been there more than quarter of an hour when I was compelled to lie down from temporary blindness and weakness through getting a dose of gas through my mouth and eyes. I was lying down for about ten minutes when a shell came somewhere near, and was struck by something in the face and on my left knee and I remembered no more until I found myself in hospital. I was all of a shake and while lying down would frequently jump up and wonder where I was.”

The patient had been mute thereafter, depressed, and given to dreams about fighting and shells. There was a fine tremor controllable by the will; the knee-jerks were increased. On lateral deviation, there was difficulty in fixing the eyes. There was a slight deafness due to an old discharging left ear. According to Wiltshire, Shell-shock is only exceptionally caused by chemical poisoning from gas.

Re poisoning by certain German asphyxiating gases, Sereysky reports in 1917 that these gases contained, among other poisons, a nerve poison. He found that poor heredity was a favorable soil for the action of this nerve poison. The clinical pictures in the gassed soldiers rather suggested cerebral arteriosclerosis. He remarks that the logical distance between the “exogenous” and “endogenous” is greatly reduced in these gassed cases, as the syndrome of “exogenous” gassing closely approximates that of various “endogenous” disorders.

Hysterical speech disorder related to mechanical disorder of auditory apparatus.

Case 217. (Binswanger, July, 1915.)

Whenever a German officer’s servant, 23 years, was addressed on the ward in the Jena Nerve Hospital, his hands would tremble and the muscles of his face would fall into grimacing associated movements. He had a peculiar infantile type of speech, talking with a fixed glance and an anxious mien. He would carefully utter, as a rule, separate words, chiefly only nouns or infinitives. He would gesticulate with both hands to make what he said understood. Thus (freely translating the German) runs his description of a battle:

“Well—because—I—we had—no artillery and so many losses—then got in position again, then we—laid down a long time—perhaps until four o’clock in the afternoon—five—and—and it happened that—lay in Rübenfeld—couldn’t go back—then shell near me—fell in and I right near, how—how far—I don’t know and—grown better. Comrade said—10 meters—don’t know—un—unconscious.”

Long compound German words could not be repeated, since after the first or second syllable there was a severe emotional excitement; syllable articulation and phonation ceased. Finally, however, the patient could be gotten to pronounce the whole word. Reading aloud was very difficult: syllable sounding and omission of difficult syllables; after a time, weeping.

The patient was a somewhat small, muscular, well-nourished man, with a murmur at the apex, a somewhat rapid pulse, increased reflexes, especially skin reflexes, painful supra- and infra-orbital points, temples painful to percussion, pressure over spine painful from second thoracic to third lumbar vertebrae. There was an increased sensitiveness to touch and pain over the whole body. There was a bilateral, somewhat marked tremor, more marked on the left side than on the right. Swaying in Romberg position was slight. Tremor of tongue.

This patient was first brought to Jena November 23, 1914. An illegitimate child, a moderately good scholar, he had worked as a mason until he went into the army, in 1912. He worked as a soldier chiefly in the officers’ casino because he got pains in his legs and knees in long drills. At the outset of the campaign, however, he withstood the heavy marching, although with difficulty. He was in his first actual skirmish September 20. A shell struck nearby and threw him several meters; whereupon he became unconscious and was carried away by the hospital corps. When he woke up he could not speak or hear. Ten days later, however, speech returned, and hearing returned in right ear; October, deaf in the left ear, and he could not hear a watch tick on the right side at a distance of 16 centimeters. He was examined at the otological clinic in Jena October 12, where the drum membranes were both found opaque, without reflexes or normal contours; hysterical attack on the caloric test. The next day, on the medical visit, there was a screaming attack. His plight seemed not so much simulation as one of traumatic hysteria.

Again, after his stay at the nerve hospital, another hysterical outburst was produced by a hearing test with vestibular apparatus, in the ear clinic, February 6, 1915. The diagnosis was nervous deafness with involvement of left ear.

The insomnia was successfully treated by sodium bicarbonate. There was a slight improvement in speech. In March body weight had improved, but there was a marked tremor of the right hand. In the next few months there was a progressive improvement in general well-being, in speech disorder, and in tremor. The auditory disorder remained unchanged. The man now works in his father’s garden.

This case appears to show a combination of psychic and mechanical injury. There are severe hysterical auditory and speech disorders. Although the auditory disorder is of mechanical origin, the speech disorder appears to be of psychogenic nature. It is somewhat remarkable that the ear tests almost every time produce hysterical attacks in the form of convulsive crying. Rather unusual is the general cutaneous hyperalgesia, more marked about the ears.

Shell-shock (distant, neither seen nor heard); left tympanum ruptured; semicoma eight days: Cerebellar syndrome and hemianesthesia. Recovery, nine months.

Case 218. (Pitres and Marchand, November, 1916.)

A lieutenant underwent “shell-shock” either at night or in the early morning, September, 1915, the shell bursting at a distance. He neither saw nor heard the shell, lost consciousness and was eight days semicomatose, failing to recognize his wife.

On recovering his senses, he could not get about, as he had lost his memory, having to write down his room number and be warned of meal times. He was led about like a child. He had a continuous headache on the right side and pains in the occiput and along the spinal column, as well as in the right leg as far as the heel. These leg pains were lightning pains. Walking was difficult, staggering, leaning to left. Weakness of right arm and leg; right-sided hemianalgesia. Complete insomnia. During November there were frequent urgent desires to urinate day or night. Evacuated to the oto-rhino-laryngological center in Bordeaux, December 13, for examination of ears. The right ear was found normal, but there was a rupture of the left tympanum. There was at this time a trismus. The jaws were opened with the dilator and the man had a syncope during this operation. The question of surgical intervention for a cerebral lesion was raised, but he was first sent to the neurologists at Bordeaux. There, December 31, he was found with a facies of anguish, unstable gait, inclination to the left in walking; no Rombergism; occasional dizzy spells. In walking, the right foot was pointed outward and on request to direct it forward he complained of pain in the loins, reaching as far as the scapula. Walking with eyes closed, he leaned to the left and lost balance. With eyes open, no disorder of balance. With eyes closed, the body leaned backward. If requested to go back, he failed to flex his legs to keep balance. If he was asked to put a foot upon the chair in front of him, he immediately fell backwards. He could not support his body on the right leg more than a few moments. He had difficulty in raising both legs from the bed at one time and he could lift the right leg not so high as the left. Movements of the legs were performed hesitatingly and slowly and with greater difficulty with eyes closed.

He could not thread a needle and could hardly dress himself. Eyes closed, he could with difficulty perform the finger to nose test; eyes open, with much less difficulty. Adiadochokinesis; muscular strength less in right than left; plantar reflexes absent; knee-jerks lively; hemianalgesia, right side. Loss of deep and bony sensibility on right side and diminution of testicular sensibility. Retraction of visual field, right; diminution of smell and loss of hearing, right; position sense absent on this side; stereognostic sense preserved. Mentally, memory was poor; he was unable to read or do mental work. He slept little and had bad battle dreams. He was very impressionable and emotional and constantly complained of occipital pain. He had lost 8 kilos weight.

He grew gradually better. In May he could go out alone. The muscular strength increased. The adiadochokinesis and synergic disturbances lessened; the hemianesthesia persisted. In June there was greater improvement; in fact, there was no sign of disorder left except irregular sleep.

We here deal with a cerebellar syndrome plus a hemianesthesia.

Mine explosion: Tremors, mutism, hemiplegia. Tremors cleared by hypnosis. Mutism replaced by stuttering. Persistent hemiplegia, probably organic.

Case 219. (Smyly, April, 1917.)

A soldier was blown up by a mine and rendered unconscious. Upon recovery of consciousness, the patient was dumb, unable to work, very nervous, paralyzed as to left arm and leg. The paralysis improved so that in the hospital at home the patient became able to get about. However, he threw his legs about in an unusual fashion. Several months later the patient was much improved.

Shortly, there was a relapse. Transferred to a hospital for chronic cases, the patient was unable to walk without assistance on account of complete paralysis of the leg. There was insomnia, a general tremor, bad stuttering, and a habit of starting in terror at the slightest noise.

Hypnotic treatment was followed by almost complete disappearance of the tremor. The patient began to sleep six or seven hours a night; nervousness diminished, and the stuttering slowly improved; but neither the paralysis nor the anesthesia of the left leg was affected by suggestion. The leg remained cold, livid, anesthetic, and flaccidly paralyzed to the hip. A slight improvement has followed upon faradization but the patient still can walk only with assistance.

Smyly regards this case as probably not a true case of Shell-shock, depending as he states “more on a lesion in the nervous system than in the psyche.”

Shrapnel bullet WOUND of skull: Unconsciousness (three weeks), followed by agraphia (three weeks), insomnia (six weeks), amnesia (six to eight weeks), hemiplegia (twelve weeks), impairment of vision (twelve to sixteen weeks), dreams (seven months). Recovery save for slight overfatiguability.

Case 220. (Binswanger, October, 1917.)

A French tailor, aged 22, of healthy stock, was wounded in the left frontal bone in August, 1914. The shrapnel bullet, from an unknown distance, made a penetrative wound. The man was able to remember how at the moment he was injured he felt a sort of strain in his brain, felt his head with his hand, found he was bleeding, took out a bandage from his kit, removed it from its cover and without unfolding it put it on his head. At this moment he fell unconscious and there was then complete loss of memory for three weeks. This patient, who was intellectually keen, distinguished exactly between what he could himself remember and what he was told by his comrades. One of these had told him that he had cried out indistinctly that in a matter of fifteen days he would be well. He estimated the interval between his wound and the loss of consciousness as about five minutes.

After three weeks, the tailor came to and remembers that the first word he heard was Munich. Astonished to be in Bavaria he asked for paper and pen to write to his people, but found he could not write, though still able to dictate a little to his comrades. Besides agraphia there was hemiplegia on the right side, marked exhaustion, rapid fatiguability of vision, power of concentration but slightly diminished, and apathy for his surroundings; emotions normal.

Three weeks later the power to write returned; after six weeks, sleep; memory was restored in from six to eight weeks; the paralysis disappeared in twelve weeks; vision became normal in three or four months; the dreams ceased after seven months. The mood for the first two months after regaining consciousness was slightly elevated; for another two months slightly depressed. The mood then became normal. There was, then, in this case complete recovery save for slight overfatiguability in a period of seven months. There were still a few residuals of hemiplegia. An operation in November, 1916, removed a shrapnel ball, one centimeter in diameter, from a dural scar.

This is a case of acute reaction psychosis of exogenous origin lasting three weeks and leading to complete recovery in an after phase of from four to seven months.

Normal subject, wounded and thrown to ground by shell explosion: Recurring MEMORIES of battle scene; persistently HYPERESTHETIC healed shell WOUND, with pupil and pulse changes on pressure of the scar.

Case 221. (Bennati, October, 1916.)

A lieutenant of artillery, student (one of his brothers dead of meningitis), suffered somewhat from diarrhœa on the battlefield. He was, however, always able to obtain the best of food. External conditions did not seriously interfere with sleep. In particular there was no excessive dampness where he was. He was preoccupied with having to act as substitute for the commandant of the battery. He was not afflicted by the thought of his parents far away; their financial affairs were entirely satisfactory.

This almost normal man was wounded after a day of incessant fighting five months after going to the front. When firing ceased, he withdrew with his soldiers to a trench. Here he was followed by an enemy gas shell which killed some and wounded others. While outside the trench shifting mutilated soldiers to the rear, he was hit by another shell of which a chip wounded him in the left thigh. He felt a terrible spanking blow that threw him to the ground and gave him great pain. He was carried on a stretcher to the medical post across the zone of fire; thence to a field hospital and from there to a hospital further from the front. He had been for almost seven hours in a sector of the fighting line which had been almost continuously active.

The wound healed in less than a week. But what he had seen and felt kept tormenting his mind. There remained slight numbness in the wound where there was to be seen a spot of pigment, the size of a two-cent coin, with somewhat obscure outlines. The pain was irritated by damp weather, in certain positions, and by touch, and the pain on pressure was reflected in the pupils and in the pulse.

No other disturbance, organic or functional, was found.

Wounds; operation: Hysterical FACIAL SPASM.

Case 222. (Batten, January, 1917.)

A 23-year old soldier was admitted to the National Hospital for the Paralyzed and Epileptic, June 18, 1915, in the following state: He sat in bed, gasping, with the left side of the face set in a strong tonic spasm and jaws tightly set. The contraction of the masseters was such that his mouth could not be forcibly opened. He himself could separate his teeth for about a half a centimeter, but the jaws came together when a spatula was brought for insertion and then failed to relax. The facial spasm increased as the jaw was clenched more tightly. The patient said he was unable to breathe excepting when sitting upright, and when put into dorsal decubitus he breathed violently through his clenched teeth and held his breath as long as he could, “assuming a purple tinge,” as Dr. Batten states, “which was apt to be disconcerting until one was accustomed to it.” Faradism and force permitted the removal of false teeth but only to the accompaniment of shrieks, foaming, and violent movements of the arms, lacrimation, and sweating. During sleep, the face was at rest. The spasm of left face and of jaw would come on a few seconds after waking, when an observer was perceived. Attempts to force the mouth open invoked the same procedure as before in spite of the fact that the patient ate well. In a month he was virtually normal.

It appears that May 13, about five weeks before, the patient had been struck by shrapnel on the right hand, forearm, and shoulder, and base of the nose, while in France. He had been dazed but had not lost consciousness, and the wounds had completely healed before arrival at hospital. It was about a week after being wounded that the patient was operated upon for removal of shrapnel from the face. Upon recovery from the anesthetic, the patient found himself unable to move the right side of the face. Unable to remove his teeth, he had been fed by rubber tube.

Shell-shock: Hyperesthesia and over-reaction.

Case 223. (Myers, March, 1916.)

A stretcher-bearer, 19, who had had 18 months’ service and 6 months’ service in France, sent to Lieut-Col. Myers the day after admission to a base hospital, showed a remarkable condition of hyperesthesia and over-reaction.

It appears that four days before, he had been blown up three times by aero torpedo mortar shells while attending the wounded. One had blown him into the air, another had blown him into a dug-out, and a third had knocked him down. Two or three hours later, having finished the job of carrying wounded to the dressing station, everything seemed to “go black” in the dug-out where he was resting, and from that time on he had been shaky. It seemed that he had hardly slept for several days before he finally gave in.

There were irregular spasmodic movements of the head, arms (especially the right), and legs (especially the left). There were coarse tremors and incoördination in moving the arms. With eyes closed, he touched his nose with uncertainty. Cotton-wool touch on arms or head provoked lively movements. “I was always ticklish,” he explained, “but never like this; I can’t stand it, Sir.” Pinpricks produced almost convulsions. There was perspiration, rigidity of legs, and spasm such that knee-jerks were unobtainable. Plantar reaction, flexor. There were also visual hallucinations of bursting shells, and these were also heard when dozing.

Improvement followed with rest, but about two weeks later, on waking to find himself being carried back to his tent to avoid a shower, he was so terrified that a special nurse became necessary. He was still jumpy the next day, alarmed at footsteps, and afflicted with headache. He improved further in three days; remained two months in hospital in England, had one month’s leave, and then returned to light duty.

Shell-shock; thrown against wall; comrades killed; no visible trauma, or loss of consciousness: Persistent TREMORS, augmented in intentional movements; CRISES of agitation following noise or emotion.

Case 224. (Meige, February, 1916.)

A corporal (an expert gunner) and his squad had just entered a mine shaft on Nouvron Plateau, January 13, 1915, when a shell, bursting above them, threw him violently against the wall and killed or wounded several of his comrades. The corporal himself was not wounded, nor is it clear that consciousness was lost. The man lay waiting on the ground for some time until a communication trench could be finished and he could be evacuated without much danger from the mine shaft. He had already begun to tremble, and trembled still more while going back in the trench.

He carried on there for a fortnight, always trembling, but not eating and no longer able to handle a gun. He was evacuated a month later and sent successively to Villers-Cotterets, to Meaux, to Courneuve (a month), again to Meaux, and finally to the neurological center at Villers-Cotterets, where he remained for two months (April 13 to June 15, 1915). Here he was given the diagnosis of hysterical chorea by Guillain, and showed lively knee-jerks and Achilles jerks and great emotionality. The tremors were greatly increased when the cannon grew loud or bombs burst nearby. Lumbar puncture here showed a perfectly normal spinal fluid. He was then sent to the Salpêtrière, June 19, 1915, and was evacuated July 13 to a civil hospital until September 24, whence he was sent for convalescence to his home village, October 6 to December 15, from which he was returned to the Salpêtrière.

Throughout these transfers there had been no change whatever in his status. For almost a year, as the result of a shell explosion, he had been trembling in precisely the same way. All four extremities trembled equally, unless the right arm and the left leg might be thought to tremble a bit more. The tremor was equally pronounced in dorsal decubitus as in the sitting or upright postures, but ceased during sleep. The tremors were worse in the evening and it was hard for the man to get to sleep. The eyelids and tongue showed a few irregular, jerking movements, not synchronous with the tremor of the extremities. The head showed few tremors. The patient was able to diminish the trembling of the arms somewhat by keeping the elbows flexed at a right angle and held firmly to his body. If the tremor of the legs got more energetic, the patient would get up and take a few steps. Any movement, such as laying hold of an object, carrying a spoon or a glass to the mouth, led to an exaggeration of the tremors in such wise that the tremor of multiple sclerosis in its most extreme form was recalled. It was very hard for the man to eat. If the eyes were closed, the tremors grew more marked. The emotion caused by sudden noise or sharp command or memory of his trench life caused motor crises, with coarse, generalized movements, and even loss of balance. This agitation grew gradually less marked, but the tremors persisted. An attempt to test reflexes led to violent generalized contractions. There was no sensory disorder. The pulse was variable; at rest it stood at 60; if a table near by was struck suddenly, the pulse would go up to 120.

Sharp gunfire: TREMORS; TREMOPHOBIA. A patient’s (an artist) description of his feelings.

Case 225. (Meige, February, 1916.)

One of Meige’s victims of shell-shock tremors was an artist. He stood the hardest sort of trench life for many months without disorder. Under particularly sharp fire, “the machine went off the track,” as the artist said, and he began to tremble. Both arms and head trembled, but especially the head, which was subject to small sidewise oscillations, variable in degree, and almost permanent,—a sort of vibration which the patient could diminish somewhat by stiffening his neck muscles. His manual tremor was not exaggerated by voluntary movements. Superficially he resembled a Parkinsonian case. He presented a curious appearance of combined vibrations and stiffness.

There was no doubt that this tremor had an emotional origin. In fact, the psychopathic status of the patient was described by the artist himself. “My nervous state, which I thought ought to last not more than a fortnight, still persists more than three, or almost four, months after being evacuated, although the trembling is a little less. I am calmer and palpitate less, and my hands perspire less when I am emotional or making an effort. At first, the slightest shock immediately ran through me, followed by an uncontrollable trembling. Now there is an appreciable delay between the shock and the trembling; I can control it for a few seconds but not longer. The subway gate noises, a flaring light, a locomotive whistle, the barking of a dog, or some boyish prank is enough to set off the trembling; going to the theater, listening to music, reading a poem, or being present at a religious ceremony, acts the same way. Recently when a flag was being raised at the Invalides, I thought at first that I was going to be cured by so moving a spectacle, but then I suddenly began to tremble so violently that I had to cry out, and I had to sit down, weeping like a child. Sometimes the trembling comes on suddenly without any cause. I went to a novelty shop to do some errands with my wife. The crowd, the lights, the rustling of the silk, the colors of the goods—everything was a delight to me to look upon,—a contrast to our trench misery. I was happy and chatted merrily, like a schoolboy on a vacation. All of a sudden I felt that my strength was leaving me. I stopped talking; I felt a bad sensation in my back; I felt my cheeks hollowing in. I began to stare, and the trembling came on again, together with a great feeling of discomfort. If I can lean against something, sit down, or better, lie down, the trembling gets better and pretty soon stops. There are three conditions in which I feel well: first, upon waking after 11 or 12 hours’ sleep; next, after a meal, especially if it is a good one; and lastly, and above all, when I get the electric douche. Then, as if by magic, my ideas get clear, cheerful, and regain color; I feel myself again. That lasts for an hour or so; then I relapse into my sad state.”

As to the tremophobia, this patient says “In the tramway or in the subway, I perceive that people are looking at me, and that gives me a terrible feeling. I feel that I am inspiring pity. Some excellent woman offers me her seat. I am deeply touched; but if they look at me and say nothing, what are they thinking of me? This anxiety makes me suffer a good deal. If I am able to speak it is less painful to me, for then it is obvious that, despite my trembling, I am not a coward. What a sad situation this is!”

Meige remarks that therapeutics is not especially successful in these cases of tremor. Sedative drugs, hyoscyamin, hyoscin, duboisin, and scopolamin, do not last long and should be used cautiously. Static electricity works well in some cases. Rest, isolation, and calm.

As for the military prognosis, a period of observation of some three to four months may be necessary to learn the nature of the tremor. If the tremor then fails to alter, a convalescent leave for one or two months may be given. The patient should then be re-observed by the same physician. Upon persistence of tremor, temporary invaliding. Tremors may be wittingly cultivated for medicolegal purposes (Brissaud’s sinistrosis.)

Letters of a German soldier about his shell-shock.

Case 226. (Gaupp, April, 1915.)

A volunteer, 21, who had been in civil life a lackey, wrote as follows upon arrival in Gaupp’s clinic:

“On account of our privations and the various terrible scenes that you have to see, my nerves went back on me. Like the rest of the front, we too had to suffer terribly heavy artillery fire from December 20 onwards. December 29 at eight o’clock in the evening, when I was about to mount guard at the camp, I was thrown down by a shell that unexpectedly struck near me across the earth pushed out into a trench. I ran at once to cover as some more shots followed directly. I couldn’t be made to do anything on the thirtieth nor can I very clearly remember the events of that day. There was a terrific cannonade again, then cries of the wounded and the sight of the dead, etc. I was told afterwards that I fell down, cried, struck about me, and remained lying, dazed. The first that I can remember was that I was lying on a floor. I was then carried into another house, into a better room. Then I regained consciousness and could hear again after the noise in the ears had stopped, but I could not talk or walk. I was unconscious for two days. I got into the hospital train at R. the next day but had to be carried in as I could not walk. Travelling in the train made me quite foolish in my head and gave me bad headaches; I could not form any clear thoughts.”

It seems that this volunteer had not been quite up to the hardships of the war from the beginning; always a weakling, he had to be spared on the marches. In fact, he had been refused by the army at the first examination as unfit. He had been a nervous, tender, somewhat anxious fellow since childhood.

At the clinic there was an astasia and an abasia without any signs of organic disease. The striking feature was mutism. He could understand things spoken and written, but he was entirely mute, nodding and shaking his head properly for affirmatives and negatives. He carried with him a few slips of paper with written requests, like: “Please, can I have salt; otherwise I can’t eat the soup;” “Are we going to ride farther, I have such a bad headache. The doctor must not come. The one who wanted to shoot me if I couldn’t speak. They are all bad.”

Treatment by suggestion (laryngeal faradization, lively verbal suggestion to pronounce single vowels, syllables, and whole words and sentences with enunciation of them) removed the mutism in a few days. At first the man’s speech was low and somewhat retarded, but later it became entirely normal. Within ten days the abasia cleared up and the patient became lively and cheerful. He was depressed on finding that he had lice, but after losing them became happy and childlike again.

February 1, however, on learning that he would be able to do garrison duty again, he took the news very soberly, and grew more quiet, trembled and seemed anxious.

February 7, he was sent to the garrison, increasingly excited. His own account of it in a letter written to a hospital nurse, runs as follows:

“As you will see, I did not reach Dn. but only got as far as here [Another hospital]. I will tell you how it happened. Probably I ought to have remained in Tübingen for a while longer and perhaps then nothing would have happened to me. You will remember that I was more nervous and excited the last days than I had been before, and the cause was also known to you. I wanted to get home in some way and so I pretended to be as well as possible. That crying attack, or whatever it was [an outcry in a frightful dream] had not been thought of by the physician any further, you know, and so I didn’t think anything about it either. Then the head doctor asked me once if I had any trouble left. Well, I spoke out everything I had to say, but no further attention was paid to that either. Then when I took a walk and after walking slowly two hours could hardly stand, was trembling all over and had a high pulse and also a violent acute pain in the region of the heart, that wasn’t of any importance either. Well, then I just got better from day to day and so I got what I wanted only too easily because they wanted the space and I certainly would have gone home and not to Dn. as I should have. [His reserve battalion was at Dn.] I got into the wrong train at St. so as to go home. I kept saying to myself, ‘You can’t do that, it will be punished.’ Nevertheless I couldn’t act any other way because I was really sick from longing for home.”

Here he described an episode in a comrade who had lain beside him in the clinic, had gone off with him and had a hysterical excitement in Heidelberg so that he had to be detrained.

“I was so awfully sorry to see him so miserable. I began to cry and was startled by every train coming from the opposite direction and by every loud noise. I was stared at by everybody in Frankfort and I could only cry more. Then a soldier scolded me because I was running senselessly up and down. Finally I got into the Leipzig train. Another guard questioned me. Everything then got more and more confused in me; I heard my mother call; then I heard shooting again; and finally I was entirely confused. I came to my senses in a room in the station toward evening, and was frightened again at a loud noise somewhere or a passing train. Then I was told what I had done in the train. I had cried out and raved, tried to get out of the car, called for my father and mother, wanted to go home, imitated shooting; allowed myself to be calmed a little, but began to shout again at every loud noise. When I was out of the train I bit a soldier and tore his whole coat open, so then I was carried to the hospital here in an auto. Up to this time I have been able to calm myself very well. The physician said that it was quite natural that I should not have very strong nerves yet. I must have beaten about and got knocked against things a good deal. There are bruises on my head and I am covered with black-and-blue spots.”

A British soldier’s account of his shell-shock.

Case 227. (Batten, January, 1916.)

A British soldier, 22 years, who went out to France in November, 1914, remained well until March 12, 1915, when after shell explosion, he became unconscious for half an hour, and on recovery found he was deaf and dumb. He was able to think of words but could not say them. He remained dazed and frightened for a time, and still wakes up with a start at night.

He was admitted to the National Hospital for the Paralyzed and Epileptic, March 25, 1915, and on March 27 recovered his speech suddenly and spontaneously. By March 29 he had completely recovered and talked well. Dr. Batten remarks “how perfect the memory may be up to the time of concussion, and how complete the mechanism is for expressing the ideas in written words when that for spoken words is abolished”; which may be seen from the patient’s own account, as follows:

I went out to France on the 3/11/14 and I was two days at Le Havre and then we went on to our 1st Batt. When we arrived at our destination the regiment was in the trenches so we had to go in. It was snowing hard and I felt it very cold. This was at Givenchy. We were relieved the following night and we went back for a rest. The next place we went to was just opposite Neuve Chapelle on the La Bassée Road and it was awful, the trenches were up to the knees in mud and water. The first night was very quiet, but the following morning about 9 p.m. the Germans started shelling and continued all day; the next was the same, but about 1 o’clock the Germans were seen to be coming up in masses. They got to within a distance of about twenty-five yards, then they turned. They commenced shelling us again and they had another try about three o’clock but they did not get far. One of the men on my left had the half of his face blown away and we had about ninety-two killed and wounded. We got relieved after being in five days, then we went back for three days’ rest. The next place we went to was Rue de l’Epinette and we had an awful time there just before Christmas. We went into the trenches and we were up to our middle in water and in some places it would have taken you over the head. We were in these trenches for twenty-four hours. There was nothing unusual happened and we got relieved by the Royal North Lancs.; but we did not get far away; we had just got into our billets and were making some tea when the fall-in went and we were told that the Germans had broken through the North Lancs. We went away without any great-coats, and into the trenches we went for other seventy-two hours, and if the Germans had attacked again we could not have fired a shot as we were hardly able to stand for the cold and with the wet kilts on our legs it was awful. We got nothing to eat except three biscuits that some of the men went out and got. When we came out of the trenches on Christmas Eve we looked all like old men and a lot of them had to be carried. We went back for a rest to (Nervaille?) about thirty kilometers from the firing line for a month. When we came back again we went to La Bassée and had a pretty hot time there. The next place we were at was at that big fight at Neuve Chapelle when 472 guns bombarded the German trench for thirty-five minutes. At about 7 p.m. the word was passed along that we were to charge the German trench in front supported by the City of London Territorials. We got the trench all right and I got orders about 4 p.m. to go back to our own trench and bring along the belt-filling machine belonging to the machine gun. There was not a proper communication trench, there was a small dry ditch that ran out in the direction of the trench we had taken for a distance of 150 yards, the other 100 yards you had to come across the open. We got into our trench all right, and I got this box on my back and started back to the trench. I was just stepping out of the trench when a shell burst just over my head and I went down. When I came to my senses I was lying in our support trench where I had been carried by two of the men of the 4th Black Watch. One of them said something but I could not hear him and I tried to tell him so, then I discovered that I could not speak.

Shell-shock by windage: Hysterical crural monoplegia, of gradual development beginning four days after accident. Recovery by suggestion.

Case 228. (Léri, February, 1915.)

A number of chasseurs were doing the “tortoise-shell” under bombardment, when the last chasseur in the line was blown forward above his comrades by a shell bursting about a meter behind him. He was projected some four or five meters, got up, walked four or five kilometers, found an automobile, and was carried to Nancy. He passed, according to his story, red urine three or four times. He was six days at Nancy, where a slight abrasion of the side was treated. He began to feel heavy in his left leg on the fourth day. At Vendôme, the paralysis got worse, and by November 17 he had apparently a complete paralysis of the left lower extremity, called “spinal contusion.” He walked upon two canes, dragging left leg behind and had to be carried upstairs on a stretcher. The reflexes were normal except that there might have been a very slight excess of the left knee-jerk. There was a slight hypesthesia of the left leg, sharply limited above.

These phenomena were strikingly modified, at a single sitting, by verbal suggestion and faradism, but the man was one of those with mauvaise volonté. He did not want to get well so quickly, so that his complete cure was delayed a while.

NATURE OF SHELL-SHOCK: At the nerve clinic the patient presents, e.g., sundry CONTRACTURES, of such a nature that they may be caused to DISAPPEAR BY SUGGESTION, e.g., by mental influences during recovery from chloroform narcosis (note battle-dreams). PAINS and ANESTHESIAS disappear PARI PASSU with the contractures. The history is of shell explosion so near as to burn patient’s clothing, fall with nosebleed, eight hours unconsciousness, crural monoplegia with anesthesia (crawled 3 meters, however).

Case 229. (Binswanger, July, 1915.)

The treatment of a German private, 22, for contracture of the left leg and other phenomena, culminated in narcosis. Binswanger lays stress upon the mental influence to be exerted upon the patient at the conclusion of narcosis, at the moment in which the patient is particularly accessible to verbal suggestion. Treatment (see diagnostic details below) was carried out as follows:

After a few days of essentially suggestive treatment with continued attempts at passive movements of the contracted joints (knee, ankle, toe), with steady concentration of the patient’s attention upon the joints, a slight mobility in the toe joint on passive movement was obtained.

After a few more days, the ankle became passively mobile to some degree; the patient exerted a certain resistance to passive flexion of toes and ankle. A week later, reflex contractions of the toes could be evoked by deep pin-prick. There had been an analgesia of both lower thighs and of the soles of the feet, and this analgesia remained unchanged. At this point, the subjective complaints of the patient, namely, noises in the head, especially in the left ear, and other cephalic sensations, tended to disappear and the patient felt subjectively better; yet there was still an intolerable itching of the head and spine.

A month after the admission of the patient to the nerve hospital of the psychiatric clinic in Jena, there had been no essential change in the immobility and contracture in extension in the left leg. Accordingly, with the permission of the patient, he was placed in deep chloroform narcosis, and the knee-joint was bent at a right angle and fixed in approximately that position with a bandage. This experiment failed because, while the patient was waking out of his narcosis, the leg slipped back into extension, breaking the bandage. Accordingly, deeper narcosis was undertaken, and the leg fixed at a right angle in a plaster cast.

While the patient was coming out of narcosis, it was evident that he had been dreaming of battle scenes. In fact, Binswanger remarks that these dream pictures and the words spoken while going under and coming out of narcosis, are curiously demonstrative of “sympathy with the enemy,” for while waking out of narcosis, he cried: “Dost see, dost see the enemy there? Has he a father and mother? Has he a wife? I’ll not kill him.” At the same time, he cried hard and continually made trigger-movements with his right forefinger. In point of fact, throughout his waking treatment, no one was able to learn what was going on in his mind, his sleep was good and deep, and his emotional state was entirely quiet and patient.

As the patient was coming out of chloroform and regaining consciousness of his surroundings, he was repeatedly and persistently assured that the bending of his leg was now accomplished and the cramp removed. All that he would now have to do was to get back the strength of his leg.

During the next few days he complained of violent pains in his left knee-joint and in the ankle-joint, but he remained in good spirits and full of confidence. Accordingly, in five days the plaster was removed and the contracture in the knee-joint was found to be completely absent; the knee was easily movable. The ankle-joint was but slightly movable. He could accomplish slight active flexion of the knee-joint while lying in bed, and the toe-joint had already, before the narcosis, been both actively and passively mobile. After a few days, exercises in walking were begun. The patient had a little difficulty with his left knee-joint in walking, walking in fact as if with knock-knee. The foot was not well raised from the ground on account of the persistent stiffness of the ankle-joint. Walking, however, improved daily. He walked for three hours, resting at intervals.

A sensory examination showed that the upper limit of the analgesia had come down five centimeters from its former level, now occupying the left foot and leg up to the junction of the lower with the middle third. There was now a zone of anesthesia interposed between the normal skin of the upper thigh and the anesthetic-and-analgesic skin of the lower thigh and leg. Upon the posterior aspect of the leg, the analgesia and anesthesia had disappeared to a point at about the middle of the upper thigh.

About five weeks after the narcotic experiment, the extended left leg could be actively raised while lying in bed, up to the full extent, with slight tremors. The patient described himself as fatigued by the active movements of this leg. The ankle-joint remained less effective. There was still a trace of resistance to passive movements. Although the passive movements of the toes were normal, active movements of these were weak and hard to execute. There was still a trace of difficulty at the knee in walking and the gait was awkward, trepidant, precipitate. He could get about without a cane, however. If unobserved, his posture was more certain and free. If he exerted himself hard, severe parietal headache on the right side would develop.

It was then proposed to the patient that another narcosis would rid him of the stiffness in his ankle-joint. He feared narcosis and was told that regular and energetic voluntary movements would also rid him of the stiffness. These will exercises consisted in his directing his whole attention to his left ankle-joint until he felt it. Then he was given the command: “Let go the joint”—whereupon he would take his attention away from the ankle-joint at once. In this way, he was told, his will would make the ankle-joint mobile. Meantime he was given twice daily a gram of bromophenacetine for his parietal headache.

The result was a rapid recovery. There were still a few traces of difficulty at date of report. The zone of sensory loss had retreated to the ankle, with a cuff-like zone of hypalgesia above the definite zone of analgesia and anesthesia.

As to the previous nature of this case, although there was neuropathic heredity on the mother’s side, there had been no sign of any individual neuropathic disposition. He had been a volunteer since 1911 in a guard regiment of infantry. His military training had been well borne; in the war he had fought through 20 battles. On November 11, 1914, in a storming attack, he had had his breeches burned from the effects of a shell. He had fallen, unconscious; the unconsciousness lasted about eight hours. He found on awaking that he had had nosebleed. When he wanted to get up, he found that his left leg was completely paralyzed and insensible; in fact, he thought it had been cut away. He crawled for about three meters to a trench in which there were several wounded. In the evening he was taken by automobile to a field hospital, and on the 17th was removed to a reserve hospital at Erfurt. Thence he was transferred to the Jena Hospital, January 25, 1915.

A strongly built man, with many reflexes increased and a lively dermatographia. The reflexes of the left, or contractured, leg were lacking; the mastoid processes were painful, and the occiput and temples were painful to percussion. The spinous processes of the vertebral column in the lumbar region were painful. The other phenomena have been sufficiently indicated above. The head sensations were peculiar; there were no pains but a peculiar itching. Contraction of the fingers of the left hand was painful. There was a feeling as if there were lice under the skin in the left upper thigh. There was itching in the nose, which the patient described as due to the sulphur “out there,” meaning shell gases. Sleep and appetite were good. Memory was imperfect: he could no longer remember the names of the battles, and of late had had to count on his fingers to find out how much was 2 times 2. As to the curious parietal headache, contralateral to the contractured leg, Binswanger inquires whether we may not here have to do with localized vascular phenomena of the brain part which might conceivably be related with the innervation of the leg. Binswanger remarks that if the plaster cast be left on too long, it may happen that hysterical contracture will take place in the new position.

As to the will exercises used in the present case, Binswanger remarks that the patients must be intelligent and attentive, and naturally they must desire to get well. Fortunately, many of the war hysterics do want to get well, since the contrary experience is had in various industrial cases.

Wound of thigh: Pseudocoxalgic monoplegia with anesthesia. Cure of anesthesia by faradism at one sitting. Cure of lameness by reëducation and electricity in one month.

Case 230. (Roussy and Lhermitte, 1917.)

An infantryman, observed at Villejuif, February 9, 1915, was suffering from a right-sided crural monoplegia of a pseudocoxalgic type, following a wound September 9, 1914. The wound had been a through-and-through one in the upper right thigh. Every active movement could be performed as well on the right side as on the left; but the strength of the movements was less on the right, especially that of leg-extension. The reflexes were normal, the lameness was slight, with toeing out; the sole came down flat upon the ground. There was an absolutely complete anesthesia of the entire right leg and side up to the umbilicus.

Energetic faradization of the skin caused the anesthesia to disappear the day the patient was brought to the hospital. The cure of the lameness required a month of reëducation and electricity.

According to Roussy and Lhermitte, crural monoplegia is less frequent than brachial monoplegia. The flaccid form is rare, and when it occurs, complete, though the patient always remains capable of executing some voluntary movements and can walk with crutches or cane. During the automatic movements of walking, some muscles may be observed to contract that remain immobile when the patient is being examined recumbent. Naturally such a difference in contractions standing and lying, would be very exceptional in a case of organic monoplegia.

Contusion of thigh: HYSTERICAL right crural MONOPLEGIA. An ORGANIC CRUTCH PARALYSIS develops in the right arm, unobserved by the patient whose main concern is his useless leg. Cure of leg by psychotherapy.

Case 231. (Babinski, 1917.)

A certain lieutenant, following contusion of the right thigh, developed a crural monoplegia of hysterical nature. In fact, although the paralysis had lasted several months, the tendon reflexes, the skin reflexes, and the electrical responses of the muscles, were absolutely normal. Moreover, the good effects of psychotherapy confirmed the hypothesis. But besides the hysterical crural monoplegia, there was a radial paralysis on the right side, clearly organic in nature, due to the nerve compression by the crutch which the patient had employed on account of the paralysis of his leg.

Babinski notes that this association of conditions was remarkable in that it demonstrated that hysteria and simulation should not be confounded with one another. To be sure, it is difficult to tell simulation from suggested phenomena, for there are no objective characters that demarcate the two. Babinski had himself said that hysteria was a demi-simulation; but a demi-simulation is not a simulation. The patient was in fact, sincere enough in his belief that he could not move his leg. To obviate this paralysis, he had in fact leaned so conscientiously upon his crutch that an organic paralysis had resulted. In fact the radial palsy had only been discovered incidentally, and the paradox appeared that a purely imaginary trouble occupied in the patient’s mind for a long time a much more important place than the genuine organic trouble which accompanied it.

Bombardment; war strain; gassing?; collapse; arthritis: Hysterical MONOPLEGIA and ANESTHESIA of leg, interpreted as a “PROTECTIVE” reaction. Later, monoplegia and anesthesia of arm.

Case 232. (MacCurdy, July, 1917.)

A corporal described as normal (“except for some shyness with the opposite sex”) adapted himself well to training and went to France in May, 1915, where he was at once thrown into 18 days of almost continuous bombardment. After some initial fright, he settled down to work well enough, but, when the weather got bad in September, 1915, grew tired of the situation. Bad dreams began (falling into a deep hole; being shelled). He thought of suicide, wanted a shell to incapacitate or kill him, began to have pains in the head, arms and legs, and was already groggy when a gas attack came. Whether he got a whiff of the gas or not, he at any rate felt giddy, got a swallow of water, and when the gas passed got out of his dugout in the open air. He was fatigued and much relieved when the company was ordered back. Now, however, he got shaky and fell in a collapse on a pile of straw, without, however, losing consciousness.

Apparently he had an attack of acute articular rheumatism. There was a sore throat and a pain in the head, radiating to left shoulder and to finger tips, with pain also in legs. The pain was worse in the right leg on moving the knee-joint. These pains lasted for a month in hospital. The leg had been like a log since the collapse on the pile of straw. Even after the pains left him a month later, the right leg was paralyzed and anesthetic. He walked with a crutch and developed a crutch palsy. After a month a hysterical paralysis of the right arm, with superficial anesthesia, supervened. During a period of eight months thereafter improvement was steady under reëducative measures.

According to MacCurdy’s analysis, the acute arthritis led to paralysis as a protective reaction. The paralyses are disabilities that would ensure absence from the front.

Lance-thrust in back, rapidly healed. Paralysis of right leg, disappearing with rest and exercises. Later, psychotic symptoms, with recovery.

Case 233. (Binswanger, July, 1915.)

N. H., 21, a laborer, industrious and sober (mother healthy, father insane and a suicide; patient somewhat sickly in childhood after pneumonia, a good scholar) volunteered at the outbreak of the war. Early in November he was on the Eastern front. November 17 to 22 he was in a number of small reconnoitring skirmishes almost daily, as a cavalryman. On the 22d, there was a clash with a Cossack patrol of far superior numbers. Eight German horsemen cut their way through, riding about 4 kilometers back to their squadron.

While dismounting, N. H. discovered that his back was wet. It occurred to him at once that he had been wounded. However, he successfully dismounted and then collapsed, feeling as if his right leg had fallen asleep. His companions found a wound in his back, which had come from a lance-thrust. The wound was bandaged. He was transported to Germany on a peasant’s wagon, the trip occupying six days, and on December 6 he came to the surgical clinic in Jena. The wound was insignificant and healed quickly.

The leg remained motionless, and on December 10 the patient was referred to the nerve hospital. He was a small, slenderly-built man, with poor nutrition, weighing 108 pounds. The scar, about 1 cm. long, alongside the thoracic vertebra, was still somewhat red and but slightly sensitive to pressure. Neurologically, the knee-jerks and Achilles jerks were greater on the right than on the left, and there was on the right side a distinct patella and ankle clonus. There was no Babinski reaction on either side.

The movements of the right leg were not of wide excursion, and flexion and extension of the knee and ankle-joints, while lying on the back, were slowly and hesitatingly performed, with an expression of pain, and with visible effort by the quadriceps muscles. Flexion and extension of the toes were likewise difficult, and when the toes were stretched there was a distinct contraction of the tibialis anticus. Electrically the muscles were normal. On passive motion, there was slight spastic tension in the musculature of the right leg, and the patient said he felt marked pain. In walking, the right leg was moved with a limp and with the evident design of sparing it. The knee was imperfectly bent and the sole of the foot was dragged along the ground. There were short out-throwing movements of the lower leg.

Pain sense was normal, or possibly slightly in excess. There were painful points on pressure on the lower part of the os sacrum and coccyx and over the right sciatic and tibial nerves. Intelligence examination showed school knowledge to be extremely poor and calculation ability poor. Critical judgment and reasoning power were deficient. Memory and perception were without marked disturbance. The patient was dull and without interest in his surroundings. He complained that his right leg was as if dead and that he felt great pain in any attempt to move it. He also complained of pains at night in the region of the right shoulder and neck. His nerves, he said, had been very weak since his trip back from the front, during which trip he had been very cold and poorly cared for.

Treatment consisted of rest in bed, application of moist packs to the right leg, active and passive exercises of the right leg. After ten days he made his first independent attempts to walk, and active movements of the right leg in dorsal decubitus became unrestricted and painless. He remained somewhat unsteady in station, showing bilateral twitchings and movements of the right leg muscles. In walking the right leg was dragged behind in a spastic-paretic fashion. Appetite improved; spasms decreased; but at the end of December foot clonus was still persistent.

Upon January 10 there was an odd mental change. He became seclusive and suspicious. January 15 he expressed ideas of poisoning; his sister, he said, wanted to poison him, and others were watching him suspiciously; his room-mates were talking about him; in fact, he thought one comrade was an Englishman. Sleep was poor. At the end of January, after a short period of improvement, he again had ideas of being poisoned, and had dream-like, unclear thoughts. His actions became incoherent: he would undress suddenly in the daytime and go to bed, getting up five minutes later and dressing. Senseless postcards were written.

This condition lasted a few days only, whereupon the mental and bodily condition greatly improved. Daily walks were then taken in the garden and in the city without exertion. The ankle-clonus on the right side was now decidedly weaker but did not entirely disappear. The muscle power on the right side was somewhat less than on the left.

The patient was very homesick, and on March 14 was sent home.

Shell-shock—six days later, crural monoplegia, cured by suggestion. “Metatraumatic” hysteria. HYPERSENSITIVE PHASE AFTER SHELL-SHOCK.

Case 234. (Schuster, January, 1916.)

On August 13, 1915, a soldier was knocked unconscious by the explosion of a shell nearby. He woke up several hours later with headache, noises in the ears, itching, but no trace of paralysis.

Six days later, on August 19, he was released from hospital, still free from paralysis. On the railway journey he met some people of his district by whom he sent greetings to his wife, meanwhile becoming greatly excited. When he tried to get out of the train he noted a weakness of the left arm and left leg; this weakness somewhat quickly grew into a severe paralysis, so that when observed in Berlin the left leg was entirely paralyzed, not a single muscle of which could be moved when the patient was examined by Schuster one month after the accident. There was also a hypesthesia on the left side with total anesthesia of the left leg, which anesthesia was related stocking-wise to the hypesthesia of the trunk. There was tremor of the hands as well as generalized increase of reflexes. The plantar reflex, though weak, was flexor. The pulse rapidly ran up under excitement. In short, the patient seemed to be suffering from hysterical palsy. Waking suggestion did so well with the man that after three weeks normal sensibility was restored to the leg, and he could walk tolerably well without a cane.

The point of interest in this case is that the symptom of greatest importance, namely paralysis of the left leg, did not arise until six days after the shell explosion and then only after the man became excited by thoughts of his home and family through meeting his town people. The term metatraumatic is suggested by Schuster for cases of this sort. The emotions and stresses of war may be regarded as labilizing and sensibilizing the nervous system sometimes for months.

Wound of left foot: ACROCONTRACTURE. Psychoelectric cure, about seven months later, at one sitting, except for some residuals that cleared shortly afterwards.

Case 235. (Roussy and Lhermitte, 1917.)

A soldier, 21 years, was observed at the Centre Neuropsychiatrique, August 30, 1916. He had been wounded in battle, March 16, 1916, near the left internal malleolus. Infection followed and inguinal adenitis, for which he was in hospital a month.

Even before the abscess began, the foot had begun to twist inward. After the abscess had been cured, a contracture set in permanently, and at entrance to hospital was irreducible. The knee-jerk and Achilles jerk were more active on the side of the equinovarus contracture. There was even a slight amyotrophy of the calf. There was no appreciable vasomotor disorder. The foot and lower part of the leg were a little warmer on the left side.

Cure followed a single sitting with psychoelectric treatment, at least so far as the contracture went. Pain and swelling remained in the evening, followed by fatigue. The patient was discharged cured, October 12, 1916.

Hysterical pes equinovarus shows the foot immobile as if frozen (figé). The foot is extended with the toes lowered and the internal border incurved, as if revolved about the axis of the leg. The surface of the sole is directed inwards and much furrowed. The tendon of the tibialis anticus is very prominent. The internal malleolus is hardly visible, while the head of the astragalus is easily made out. No passive movement is possible and the tibiotarsal and mediotarsal joints are quite out of function. Upon palpation, the excessive contracture of the anterior muscles of the leg is striking. Upon request to move the foot, the foot is not moved, but muscles of the lower leg may contract, and even those of the thigh.

There were no sensory disorders in the present case, though they often do occur in this form of acrocontracture. It is doubtful whether the skin changes sometimes seen, such as hypothermia, hyperidrosis, cyanosis, and glossiness are due to circulatory disorder induced by the contracture or to the prolonged immobility. It has been proved by Meige, Benisty and Lévy, that even in a normal subject prolonged immobility may cause a difference of temperature of several degrees. Circulatory disorders sometimes cease immediately upon cessation of the contracture. Roussy and Lhermitte insist upon energetic and early treatment of these psychoneuropathic acrocontractures, which are apt to proceed less favorably than the acroparalyses. If not treated energetically and early, actual nerve, tendon, and bone lesions may ensue.

Shell-shock; shell-wound; emotion: Hysterical paraplegia. Approximate recovery.

Case 236. (Abrahams, July, 1915.)

A private of the First East Lancs could remember a shell’s bursting and striking a wagon near him when he was carrying food to the firing-line. He also thought a spare wagon wheel might have fallen on him. A period of unconsciousness of four or five days duration elapsed, on recovery from which he found himself suffering from a shell-wound in the left buttock, complete paralysis of both legs, and pain in the back, by the fourth lumbar vertebra. He thought that he had suffered from sphincteric paralysis for eleven days after the accident; but by September 25, there was no sign of this. Besides the paraplegia, there was complete loss of sensation below Poupart’s ligament in the right leg, reaching as high as the iliac crest behind; and an anesthesia of the left foot including heel and sole, with anesthesia to light touch throughout the limb (pin-pricks being appreciated in a normal way as far as the ankle); and there was an anesthesia to touch and pain in the ulnar distribution.

April 20, 1915, the patient was found to be a robust, somewhat microencephalic slowly cerebrating subject. Total flaccid paralysis of legs; right knee-jerk slightly exaggerated; no plantar response of any sort was obtainable. Right leg entirely anesthetic; left leg and both arms showed a diminution of sensibility; suggestion of glove and stocking anesthesia; trophic changes absent. The scar of the healed bullet-wound lay over the trunk of the left sciatic nerve.

It seems that the man’s companion had both his legs blown off at the time the shell burst. It is questionable whether the paraplegic patient actually saw the legs blown off, or merely heard about the accident. Another psychic feature lay in the fact that the patient had a paralyzed sister—a possible financial burden.

April 30, nitrous acid anesthesia. During the temporary rigidity, the legs were found to stiffen slightly; the legs were flexed. Upon the return of consciousness, the patient was told that the legs had moved during anesthesia, and was asked to place them in a more convenient position. The thighs moved slightly, and throughout the day movements were encouraged against resistance.

The next day he was gradually raised to the vertical position and supported upright. But at this stage he had become mentally resistant and resentful. During the day the upright position was at intervals resumed, and the patient was made to walk between two attendants. The next day he walked alone and his mental resistance had broken down. There was no longer any evidence of exhaustion and effort in the movements, and the patient began to take pleasure in his recovery.

Improvement was progressive. A pronounced hysterical element persisted, encouraged by the perpetual attentions of visitors. When discharged, there was a slight hemi-anesthesia throughout the right side, and a doubtful patch of anesthesia on the dorsum of the foot, sole, and plantar surface of the heel.

Shell-shock; burial; flexion of spine: Paraplegia.

Case 237. (Elliot, December, 1914.)

A reservist, 34, formerly army instructor in gymnastics, a member of the 1st Battalion King’s Royal Rifles, was subject to injury from the bursting of a “Black Maria” on his trench. He was sitting with bent back in his shelter, with legs fully extended. He was in a small dug-out, a recess excavated under the earth backward from a narrow trench and not timbered. The “Black Maria” burst and covered him up to the chin in a heavy clay soil. After building up the breach twenty minutes later, his comrades dug him out.

He had received on his body the violent impact of the mass of earth pushed laterally from the crater excavated by the bursting of the shell. Accordingly his vertebral column was forcibly flexed, its ligaments were stretched, and hemorrhages were produced in the great muscles of the back. As the twelfth thoracic vertebra is the weakest spot in the spine, the roots of the cauda equina opposite this weak spot were probably injured. Such accidents are met in mines.

The legs were powerless and numb. There was nausea, no vomiting, no gas, no dizziness or trouble in the head, not even pain in the small of the back. The accident had occurred at 8 A.M. Upon nightfall, he was removed on a stretcher to the field hospital, arriving at the base hospital four days later; and on the fifth day power began to return to the legs. Knees, ankles, and toes would move slightly November 6, though passive movements of the legs caused pain in the back. The deep reflexes were weak, the plantar reflexes flexor. The left cremasteric reflex was weaker than the right. Impairment of sensation was slight in both extremities, but the left leg was a little more numb than the right. The left lower abdominal reflex was lost. A band of hyperalgesia corresponded with the left eleventh and twelfth thoracic segments November 12, slight reflex disorders and some degree of paresis of the legs.

Shell explosion: Paraplegia; sensory symptoms.

Case 238. (Hurst, January, 1915.)

A lieutenant, 23, came to the ambulance September 15, 1914, having the morning before been to the firing-line with his company and thrown to the ground on his back by the explosion of a shell which he had seen falling behind him. He had not lost consciousness, but was unable to rise. After a night in the relief post, he was brought by automobile 12 kilometers to the ambulance. He complained of pain in the back, though no wound or ecchymosis could be found there, nor any painfulness of spinous processes or irregularity of bone. He had not emptied the bladder from the time of the shock. Preparations were made to catheterize on the morning of the 16th, when the patient after effort became able to micturate. There was crural paraplegia such that he could not sit or walk even when supported. Lying down, he could move his legs slightly sidewise. Anesthesia to pin-prick and temperature was complete to the groin; but tactile anesthesia was found only in the sacral root territory, namely in the feet, the outer aspect of the legs, the posterior surface of the thighs, and the scrotum. There was loss of sense of position for the toes. The plantar reflexes were abolished; but there were no other reflex disorders; nor was there any evidence of other disorder.

September 20, the man was evacuated by sanitary train in the same status as at entry. January 27, 1915, the patient could walk on crutches, supporting himself in part on the left leg. The lumbar pain had largely disappeared.

Hurst regarded this case as one of organic origin due to commotio spinalis.

Wet, cold, heavy marching; leg pains, rheumatic; no other somatic factor or any emotional factor discoverable: Transient paraplegia; two months after period of exposure, brachial tremor, hysterical. Recovery incomplete.

Case 239. (Binswanger, July, 1915.)

A German soldier, 34 (non-alcoholic; married, father of five healthy children; on military service 1901-3; regarded as a very good soldier; father alcoholic), got bad leg pains from wet and cold in West front trenches September 8-13, 1914. Still he was able to march some 30 kilometers. But two days later (he had lain down in wet clothes in a barn), his legs became quite immobile. He was in a reserve hospital from November 3. The rheumatism disappeared, and suddenly, early in the morning of November 8, when he was washing, a lively tremor and shaking of the right arm set in.

Examination at Jena January 30, 1915, showed no special physical disorder. The sense of touch was slightly diminished on the right side; the pain sense was normal; movements were free. While at rest there was a continuous shaking tremor of the right arm and hand, which consisted of very rapid pronations and supinations, and shaking movements of the upper arm. At times the tremor would completely cease, and when attention was diverted the tremor became slighter or quite disappeared. The tremor increased when it was talked about in the man’s presence. The left grip was stronger than the right.

January 31, after he had been in bed one day and treated with moist packs, the shaking suddenly ceased. He then complained only of mild pains in the right shoulder and wanted to get up.

February 23, he was given three days’ home leave, which he stood very well. He now began to take part in the medical gymnastic work, but complained afterwards of more pains in right shoulder and arm. There was a lapse into the shaking tremor, which lasted with varying intensity for several weeks. Loud noises or calling made it worse.

Hypnotism and suggestive treatment of the tremor were without effect March 25. March 26, on passive extension of the right arm, patient complained of pain in shoulder and arm. Next day the tremors were more marked, but March 29, the tremors suddenly stopped altogether. April 4, the pains stopped never to return. April 15, he was given leave to go home for spring farm work.

Four weeks later he returned, sparing his right arm, which he held stiffly beside his body when walking. If he let the arm hang free in walking, rhythmical movements in it began. He complained of painful involuntary contractions in the right arm even when in complete rest. Nor did the condition afterward essentially change; the patient went home at the beginning of July.

The remarkable feature of this case is the complete lack of any emotional shock. The total genesis seems to have consisted in the prolonged exposure to wet and cold, and the heavy marching. The tremors, limited to the right upper extremity, occurred without any demonstrable psychic or bodily trouble, and set in after the disappearance of the so-called rheumatic disorder. Although there is no one psychogenic factor to single out, the psychic influencibility of the case is unmistakable; moreover, the incompleteness of the cure is doubtless, according to Binswanger, a matter of the imperfect suggestive therapy employed.

Fever patient watches barrage coming: unconsciousness, paraplegia: recovery.

Case 240. (Mann, June, 1915.)

A lieutenant was lying with fever in a farmhouse in upper Alsace, watching from his window the shelling of a battery about 400 meters away. He saw that the enemy was to reach the farm with shell in due course of time. The shells came nearer, say up to about 100 meters, and the lieutenant was able to reckon closely when he would be reached. He was quite defenseless and unable to get to safety. At the very moment, he thinks, when the shells began to strike the house, the lieutenant lost consciousness from fear. He was unconscious an hour before being carried to the cellar. The shelling lasted several hours more. Immediately upon coming to the patient found that, although he bore no external wound, both legs and the right arm were paralyzed.

There were never any signs of organic disorder. The patient recovered completely with purely suggestive treatment.

Incentives to paraplegia.

Case 241. (Russel, August, 1917.)

A young Canadian paid $150 to have his teeth repaired to be accepted for service and then married. The wife became pregnant. He reported sick after falling out on a route march in a heavy rainstorm. The medical officer said he had weak feet and ankles. He lay around the huts, was excused duty, and got worse in the wet and cold. He was admitted to hospital and came to Russel’s wards on a stretcher showing paralysis of both legs with slight power of movement at the knee. Stroking anesthesia to pin prick from the knee down. Reflexes not abnormal. He walked back upstairs!

According to Russel the wife’s pregnancy had furnished a sufficient incentive, and the M. O.’s suggestion had fallen on fertile soil.

Bullet wound of back: Hysterical bent-back—camptocormia.

Case 242. (Souques, February, 1915.)

A man was wounded September 6, 1914, by a bullet that entered along the axillary border of the scapula and emerged near the spine. He spat blood for several days; but the skin wounds quickly healed.

When he got up, his trunk and thighs were found to be in a state of moderate flexion upon the pelvis, the trunk being bent almost at a right angle; the legs were flexed somewhat upon the thighs. The man could not voluntarily extend his trunk, but he could extend his thighs to a moderate degree. He could bend his trunk still further forward than its habitual contractured position, being able to pick up an object from the ground. If the man was put in the ventral position, the trunk could be straightened to a considerable degree. Curiously enough, the man felt no pain, nor had there been any pain since the healing of the wound. No motor, sensory, reflex, trophic, vasomotor, electrical, visceral, or X-ray disorders could be found. It was evident that there was a contraction of the muscles of the abdominal wall and of the iliopsoas, yet it was also clear that these muscles were not contractured on account of the subject’s ability to flex his trunk and to extend his thighs.

Here, then, is a vicious attitude crystallized (in the phrase of Souques) in the form of a pseudocontracture.

Blown up by shell; unconsciousness: Camptocormia (bent-back, “cintrage”). Cure by corsets.

Case 243. (Roussy and Lhermitte, 1917.)

Camptocormia with antero lateral bending is described by Roussy and Lhermitte in an infantryman observed at Villejuif, February, 1915, after having been wounded September 3, 1914. The infantryman had been thrown into the air by the bursting of a shell, had lost consciousness, and came to with violent pains in the back. The trunk was found to be bent strongly forward and to the right side, and remained in this position thereafter. There was no evidence of wound.

In February, 1916, a plaster corset was applied by Souques, which brought the patient partly to normal station in three weeks. The trunk was now no longer bent forward, but was still bent to the right. A second corset was applied for three more weeks, with which the patient became absolutely straightened out again. He was discharged cured and sent to the Grand-Palais for the reëducation course.

This condition is a form of trunk contracture in the nature of a kyphosis (scoliotic and lordotic forms of contracture are also found in the hysterical group), for which the terms plicature of trunk, traumatic kyphosis, pseudo-spondylitis, and camptocormia have been in use. The term camptocormia has been proposed by Souques and Rosanoff-Saloff. The poilus speak of the condition as cintrage (arching). In these cases the trunk is held almost horizontally, with the head in hypertension and neck muscles and thyroid cartilage jutting. The patient looks fixedly straight forward, with eyes wide open, and carries his legs extended or half flexed. The normal folds of the abdominal wall are very deeply marked, and at the level of the groins, the epigastrium and the pubis, there are deep folds. Viewed from behind, the median lumbar fold has disappeared or is faintly marked, as are the sacro-lumbar and other masses of spinal muscles. The whole lumbar region is elongated and flattened. The dorsal spines of the back are accentuated; the buttocks are flattened and broadened transversely. The back of the neck is marked by deep transverse folds, and the seventh spine does not stand out. The patient can walk perfectly, though sometimes there is a pseudocoxalgia and lameness. Attempts to straighten the body lead to visible forcible contractions of various muscles, but the kyphosis remains persistent. There is a sense of active resistance on the part of the patient, which can be demonstrated by palpation. If an active attempt at straightening is made, lumbar or sacral pain develops, followed by a very lively and emotional state of anxiety on the part of the patient, with interrupted and accelerated breathing, an expression of terror in the face, and a rapid pulse. The patient then subsides into his earlier attitude, and his anxiety disappears in a few seconds. It is much easier in many subjects to reduce the camptocormia in the position of dorsal decubitus than upright.

Burial after shell explosion; lumbar ecchymoses; regionary pains; camptocormia, 5½ months. Cure by three months’ plaster cast about trunk.

Case 244. (Roussy and Lhermitte, 1917.)

An infantryman was buried after shell explosion August 25, 1914, but he sustained no wound or bone injury. There was, however, a large ecchymosis of the lumbar region, and he had felt violent lumbar pains. The trunk was carried flexed, symmetrically bent over and quite incapable of being straightened completely. A plaster corset was applied March 16 by Souques. Three months of this was followed by a complete straightening, which lasted after the corset was removed. The patient was discharged well.

As to these cases of camptocormia, some authors regard them as due to anatomical changes in the vertebral column itself, or in the ligaments and muscles, and accordingly regard the condition as a form of spondylitis, syndesmitis, or psoitis. This view is held by Sicard, who bases the idea upon the local pains and the results of cerebrospinal fluid examination. According to Roussy and Lhermitte, hyperalbuminosis of the fluid is extremely rare, and one case of their own with hyperalbuminosis was nevertheless cured with great rapidity. Roussy and Lhermitte even inquire whether the fluid albumin may not be due in some way to an interference with venous and lymphatic circulation.

In some cases, this condition may be at first a response to pain, a pseudospondylitis dolorosa, such as may be sometimes observed in hospitals near the front. Later, however, the suffering in camptocormia is due more to the abnormal position of the trunk, with strain upon vertebral ligaments, than to the persistence of any original pain. Moreover, these patients recover almost immediately from their pains when the contraction is relieved.

In differential diagnosis, one has to consider, according to Roussy and Lhermitte, Pott’s disease, traumatic spondylitis, as well as Bechterew’s vertebral ankylosis, Pierre Marie’s rhizomelic spondylosis, Kocher’s intervertebral disc contusions, and Schuster’s myogenic ankylosis of the vertebral column; but in Pott’s disease, the fixed pain points, rigidity of column, fluid examination, and signs of myelitis, should suffice for the differential diagnosis. Traumatic spondylitis follows the contusion after months and after a phase of neuralgia. Ankyloses do not so much concern the trunk as the vertebral column itself; disc contusion produces disorders in standing and gait as well as pains and edema. Schuster’s disease shows paresis, hyper reflexia, and amyotrophy not shown in camptocormia.

Shell explosion; partial burial; forcible flexion of spine. Paraplegia, cured by suggestion. Then camptocormia, also cured.

Case 245. (Joltrain, March, 1917.)

An infantryman in the Côte du Poivre was sitting on the ground in the opening of a dugout eating soup, when a shell burst and the roof of the sap fell in on him. The planks and the stonework fell heavily on the dorsolumbar region. The patient was almost bent in two, head to knees, legs buried, hardly able to breathe. He did not lose consciousness and cried out, feeling for a moment very anxious and fearful that his comrades had left. Only two hours later was it possible to dig him out. He said he had been absolutely unable to make any movement, had kept his body bent, and felt violent pains in the back. He was carried back twelve hours later and reached the dressing station in eight more hours, eventually reaching the neurological service two days and a half after the accident. On entrance he was prostrated, complained of lumbar pains and of inability to move, and was able to make only a few contractions on the left side when asked to try. The right leg was flaccid. The left knee-jerk was stronger than the right. Other reflexes normal. Hyperesthesia to pin prick on the right side. Slight saddle hypesthesia, reaching to the iliac crests above and perineum below with preservation of touch sensation. Slight forward posture of vertebral column. The patient complained of pain on pressure of the spinal processes and the lumbar spine. There was slight ecchymosis about the left iliac crest.

Lumbar puncture showed clear fluid without hypertension, in which were a few lymphocytes. There was a large amount of albumin. The blood pressure was normal. There had been a slight diarrhea following the accident which disappeared on entrance to the hospital. The question was raised whether the case was one of slight hematomyelia or was pithiatic.

Suggestive therapy was tried, and liquid was injected into the muscles of the lumbar region and the posterior surfaces of the thighs. In a quarter of an hour the patient found himself able to raise the foot above the bed. There remained an extensor paralysis of the right leg. When the patient was made to raise the foot he began to show the phenomenon of Souques, called camptocormia. He could walk, nevertheless, and took a few steps sustaining the weight of his body by placing his arms on his thighs. Though he complained of lumbar pain, it was finally possible for him to pick up an object from the ground and lean sidewise. He could not, however, stand up. Yet when the patient was made to lie down, his back was spontaneously straightened. Treatment of the camptocormia was also successful.

Astasia-abasia: Two cases from (a) thigh wound, and (b) shell-shock and wound of thorax. Cures by faradism.

Case 246. (Roussy and Lhermitte, 1917.)

An infantryman was wounded September 23, 1914, by a bullet in the anterior and middle part of the left thigh. From the moment of the trauma, he had not been able to walk, but gradually regained his ability to stand, and then to walk. He was returned to the front (January, 1915).

Slightly wounded again in the neck, January 6, 1915, he was evacuated and operated on. After the operation he could neither walk nor stand. His reflexes were normal; he could perform all movements when lying down, although the movements were executed very slowly. As soon as he could sit upright, he was taken with tremors and could not hold himself in a vertical standing position, nor take a single step. If he was given crutches, he dragged the two legs.

Under the influence of electric treatment—a mild faradic current—he was cured at a sitting so that he could both stand and walk (March, 1916).

Case 247. (Roussy and Lhermitte, 1917.)

Astasia-abasia after shell explosion occurred in an infantryman observed by Roussy and Lhermitte at Villejuif, July 8, 1915.

The patient had been wounded September, 1914. The wound was a superficial one in the thoracic wall, under the right nipple. He had been cast into a very deep shell hole, but had been able to get back to the aid station alone, taking very short steps only.

As soon as he reached the station, his gait became spastic, trembling and hesitant. Given two canes, he could walk painfully, trembling. At each step, he would balance his body back and forth. He gave the impression of a man drawing some sort of vehicle, who had to make a considerable effort at each step.

The faradic treatment cured this patient at one sitting.

War strain; fall into water-filled trench: Dysbasia, tremors, vasomotor disorders. Cure by hypnosis. Case to demonstrate “traumatic” hysteria WITHOUT somatic TRAUMA.

Case 248. (Nonne, December, 1915.)

An artilleryman (without hereditary or acquired neuropathic taint) underwent much stress and strain in the war in Belgium, Lorraine and Flanders. One night, on leaving his observation post, he fell into a trench filled with water. He felt pricks in the groin and gradually developed a pseudospastic tremor of the lower extremity, paraparesis inferior, depression, irritability, pressure sensations in the head, and sleeplessness. He passed through three hospitals before arriving at Hamburg and received the diagnosis of concussion of the brain and cord.

Nonne found an emotional state of depression with hypochondriacal fear, disturbance of sleep, deficient appetite, constipation and pollakisuria. He walked upon two crutches, dragging his legs inertly after him. There was marked cyanosis, lowered temperature and hyperidrosis of the feet and lower legs; exaggeration of tendon and skin reflexes and pseudoclonus; no Babinski or Oppenheim reaction. There was anesthesia of the lower extremities and of trunk as high as the ribs. Pulse 130. Visual fields normal. Sensory disorders absent.

After the first hypnotic treatment the patient was able to stand and take a number of steps, and the tremor gradually diminished. After two treatments standing became normal and walking was much improved, the tremor ceased, cyanosis and hyperidrosis disappeared, and the movements of the bowels and urination became normal. Thereafter the patient had no attention paid to him deliberately and in a week’s time became well.

Here is a case in which, as Nonne states, the somatic trauma required by Oppenheim as the basis of every traumatic neurosis did not occur. Moreover, the sudden cures by hypnotism, or by any other method in these cases, warrant us in supposing that there are no such fine molecular changes as Oppenheim and von Sarbo assert. Such experience as the cures in this group of cases confirms, according to Nonne, the surprising result first achieved in this war (Bonhoeffer, Wagner von Jauregg, Karplus, Wollenberg, Westphal) that the most severe neuroses produced by somatic and psychic traumata can be cured in an astoundingly rapid manner without residuals.

Re the controversy over Oppenheim’s traumatic neurosis, Nonne holds with the Charcot school that traumatic neurosis is clinically identical with hysteria. Oppenheim admits the part played by psychogenesis, but has always laid a greater emphasis upon the actual injury of the neuronic apparatus in which he believes. He thinks that small hemorrhages, inflammatory processes, and degenerative processes affect the neurones unfavorably, and permit the psychogenic effects to occur more readily. Of course the insurance-company attitude and the attitude of railway corporations saw malingering in all cases, and to this day, neurologists are inclined to see a great deal of “indemnity neurosis” in these cases. Opposed to the corporation men and the neurologists were the psychiatrists, who chiefly upheld an emotional theory of genesis—whence we began to hear of the neuroses of fright and of accident.

Oppenheim claims to have established with war cases the fact that an entirely normal person without heredity and without antebellum acquired soil, may develop a neurosis through war stress. Oppenheim concedes that there may be purely psychic cases, but holds that there are nevertheless, numerous purely physical cases and a great number of cases of a compound nature, which are both physical and psychical in their etiology. Oppenheim’s point is not that every single symptom described may not be upon occasion psychogenic, but that the data of this war prove that neuronic injury, particularly injury of the peripheral neurones, can also produce these effects. Nonne, Forster, Lewandowsky, and others, opposed Oppenheim’s views vehemently. See especially comments by Zeehandelaar.

Shell-shock; BURIAL HEAD DOWN: Brachial monoplegia, head-shaking, speech disorder, corneal and conjunctival reflexes absent. Determination of hysterical phenomena to parts buried.

Case 249. (Arinstein, 1916.)

A Russian private was buried after a shell explosion, September 13, 1915, head down, so that only his legs stuck out of the débris. Afterward his right hand refused to move, and there was edema of the right wrist, with pain referred to the shoulder joint. The head shook and made jerky movements during the day, but ceased them in sleep. Speech was retarded; words were uttered clearly enough but in a sing-song fashion; sometimes the man stammered. Hearing was diminished in the right ear. Pupillary responses were lively, but the swallowing reflexes were diminished, and the corneal and conjunctival reflexes were absent. The tendon reflexes were lively on both sides. There were no pathological reflexes.

At the end of October—six weeks later—the patient was sent home on convalescence for three months, and improved rapidly after a short time in family surroundings. He was examined again, two months after discharge, and found normal in all respects. He returned to the ranks.

Re Shell-shock in Russians, Arinstein concludes that concussion hysteria may occur in a perfectly normal person, yet be innocent of all organic signs indicating destruction of peripheral or central neurones. Rifle or machine-gun fire had not in his experience brought about concussion hysteria, which was invariably due to the bursting of a large projectile. With reference to Schuster’s remark that a sleeping man never acquires hysteria from the bursting of a shell near by, Arinstein confirms Schuster, finding amongst 2000 cases no instance in a soldier sleeping at the time the shell burst.

Re effects of cannonading, Gerver reports Russian instances of a kind of hysterical clavus, or sensation of a nail being driven into the back of the head, in men who have been a number of days under stiff shelling.

Multiple wounds and bullet wound of palm: ACROPARALYSIS. Cure, five months.

Case 250. (Roussy and Lhermitte, 1917.)

A patient was observed at Villejuif, February 5, 1915. He had been wounded, January 2, 1915, and showed scars of a bayonet wound on the anterior surface of the right thigh, of a lance wound on the dorsal surface of the right foot, and of a bullet wound in the palm of the left hand.

There was left wrist drop with fingers extended. On the sensory side, there was a glove anesthesia and analgesia up to the bend of the elbow. The right leg showed a paresis and contracture, but there were no sensory disorders in the legs. Reflexes were normal. The patient was discharged cured, in May, 1915 (psychoelectric method).

This is an example of the so-called acroparalyses, paralyses limited to the hand or foot, many of which have developed in this war, after grazing wounds or more severe injury. More rarely they appear as if spontaneously. Sometimes they are preceded by slight arthralgia or vague pains.

The condition in the hand suggests a radial paralysis. The patient is unable to flex his fingers, though he probably is able to make some movements with his thumb. Sometimes, on request to move the hand, a series of coarse oscillations follows, somewhat like a tremor. These oscillations are, according to Roussy and Lhermitte, apparently pathognomonic, and depend upon the contraction of the muscles antagonistic to those whose movement has been requested. These antagonistic muscles, themselves entirely incapable of voluntary movement, are seen to be contracting effectively and jerkily to meet the action of the agonists, also seen making jerky movements. If the forearm is moved passively and rapidly, the hand flops about inert, like the hand of a marionette, although not to the degree of hypotonia in organic paralysis. The hand is often cold, moist, and cyanotic, and even possibly analgesic and hypesthetic.

Bullet wound of arm: Apparent radial paralysis, not resolved by self-preservative swimming movements. Paralysis actually hysterical.

Case 251. (Chartier, October, 1915.)

A professional acrobat, 22, Corporal in an African Chasseur regiment, was rather instructively tattooed and had apparently performed some of his service in disciplinary companies. In short, one might have a legitimate suspicion of the objective value of any manifestations he might present. However, one of his chiefs had written a favorable letter concerning his services. He had had various crises of a hysterical character since adolescence, and there was alcoholism in the family.

He was wounded May 4, 1915, by a bullet which passed through the outer and lower part of the right upper arm, and thereafter the forearm and hand became completely inert, both for flexion and extension. There was a considerable hyperesthesia. The wound healed quickly, without complications.

August 5, about 10 o’clock at night, the man—then at his dépôt—tried to commit suicide (motive not related with the war). He threw himself into the Rhône from a height, where the water was deep and the current rapid. His brother and a comrade, who knew that he was going to make the attempt, saved him. Chartier himself happened to see the whole scene, and noted that throughout the affair the forearm and hand of the patient remained inert. It seemed as if there was a radial paralysis. This was the more likely as the man had been wounded in the arm. First care was given. The man had not known of Chartier’s presence. He had been under water about two minutes.

From hospital he was evacuated three weeks later with a diagnosis of radial paralysis, coming on service September 11. Examination showed a slight paralysis of the extensors and flexors of hand and fingers, and of the hand muscles. There was also a slight contracture of these muscles, more marked in the flexors. There was pain upon reduction, with some jerking of the muscles. Electrical reactions proved normal in nerves and muscles. There was a segmentary anesthesia to pin prick, reaching to the level of the elbow; deep hyperesthesia of the finger joints. There was no trophic or vasomotor disorder.

In short, here was a case of functional paralysis with contracture of the right hand, to be regarded as hysterical in the classical sense of the term, both by reason of the anesthesia and absence of trophic disorder, and on account of the hysterical history of the patient. Functional reëducative treatment quickly improved the paralysis, so that two weeks later the patient was able to extend fingers and hand. His total recovery was hoped for, when, September 26, wishing to get out of the hospital without leave, the patient jumped from a window and broke his right leg. The functional paralysis of the hand persisted and even grew more marked.

The interesting point in this case is that despite the powerful nature of instinctive efforts with drowning persons, this patient, subject to an hysterical arm paralysis, did not make defensive movements with the paralyzed arm; yet this paralysis was such as to be greatly improved by psychotherapy.

Bullet wound in brachial plexus region: SUPINATOR LONGUS CONTRACTURE, hysterical-looking. Callus of fractured rib probably at fault: Treatment surgical.

Case 252. (Léri and Roger, October, 1915.)

A man was wounded, December 21, 1914, by a bullet which entered about the middle of the spinous process of the left scapula and was extracted a few days later from the posterior border of the sternocleidomastoid muscle, two finger-breadths from the left clavicle, that is, at about Erb’s point. The left upper extremity was inert for ten days, but then began to move again, although extension and flexion of the fingers did not begin at once.

October, 1915, movements were normal, except those of extension of the forearm, due to contracture of the supinator longus muscle, a contracture that had developed about three weeks after the wound and stood out along the external border of the forearm, almost suggesting a musculotendinous retraction. There was a palpable, hard callus of a fractured rib, presumably a cause of the permanent irritation of the supinator longus, being precisely at the point where lesions usually produce superior brachial plexus palsy.

Why should the supinator longus alone of the Duchenne-Erb group be affected? Perhaps a single root was involved in the irritative lesion. The biceps showed also a partial R. D. The deltoid was normal electrically and in contraction.

The treatment planned for this case of isolated contracture of the supinator longus was surgical operation of the irritative focus. According to Léri and Roger, it is sometimes dangerous to use such measures as massage and electric baths for a paralyzed limb, since the massage or electricity excite not only the affected muscles, but also the other sound muscles,—muscles that are already more powerful than the paralyzed muscles and may go into antagonistic contracture. Even in limited galvanization, it is desirable to work with weak currents, so as not to diffuse the current into non-paralyzed muscles. In case of radial or sciatic paralysis, apparatus permitting the extremities to rest without over-action of the muscles antagonistic to the paralyzed ones may well be applied.

We here deal with a case, therefore, which looked purely functional, but in which careful examination and X-ray served to show an organic focus of irritation.

Re nerve concussion, Tubby offers the following definition: Nerve concussion is damage to a nerve trunk without actual destruction of the axis cylinders. The damage may consist of an effusion of blood between the nerve fibres following compression of a nerve against the bone by rapid passage of a foreign body near the nerve. Sometimes, however, the lesion which causes damage to the nerve trunk without actual destruction to the axis cylinders is nothing more than a temporary anemia or hyperemia. In most instances, both motor and sensory function are together interfered with, but in the case of large nerve trunks, e.g., the popliteal, there may be a separate concussion of motor or sensory bundles.

Contusion may effect a sort of STUPEFACTION OF MUSCLE and paralyze it by a non-psychic process: The SYNERGY in contraction of biceps and supinator longus is thus SPLIT. Biceps restored to synergy with the supinator by massage and faradism.

Case 253. (Tinel, June, 1917.)

A man was wounded at about the middle of his biceps and three weeks later was found to be able to flex the forearm only by means of the supinator longus. The biceps remained absolutely flaccid and soft, so that the diagnosis of a lesion of the musculocutaneous nerve (unlikely as this seemed on account of the low site of the wound) was entertained.

However, the biceps and the musculocutaneous nerve proved electrically normal. In short, this paralysis of biceps was functional in nature. But, according to Tinel, there could be no voluntary suggestive or hysterical element in such a paralysis, since flexion of the forearm is normally produced by a synergic contraction of biceps and supinator longus that cannot be separated voluntarily.

Treatment by massage and rhythmic faradization caused the biceps function to return to normal, so that voluntary synergic contractions of the biceps took place along with those of the supinator longus.

We here deal, according to Tinel, with a genuine functional paralysis, nonhysterical—a paralysis due to a kind of stupor of the muscle. Such paralyses due to muscular stupor ought to get well in a few days or weeks. Should they persist, it is clear that a stuporous paralysis might be transformed into a hysterical paralysis. In short, the direct contusion of a muscle or group of muscles may be the point of departure for various persistent paralyses.

Wound of arm: Blocking of impulses to certain hand movements. Recovery with splint.

Case 254. (Tubby, January, 1915.)

A private was wounded by a shell fragment, September 16, 1914, and admitted to the London General Hospital, September 27. A high-velocity shell fragment had passed through the soft parts of the left arm at a spot exactly corresponding to the musculospiral groove. He could extend the middle finger of the left hand, but the other fingers were held in flexion. The last two phalanges of index finger could not be moved, it was found, on account of severance of the extensor tendon some years previously. Accordingly, the loss of function due to the shell injury was that of thumb, ring, and little fingers. Supination could not be executed completely to the extent of 15 degrees; there was no R. D. upon electrical test, October 2. The sensation of affected fingers was woolly. November 3, the little finger had recovered, but supination could not be completely executed.

The treatment consisted in a bent malleable iron splint, with the wrist and affected fingers hyperextended. November 20 all power had returned with full supination, except for the two phalanges of index finger previously injured.

Major Tubby thinks this a case of physiological blocking, as from a small hemorrhage amongst the fibers or around the nerve.

Re inhibition, Myers thinks it is the functional cause of the effects of shell-shock. He thinks it is not a fixation of the idea of the paralysis of volition, but that it is a fixation of the process of inhibition itself that produces the effects we see in Shell-shock. It is a block of ascending paths that produces the anaesthesia so characteristic of Shell-shock. It is a blocking of sensory paths that produces mutism or aphonia. But according to Myers, there is also a block in certain cases of descending paths that control and coördinate various mechanisms. The result of a block in the descending paths is shown in spastic, clonic, or ataxic phenomena of, e.g., functional dysarthria. See also Case 253 (Tinel).

Eight months of war experience (often under heavy fire) without reaction; then, shell-shock; unconsciousness: Right hemiparesis; pain in the left side of head; heat sensations of right half of body; diminution of hearing in left ear; a variety of asymmetrical bilateral phenomena.

Case 255. (Gerver, 1915.)

A Russian private, 24, sustained shell-shock April 14, 1915. He was observed, when the shell burst, to crouch down, and then to fall to the ground, unconscious. The unconsciousness lasted about two days, after which he was found to be oriented, though slow and stammering of speech, hardly able to concentrate attention or sustain a conversation, and giving the impression of a man stunned. There was difficulty in the expression of thoughts, and a marked over-fatigueability. After adding and subtracting accurately two-digit figures for a time, the man quickly grew confused and said that trying to solve such a problem made him dizzy.

His imagination was filled with gunshots, shell-bursts, and the killing of comrades, and during any conversation the man frequently shuddered. Concerning the shell-shock, he remembered only that a number of shells had burst near him and that he came to in the hospital. He kept looking to one side and to a distance, as if listening, sometimes bending his head downwards. He would cry and sigh during conversation, and then be quite unable to explain why. He said there were loud noises in his ears, and that his head and the whole right side of his body felt hot. Pain was felt in the left side of the head. The right hand and the right foot were weak (on distraction, this hemiparesis remained unaltered). Tremors affected all the extremities. He had a sensation, possibly hallucinatory, of the creeping of insects on his skin. The hearing of the left ear was objectively diminished. There was palpitation of the heart and difficulty of breathing. Tendency to Romberg. There was a general hypalgesia, more marked on the left side of the body. Both conjunctival reflexes were diminished. Knee-jerks and Achilles jerks were exaggerated. All the reflexes on the right side were livelier than on the left. There was a moderate Babinski reaction on the right side. Mechanical over-excitability of muscles. Dermatographia. Both sides of the skull were sensitive on tapping, but especially the left side. Mannkopf sign on pressure of the left side of the cranium.

Hemorrhagic points without injury to the skin were noted on the skin of the left hand and foot. Speech was stammering. There was a marked digital tremor, sometimes spreading to the rest of the body during examination. The muscles of the face, eyelids, and tongue showed sharp fibrillary twitching. The pulse stood at 100 and frequently missed beats. Battle hallucinations, visual and auditory, sometimes occurred, the commands of superiors and the noise of guns, rifles, yelling, and groans; the man would see trenches or redoubts, or a field full of wounded soldiers or attacking columns of the enemy. He recognized the hallucinations as such. His sleep was troubled by nightmares of the same general description.

For eight months the man had been in action at the front, under heavy gun and rifle fire. He was a courageous man, who had never felt fear, regarding himself as used to battle and the bursting of shells. He had not been wounded. The entire situation seems to have developed after the single shell burst of April 14, 1915.

LOCALIZATION OF SHELL-SHOCK SYMPTOMS: Hemiparesis and hemianalgesia on side of body exposed to explosion; contralateral irritative symptoms of face and tongue.

Case 256. (Oppenheim, January, 1915.)

A soldier had a shell explode to his right, October 23, 1914. He declared that the concussion launched him through the air. When he recovered consciousness three hours later, he lay in a bog and was unable to move either leg. Gradual improvement followed. The symptoms were sensations of formication in the legs, pain in the back, blurred sight, hardness of hearing, disturbance of speech, headache, vertigo, weak memory. After a fortnight weakness in right arm.

He was admitted to hospital a week after the injury, unable to walk, restless, given to palpitation and attacks of anxiety. On attempts to walk, leg spasms and tachycardia.

Transferred to nerve hospital, December 2. Sleep poor, uneasy with dreams. Tic on left side of face. On opening the mouth, left-sided faciolingual spasm. Paresis of right arm. At first, right-sided ankle-clonus and paresis of leg. Knee-jerks increased. Speech hesitating. Right hemianalgesia. Concentric contraction of visual fields. Tachycardia (120). In walking the right arm failed to swing normally. Attacks of vertigo, with falling. Patient got up at night and pushed against objects in his room.

There was only slight improvement while under observation. He became psychically more frank and even talkative, and was moving more readily when transferred.

Re Oppenheim’s conception of the strongly peripheral element in traumatic neurosis, he sums up by saying that a traumatism attacking the organism at its periphery is in line to produce a neurosis without any psychic mediation whatever. The rôle of the psychic process, in Oppenheim’s view, is contributory to the fixation of neuroses. Even when there is a free interval betwixt shell burst and neurosis, still there are physical effects of trauma upon neurones.

Shell-shock; unconsciousness; after improvement in symptoms (4 months) return to trenches; more symptoms after 5 days: Sensory disorders, especially on left side (the side more exposed to explosion); exaggerated reflexes on right side with slight clonus and with Babinski sign. Improvement.

Case 257. (Gerver, 1915.)

A Russian Captain, 45 (heredity good; non-alcoholic, non-syphilitic; always in good health) sustained shell-shock in a battle in southeastern Prussia, August 13, 1914, and was unconscious for two days. He was carried to one of the provisional field hospitals, and then evacuated to Petrograd, where during a period of four months, he was given electricity, suggestion, and baths. He was feeling so much better in December, 1914, that he went back to the front and headed his company in the trenches. He stood only five days of trench work, and was sent for mental examination December 29, 1914.

The captain was of middle height, well developed but poorly nourished, of a dejected and preoccupied appearance, looking to one side in conversation, and finding difficulty in the expression of his thoughts. He talked almost exclusively of his illness. He found difficulty in adding or subtracting 2-digit figures. He seemed to have amentia, frequently being mistaken as to the most important dates in his life. He complained of general weakness and inability to work. Any endeavor to concentrate caused vertigo, irritation, and pains in the head. Day and night he was troubled about his health, his future, and his family’s future. He was going to become an invalid and a burden. He was tormented with the idea that people thought him a simulator. He complained of lumbar pains. It seems that the explosion had affected the left side of the body more than the right and he complained more of pains upon that side. In the dark his gait was unsteady, and he often had marked tremors of feet and hands. In excitement the tremor would increase uncontrollably. The patient thought that his hearing was diminished, especially upon the left side, and that his left ear was weaker than the right. He slept poorly and had many nightmares; his appetite was poor, and he was constipated. There was difficulty in respiration; the pupils were slightly dilated and sluggish in their responses. There was a marked tendency to Rombergism; dermatographia marked; the skull and especially the lumbar spine was painful on tapping; hyperesthesia of the lumbar skin; paresis of left hand and left foot. The tendon reflexes were more marked on the right side than on the left, and there was even a slight ankle and patellar clonus. The Babinski sign was present on the right side. There were frequent fibrillary contractions of the muscles of the trunk and back.

Objectively the hearing was somewhat decreased in the left ear, and the vision of the left eye appeared to be somewhat impaired also. If the eyes had been held closed for a time, there was difficulty in opening them quickly. Aside from a somewhat elevated pulse and slight cardiac arrhythmia, there was no disorder of the internal organs.

This patient remarkably improved but was not absolutely well at the date of the report.

Re organic signs in Shell-shock cases, Oppenheim warns practitioners and experts against undervaluing war neuroses. He does not like to have them set down in too offhand a way, as hysteria, wish-fulfilment, and simulation. Hysteria is not likely, according to Oppenheim, in cases with permanent cyanosis, disappearance of the radial pulse, trophic disturbances, hyperidrosis, alopecia, fibrillary tremors, myokymia, cramps, dilated and sluggish pupils, and weakening of tendon reflexes. Hyperthyroidism also has been found by Oppenheim.

Shell-shock, explosion on left side: Sensory disorders especially on left side; ecchymosis of right (uninjured) leg, possibly conditioned upon shock of left hemisphere.

Case 258. (Gerver, 1915.)

An artillery officer had had a shell burst to the left side of his horse, which veered to the right but did not fall. The officer’s left hand immediately became so numb and weak that he could not hold his reins with it; it shortly became more painful. The left foot showed a tendency to the same anesthesia and paresis.

Curiously enough, a number of punctate hemorrhages appeared on the right thigh and lower leg, upon the outer aspect. According to Gerver, these hemorrhages into the skin of the right leg may have something to do with a disturbance of circulation related with effects wrought upon the left hemisphere. During the course of the disease, pains occurred not only in the left arm and leg but also in the right leg.

Re brain injuries produced by shell explosions without external wound, Roussy and Boisseau have not found a single clinical instance amongst 133 cases observed, which suggested cerebral softening, or even hemorrhage into the brain substance, the cord substance, or the meninges. These 133 cases were observed in army neurological centres and contained instances of (a) mental disease (confusion, delirium, amnesia), (b) nervous disease (astasia-abasia, tremors, paralyses, contracture), and (c) an intermediary group (either mental confusion with stupor, or hysterical deafmutism).

Shell-shock; unconsciousness: Hysterical deafness, speech-disorder, gait. Recovery by reëducation. Brief relapse to deaf-mutism at noise of drums. Improvement. Relapse to numerous and severe hysterical symptoms at small guns fired on King’s birthday. Improvement. Speech wholly regained in a quarrel. Recovery.

Case 259. (Gaupp, March, 1915.)

A musketeer, 22, had been blind for a time at 11 on account of some spinal cord disease.

He was a soldier up to Christmas eve, 1914, when he was hurled backward in a trench in the Argonne by an exploding hand grenade. He lay unconscious for several hours, though without sign of physical injury. Coming to his senses, he worked himself out of the trench and crawled to another, but again fell unconscious. When he awoke he was in a physician’s care in quarters, to which he had been taken by ambulance men. Thence to the field hospital, and then to a private hospital at B.

Upon admission, January 17, he was hard of hearing on both sides, and his speech was peculiar: choked off and retarded. His gait was heavy, on a broad base. He was subject to headaches.

Exercises gradually improved the speech and the walking disorder was quickly overcome. February 5 came a relapse through fright at the rolling of drums near by. Speech was completely lost, deafness set in, and the patient ran restlessly to and fro in tears. After a few hours speech returned with still some minor difficulty.

From time to time came fainting spells and attacks of disorder of consciousness, with loss of orientation and the idea of being in the trench or under cover. He would ask whether it were raining through. His mood herein was at times cheerful and excited. Speech further improved from the middle of February, as well as did the other symptoms.

On the King s birthday, February 25, occurred another relapse due to his hearing small guns fired: Apathetic stupor, clonic spasm, aphonia, abasia, severe deafness, poor sleep, refusal of food. The next day he was still mute, but the spasms had ceased. He lay apathetically in bed, taking a little liquid food. February 27 he was still mute, though more active, not deaf, getting up alone, walking unsteadily on a broad base, and playing cards at the table. March 2 the word yes was again enunciated. March 3 he talked more freely and took a short walk. March 4 speech of a sudden came completely back on the occasion of getting excited in a quarrel among some other patients. The patient thereafter began to talk a great deal, was bright and cheerful, but still complained of a variety of nervous troubles. Speech was somewhat difficult, but he was free from any definite aphasia or paraphasia.

Re Shell-shock deafness, Jones Phillipson states that concussion deafness is due to three contributory factors: (a) cerebral concussion, (b) fatigue (violent oscillation of the perilymph, continued noises, strain of organ of Corti), and (c) temporary or permanent disorganization of the conductive apparatus.

Re concussion deafness, J. S. and S. Fraser found in four cases of actual explosion injury, a ruptured drumhead and hemorrhage into the fundus of the internal meatus in three cases. They did not find evidence of neuro-epithelial changes. Possibly the fundus hemorrhages, besides giving rise to deafness, may start up the tinnitus and giddiness that are sometimes found. In one case, there were changes in the delicate nerve endings of the auditory ampullae.

Shell-shock: Deafness

Case 260. (Marriage, February, 1917.)

A shell burst behind an English lieutenant in 1914 without causing any wound but making him unconscious for an hour. During the hour the Germans passed by and stripped him of all articles of value. He came to and felt himself markedly deaf in both ears with an intense headache. There was no hemorrhage, no discharge, no tinnitus, no vertigo. Four days after the shell burst he could hear spoken words on each side at two feet, but could not hear a watch that could usually be heard from 3½ to 4 feet. With tuning fork C air and bone conduction proved much subnormal, though air conduction was better than bone conduction. With tuning fork C-5 air conduction was subnormal. Drums healthy. Improvement followed; hearing became normal eighteen days after explosion. The treatment was rest in bed with bromides early and strychnine later.

Marriage states that the psychical deafness due to shell-shock is usually bilateral and absolute. It is accompanied also, as a rule, by other nervous signs and symptoms, such as aphonia, tubular vision, paralyses, and anesthesias. Milligan and Westmacott state that the deafness is due to a functional suspension of neuronic impulses. They regard the brain as in a state of physical fatigue, and the mind as in a state of strain. There is no organic lesion. The neuronic impulses which are temporarily suspended are those which run from the higher cortical cells to the periphery.

Mine-explosion: Unconsciousness: Deaf-mutism. Recovery of speech after epistaxis and fever.

Case 261. (Liébault, October, 1916.)

A soldier, 24, teacher in civil life, was in a mine explosion November 27, 1914, at Vienne-le-Château. He was unconscious six weeks and remembered nothing of what had passed. They had told him that he had been blind for a month. After regaining consciousness he was a deaf-mute and for seven months he did not speak. His mutism did not bother him, as he thought he had always been mute. He had always been able to write. He could not remember what had interfered with his speech or tell whether he could think the words which he could not utter.

May 22, 1915, there was considerable nasal hemorrhage, with fever. Upon this day he began to speak, at first a few words, telegram style, and with aphonia. A week later his voice returned. He was very irritable during the period of mutism and had ideas of persecution and of suicide and complained of becoming easily fatigued and exhausted.

His voice, however, became completely normal again and his respiration better. On the spirometer he breathed four liters, but still got out of breath easily. His diaphragmatic respiration was still imperfect. His deafness remained at the time of report about as before, though he had now been hearing for some time a slight resonance of his own voice and could hear sounds emitted a few centimeters from his ear. At time of report there was still general fatigue with insomnia.

Re war deafness, Castex states that not merely shell bursts and explosions are able to cause deafness, but the din of battle alone. There are two big groups of war deafness: one due to drum rupture, and the other due to labyrinthine shock. Labyrinthine shock—a much more serious matter—is produced when a big shell bursts. In these cases, the labyrinthine disorder is simply of the same general nature as commotio cerebri. The labyrinthine shock cases often need to be retired permanently from the front.

Shell-shock: Deaf-mutism.

Case 262. (Mott, January, 1916.)

A deaf-mute, 24, not of a neurotic temperament or of a neuropathic predisposition, was admitted to the Fourth London General Hospital November 16, 1915.

He wrote, “I left England the 8th of March, and went to Gallipoli on the 26th of May, and about the middle of August, one of our monitors fired short. I felt something go in my head; then I went to the Canada Hospital. They said it was concussion.” He had seen the monitors firing. He came to in a dug-out about an hour afterward. He was quite deaf and his head felt as if it would burst.

He could see and speak a little but lost his speech completely when Barany’s tests were applied. The headache then passed away, leaving the deaf-mutism. The ears, on examination, proved normal. The patient was able to cough and whistle. He wrote his wife a letter, telling her how he killed a Turkish woman sniper, but he did not remember that he had written the letter. Although he said he did not dream, while asleep he would assume the attitude of shooting with a rifle, as if pulling a trigger, and then the attitude of using the bayonet: the right parry, the left parry, and the thrust. Sometimes while asleep he would jump as if a shell were coming, and he would catch his right elbow as if hit there. He would then open his eyes wide and look under the bed. Then he would wake up and begin to cry, but without sound. Just such habitual attitudes occur in soldiers under anesthesia. In hypnotic sleep, although he trembled at his trench experiences, he did not assume these defensive attitudes.

Mott states in his Lettsomian lectures that hearing is often absolutely lost, but that sometimes a man is absolutely deaf on one side alone, either from the ruptured drum or from the violence with which wax has been driven against the drum. Mott speaks of the frequency of auditory hallucinations, and of hyperacusis—part of the patient’s general hypersensitivity—which may increase the violence of the neurosis and especially aggravate the headache.

Shell-shock: Deaf-mutism; convulsions and dream.

Case 263. (Myers, September, 1916.)

A private, 28, was seen by Lt. Col. Myers at a base hospital. This deaf-mute wrote, “I was standing and a shell bursted and that is all I can remember.” This might have happened six days previously. The patient wrote vaguely about a walk to “windy corner”; about being billeted in a dug-out, a train journey, and another hospital. He was deaf, deficient in sensibility throughout, especially in the left arm and left side of the face, and had severe headache. Two days later he started distinctly when hands were clapped while he was writing, but at the next hand-clapping there was no response.

After Lt. Col. Myers wrote down, “Imitate me,” and made consonant sounds, the patient succeeded imitating them. “You hear me a little now,” Lt. Col. Myers wrote. “Is this the first time you have spoken?” Patient replied, “I hope the Lord I can get my speech.” “But you did speak just now. Read this word. Say it.” Whereupon he was got to say his name and number.

The therapy was proceeding properly when suddenly he was seized with convulsions, limb movements chiefly clonic, back arched, eyes starting, later upturned. The patient pulled out a crucifix from a locker near the bed and regarded it ecstatically (pulse 85, corneal reflexes preserved). Three minutes later there was quieting down, and the patient was induced to talk. He began to talk about his wife. He had just been “seeing a farm and all the fighting.” A shell must have come in there. He had “seen the Lord Who saved him.” Intense headache and thirst followed. According to the patient the excitement was due to recovery of speech.

He later said, “It was just like a dream when I came to. I was sweating awful. I was seeing the Lord while I was in the farm by the Captain. I dreamed that I had the cross in my hand to meet him coming. I saw the trenches and the dug-outs and the wife.” In point of fact, the Captain at the farm had had his arm blown off, and he had found him lying on the straw unconscious. Under hypnosis it appeared that he had gone to a dugout from the farm and that at the clearing station he had been “raving, seeing things, shells, trenches, and things like that, sir.” A slow recovery was made after evacuation to England. Seven months later he returned to the front.

This case appears to belong to the B group of mutism cases, according to the classification of Myers, namely, to the group in which the effects are psychical rather than physical. According to Myers, whether mutism occurs as an apparent result of physicochemical or of mental causes—that is, as an A or a B case—it is actually always the result of mental—that is, psycho-physiological shock. Mutism in the A cases of physical nature, where the shock must have been grosser and more profound, generally proves more severe than in the B cases. As to the appearance of unconsciousness, apparently confirmed by the patients’ statements that they “lost consciousness,” it is a question whether these cases are not really cases of deep stupor. According to Myers, the mutism is in nearly every instance closely dependent on some form of stupor, being generally the relic of such stupor after it has passed off. Let the loss of consciousness be a profound stupor due to the lifting or burial of the patient, then from this stage there will be a transition to a state of ordinary stupor in which intelligence is active but the patient is unresponsive to stimuli. The patient is in a condition called by Myers excommunication, in which the inhibitory process may be regarded as protecting the individual against further shock. As the stupor now passes away, it is natural that the inhibition should appear lost in the case of hearing and speech, which are two main channels of intercourse with others.

Dumbness is, by far, the commonest disorder of speech, occurring in about ten per cent of shock cases in the first thousand cases of shell-shock seen by Lt. Col. Myers. Stuttering and jerky speech have occurred in about three per cent. Loss of voice is rarer.

As against the view of Babinski, that mutism, being curable by suggestion, must have been produced by suggestion, Lt. Col. Myers argues that the stupor preceding mutism is the antithesis of suggestibility and is, in fact, a condition of extreme autofixity.

Naval gun-fire effects on seaman: Aphonia. Two recurrences.

Case 264. (Blässig, June, 1915.)

A seaman from the Derfflinger was brought into a naval hospital with loss of voice, December 22, 1914, able to speak only in a whisper. As a child he had had diphtheria, but recovered without complication. He had always had a very well-controlled voice. Early in December he had had a cold owing to sentry deck duty in bad weather. Two days after the shelling of Scarboro,—December 16,—while in the munition chamber of the big guns, he suddenly lost his voice. He had been greatly upset during the firing of the guns. In two weeks he recovered speech.

February 12, 1915, he returned to the hospital with a complete aphonia. This was immediately after the naval engagement in the North Sea. Three days later he was treated with electricity directly applied to the vocal cords. March 20 he was discharged with speech completely recovered. As soon as he went on leave, however, his voice was lost for the third time, and he was still aphonic at time of report.

Shell-shock MUTES observed, then DREAMED OF: MUTISM developed the SECOND NIGHT after shell explosion.

Case 265. (Mann, June, 1915.)

A volunteer of 20 was made unconscious for a short time by a shell explosion, but was still fully able to speak when brought to the field hospital.

In the second night after the explosion, however, he dreamed that he had lost his speech. In the ward, meantime, he had seen a number of shell-shock mutes. Following this dream of aphasia, came several weeks of mutism, which then cleared up. According to Mann, this is experimental proof of the psychogenic origin of a mutism.

Mortar explosion: Hysterical deafness.

Case 266. (Lattes and Goria, March, 1917.)

A young soldier, a peasant, fell down unconscious when a mortar exploded killing several men. He regained consciousness a few hours later but was deaf on both sides. He looked dazed and did not spontaneously move, having to be called for meals. Communicating by writing, he could tell all the details of the accident.

The laryngeal and corneal reflexes were absent and there was a hyperesthesia and hypalgesia of the right side of the body. No anatomical basis for the deafness could be determined.

Shell explosion: Onomatopoeic noises in ears.

Case 267. (Ballet, 1914.)

A Zouave was with his squad at Tracy-les-Val Church, October, 1914, when the roof was burst in by a shell which wounded four men. The Zouave felt a strange emotion with trembling, and whistling in his ears. However, he helped his comrades into a neighboring car. From that time forward, he was very emotional, and felt noises in his ear, sometimes humming, sometimes whistling. At Compiègne Hospital a lumbar puncture was made, perhaps with a therapeutic purpose, but this gave no results. The noises were heard as a whistling pseeee followed by a boom,—an onomatopoeia recalling the whistling and bursting of the bomb. There was, in short, no labyrinthine lesion, but merely an obsessive mental phenomenon. There were no ear lesions objectively. The man developed a stuttering some time after the humming and whistling in the ear.

Injury of eyes by gravel from shell-burst: Photophobia, blepharospasm, facial anesthesia, pains.

Case 268. (Ginestous, January, 1916.)

A soldier of the Ninth Engineers, 28, a Beaux-Arts student, was wounded, December 19, 1915, by stones and gravel thrown in his eyes by a shell-burst. The eyelids swelled and the eyes filled with tears. He was treated at the relief station and then evacuated to Verdun. The edema disappeared in five weeks, but it was impossible for him to look at light. February 2 he was evacuated to Nice, where he received the diagnosis of traumatic keratalgia, blepharospasm, and photophobia. After eight days’ leave he went back to his corps; but the eye troubles persisted and he was sent to the ophthalmological center at Angers, May 18, 1915.

Both his father, 67, and his mother, 58, were irritable and odd. Three brothers and three sisters were also more or less neuropathic, and one of the sisters had been in a hospital for the insane with a persecutory mania. The patient had a daughter, fourteen months, well.

The man was a nervous, impressionable person, who wept at the slightest emotion. With an effort of will he could open his eyes, but if one tried to open them passively there was stout resistance. In the dark the occlusion was not so complete. Both eyelids were wrinkled and folded and made jerky, fibrillary movements. The conjunctiva and cornea were normal (fluorescein test), but the palpebral conjunctiva was red and injected. The patient said he had subcutaneous pains recurring at irregular intervals above and below the left orbit, brought out or exaggerated by pressure; but such pressure had no effect upon the lid movements. Visual acuity was normal, but the use of ophthalmometer was impossible, as was measurement of the visual field. There seemed to be no disorder of chromatic sense. The reflexes could not be fully examined; knee-jerks preserved. There was a zone of anesthesia to pin prick, less marked to heat, on the whole left side of the face. W. R. negative.

Shell-shock; burial; blow on occiput: Blindness.

Case 269. (Greenlees, February, 1916.)

A man in the third Wiltshire regiment was buried in a shell explosion and struck by a large mass of earth on the back of the head. When dug out, he was found blind. It was thought at the time that the severe blow at the back of the head had “concussed” the occipital cells for sight.

Some months later the man was sent to Mr. Pearson’s home for blind soldiers in London; but two months later was returned to Weymouth, under Greenlees’ charge. He thought himself worse, since now he could not see light at all. He had trained himself to take care of himself and steered confidently aside from obstacles in walking about. He was able even to learn the various colors by the sense of touch, according to Greenlees; thus, blue was diagnosticated against red: according to the patient, a piece of colored card always had a rougher feel if it was blue than if it was red. In fact, his work consisted of making colored net bags.

As to the possible interpretation of such a case, see Case No. 433 (man who could see large letters sometimes).

Re blindness, H. Campbell states that the number of cases of hysterical blindness appears to be decreasing as the war continues. The blindness he finds to be rarely an absolute one. As a rule, the vision is merely blurred or there is a contraction of the visual fields. The condition is much less frequent than that of deafmutism.

Re hysterical blindness, Dieufaloy is cited by Crouzon as describing a triad of conditions characteristic of hysterical blindness, namely, (a) sudden onset, (b) preservation of pupillary reflexes, and (c) normal fundus.

Shell-shock amblyopia (composite data).

Case 270. (Parsons, May, 1915.)

Parsons describes a typical case of shell explosion amblyopia. After more or less prolonged fatigue from marching and trench exposure, the soldier is knocked down or blown into the air, and more or less severely injured or wounded by concussion, fracture, bullets, or shell splinters, losing consciousness, but perhaps not enough to prevent automatic walking in a dazed state to the dressing station. Memory of this phase is lost. The man is instantaneously stricken blind, possibly also deaf; and possibly smell and taste are also lost. Blepharospasm is intense; there is lacrimation; the lids are opened with such difficulty that examination of the eyes is almost impossible (nor, according to Parsons, have the pupils yet been examined at this stage).

In a week or two the blepharospasm diminishes, and the fundi, which are found to be absolutely normal, can be examined. The eyes may be found to be quite normal, the pupils reactive to light though perhaps sluggishly and perhaps unequally. Sight is now somewhat restored, light can be perceived, and large objects distinguished. The patient can grope about and usually does not stumble against obstacles. The fields of vision are markedly contracted, and more so than the avoidance of obstacles in walking would suggest.

Vision is eventually recovered completely. The right eye (the shooting eye) is often more deeply affected and recovers more slowly. Perhaps a central scotoma may persist. Sometimes on manipulation of lenses the full vision can be produced for the types. Parsons seeks to explain the psychology of traumatic amblyopia in the light of deductions of Lloyd Morgan, Mark Baldwin and McDougall.

Shell-shock amblyopia (excitement, blinding flashes, fear, disgust, fatigue).

Case 271. (Pemberton, May, 1915.)

Pemberton calls attention to the following factors in a case of amblyopia: First, excitement during a prolonged and somewhat critical attack; second, overstimulation of eyes and ears due to brilliant flashes, night firing from many batteries close together (the gunners are always subject to temporary deafness from this firing); third, natural fear from close bursting of shells; fourth, disgust at decapitated and disemboweled soldiers; fifth, fatigue from twelve hours’ work.

The artillery sergeant worked under heavy shell fire at Gun No. 1. A direct hit killed three men serving No. 2 gun. The sergeant became somewhat excited but worked his gun until the following dawn, when he collapsed across one of the disemboweled corpses. He thus had been at work for about twelve hours. The battery had fired 400 or 500 rounds.

A few hours later, the man was conscious but very feeble and much shaken. There was amblyopia and contraction of the fields of vision to rough tests, but no change in color vision. Taste sense was blunted, and salt could hardly be told from powdered quinin tablets. Smell also was practically absent, although he had never been able to smell accurately. Hearing was not more affected than that of other men in the battery, and there were no tympanic fractures. Both thighs, from about the apex of Scarpa’s triangle to the knee, showed partial anesthesia, such that a pin prick that should have been painful was felt only as a tactile sensation, whereas lighter stimulation caused no sensation whatever. The patient himself complained of numbness in these areas. The gait was slow and spastic. The knee-jerks were brisk. Sent back to the wagon lines for a week, the patient lost his sensory disturbance, but the symptoms of mental distress increased. He walked weakly and stiffly; he continually thought of the dead men at the next gun, one of whom was a friend. He was finally sent to a hospital in England.

Shell-shock amblyopia.

Case 272. (Myers, February, 1915.)

A private, 20, lay in the booking-hall of a station, October 28-29, not securing much sleep; motored in a bus next day to another place at 7.30 p.m.; went into billets at 8 p.m.; mounted guard 10-11.30 p.m. and 1.45 to 3.45 a.m.; and went to the firing-line for the first time at 11 a.m. October 31. The platoon advanced through two sets of trenches, which were full, and had to retire. About 1.30 p.m. they were found by the German artillery.

This man had been rather enjoying it and was in the best of spirits until the shells began to burst. The platoon was retiring over open ground. He was kneeling on both knees, trying to creep under wire entanglements, when two or three shells burst near by. Three more shells burst behind and one in front. The escape was described by an eye-witness as a miracle. He managed to get back under the entanglements and into the trench, and shortly, as the fire slackened, rejoined his company.

His sight had become blurred immediately after the shell burst. Opening his eyes hurt him, and the eyes burned when closed. The right eye “caught it” more than the left. At the same time, he was seized with shivering, and cold sweat broke out, especially about the loins. He thought the shell behind caused the greater shock, like a punch on the head without pain. The shell that burst in front had cut his haversack away, bruised his side, and burned his little finger. This shell he thought caused his blindness.

He was led to the dressing station by two comrades, opening his eyes to see where he was going but finding everything blurred except immediately after opening his eyes. There was no diplopia. Objects seemed to dissolve. He was weeping and worrying about becoming blind. The horse ambulance took him to a hospital and thence to another hospital, and thence he went by motor ambulance at night to the starting point, where he arrived five days after he had entered the field. He could remember nothing about the ambulance trips. There was a slight deafness which soon passed off. In hospital he shivered almost incessantly in bed, and he kept thinking about his experience and the shell bursting. The shivering ceased November 3. No micturition from the afternoon of October 30 until the afternoon of November 2. No movements of bowels from October 30 to November 5.

It seems that this soldier had been for two months in the Aisne district, sleeping badly on account of lumbar pains and toothache. There had been albuminuria, and the patient said he had failed to pass a medical examination. The fields of vision were found to be distinctly contracted. There was difficulty in taste and smell, which the patient said he had lost since the shell-burst.

Hypnosis was tried but the patient “insisted on resisting.” The suggestions were offered during the concentration period. November 13 taste and smell began to return and the fields of vision were less contracted. He was transferred to England for further treatment, and by November 27 had become much improved and not so “nervy.” February 1 he had begun to attend hospital as an out-patient.

SHELL WINDAGE (NO EXPLOSION): Multiple affection of cranial nerves.

Case 273. (Pachantoni, April, 1917.)

August 22, 1914, a French officer was leading his company to an attack and carried on, though wounded in the side by a bullet. Suddenly he felt as if he had received a terrible blow with a hammer on the left cheek and eye and as if his arm had been torn off. He fell to his knees without losing consciousness. There had been no explosion, and none of his soldiers had been hit. He felt of his arm and carried his hand to his head to make sure of the wounds. There were none, but he was bleeding from the nose and the mouth. His left eye was closed and his left cheek drawn “by an invisible hand.” His tongue had swollen until it had to be pushed out of his mouth. He was breathing hard. He fell upon his side without losing consciousness and he was carried by his men to shelter in a trench. Placed on his back he felt that he could not lift his head as “it had become too heavy.” His voice was lost. He could neither cough nor spit. In order to get air he had to remove bloody saliva from his mouth with his finger. The left side of the head was swollen. On opening his eyes he could no longer see with the left eye. His cheek was covered with ecchymoses but without wound. A few hours later he was made prisoner by the Germans. For two months he had an increase of temperature every evening and for three months he lost his voice. Six months later there was still visual impairment. He was anesthetic in the left cheek, unable to chew, paralyzed in the left facialis region. There was alteration of taste, with atrophy of the left side of the tongue deviating to the paralyzed side, and nasal regurgitation. There was continual drooling and convulsive coughing. In dorsal decubitus the head could be lifted with difficulty. There was a kind of paresis of the esophagus, as he felt the bolus stop at the level of the third ribs so that with each mouthful he had to swallow a little water. Apparently he had a paralytic state of the following nerves: optic, oculomotor, trigeminal, glossopharyngeal, pneumogastric, spinal accessory and hypoglossal. There was evidence of a slight old tuberculosis at apices. The man was slightly pale. There was an atrophy of the optic nerve and some retinal swelling. No pupillary reactions to light on the left side; but the accommodation reflex and sensory reaction were preserved. Divergent strabismus of the left eye. The taste on the left side and on the anterior part of the tongue was slightly diminished. Diminution of galvanic and faradic excitability on the left side of the face. No reaction of degeneration. Bitter, salt and sweet tastes altered. Left-sided atrophy of the tongue. No reaction of degeneration in the tongue and thyroid muscles although there was a marked diminution in faradic excitability.

The author records this case of multiple lesions of cranial nerves as due to shell windage. Thirty-one months after the onset of the paralysis the cranial nerves, although manifestly regenerated, had not regained conductivity. The officer was examined by Pachantoni at Louèche-les-Bains in Switzerland.

Re windage, see remarks under Case 201.

Wound of thigh: Claudication, vasomotor disorder, hypothermia, but no exaggeration of tendon reflexes. Under CHLOROFORM, ELECTIVE EXAGGERATION OF REFLEXES, i.e., in this case, hyperreflexia of affected thigh, including patellar clonus, after other reflexes (including conjunctival) had become extinct. The case described led to the new formula of THE PHYSIOPATHIC SYNDROME (BABINSKI).

Case 274. (Babinski and Froment, 1917.)

Babinski examined in August, 1915, at the Pitié, a soldier who had been wounded in the upper and outer part of the thigh. He showed a most marked claudication with outward rotation of the foot. There was a muscular atrophy of the thigh but no appreciable disorder of the electrical reactions. There was a slight limitation in the movements of the hip, namely, the movements of flexion and internal rotation of the thigh upon the pelvis; yet this limitation of movements did not seem to be in proportion to the rest of the motor disorder. The X-ray showed no joint lesion. The right knee-jerk was a bit stronger than the left, though this was controversial. Achilles reflexes were normal and equal; epileptoid trepidation of the foot, and clonus of the patella absent; the limb showed marked and permanent vasomotor disorders and local hypothermia; both phenomena were of a sharp and definite nature.

On the basis of the intensity of these vasomotor disorders, Babinski felt that, in accordance with his general ideas, he was not dealing with hysteria, and that he was in fact dealing with the so-called physiopathic syndrome. Lacking for this syndrome was the exaggeration of the tendon reflexes of the affected limb. Might it not be that the improper attitude and muscular stiffness of the limb were based simply on retractions of tendons? The patient was chloroformed. This procedure was the more warrantable as a number of physicians had thought of the patient as an exaggerator or even as a simulator. Under chloroform there was in fact a slight tendon retraction; yet on the whole it was clear that the attitude and stiffness of the limb were largely dependent upon a contracture. When during narcosis all the other tendon reflexes and skin reflexes had become extinct, there was still to be observed on the affected side a hyperreflexia, and even a clonus of the patella; and the clonus lasted an hour after recovery from the anesthetic. This curious phenomenon of elective exaggeration of tendon reflexes in narcosis, Babinski has observed to be not infrequent. It is a valuable diagnostic sign for a sure proof of excess tendon reflexes in cases where doubt prevails under ordinary circumstances. Sometimes the contracture will yield, but only in the deepest sleep, outlasting even the conjunctival reflex and the reactions to pricking of the normal extremities. Moreover, the contracture would return from 20 to 25 minutes before any manifestation of consciousness. If an endeavor was made to reduce the contracture under full anesthesia and in complete unconsciousness, a spasmodic movement was provoked which exaggerated the abnormal attitude of the limb. Sometimes even the leg would be thrown into flexor contracture.

The case above described was the one which led Babinski to his new formula of the Physiopathic Syndrome. This he describes in general terms as follows:

These disorders consist in post-traumatic contractures, paralyses or paretic states, but are not attended by any of the signs of the so-called organic diseases, either of lesions of the central nervous system, or of the peripheral nervous system, or of the great arterial systems. In fact, these disorders somewhat resemble hysterical manifestations. The underlying lesions appear to be sometimes extremely small; in fact, so minimal as to be out of proportion with the functional disorders that they produce. These disorders do not correspond with any known anatomical regions, but they are singularly tenacious, and, unlike truly hysterical (pithiatic) phenomena, they are completely resistant to suggestion. Yet it is not merely in resistance to suggestive therapy that these reflex disorders differ from hysteria; for besides the contracture and the paralysis or paresis found in the different segments of the extremity concerned, the complete Babinski syndrome includes also muscular atrophy, exaggeration of tendon reflexes, alterations of skin reflexes (even amounting to areflexia), hypotonia, mechanical over-excitability of the muscles with retardation of the muscular contraction; quantitative changes in electrical excitability of muscles (excess or diminution without R. D.), mechanical over-excitability, and occasionally electrical over-excitability of the nerves, disturbances in objective and subjective sensibilities (anesthesia and pains), heat regulation disorders (especially hyperthermia), and disorder of the vasomotors (cyanosis, skin redness, oscillometric lowering at the periphery of the extremity in the presence of low temperature), secretory disorders, and various trophic disorders of the bony system, the skin, and the nails.

Despite the permutations and combinations of these symptoms, according to Babinski they amount to a new group of disorders and represent a nosological species: a species of disease phenomena that lies midway between the organic affections and hysterical disorders. Babinski proposes the term physiopathic for these phenomena, a term which excludes the connotation of hysteria and all forms of psychopathia, on the one hand, and seems, on the other, to express the fact of their correspondence to a physical material perturbation in the nervous system of a novel sort.

Bullet wound of ankle: Contracture effect of chloroform.

Case 275. (Babinski and Froment, 1917.)

A man was wounded, September 1, 1914, by a bullet in the left ankle. Contracture of the foot and of the four outer toes in extension followed, with a flaccid paralysis of the great toe. The left knee-jerk was a little stronger than the right; the left Achilles jerk also appeared weaker but observation was difficult on account of contracture of the foot.

Chloroformed, October 22, 1915: There was no sharply defined asymmetry of the tendon reflexes. The left Achilles reflex appeared a little weaker. In the phase of muscular resolution, the contracture disappeared entirely, but it reappeared a little after the return of the tendon reflexes. The reappearance of the contracture preceded the reappearance of consciousness from twenty to twenty-five minutes.

Post-typhoidal reflex or physiopathic disorder of right leg. Elective exaggeration under chloroform.

Case 276. (Babinski and Froment, 1917.)

A typhoid patient, October 20, 1914, showed phlebitis and abscess of the right buttock with contracture of pelvic trochanteric muscles. He was sent to the Pitié on medicolegal grounds.

September 22 there was found a slight laxity of the patella tendon, as well marked on the left side as on the right. The right side was more cyanotic, due to the inactivity of the limb. There was no edema. Tendon and skin reflexes were normal. The lack of power was diagnosticated as purely functional, and the report was rendered that the soldier could begin to walk as soon as he desired. The two knee-jerks were noted to be stronger and polykinetic, and the right knee-jerk appeared a little stronger.

The patient was chloroformed, October 25, 1915. Almost immediately, the knee-jerks, Achilles jerks, plantar, and cremasteric reflexes disappeared. During the first period of anesthesia, there was no accentuation of the reflexes, but at the beginning of recovery the anticipated reappearance of the right knee-jerk was observed. This knee-jerk was already sharply defined at a moment when the left knee-jerk was still abolished. In a later phase of recovery, the right knee-jerk was very markedly exaggerated and a patellar clonus was demonstrable on the right side. Even percussion of the left patellar tendon brought about a contraction of the right adductors. There was a true clonic and tonic spasm of these muscles. On the other hand, percussion of the right patellar tendon was able to provoke no contraction of either right or left adductors. Nor was there at any time any ankle clonus.

Hysterical lameness (bullet wound of calf) cured, but the associated “reflex” disorder (in the sense of Babinski and Froment) NOT cured.

Case 277. (Vincent, April, 1916.)

A corporal was wounded by a bullet in the calf, September 8, 1914. At the end of July, 1915, his lameness continued and he disliked to lean on his left leg which bent under him. There was a slight atrophy of the left calf. The lower leg could not be extended upon the thigh if the foot was in dorsal flexion, and the dorsal flexion of the foot was itself limited. There were no reflex, vasomotor or electrical disorders. The man was given the usual treatment by Vincent and soon learned to carry his body on either foot, and, being well disposed, speedily abandoned his lameness, acquiring such skill in movements that he became monitor over the other soldiers, watching over them in his capacity as corporal.

For about a year he thus served as monitor, and when fully dressed did not seem abnormal or look as if he were walking lame. However, after walking, say 6 kilometers, rapidly, he dragged his leg; nor was extension of the lower leg upon the thigh absolutely complete in habitual walking, though he was able to extend perfectly if requested. Dorsal flexion of the foot was also still somewhat limited, and the measurements of the two lower extremities at both calf and thigh showed a persistent slight atrophy on the left side. He was then sent into the auxiliary service and did good work as draughtsman. In the winter the left foot got cold rather easily.

This case is instanced by Vincent to support the contentions of Babinski and Froment that the truly “physiopathic” or “reflex” disorders do not completely clear up in the recovery from the associated hysterical disorders. That limb, which is the seat of physiopathic disorder, is not in a state of meiopragia.

Foot trauma: Pains and dysbasia, hysterical; slight atrophy of calf, physiopathic. Differential disappearance of hysterical symptoms; increase of physiopathic symptoms.

Case 278. (Vincent, April, 1917.)

Clovis Vincent examined a man who had been wounded in the foot but without injury to the bones. He was first examined in July, 1915, when he complained of foot pains and was walking with crutches. The left calf was smaller than the right (4 cm.). The tendon reflexes were normal. There was no abnormality of electrical reaction. There was no proportionality between the trouble with walking and the organic status. A large part of the trouble appeared to be hysterical. In fact, upon treatment, the man was soon able to abandon the crutches and to walk, though lamely. He was put into the auxiliary military service.

However, the pains grew more marked and the lameness increased. Incapable of working, the patient was sent to the neurological center at Montpellier, whence he came to the neurological center at Tours in September, 1916. He had never been confined to bed, and had never ceased his daily walking, aided by a cane. The walking disorder was very pronounced. The patient said he was still suffering much. The difference between the two calves was now 8 cm. and the thigh was atrophied, though the atrophy had been absent in July, 1915. There was hyperexcitability of leg muscles. The right foot was colder than the left. The hysterical phenomena, so pronounced in July, 1915, were now absent, yet the reflex phenomena were sufficient to invalid the man.

Shell-shock paraplegia may AFTER TWENTY MONTHS develop vasomotor and secretory disorders: The whole to vanish on treatment.

Case 279. (Roussy, April, 1917.)

A foot chasseur, 22, a farmer in civil life, sustained shell-shock à distance, June 2, 1915. He had no wound, but lost consciousness. He was evacuated for “contusion of back” to a hospital June 4 to 12; for “contusion of back and commotio cerebri” to Portarlier, to July 21; for “internal contusions and commotio cerebri” to Besançon, where he was in three hospitals up to May 31, 1916, and the diagnosis “hysteria, old commotio cerebri and trepidant astasia-abasia” was rendered and psychotherapy tried. The man was then evacuated to Saint Ferréol and the diagnosis “hysterical paraplegia” rendered. He finally reached Veil-Picard in February, 1917, still victim of paraplegia.

Up to this point there had been no signs suggestive of organic lesion of the spinal cord or any hysteroörganic intimation whatever. But in February, 1917, besides the motor disorder there was a hypothermia of several degrees, with cyanosis and hyperidrosis of both feet, with a marked diminution (and absence on one side) of the plantar cutaneous reflexes. The man was also victim of “hysterical pregnancy.” The cyanosis, hypothermia and hyperidrosis lasted six weeks.

March 23 the man was given treatment and for the first time in 21 months was able to stand and walk. The foot now turned from blue to red, and instead of cold became warm, even hot. In about a week the hyperthermia diminished, and, with the other troubles, disappeared. There remained only a slight swelling of the foot and ankle joints, due to the painful exercises given the patient.

It would seem, then, that a hysterical paraplegia of long duration may finally associate itself with marked vasomotor and secretory disorders and that these may be altered with extreme rapidity on the very day in which the hysterical phenomena are removed, and quite disappear in a fortnight.

Tetanus clinically cured: Phenomena in part reproduced UNDER CHLOROFORM ANESTHESIA five weeks afterward.

Case 280. (Monier-Vinard, July, 1917.)

An infantryman, wounded at Notre Dame de Lorette, May 9, 1915, by a shell fragment in the right popliteal space, was given a preventive injection of 5 c.c. of antitetanic serum, evacuated to a hospital, May 12, and developed signs of tetanus August 1, with trismus and pains and spasms in the right leg.

The disease progressed with dysphagia, stiffness and paroxysmal hypertonia of the legs, especially of the right leg, fixed orthotonus of the trunk, neck hyperextended, arms stiff but able to move. Antitetanic serum was given daily. At the end of eight days there was a marked improvement and the whole course ran to approximate recovery in 25 days from the onset of tetanic symptoms, at which time the man was able to get up and walk on a crutch. The external popliteal nerve had been sectioned, and the foot was in a marked equinovarus.

Chloroform was administered for the purpose of straightening the foot, September 2, that is, about five weeks after the apparent end of the tetanus. The first stage of the anesthesia lasted about two minutes, but at this point the trunk and leg muscles passed into a state of diffuse contracture. In fact, a tetanic syndrome took place in the midst of the anesthesia. At a time when the corneal reflex was completely abolished, it was still impossible, with the exertion of the greatest strength, to flex the segments of the lower extremities. Moreover, the trunk was stiffly extended and the jaws were in trismus. Tonic and clonic contractions were produced by the efforts made to straighten the foot, and these contractions passed from the right side to the left. The chloroform was now increased and a transient resolution of the muscles was obtained, lasting hardly more than a half minute. As all efforts to reduce the pedal deformity failed, anesthesia was stopped. The contractures and paroxysms lasted a few minutes. The knee-jerks were extremely exaggerated and there was a bilateral ankle clonus. After a brief phase of excitement, the patient emerged from anesthesia, began to talk with his comrades, and ate his usual meal without inconvenience. The chloroform anesthesia had lasted twenty minutes, and 60 grams had been administered.

It was now determined to section the tendo Achilles and the tibialis posticus. September 8 the man was chloroformed again and the same phenomena were exactly reproduced. Sixty grams of chloroform was again administered. The tendon resections permitted placing the foot in the proper attitude. Next day the patient was examined neurologically. The skin reflexes were found normal. The Achilles and knee-jerks were somewhat exaggerated, but equal on the two sides. There was no ankle clonus. Sensations proved normal. There was a mechanical hyperexcitability of the muscles of the anterior aspect of the thighs and of the calf.

In another case chloroformed 17 months after recovery from tetanus no such phenomena appeared. It would seem that the impregnation with tetanic virus or toxin must last in the nervous system a good deal longer than the apparent disease clinically lasts, but that this belated and concealed intoxication eventually passes.

The phenomena are perhaps analogous to those of Babinski and Froment’s so-called post-traumatic physiopathic or reflex phenomena. It was following the special work of Babinski and Froment upon the use of chloroform anesthesia in detecting physiopathic conditions that Monier-Vinard made his observations in cases of tetanus.

Shell-shock from falling of shell at a distance: Hysterical hemiplegia, terminating in brachial monoplegia. Case to show that the reflex or physiopathic disorders of Babinski and Froment may occur without mechanical injury in the region involved.

Case 281. (Ferrand, June, 1917.)

A soldier of the class of 1917 who never went to the front, while in training at Belfort, felt violent emotion on the occasion of the falling of a big shell in the town of Belfort. The explosion was a good distance from him. He lost consciousness a few moments, February 23, 1917, and almost at once found himself unable to move his left side. He was hemiplegic three months, but his leg shortly regained power. December 23 he entered a neurological center with his arm flaccid and a paralysis affecting the shoulder also. There was an almost complete anesthesia of the arm terminating in segmentary fashion about the shoulder, and the whole of the left side was slightly hypesthetic, although there was no disorder of motion except in the arm. The tendon reflexes of the left arm were exaggerated, and there was even contracture upon percussion of the muscles themselves. Percussion of the thenar and hypothenar eminences produced movements of the hand. There were several vasomotor disorders. Percussion led to large vasomotor plaques, and rubbing of the skin produced a reddening which passed away slowly. The hand was red and cold. Slight electrical hyperexcitability of flexors with feeble galvanic current; excitation of the extensors not associated with any contractions of the antagonist muscles. Threshold lower for flexors on the affected side in the forearm. Half centimeter atrophy of the biceps. The forearm and hand were possibly slightly increased in volume from a blue edema of the dorsal surfaces. The man was very timid, complained little, and accepted all treatment, which, however, was not very effective. This is presented by Ferrand as a case with physiopathic disorder in the sense of Babinski and Froment, though it does not present any sign of organic lesion whatever.

Shell fire: Delayed shell-shock symptoms, sub-lethal, appearing in England.

Case 282. (McWalter, April, 1916.)

A soldier was picked up insensible in the public street and brought to hospital by ambulance, unconscious, breathing stertorously, pupils dilated, lips parched, unresponsive to stimuli, but without signs of injury or alcoholism.

The pulse grew slower, the respirations more sighing, the heart-beat more diffused and labored; but towards evening, about eight hours after admission, he began to move the eyelids and lips, and muttered a response to the request for his name. After ten more hours, respiration grew better, and Croton oil led to a movement of the bowels. Natural sleep intervened, and 18 hours after the onset of unconsciousness, the man woke up, and in the course of a few days became fairly well though still dazed and confused.

This soldier had never received any definite injury in his war service, but McWalter attributes his break-down to the effects of the constant shocks from the bursting of shells, and the scattering of shrapnel.

McWalter generalizes that a soldier, in the course of some civil occupation after the war, might develop symptoms, even fatal symptoms, and still the death in the case would be a direct consequence of the war.

Shell-shock symptoms, some initial, with recovery—others late and gradual, with deterioration.

Case 283. (Smyly, April, 1917.)

A soldier became blind, deaf and dumb, as well as paralyzed, as a result of shell explosion. When he arrived at the hospital, he was able to see but had visual hallucinations. In a few days he recovered his hearing. There was a fine tremor of the hands, controllable by suggestion. There was an almost complete amnesia, but the patient remained able to read and write.

The pain persisted several months. The patient was physically well and seemed perfectly intelligent despite his aphasia and amnesia. One night, he sprang out of bed, shouting, “The guns are coming over us!” and from that time forward was able to speak. Amnesia, however, supervened for the months in the Dublin Hospital, and the patient believed that he was still in France. He also became unable to read or write, and was unable to recognize any letters except those he had been taught to speak during his period of dumbness. Still later he got a flaccid paralysis of the legs. From seeming perfectly intelligent, he began to seem markedly deteriorated. Hypnosis with waking suggestions had no power upon him. After a time, intelligence reappeared, but there had not been any recovery of locomotion at the time of report.

Wounds, gas, burial: Collapse on home leave.

Case 284. (E. Smith, June, 1916.)

A non-commissioned officer went through the first eleven months of the war in France and Flanders and was subjected to every kind of strain therein. He was wounded twice, gassed twice, and buried under a house, in each instance being treated in the field ambulance and returning to the trenches. Some time thereafter he was granted five days’ leave.

On reaching home, while waiting for a train, the officer suddenly collapsed and became unconscious. For months thereafter, he was the subject of a severe neurasthenia; “the whole of his trouble seemed to be due to the dread, lest on his return to the front, the added responsibilities which would fall upon his shoulders might be too much for him.” He thought his intelligence had been numbed by his experience. He thought his memory was unreliable, and that he could understand neither complex orders nor even the newspapers.

As to the reason for his maintenance of composure at the front, this may be laid to the excitement, the officer’s sense of responsibility, and the example he felt he should set his men. This kind of case “demands a great deal of patient and sympathetic attention before the real cause is elicited, and then months of daily reëducation to build up anew the man’s confidence in himself.”

Bullet wound of neck: Late sympathetic nerve effect.

Case 285. (Tubby, January, 1915.)

A Belgian was wounded, October 21, 1914, at Dixmude. The bullet wound was just below the right mastoid process. He was admitted to the London General Hospital, October 29. He said that the bullet had passed into the tonsil, lodging there, but that on the third day, while vomiting, he brought up the tonsil with the bullet in it. There was in fact a large ragged wound at the site of the right tonsil. He could swallow fluids only, but articulated clearly. There was a question of injury to the following nerves: facial, glossopharyngeal, vagus, hypoglossal, spinal accessory, and sympathetic. None of these nerves, however, appeared actually to have been injured. The difficulty in swallowing was due probably to the faucial wound, and it is hard to see how the pharynx could have been involved on account of the perfect articulation. November 3 the right sympathetic nerve was slightly affected; the right pupil was smaller than the left although it reacted to light. November 12 the patient left the hospital and nothing further is known of his history. Thus there was a late effect upon the sympathetic nerve thirteen days after the wound.

Re peripheral nerve disorders, see remarks under Case 252 (Tubby).

Fall from horse under shell fire: Crural monoplegia, hysterical. Reminiscence? Autosuggestion?

Case 286. (Forsyth, December, 1915.)

A patient of Forsyth had been exercising a high-spirited horse. Artillery fire close by made the horse leap sidewise, and the rider fell, his back striking the ground. He seemed to be curiously shaken out of proportion to the gravity of the fall. In a day or so, he lost the use of one leg.

He recalled a rather similar incident: He had taken a hand in a local uprising in a distant quarter of the world. While he was escaping up a mountain track, a rifle-shot from the enemy brought down his horse, which rolled over and threw him violently against a boulder, where the small of the back met the force of the impact. He felt intense pain and lost consciousness. Upon recovery he found he was paralyzed. At the end of several days, in a hiding-place in the rocks, he found himself still unable to move his legs. The friend who had carried him to the hiding-place refused to leave him. He thought of suicide, but then discovered that he could move: at first, the big toes, then the ankles, then the knees, and finally the hips. He was finally able to get into the saddle.

Moreover, years before, he had heard that a man who broke his back was paralyzed in the legs.

Re autosuggestion, Babinski remarks that suggestion may work in hystero-organic cases not precisely as in hysterical cases. Autosuggestion may here replace or accompany the ordinary heterosuggestion. Some temporary disturbance—a slight pain, a trivial injury, or a mere bruise—may start up a complex process of autosuggestion in which it may be difficult to unravel the part played by the patient’s own reflexes, his previous experience and beliefs (in this case, the reminiscences of a similar accident), the solicitude of his friends, and the medical examination itself. Babinski believes that hysterical paraplegia or monoplegia never appears automatically under the influence of emotion; never appears after the manner of sweating, diarrhea, or blushing.

Shell explosion; struck in cave-in: Symptoms in right leg (antebellum experience).

Case 287. (Myers, March, 1916.)

A private, 26 years old, had 11 months’ service and one month’s service in France. He arrived at a base hospital the day after his shock. Concussion had caused the dug-out in which he was standing to collapse. A beam struck him on the left side of the face, and pinned him to the ground on his right side. A piece of iron fell on the left side of his back, and his right leg was pinned by a cross beam on the back of his thigh. He was dazed by the shock; was released and was able to walk, but complained of a pain in the right groin and a giving-way of the right knee. The medical officer arrived about an hour later. A numbness, or state of no feeling, in the right thigh appeared, and increased to the point of total analgesia to the level of the upper margin of the patella save for a narrow strip in the mid-line on the posterior aspect of the leg. The only area of complete anesthesia and algesia was on the outside of the lower half of the leg.

According to the patient, it seems that about three years before, he had been buried four feet deep in a brick yard, beneath a heap of clay. He had felt it most in the right leg, but the thigh had been merely stiff and sore, and not numb. The patient admitted that the present accident immediately reminded him of his previous experience. There were no tremors or sensory disorders in the face, arms, chest, back, or abdomen. There was diminished sensibility to cotton wool of the left buttock (across which a plank had fallen), and there was a degree of hypalgesia of the buttock. The right thigh showed a degree of thermanalgesia and slight loss of vibratory sense. The corneal and conjunctival reflexes were diminished, and the knee-jerk was unobtainable on the right side. Three days later, there was a marked improvement with almost complete return to normal, whereupon the patient was sent to a convalescent camp.

Emotional subject, ALWAYS WEAK IN LEGS; shell explosion; wound of back: PARAPARESIS.

Case 288. (Dejerine, February, 1915.)

A Lieutenant, 25, was wounded at Arras about 10 a.m. October 20, 1914, just as he was leaning on another officer’s shoulder looking at a card in a chateau room. A shell burst in the court yard. A fragment came in the window, struck him in the back and pushed him forward, whereupon he felt pain in the back and a severe dyspnea, due to the gas from the shell. He lost consciousness several times and the dyspnea lasted for about two hours. When he was picked up he could not walk.

He was carried on a stretcher to the ambulance at Avin-le-Compte. During the fortnight there, he was also several times dyspneic. Strength left his legs and he could only get about on crutches. There was now a suppurating wound in the interscapular region where he had been struck by the shell fragment. Evacuated to Paris, he was operated upon on account of a tremendous abscess in the back, and the shell fragment and some bits of cloth were removed. The wound healed; but vague pains in the left thorax remained, especially when the man walked.

On examination, July 28, 1915, he would in the standing position hold his legs together with the feet resting on their external borders, especially on the left side. The toes were in plantar flexion, and the soles were arched upward more on the left side than on the right. In walking, the legs were always held in extension, the feet twisting outward. If an attempt was made to walk quickly, the man walked more and more upon the external borders of his feet, in such wise that the plantar surface and the heel turned up and became visible from above. He would get tired after five minutes’ walking even if he spread his legs out for a broader base of action. He could lift his legs only about 10 cm. from the bed, but could flex and slowly extend his lower leg on the thigh. He could not adduct or abduct the feet. Movements of extension and flexion of leg on thigh were jerky and abruptly terminated, as also movements of thigh on hip. The patient could not sit, and when leaning forward he could not straighten up against resistance. The reflexes were normal. There was no sensory disorder. The electric reactions were normal. Pupils normal. There was slight hypertension of the spinal fluid and a slight excess of albumin. There were no lymphocytes.

In accordance with Dejerine’s idea that these neuropaths always have antecedents looking in the same direction, it was found that he had always been an emotional person, easily affected, sympathetic with other people’s troubles, given to weeping. As Lieutenant, he had not had the courage to harangue his soldiers. He had often during his life felt his legs weaken during times of emotion and had sometimes been unable to walk, though nothing of the sort had happened during the campaign. He was sure he could get well, and wanted two months’ leave in order to get back to the front. There were no hereditary features in the case. A physician had told him that he had had meningitis. This possibly followed whooping cough. He had had orchitis after mumps at 16. He had not had children, nor had there been miscarriages since marriage at 21.

Wound near heart; delayed medical care; fear of having been shot through heart: Paraparesis (antebellum always “hit in the legs.”)

Case 289. (Dejerine, February, 1915.)

An infantryman, 20, was sent as a Colonel’s bicyclist about 1 p.m. September 30, 1914, with a message to one of the battalions. He was exposed on the way to shell and rifle fire, and was wounded by a bullet which entered 8 cm. below and internal to the left mammillary line and came out in the region of the left hypochondrium. He crawled to some village houses 20 or 25 meters away. Another cyclist came to transfer the order, but could not help him. A friend came to his aid but was struck by a bullet 10 meters off and remained on the ground for an hour while the young cyclist lay behind a tree on the roadside. At 3 o’clock it was possible to take him to a house around which shells were raining. Shortly afterward the house caught fire. The man was evacuated 6 kilometers to an ambulance in the night, and that night six of his wounded comrades died in the same room. The man had lost much blood and began to think that his heart had been hit. He choked, had violent palpitations, and intense thirst. By automobile next day he was taken to the railway station at Maison and was there for a day practically without food.

That evening, 36 hours after the wound, he was evacuated to Juivisez and stayed there one night in the temporary hospital. The hemorrhage had now practically ceased. When he arrived next morning at Vincennes he could hardly move, was unable to walk, had violent palpitation, precordial pain, and two nervous seizures, with outcries and weeping. Several days later he could not walk at all or raise himself in bed. He was operated on May 29; he afterward felt the same leg weakness and was still unable to walk. Early in December, when observed by Dejerine, he was able to stand on crutches with legs flexed, toes on the ground, and heels up. In walking he would scrape the ground with the dorsum of the foot. The wound was now healed. Suppuration had been intense and the scars were extensive. Lying down, the man could move, though slowly, his lower extremities in every way, nor was there any diminution in the strength of his flexors and extensors. The patient in making movements against resistance would let go quickly and jerkily. The plantar reflexes were flexor but weak. There was no other reflex disorder, no evidence of sensory disorder, nor any sign of neuritis or arthritis. Lumbar puncture gave a normal fluid without tension.

There were no hereditary features in the case. The man had been in childhood nervous and irascible, rolling on the ground, crying and weeping when crossed. He had had three attacks of appendicitis—one at 15 years and two at 19 years. After each attack he had felt weakness in the legs. He remembered, too, that after his nervous crises on being crossed, he had always felt this same weakness.

According to Dejerine, these paraplegic neuropaths, like functional gastropaths, cardiopaths, and victims of urinary disorder, have had earlier spells of the same kind, though milder than the attack which brings them to medical notice.

Wounds: Tic on attempts to walk; tremors. Recovery except for frontalis tic (ANTEBELLUM HABIT emphasized).

Case 290. (Westphal and Hübner, April, 1915.)

A substitute officer (mother nervous; always slightly excitable, easily fatiguable; had had a habit of wrinkling his forehead) sustained wounds September 8, 1914, in the foot and thigh. The wounds healed well, but in the hospital he slept badly and had battle dreams. When he essayed to walk, he had contractions of face muscles. There was a lively tic involving both face and neck muscles, with the head pulled to one side and backward. This grimacing was but slightly influencible by the will. There was a marked tremor of the arms. Gait was trippelnd. There were tremors of the whole body. There was also a slight hemi-hyperesthesia. The tendon reflexes were very lively; vasomotor disorders (feelings of cold and perspiration).

Seven months later the phenomena had all disappeared except for slight tic-like frontalis contractions.

Re heredity and soil, Mairet investigated 22 cases of Shell-shock, and found a hereditary taint in eight, and an acquired predisposition in nine. He found hereditary taint definitely absent in seven, and acquired soil definitely absent in six; whereas the rest of the cases were doubtful. He found both the taint and the soil in five cases; two cases with hereditary taint alone; no case acquired, non-hereditary.

In eight cases with head trauma, Mairet found three with hereditary taint, four without such; against one with an acquired predisposition, four without such, others doubtful.

Re cases of somatic trauma (not affecting the head), among five examined, there were none with hereditary taint, three definitely without taint, and five definitely without predisposition. According to Babinski, neither hereditary taint nor prepared terrain needs be found in hysterics.

A predisposition is not thought important by Oppenheim, especially as so many normal persons are predisposed.

War strain (fatigue, emotion): Hysterical hemiplegia. Precisely similar hemiplegia ANTEBELLUM.

Case 291. (Roussy and Lhermitte, 1917.)

A sergeant in a regiment of cuirassiers was observed at Villejuif, January 25, 1915. He had lost power on the left side as a result of fatigue and emotion, November, 1914. He had a complete paralysis of the left arm and a paresis of the left leg. There was an anesthesia of hysterical type in the left arm, and also of the left leg as far as the middle of the thigh. He dragged his leg in walking (démarche en draguant: the toe is dragged along the ground, the trunk is bent forward, and at every step plunges somewhat toward the paralyzed side. The patient is able to walk, however, by means of a cane or crutches. This walk is characteristic of hysterical hemiplegia. According to Roussy and Lhermitte, the number of cases of hysterical hemiplegia (better, hemiparesis) is not large). The plantar reflexes on both sides were those of flexion. Upon treatment (not specified), at the end of six months he went back to service in the cavalry.

The point of note in this case is that this patient had had a precisely similar phenomenon on the same side, which lasted a month, at the age of sixteen years and a half. It is noteworthy that in this case there was no traumatism and only the factors of fatigue and emotion to serve as an occasion for the hemiplegia. In fact, hysterical hemiplegia is said very rarely to follow physical trauma to an extremity. There are, however, some cases in which hemiparesis follows a slight head wound, particularly if over the region controlling the paralyzed limbs.

During the six-months’ course of successful treatment, no atrophy of limbs appeared, and there was never any inequality of the reflexes.

A good soldier (son of a tabetic sometimes hemiplegic), at 17 victim of hysterical hemiplegia, has AT 24 A RECURRENCE after two months’ field service. “Functional excommunication” of left arm and leg.

Case 292. (Duprés and Rist, November, 1914.)

A cuirassier, 24, one month in the field, began to feel in September, 1914, crawling sensations in left arm and leg; then fingers, later hand and forearm, and finally upper arm began to work awkwardly and feel heavy, and there was a little of the same sort of thing in the leg. Hand and forearm were by the middle of October completely paralyzed, whereas the arm and shoulder were only paretic. Anesthesia at this time reached the elbow. The man had to be evacuated, after two months’ active and skilful field service, in one instance (September 19) carrying out a clever and useful interception of hostile telephone messages.

It seems that at the age of 17 also the man had had a left-sided hemiplegia, with sensory and motor symptoms, lasting two months, cured by electricity applied with a small electrode in his village. The war situation was therefore actually a recurrence of the transient hysterical paraplegia.

Moreover, the patient’s father, 52, an old tabetic, had also several times shown a hemiplegia (however on the right side), a phenomenon which had strongly affected his son.

It was curious that the slight residuals of movement which the cuirassier could perform could be made only while he was looking at the parts he was requested to move, and were impossible with eyes closed. The anesthesia was a total one when observed in November, 1914, coming to a sharp and circular termination at the shoulder and garter-wise above the knee—tuning fork insensibility in the same areas. The left patellar reflex was diminished when the eyes of the patient were leveled at the knee; but a surprise test brought the knee-jerk out normally. The hand and fingers were a little darker in color, and the whole left arm a little colder than the right. There was also a slight amblyopia on the left side.

This hysterical paraplegia proved rather resistant to psychotherapy. The patient seems to have systematically eliminated from consciousness and from action the entire function of the left arm and a good deal of the left leg. Duprés and Rist speak of this as a kind of functional excommunication of the parts.

Re relapses, Wiltshire remarks that the frequency of relapses and the ways in which they are produced favor the conception that the original cause of Shell-shock must be psychic. Sir George Savage remarks that cases of Shell-shock should not return to the service under a period of six months on account of the frequency of relapse. Others have recently argued that such cases should not be sent back to the front at all. Harris notes that relapse may follow so apparently slight a factor as a vivid dream. Remarks concerning the true nature of relapses are made by Russell. Russell, for example, disapproves anesthetics in curing such a hysterical phenomenon as deafmutism. This sort of treatment does not get at the real cause of the condition, so that the man is very liable to relapse with the same symptoms. Ballet and de Fursac note the many cases of relapse after treatment and after discharge. Sometimes the relapses were due to some unfortunate happening, but in other instances no external cause could be made out. Fear of having to return to the front is a factor in certain cases, so that the true answer to the relapse question may not come until after the war.

Roussy and Boisseau insist upon the value of rapid cures (psychotherapy, electricity, cold shower, etc.), in diminishing the number of relapses. They maintain that these rapid cures abolish any chance for the man to brood over symptoms and thus to exaggerate and fixate them. These workers send their hospital return back to the regiments with a statement relative to diagnosis and the request that he be immediately returned to hospital if neurotic symptoms appear.

War strain; burial: Deafmutism. ANTEBELLUM speech difficulty.

Case 293. (MacCurdy, July, 1917.)

A private 20 (always rather tenderhearted, disliking to see animals killed; rather self-conscious; a bit seclusive; “rather more virtuous than his companions”; shy with girls; sore throat a year or more before the war, with inability to sing or talk; always a lisper) enlisted in May, 1916, spent five advantageous months in training and became increasingly sociable. However, on going to the front October, 1916, he was frightened by the first shell fire and horrorstricken by the sight of wounds and death. He grew accustomed to the horrors and five months later was sent to Armentières, where he had to fight for three days without sleep. He grew very tired and began to hope that he would receive wounds that might incapacitate him at least temporarily for service.

He was suddenly buried by a shell, did not lose consciousness, but on being dug out was found to be deaf and dumb. On the way to the field dressing station he had a fear of shells. The deafmutism persisted unchanged for a month and then was completely and permanently cured in less than five minutes. He was made to face a mirror and observe the start he gave when hands were clapped behind him. He was assured that this start was an evidence of hearing; that his hearing was not lost, nor was his speech. He had no relapses during two months.

According to MacCurdy, this case is a typical one of war neurosis of the type of a simple conversion hysteria. The man never suffered from anxiety or nightmares.

Re burial cases, Grasset suggests that some of the patients probably think that they have actually died; both sensation and motion have been lost, and it is naturally these that permit a man to believe that he is still alive. The classical case is recalled, of the almost absolutely anesthetic boy who, with eyes closed, at once fell asleep. Foucault’s patient also said he actually thought he was dead after an explosion.

War strain: Shell-shock and psychotic symptoms, with determination to parts injured ANTEBELLUM.

Case 294. (Zanger, July, 1915.)

Several years before the war, a cavalry officer had a severe concussion of the brain after a fall from his horse, but got no manifest symptoms therefrom except a mild transient deafness. There must have been a vestibular nerve injury, however, since there was a marked bilateral subexcitability of this apparatus later determined.

In September, 1914, as the result of strains and privation in the field, he got vertigo and lachrymose spells, with some obsessions as though he would have to shoot himself in the foot or spring out at the enemy from the trench.

In hospital at Jena, insomnia, anxiety, excessive perspiration and salivation, feelings of the death of various parts of the body, especially the forearms and hands, associated with hypesthesia of the parts, were determined. He had a feeling of vertigo on walking and was very sensitive to noise. He now developed a very intense and very variable degree of deafness on both sides, diagnosticated as nervous deafness. The caloric test demonstrated vestibular subexcitability above mentioned. We may suppose that in this already injured organism fresh disorder had set in on a psychogenic basis in the same region that had been injured years before.

Mine explosion; emotion at death of comrades: Unconsciousness eight days with hallucinatory delirium; later, dizziness. History of previous trauma to head with unconsciousness and dizziness.

Case 295. (Lattes and Goria, March, 1917.)

Sent at end of May to the front, an Italian soldier (Class 1895, laundryman) was placed in an advanced post where he at once sustained great hardships.

Father drunkard, mother healthy, sister nervous. Two brothers healthy, one brother died of tuberculosis. Patient had scrofula, scarlet fever, and bronchitis (tendency to rave intensely when in fever). At four, sustained a trauma on the head (skull depression), dizziness, loss of consciousness.

June 7, a mine exploded in his vicinity, smashing several of his comrades. He did not himself fall to the ground, but was overwhelmed by a violent feeling of anguish. After a while, he lost consciousness. He woke up at Bologna, June 15, as after a long sleep. During the interval he had been in a state of intense hallucinatory delirium day and night. Then his mind began gradually to clear, first with amnesia of the shock which had caused the trauma. Then he recalled this fact too. Dizziness, however, grew in intensity so that he fell to ground many times during the day. There were intermittent tremors in the limbs.

Under observation, August 7, a sturdy, robust man. Somewhat dull in demeanor. Senses intact. Cranial nerves negative. Tendon and skin reflexes lively, especially on the right. Memory intact, except for above-mentioned oniric delirium with restlessness and shouting at night, especially while falling asleep and waking up. Frequent intense dizziness.

The condition remained unchanged for a week. Patient transferred to another department, for acute catarrhal bronchitis with fever.

Sniper stricken blind in shooting eye.

Case 296. (Eder, March, 1916.)

An Australian, 19, was admitted to hospital for loss of sight in the right eye. There had been a right ptosis from childhood. January 7 nothing could be perceived but light.

According to the patient, he was sniping through a loop-hole, November 15, when a bullet knocked a piece from the stock of his rifle. He continued at his post. There were five more shots, when another bullet struck the sand around the loop-hole. His right eye began to water. He shut the loop-hole and retired for an hour. His eye improved, he returned, opened the loop-hole, braced the rifle, and found he could not see the sights. He went to the physician. Vision grew rapidly worse, and in a few hours perception of light failed. He had been stricken blind in the shooting eye (the seat of a congenital deformity).

Anticipation of warfare: Hysterical blindness.

Case 297. (Forsyth, December, 1915.)

Anticipation of warfare may provoke a neurosis as in a case of Forsyth’s. The man went blind training in England.

It seems that four months before, while mounting sentry at night, marauding gypsies had felled him by a blow on the head from behind. He had returned to duty after a day or two and was now expecting to be moved to France. He said that while sitting with a friend, he began to feel giddy, turned a somersault, and fell unconscious; and that on coming to, his mind was clear but everything was dark. For ten days he had been blind, although once he could see his parents, who visited him in hospital, almost clearly. His appearance under examination strongly recalled that of a blind man. He was induced to read some large print, then smaller print, and finally very small print. He then lapsed into blindness.

He remembered that before enlisting, he had trained in a smithy, and heard that blacksmiths often went blind at the forge.

Bareback riding: Spasmodic neurosis (similar ANTEBELLUM episode).

Case 298. (Schuster, December, 1914.)

A soldier, 32, had to do a long stretch of riding bareback. As a result, he later suffered from tonic muscular spasms whenever he had to exert himself seriously, especially whenever he had to move his legs and when sudden movements or sudden strong contacts were made. The attack appeared to be reflexly dependent on the pain. The case is regarded as one of the Wernicke Crampusneurosen, a disease somewhat related with hysteria.

A condition somewhat like the one developed in the war had occurred in this man at the age of seventeen after a drenching, but the attack was at that time much milder. He had, however, frequently had cramps in his legs.

ANTEBELLUM spasm of hands, functional.

Case 299. (Hewat, March, 1917.)

A boy, 19, had been passed as fit for laboring work at home. He had been a farm boy from 14. Once at 17 he had developed whilst working amongst turnips in wet weather, pain in the hands, which got worse and was followed by pains in legs, arm, and neck, that kept him in bed a week, and from work ten days. Even on returning to work, his hands were swollen, though he was able to drive a horse. The fingers had been somewhat firmly flexed on the palms ever since this illness at 17.

He was sent to Netley after three weeks of army work, as having a spasm of both hands. He was found to be mentally below par, nervous, apprehensive, stuttering in speech and not readily responsive, with defective vasomotor control, though of good average bodily development except for asymmetry of chest.

Both hands were found firmly closed; tips of fingers applied to palms; thumbs freely movable; forearms well developed, especially the flexors. Counterforce was exerted upon passive extension of fingers. There was no sensory or reflex disorder, and while the patient was asleep, it was found that the first and second fingers of both hands could be fully extended. Yet there was a definite contracture of the palmar fascia which prevented full extension of the third and fourth fingers. He was awakened by this test and the fingers became firmly flexed at once.

The man was treated by milk isolation behind screens, without permission to read, smoke, or talk. Twice a day he was encouraged to move the fingers and made to perform finger exercises. He became able to extend the fingers over half their normal excursion in three days, and was then able to abduct and adduct the fingers. He was allowed up in two weeks’ time, with full diet and screens removed. The contracture of the palmar fascia was still in evidence, but the power of movement in the hands and fingers was so satisfactory that he could be sent back to duty in three weeks. The interpretation of Fergus Hewat is that the painful condition of the hands which set in in the illness at the age of 17, had caused an obsession which had developed into a functional spasm of the hands.

Quarrel: Hysterical HEMICHOREA, DOUBLY REMINISCENT, of a former hysterical chorea, itself related with an organic chorea of the patient’s mother.

Case 300. (Dupuoy, October, 1915.)

A nineteen year old soldier, for some months a bit distressed and irritable, had a dispute with an old man whose jug he unluckily happened to smash. The old man said something was going to happen to him for that. That day, in point of fact, he fell and sustained an injury with water on the right knee. He was upbraided by the captain and evacuated to the ambulance. The fellow thought the old man with the broken jug had interfered, dreamed of the old man’s threats, and felt his hand on his shoulder.

Next day hemichorea developed on the right side, a partial and rhythmic chorea with jerky, regular contractions, fifty to sixty per minute, affecting synchronously the muscles of the leg, arm, face and tongue.

Dupuoy speaks of the reason for the hysterical “choice” of this disease, since his mother had had a probably organic hemichorea, also on the right side, with which she died at thirty years in a stroke. The boy was at that time thirteen years old and had had a rhythmic chorea six weeks, limited to the extensors of the hand on the forearm, treated in hospital.

This new hemichorea was quickly and completely cured by psychotherapy.

Hallucinations and delusions in a soldier, of antebellum origin. Treatment by explanation of causes.

Case 301. (Rows, March, 1916.)

A private, 31,—a case of Capt. W. Brown,—was admitted to hospital suffering from hallucinations of hearing and delusions of supervision by his family and friends; he heard his relatives telling him what to do and what not to do. He thought they belonged to a secret police entrusted with the task of supervising his actions and seeing that he did not again transgress as he had done. An inquiry into his past revealed the following facts:

He had been a bank clerk before the war and once because of a nervous breakdown as a result of drinking and smoking had been given a three months’ vacation. On this occasion he went with a prostitute—his first and only offence in sex matters. He later thought the behavior of his family indicated that they knew of his misdeed. He heard the voices of members of his family, became rapidly worse and more depressed, and attempted suicide.

He went to a private asylum. Later, he emigrated to Canada, but he was still pursued by the voices and he returned to England. He enlisted at the outbreak of the war and went to France. He was soon invalided and sent to Maghull.

The cause of his condition, according to Rows, was his affair with the prostitute and his previous drinking. This was explained to him as the basis of his strong feeling of self-reproach. The hallucinations and idea of suicide had developed therefrom. Recovery “to a large extent.”

A poor risk (hereditary and acquired); emotionality: Tremors and convulsive crises with lowering of pulse.

Case 302. (Rogues de Fursac, July, 1915.)

A man, 36 (boat painter to 30 and thereafter a wine seller; paternal grandmother insane, father alcoholic and suicide; gonorrhea, 20; two attacks of lead colic, 25 to 30; purulent pleurisy, 31; phlegmon of mouth, 34; also a chronic alcoholic), at the time of examination showed arteriosclerosis and slightly hypertrophic liver; unequal pupils, slightly contracted and sluggish to light. He complained of frequent headaches, possibly due to a combination of plumbism and alcoholism. He was not in any respect demented, and had an excellent memory. He had always been emotional, being unable to go to a funeral without many tears, or remain in a house where there was a corpse without threatening to faint. He was always overcome if he saw a fight going on; and even in his wine shop he would escape when there was a fight and get a neighbor to bring the police.

He was mobilized on the fifth day, sent first to a territorial regiment and then, in October, put into the reserve of an active regiment and sent to the front. He reached the first line trenches in the night, greatly affected by ruins he saw on the road. He slept poorly and had nightmares. At daybreak he woke up to see a pile of corpses near by, and felt an indescribable terror on account of the corpses and the noise of bullets, machine guns, and shells. By superhuman efforts—according to the man—he mastered his emotions and took his turn at the observation post. Another sleepless night. Next day he got such tremors that his sergeant sent him to the hospital where he was at first thought to be suffering from a fever. But his temperature was found normal, and he was sent back to the trenches.

He passed another night without sleep, and next day he could not hold his gun for trembling. The Captain sent him back to be a kitchen man in the rear, and here he remained six weeks—restless, trembling, eating very little. He would have anxious spells. In the morning, as he was carrying coffee to the men in his company, on seeing a pile of corpses, he dropped his pot and ran back to the kitchen declaring that whoever wanted to carry coffee might, but he would not go back. He spilled a pot of soup on his left foot. The Captain had him evacuated, saying: “Go! when you come back, I hope the war will be over!”

He was sent back to a hospital near Paris, where he was all right for a few days, happy as a prince. The burn got well, and as the time approached when he would probably have to go back to the front, the terror returned. He had visions of corpses, and imagined bullets whistling, machine guns popping, and shells bursting. He wept, lost appetite, hid in corners, made three suicidal attempts by poisoning,—though the sincerity of these attempts was doubtful (zinc oxide ointment; rose laurel leaves; verdigris). Sent back to a dépôt before getting leave, he had crises of tremor with anxiety, and was then sent to Val-de-Grâce on the mental service, and finally to Ville-Évrard. He unhesitatingly confessed his terror, becoming more and more anxious and tremulous, and almost losing his pulse while describing his experiences. He said he would commit suicide rather than return to the front. He stayed at the Hospital, working in the garden rather calmly, but when it was a question of leaving, even on convalescence, his terror and anxiety returned. Every time he was examined there was an emotional explosion, with expressions of anguish, generalized tremors and crises of clonic convulsions with respiratory disturbance even of threatening suffocation, depression of pulse. It is this latter which is the most important element in the proof that such a case is not a case of simulation.

Re war cases, Bennati remarks upon the great number that do not fall into known categories. There is, he thinks, an anaphylactic group in which the trauma acts as the secondary toxic agent; and there is another group in which exhaustion works after the manner suggested by Edinger: that is, by a physiological overwork of certain structures.

Martial misfit, dwelling on horrors of war at home; exposure; shell fire: Mental exhaustion with depression, emotionality, tachycardia.

Case 303. (Bennati, October, 1916.)

An Italian corporal, in civil life a writer (mother very nervous; patient himself rickety, unmarried; relatives well off), was in front line trenches for some fifty days. He was repeatedly excused from service on account of fatigue, distress, poor appetite, insomnia, depression and even confusion (aimless shots fired off in the night). It turned out that he had been in just this state of mind when he left home and family and that the very thought of war had seemed dreadful to him. He did not at all enjoy leaves at night, as he stumbled and fell about in the darkness and had shells burst near by. He lived immersed in mud. He reacted unfavorably to antityphoid injection.

The very day he went on winter furlough he greatly improved, but then suddenly relapsed into depression, emotionality, inattentiveness, sluggishness of mind, and exhaustion. The tendon reflexes were lively, the abdominal reflexes sluggish. There was tachycardia (120), the Mannkopf-Thomayer tests were positive at 76 and 80, oculocardiac reflexes 84 and vagotonic. Stellwag and v. Graefe symptoms.

Hereditary instability.

Case 304. (Wolfsohn, 1918.)

An English soldier, 23, had been ten months on active service in France, when he was buried by a shell December 19, 1915. He became unconscious and later suffered from nervousness and stuttering, depression, insomnia, frightful dreams, and tremor. Improvement was such, under treatment, that he was again returned to the front. A shell burst near him once more and again he grew dazed, trembled, had lapses of memory and fell into a state of general nervousness. He improved again in hospital.

On returning to the front in a few days he saw a bomb burst some distance away. He began to stammer and to wander about aimlessly. Insomnia, tremor of legs, arms and head, fatiguability, feeling of lassitude, occipital and vertical headache, fear of aircraft and crowds, frightful dreams, absences and aimless wanderings appeared. There was one attack of deafmutism. Whenever the patient saw aircraft he ran. He was easily startled by noises.

He was the son of an excitable, alcoholic father and of a nervous and bad tempered mother. A sister had had nervous prostration. The man himself had always been more or less moody and a nail-biter. According to Wolfsohn, 74 per cent of the war neuroses have a family history of neurotic or psychotic stigmata, including insanity, epilepsy, alcoholism and nervousness; 72 per cent show previous neuropathy.

According to Wolfsohn, wounded soldiers do not show war neuroses except in rare instances. In the wounded soldiers studied by him no neuropathic or psychopathic stigmata occurred in the family history and previous neuropathic tendencies in the patients themselves were found in about 10%.

A soldier that is excessively fatigued or has been under undue mental anxiety, expecting to be blown to pieces, may go into psychoneurosis more easily than one without such emotional strain.

Genealogical tree of a shoemaker.

Case 305. (Wolfsohn, 1918.)

An English private, shoemaker, 37, was partially buried in a shell explosion and came to, stupid, shaky, weak and fearful of the dark. Twice, in a dazed state, he attempted to murder companions and was afterwards amnestic. He had always been of a violent temper and his outbursts had been followed by petit mal. He had also always been afraid of the dark. One of his children had fits; three were hysterical and had temper fits. The man’s father was in an insane hospital. Sundry other facts are shown in the genealogical tree presented herewith.

Fall from horse in battle; fear of being crushed: Hysterical crises. Case offered as showing TRAUMATIC HYSTERIA in a young physician WITHOUT HEREDITARY OR ACQUIRED PSYCHOPATHIC TENDENCY.

Case 306. (Donath, 1915.)

A physician of twenty went into the war as a volunteer Hussar. During an attack, he fell from his horse without losing consciousness, though he was at the time much afraid of being crushed. The attack ceased and he returned to the lines on horseback.

Immediately there developed an emotional crisis, and thereafter he broke into weeping on the slightest occasion. He was afraid he was going to lose his reason; that some spiritual power was going to suppress his ego and madden him. He wept as he was going under narcosis to be operated upon for an intercurrent appendicitis. He became so sensitive to noise that he wanted to choke the offender. One day he bit himself on the arm in his excitement. Sensory tests could not be executed on account of his fear of the brush. Reflexes were normal.

It took four hypnotic seances to get him in proper rapport with his physician for psychotherapy.

This case is cited by Donath as one in which traumatic hysteria has been proven to exist in a man without any sign of neuropathic or psychopathic taint, either in his previous history or in his relatives.

A perfect soldier type. Mine explosion; burial; superficial wounds: War neurosis.

Case 307. (MacCurdy, July, 1917.)

A lieutenant, 29, had been a regular soldier for eight years before the war and was made a non-commissioned officer almost at once after enlisting. He went out as a sergeant with the original expeditionary force and got through the retreat from Mons and the first battle of Ypres intact. He enjoyed the fighting hugely and even got indifferent to the burial work. The death of chums saddened him, but he carried on and soon forgot about the incidents. He might be regarded as a perfect soldier.

In August, 1915, there was a slight touch of rheumatism. Two or three months later the Germans exploded a mine immediately in front of the trench where he was. He went pale for the first time in his life, but kept his men “standing to.” Thereafter he began to think for the first time about danger. Mining was hereabouts the chief form of attack, and he frequently heard Germans digging beneath a dug-out. He slept well in billets, but was too restless for sleep on active duty.

He got more and more on edge during the next weeks. Six weeks after the mine explosion he was buried in a dug-out. Though he did not lose consciousness, he was dazed and had to lie down for two hours. Nervousness, chronic headache and insomnia, even in billets, followed. His imagination played upon the blowing out of dug-outs and the bowling over of men by shells. He had become company sergeant-major and the responsibility made him grow worse and worse. At times he tended to jump when the shells came, but was outwardly perfectly calm. He began to take morphia, though with little result. He had suicidal thoughts.

After two months of these symptoms he was sent to England. He began to sleep fairly well and three months later applied for light duty; was greatly bored by the company accountant work given him; got a commission and was sent back to the front nine months later, January, 1917. He got on with the active fighting very well, sleeping four or five hours a night. In April he was sent to Arras. He had had a dream that he was going to be bowled over, buried and wounded in the neck. Sleep got poorer. In April he led his men in an advance and actually was bowled over, buried and hit in the neck as well as in the knee and the hand, though all the wounds were superficial. He was carried back, dazed, to hospital, where he grew fairly comfortable in ten days and even undertook a journey down to the base.

He arrived in collapse, remained in camp at the base three weeks, getting steadily worse. Something, he could not tell what, was going to happen and kill him. He could not concentrate, even to read. He thought of suicide. He slept practically not at all, waking from a doze with a start, feeling that something had hit him. He had dreams of being taken prisoner and on waking would in fancy start a fight to escape from imagined imprisonment back to the British lines. After two weeks in various hospitals he spent ten days in a hospital for nervous cases and grew better. Riding on trains he was terrorized in every tunnel lest he should be crushed.

According to MacCurdy, an anxiety neurosis would have developed had not his superiors sent the lieutenant back to hospital after the final burial in April. As this perfect soldier said: “There is no man on earth who can stick this thing forever.”

Shell-shock; thrown against a wall: Tremors—TREMOPHOBIA.

Case 308. (Meige, February, 1916.)

Meige has studied shell-shock tremors, especially those occurring without external wound.

A corporal was with his squad on the Nouvron Plateau, January 13, 1915, when he was thrown against the wall by a bursting shell, which killed or wounded several comrades but did not wound the corporal. Whether he lost consciousness is unknown, but he lay on the ground for some time, until he could be moved through a communication trench. After the explosion he began to tremble, and was still trembling on his trip back. Constantly trembling, he lived on at the front for a fortnight, but without eating; and, although he had been a good rifleman, he had lost all his former skill with a gun.

There was a delay of a month before evacuation, but the trembling did not cease, and he was passed through various units, to the neurological center at Villers-Cotterets, where he remained for two months,—April 13 to June 15, 1915,—with a diagnosis of hysterical chorea. He was examined by Guillain, who found, besides the generalized tremors, lively knee-jerks and Achilles jerks, an excessive emotionality, particularly marked when the guns were going or bombs bursting. Lumbar puncture yielded a perfectly normal fluid.

June 19 the corporal went to the Salpêtrière under P. Marie. July 14 he was evacuated to the civil hospital of Arcueil, where he remained till September 24, when he was sent home to convalesce, from October 26 to December 15.

He returned to the Salpêtrière December 15, 1915. Throughout these various movements from hospital to hospital, his status was unchanged. At the time of report about a year after shell-shock, he was still constantly and uniformly trembling. All four limbs were affected, perhaps the right arm and the left leg more markedly. There was no tremor during sleep, but there was a tremor when the patient lay awake in dorsal decubitus just as when he was sitting or standing. The tremor was worse in the evening than in the morning, and the patient could get to sleep only very late. There was slight tremor of the head; the eyelids and the tongue showed a few tremors, which were not synchronous with those of the limbs. Nystagmus was absent. To diminish the effect of the trembling, the patient held his forearms flexed and kept his elbows close to his body. If the trembling of the legs got intense, the patient would rise and walk a few steps. Any movement, such as carrying a spoon or a glass to the mouth, led to an exaggeration of the tremors; and there was at this time a suggestion of the intention tremor of multiple sclerosis. The tremor was increased when the eyes were closed. Any sudden noise or sharp command, or recalling to mind of trench service, would bring about extraordinary motor crises, in which there was an intense and generalized tremor, so the patient would lose his balance. Any attempt at eliciting reflexes would produce generalized violent tremor. Sensations were normal; tendency to hyperidrosis; pulse in repose, 60, rising to 120 if one struck the table sharply.

Meige remarks that a number of examples of tremors suggestive of Parkinson’s disease were observed in the War of 1870. Might the explosion have caused properly situated lesions in the encephalon of such a nature as to produce a Parkinsonian tremor? The tremors were stationary, and if due to some lesion, the lesion remains now exactly what it was at the beginning. There was no digital tremor such as is characteristic of Parkinson’s disease. Moreover, the intention tremor of such a patient, rather than Parkinson’s disease, suggests multiple sclerosis, of which latter disease, however, there is no other sign. Nor does there seem any evidence that these tremors were of cerebellar, paretic, goitrous, or of any definite toxic origin. On the whole, Meige regards it as a neuropathic manifestation resembling what is found in traumatic neurosis. He believes that there is not sufficient evidence that it is the consequence of any structural change in the nervous system.

Meige remarks that the analysis of any case of tremor must take the mental state into account. This patient, perfectly conscious of his tremors and their critical exacerbations, was much chagrined thereby. He suffered mentally from his impotence, especially when bystanders would intentionally bring about his paroxysms. He looked like one shuddering from fear, and it is actually probable that he was afraid of his own tremors and shuddering. He was, besides subject to tremor, also a victim of tremophobia,—a kind of phobia described some years since by Meige, somewhat resembling ereutophobia, or fear of blushing, described by Pitres and Régis.

Four hours in a freezing bog: Hysterical glossolabial hemispasm twelve hours after rescue. No sensory disorder of face or tongue; sensory disorder of arm, but no motor disorder.

Case 309. (Binswanger, July, 1915.)

A man, 27, in good health, called on the second day of the mobilization, got into the line two weeks from mobilization, first in the West, and then, from mid-September, in the East. He was in the artillery and stood shell fire in a big battle very well.

However, December 27, 1914, while engaged in transport service, on the way back with his horse, he fell into a bog and gradually sank to his neck. Attempts to get the man and his horse out failed. All that saved him from drowning was the freezing of the bog surface. After four hours he was freed by his comrades, apparently frozen stiff, but with consciousness completely preserved. On the next day, at about five o’clock,—twelve hours after his release from the frozen bog,—he had a seizure. It began with headache on the left side and loss of consciousness that lasted 24 hours. The right leg was paralyzed and very painful. He passed through various hospitals and finally arrived at the Jena Nerve Hospital, January 25, 1915.

He was a tall, powerful man, with a slow regular pulse, accelerated heart sounds, lively dermatographia, increased muscular excitability, general increase of knee and Achilles reflexes (left greater than right), slight patellar and ankle clonus present on the left side, Babinski reaction absent, plantar reflex more lively on the left than on the right, but abdominal reflex more lively right than left. Head painful to percussion in the left temporal region. Touch and pain sense segmentally absent in both right extremities. Arm movements free; tremors absent. Active movements almost impossible in the right leg; on passive movement marked pain. Slight muscular tension about knee-, hip-, and ankle-joints. The patient got about with a cane, trailing the left leg. Romberg sign.

The right angle of the mouth was withdrawn slightly upward and outward, and lagged a little in active movements. The protruded tongue deviated completely into the right angle of the mouth and there remained, but without tremor. The uvula deviated to the right, and the right palate was held higher than the left. Lively palatal reflex. Speech intact. The patient’s chief complaint was attacks of coughing, which increased his headache to the point of intolerability. A harmless drug caused the coughing and headache to disappear. The patient was a quiet, willing man, who industriously went through his exercises, and on the Kaiser’s birthday was already walking in the marketplace. His tongue contractions gradually improved. His body-weight increased.

In the course of two months the glossolabial and palatal contractions had largely disappeared. The walking movements of the right leg had improved, although there was still a distinct paresis, and a stiffness in the right knee and ankle joints. Climbing stairs was impossible on account of difficulty at the hip. March 30, 1915, the sensory improvement was marked. There was a feeling as though the last three fingers of the hand were asleep; walking was improved; he could walk one or two hours a day. The walk was still slightly spastic-paretic, May 28, when he was discharged.

It is remarkable that the hysterical attack had such a long incubation period in this case: twelve hours after his removal from the marsh. There were doubtless physical factors of refrigeration, on the one hand, and on the other, psychic factors of fear of sinking alive in the marsh, at the bottom of the phenomenon. The most marked feature, of course, was the glossolabial hemispasm. In the presence of this hemispasm, it is remarkable that there should have been no anesthesia or analgesia of the face, cheek, or tongue; and moreover the paresis of the right mouth and tongue was far less marked than the contracture. It is also striking that the right upper extremity, although it had sensory disorder, failed to show motor disorder.

Slight bruise by horse: Apparently invincible complaints of pain. Cure by single-handed capture of many Russians.

Case 310. (Loewy, April, 1915.)

An infantryman was standing below an embankment when a horse fell upon him, bruising him slightly on the left hip. This infantryman later continually complained of pains in the opposite hip though there had never been a contusion there, nor anything felt there. These complaints could not be influenced by exhortation, by diversion, or by drugs. If they were purposely ignored, the patient reacted complainingly and in a way to suggest delusions of persecution.

Nevertheless, this querulous man soon proved an effective soldier in a storming attack in which the whole battalion distinguished itself, putting himself forward particularly. In fact, by himself he captured a whole group of Russians!

Thereupon all the pains in the hip ceased, nor did they recur so long as he was under observation. Morose and complaining before, he now became cheerful.

Kick in abdomen by horse: General spasticity; tremors; eye symptoms (e.g. monocular diplopia); convulsions. Improvement.

Case 311. (Oppenheim, July, 1915.)

A cuirassier was kicked by a horse on left side of abdomen, November 24, and lost consciousness. A month later, in hospital, hardness and tenderness to pressure of abdominal wall, spastic muscles everywhere, pseudospastic tremor of legs, and complaints of double vision were noted. He also had attacks of convulsions, in which he became unconscious, twitchings appeared, but the tongue was not bitten. Urine was often involuntarily passed in these attacks, but he was not always continent outside attacks, as, for instance, in coughing.

On admission to nerve hospital: Right-sided monocular diplopia; mild ptosis; ocular movements free. Rapid tremor on shaking hands. Stood with straddling legs affected by vibrating tremor. Knee-jerks considerably increased. In the dorsal position movements of the left leg were accompanied by marked tremor. He even could not go to sleep easily on account of twitching of the left leg.

His comrades observed that he had convulsions at night, and often spoke in his sleep. Inoculation against typhoid fever was made early in December. Later, permanent rise of temperature to 37.8. Several attacks, lasting about ten minutes, came under observation of the physician.

In January, progressive improvement in the motor sphere and also psychically. The urinary disturbance likewise disappeared, but the spasms persisted.

Windage from a shell; fear; fall, unconscious: Homonymous hemianopsia (organic? functional?) with blinking and vasomotor excitability.

Case 312. (Steiner, October, 1915.)

A volunteer, 19 (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 near his trench, but failed to explode. Up to that time everything had been quiet. The soldier had been looking out of the loop-hole, surveying the landscape. He felt a great fear, felt a blow in the neck, and fell down unconscious. How long he was unconscious is unknown. Sometime later he walked back with his comrades.

About an hour later, this volunteer—who was a very intelligent young man, possessing some 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.

Shell-shock PSORIASIS. Post-traumatic eczema.

Case 313. (Gaucher and Klein, May, 1916.)

A soldier, 28, came to the Saint-Louis skin clinic, May 15, 1916, for leg lesions three months old. These lesions were cicatricial, squamous, irregular-contoured, and had developed following a wound. The lesions were eczematous.

On the trunk, arms and elbow were lesions of psoriasis. These lesions had appeared after shell-shock. The man had been bowled over June 16, 1915, by a marmite. The psoriatic lesions appeared shortly afterwards. The patient had never seen anything of the sort before.

In this case the trauma provoked eczema; the emotion, psoriasis. Gaucher and Klein say that they have been struck by the recrudescence of psoriasis since the outbreak of the war, and remark, also, that there has been a relative increase of new cases since July, 1914.

There are cases of psoriasis following nervous shock, emotion and trauma. Sometimes the psoriatic lesion develops upon the scar of a wound. In the above case, as in the case of a woman of 25, a refugee from the Arras bombardment, the psoriasis began de novo and slowly developed immediately after the catastrophe of the Jena. Five, possibly six, out of eight cases totaled, appear, unlike the case sketched above, to have developed in cases either tuberculous or of tuberculous stock.

Re psoriasis, Vignolo-Nutati remarks that this is a relatively frequent skin disease amongst Italian soldiers. He states that many of these cases are due to nervous shock. Some are related to wounds appearing near the scars. In all cases an emotional disturbance is the chief cause. Vignolo-Nutati had 86 cases of psoriasis in six months, 52 of the men coming from the front. Eighteen of the men said that they had not previously suffered from the disease.

A sergeant gets the CROIX DE GUERRE and SHELL-SHOCK together: Transient deafness; later pseudohallucinatory electric bell ringing, reminiscent of civilian work; stereotyped movements, reminiscent of war experience.

Case 314. (Laignel-Lavastine and Courbon, May, 1916.)

A sergeant, 24, had worked about Parisian hotels from the age of thirteen and a half. He won the croix de guerre and was evacuated for his wounds April 24, 1915.

It seems that he carried the remains of his company, which had been decimated the night before by a mine explosion, on to the enemy trench, getting there first and facing three Germans, whom he beat down. At this time, gas shells began to rain about. Making a number of violent expiratory movements to get rid of the gas, he found himself unable to progress on account of the fall of the shells, and sat motionless with his hands before his face. He was cast to the earth by an explosion, which at the same time blew off a revolver which the wounded lieutenant had passed to him. He sat up, and, observing that the soldiers had gotten the trench, went back to the lines, where he told his story.

He then found that he was deaf, and wounded in the left leg. The wounds rapidly healed, but sundry other symptoms developed. He had a peculiar sensation back of the forehead. He could not think, read or write and was very weary. He got better in a few months, but disorders kept returning.

His deafness had left him in about a fortnight, but when his hearing came back spontaneously, there were peculiar sensations. He constantly heard an electric bell, intense and continuous, like that of a French cinema advertising its films. The sounds seemed to begin in the ear and to run out as a sort of whistling. This sensation was preceded by buzzing and associated with noises like those of a musical triangle or a steam whistle. The noise kept up during waking hours, but was often forgotten while he was at work. In sleep he heard nothing, except sometimes battle noises. August 20, 1915, he was given the diagnosis: labyrinthine shock—hearing returned.

About ten weeks after evacuation, when the headaches and thought blocking began to disappear, a generalized tremor, especially of the head, set in, which the patient called St. Vitus’ dance. Then a peculiar gait began, which lasted several weeks and then transiently reappeared. Every few steps his legs would bend, and he could only walk forward in the attitude of a man who is concealing his height. After resting a few minutes he began to walk regularly again and the cycle began over again. He had to walk with two canes. If he felt some sudden emotion, or sometimes without any obvious reason, he would stop short and look straight ahead, with body bent, and arms before his face. This would last but a moment, whereupon he would walk again normally.

When this anomalous walking disappeared, curious face movements and gestures began. If a strange person arrived, the forehead and eyebrows would contract, the eyelids would stand wide, which gave him an expression of surprise lasting a few seconds. At the same time the mouth would open and remain so for some moments. A forced expiration would be executed, suggesting a fish out of water. He would then imperatively strike the table with his fist, or the ground with his foot.

Laignel-Lavastine and Courbon explain the anomalous movements as stereotypies due to secondary automatism. They are not convulsive, are not preceded by emotion or followed by a sense of relief, and are not tics. They are gestures and postures without present significance, but adapted to certain former circumstances. The electric bell effect is a sort of pseudohallucination, differing from true hallucinations in little except the absence of the externalizing feature. The stereotypical movements are reproductions of things done in the battle, and the pseudohallucinations relate to the former hotel work of the soldier.

Cinema worker, two days after being waked up by a shell, develops a nystagmiform tremor of eyes and tachycardia. Graves’ disease? Tic (“occupational virtuosity”)?

Case 315. (Tinel, April, 1915.)

A soldier was waked up with a start Sept. 22, 1914, by a shell burst. The man was not wounded or shocked, and merely felt a good deal moved. The next day but one he felt a little movement of his eyes, which was at first intermittent but in three or four days became continuous and troublesome. These movements were those of nystagmus, almost transverse and very rapid, and suggestive rather of a vibratory trembling than of a true nystagmus of the eye or of labyrinthine disease. When the patient fixed an object, the nystagmus would stop for a few seconds and then immediately reappear. There had never been any vertigo, nausea, vomiting, deafness, ocular disorder, or disorder of equilibration. During the tests for nystagmus, the morbid nystagmus would stop and be replaced by the normal nystagmus which was obviously slower and more regular. The condition had persisted from September, 1914, to the meeting of the Neurological Society, April 15, 1915. The patient said he had become very emotional and got palpitations on the slightest occasion, such as a fast walk, going upstairs, or hearing a loud noise. There was also a slight vibratory trembling of the fingers and a permanent tachycardia (120-140 beats). Tinel regards the case as one of neurosis, due to a neuromuscular hyperexcitability comparable in some ways with that found in Graves’ disease.

Meige, in discussion, called attention to the fact that not every nystagmus is of organic origin and that there is a rare form of tic of nystagmiform nature. The victim in this case was an employee in a moving picture house, and very possibly his occupation had permitted him to utilize what Meige speaks of as a “occupational virtuosity” of the eye muscles.

Synesthesialgia: FOOT pain on rubbing dry HANDS, following bullet wound of leg.

Case 316. (Lortat-Jacob and Sézary, November, 1915.)

A foot chasseur was wounded, September 15, 1914, low in the right thigh, a bullet entering outside the biceps tendon and emerging on the inner aspect of the leg, 4 cm. below the knee joint. He at once began to feel pains in the right foot, which grew swollen and red. The leg began to flex upon the thigh and, after straightening under anesthesia, was placed in plaster. An arteriovenous aneurysm developed in the popliteal space; operation, October 22nd, followed November 1, by ligature. The pains in the foot grew better after this operation; but as soon as the wound was cicatrized they came back again as before.

For seven months the foot pains remained sharp and continuous, such that the man could not leave his bed. If a bright light struck his eyes, the pains grew much more marked, especially in the morning on awakening. The patient found that when his hands were dry he could not use them because of the violent pains which rubbing them would cause in the right foot. Accordingly he kept putting his hands to his mouth to moisten them. Finally he kept a wet rag by him which he could pass from one hand to the other.

The pain was what made walking difficult. Foot movements were only a bit less ample on the affected side than on the normal side. There was a general muscular atrophy of the lower extremity (30.5: 34 about calf, and 40: 49 about thigh). Right knee-jerk more lively than left. Right Achilles jerk absent. Negligible disorders of electrical excitability in the territory of the right sciatic nerve. The skin of the foot was a little thin and pale; the temperature was low; and the nails had transverse striations. The pains grew gradually a little less marked, but if the room temperature was increased or lowered or if the foot became cold, the pains became extreme. Pressure on the popliteal space produced pain on the external border of the foot; likewise pressure on the calf. Lasègue’s sign could not be tested for on account of the contracture of the flexors of leg on thigh. Due to the direct action of the bullet, there was an objective hyperesthesia of the dorsum and sole of the foot. The toes were anesthetic. A cold foot bath increased the pains, and a warm foot bath diminished them (contrary to experience in analgesias).

This was a case of synesthesialgia in the right foot, brought about by rubbing dry hands, exactly as if there were a direct contact with the foot. Milder painful reactions were brought about by bright lights and loud noises; but on the whole, these other effects were insignificant. It must be remembered that the man was wounded and plainly had also organic nervous disorder. He sometimes complained of radiations of the pain up to the left hypochondrium, and sometimes he showed the classical sensation of “esophageal globus” (lump in the throat). In short, there was in him a special excitability of the nervous system which may partly explain the synesthesialgia.

Shell-shock; burial: Clonic spasms; later, stupor with amnesia.

Case 317. (Gaupp, March, 1915.)

A reservist, 28 (laborer in civil life, of a nervous family; even before mobilization had attacks of weakness at his work or in the company of others) January 3 or 4, 1915, fainted in the trench while shells were striking around him. On January 5 he was brought to hospital in deep stupor. He went to the reserve hospital at N. by hospital train, January 8, and arrived at the Tübingen clinic January 18.

A slip of paper stated that after burial in the trench he had been brought from the field unconscious. Clonic spasms of the upper part of the body are said to have occurred. At the reserve hospital in N., January 10, he was still unconscious, at times twitching his face and the upper part of his body, and once at night excited and delirious.

At first in the clinic he was apathetic, speaking not a word, looking vacantly into the air as if lost in a dream. He went to the section passively, and lay passively in bed.

In the examining room, he stood speechless with unemotional face, sometimes looking up to the ceiling, slowly scratching his head, failing to answer questions, although fixing his eyes upon the physician. He could not be communicated with in writing, playing uncomprehendingly with the pencil or scratching his head with it. He would start with fright at a sudden noise or an unexpected touch. Sometimes he would heave a deep sigh, grasp his head in his hands, or lay hold of his hair with a hopeless expression of face and shake his head to and fro.

Next day, January 19, he made a few slow, low answers. He was found to be entirely disoriented and with associations impeded, although he could get out his name and residence with difficulty. Some of his color identifications were correct, such as red and green; some impossible, as yellow, brown, violet. A comrade who was called in and could speak the Cologne dialect, was talked with at first with difficulty, later more easily. Although the patient was visibly freer, he remained without apparent emotion, retaining a rigid and dreamlike expression of face. It was hard to find words, although objects were named correctly, and there was no paraphasia or agnosia. Vision and hearing were normal; walking, manual movements, eating were all undisturbed though slow. The patient had to be led to the toilet. It seemed as if all intellectual life was at rest, and that in the absence of impulses from without, there would have been complete apathy. It was made out that the patient thought he was still in the trenches.

Next day, the stupor had decreased and the patient spoke, getting his bearings for a time. There was a complete amnesia as to the cause and duration of his condition. During the next period, up to the beginning of February, 1915, consciousness cleared and the apathy was replaced with anxiety, weariness, and a dull headache.

During February, the patient gradually returned to his senses, and remained in a state of general nervous exhaustion. Amnesia was complete for at least two weeks of his life and recollections were fragmentary for the first three days of his stay in the clinic. He worked willingly in the garden with the other patients. On February 26, the patient was cured and went back to the reserve battalion in a much strengthened condition.

Battles (including liquid fire); eventually shell-shock: Hallucinatory delirium, mutism, asthenia—after a few days puerilism (history of convulsive crisis in adolescence) with regression of personality to late childhood.

Case 318. (Charon and Halberstadt, November, 1916.)

Puerilism (Dupré) appeared in a soldier, 21 (uncle and cousin insane; patient had difficulty in studies at fourteen and nervous spells for two years, with loss of consciousness, fall and convulsions probably at rare intervals; a student at eighteen) after he had taken part in a number of battles with the Chasseurs Alpins. He was exposed once to liquid fire July 21, 1916. He entered the military psychiatric center at Amiens. Mental troubles had followed the bursting of a shell near him. He said a few words, such as, “Alsace; fire; blood; snow; it hurts.” These phrases, spoken in a low tone, with an anxious appearance, eyes fixed, suggested hallucination. He seemed to be listening. Aside from the isolated words above mentioned he showed complete mutism. There was physical weakness, difficulty in walking without support, exaggeration of patellar reflexes, pains in the head and limbs. After several days, he said, “Milk; bread.” After this the anxiety and the slow and difficult walking disappeared, whereupon the puerilism appeared.

Now the soldier began to run instead of walking. He galloped and gamboled like a child imitating a horse, or he would sit on a board seeming to paddle. He would skip along the halls. The puerilistic phases were rather brief and for the most part he lay in bed. There was still a certain asthenia. He made little paper boats in bed, keeping them in a small metal box along with bits of bread, looking glass and the like. If a gesture was made to take them away, he would protest and press the box to his breast, looking childish and anxious, and if the box were taken he would weep hot tears. Sometimes he would stick out his tongue at the attendants. His mother came to see him and afterwards he would say, “Mamma told me to be good, to eat well, to get well and to go home.” He would use childish grammar,—“Me eat much.” Asked why he had hollowed out a small hole in the wall of the room, he answered, “I did it for fun, but I will not do it any more. Mother doesn’t want me to.” The patient was unwilling to answer a question correctly; would sometimes answer incorrectly at first and correctly afterward.

It appears that the man had adopted the language, occupations and attitude of a child, showing a regression of personality ten to twelve years backwards. There was a neurotic basis in the convulsive crises of adolescence. On the basis of this predisposition following shock there appeared an attack of confusion, upon which, several days later, supervened ecmnesic phenomena of hysterical nature assuming all the features of puerilism.

Bomb-dropping from airplane; unconsciousness: Battle dreams. Leaves of absence failed to relieve. Episodes of dizziness and fugue.

Case 319. (Lattes and Goria, March, 1917.)

M. Alessandro, Class ’79, baker (father a drunkard; brother an idiot, in asylum), had typhus in youth, and as a boy had periods of intense “pavor nocturnus,” but no convulsions. He enjoyed good health in the army before the following event:

On July 13, 1915, a bomb, dropped by an airplane, fell near an Italian soldier, killing many comrades, and throwing the man to the ground unconscious. He awoke several hours later at a hospital in a stunned condition. During the night, under the influence of terrifying dreams, he would leave his bed to look for enemies who, it seemed to him, were throwing stones and firing. He managed to grasp a rifle and fire at the images he saw. He was given a 60 days’ leave of absence during which he did not improve; and then again 90 days’ furlough, which he spent at his home, where terrifying dreams, tremor of limbs and asthenia continued.