Part 24

He returned four months later; he was still occupied with his disease, still going to physicians and buying drugs. It took six months more before the man could be discharged from the service, at the end of 1916.

This man appears to be a hereditarily predisposed subject, who simply affixed his delusional ideas to a disease which had begun some time before the mental trouble itself. The family plight is important and practically constant in this group of cases. The fear lest the disease shall be revealed by the physician to the family is deep-grounded and impossible to overcome by mere statements concerning professional secrecy. The impulse to suicide is extraordinarily keen.

A soldier (neuropathic taint) after hardships for two days stumbles over a corpse; unconsciousness: Stupor; episodes of fright with war hallucinations; look of premature old age; paresis; anesthesia.

=Case 196.= (LATTES and GORIA, 1917.)

An Italian soldier (a shoemaker with an epileptic mother and two nervous brothers; himself always irritable and for long periods melancholic; at 15 condemned to nine years in prison for homicide in a quarrel) took part in a number of attacks at the beginning of the war. His company was heavily engaged in October, 1915, and there was no sleep two nights, and only a bit of cold food. He was dazed.

October 24, the company had to advance at night in the rain and under a heavy rifle fire. The shoemaker stumbled over a corpse, fell, and lost consciousness for a time that he thought was very long. He woke up in a camp hospital, remembering all the experiences he had undergone up to the time of losing consciousness. He now fell into a state of torpor, occasionally jumping out of bed and shouting with fear, hurling himself at non-existent persons, assuming a position of defence, and suddenly awaking in anxiety.

October 29, he was transferred to a second hospital, and October 30, in a third hospital, was examined and found well and strongly built, but looking prematurely old. He was inactive, depressed, and stuporous looking. He fell to weeping often and rarely gave any answer to questions. Sometimes he refused food. There was a slight paresis of the left arm, and the left pupil was smaller than the right; both pupils reacted poorly to light. The larynx and cornea did not respond to stimulation. Skin reflexes were poor, and the plantar reflex lacking. The left side about the shoulder and hip showed large patches of anesthesia to touch, pain and heat; but deep sensibility was present in these areas. He slept well at night. Status unchanged for two weeks. He was experimentally sent to the guardhouse, but was soon back in hospital with the same symptoms as ever.

B. SHELL-SHOCK: NATURE AND CAUSES.

--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

SHELL-SHOCK ^ | +----+-----------------------------+ | | | | | SUGGESTION | ESSENTIAL! | (AUTO-, HETERO-, MEDICAL) | (Babinski) | | | | SOMETIMES SOLE | | FACTOR? +----------------------------------+ ^ | ^ | | | | | | +------------+ | +------------+ | | | | | INTRABELLUM | | | | | FACTORS | | | | | USUALLY | EMOTION | | | SHOCK | ONE OR | | | | | BOTH | | | | | | | | | | +------------+ | +------------+ ^ | ^ -------|--------------------|---------------------------- | | +------------------------------------+ | | | SOIL | FREQUENT BUT | (ACQUIRED, ANTEBELLUM) | NON-ESSENTIAL | | +------------------------------------+ ^ | ------------------|-------------------------------------- | +-------------------------------------+ | | | TAINT | FREQUENT BUT | (HEREDITARY) | NON-ESSENTIAL | | +-------------------------------------+

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.

HISTOPATHOLOGY OF CASE OF SHELL-SHOCK, BURIAL, GAS POISONING? (F. W. MOTT)

HISTOPATHOLOGY OF SHELL-SHOCK (F. W. MOTT)

NOTE THAT THE CHANGES IN CELLS OF FIG. 3 ARE DIFFERENTIAL FOR NUCLEUS AMBIGUUS: CELLS NEARBY PROVED NORMAL

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 (198), Roussy and Boisseau’s (199), Claude and Lhermitte’s (200), as well as Ravaut’s own case (202) are in point.