Shell-shock and other neuropsychiatric problems

by Elmer Ernest Southard

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.