EXPERIMENTAL LUMBAR SPINAL STENOSIS - ANALYSIS OF THE CORTICAL EVOKED-POTENTIALS, MICROVASCULATURE, AND HISTOPATHOLOGY

An animal model of lumbar spinal stenosis was developed in which the pathophysiology of this condition could be examined. Four experimental groups, each containing six dogs, were studied. One group had a laminectomy of the sixth and seventh lumbar vertebrae only; these animals served as controls. In the three other groups, a laminectomy was performed and the cauda equina was constricted by 25, 50, or 75 per cent to produce chronic compression. Cortical evoked potentials were recorded preoperatively, immediately after constriction, and at one, two, and three months postoperatively. Daily neurological examinations were carried out, and the neurological deficits were graded using the Tarlov system. After three months of constriction, the cauda equina of three dogs in each group was examined histologically, and the vascular circulation was examined by latex and India-ink injection with a modification of the Spalteholz technique. The animals in the control group showed no neurological abnormalities, no changes in cortical evoked potentials, normal microvascularity, and no histopathological changes in the nerve roots or the spinal cord. The dogs in which the cauda equina had been constricted 25 per cent had no neurological deficits, mild changes in cortical evoked potentials, slight histological changes, and venous congestion of the root and dorsal root ganglion of the seventh lumbar nerve. The dogs in which the cauda equina had been constricted 50 per cent had mild initial motor weakness, major changes in cortical evoked potentials, edema and loss of myelin in the root of the seventh lumbar nerve, and moderate or severe venous congestion of the root and dorsal root ganglion of the seventh lumbar nerve. The dogs in which the cauda equina had been constricted 75 per cent had significant weakness, paralysis of the tail, and urinary incontinence; two dogs recovered by the third month, but all had neurogenic claudication for three months. All six dogs had dramatic changes in cortical evoked potentials and had complete nerve-root atrophy at the level of the constriction. There was blockage of axoplasmic flow and wallerian degeneration of the motor nerve roots distal to the constriction and of the sensory roots proximal to the constriction, as well as degeneration of the posterior column. Severe arterial narrowing at the level of the constriction and venous congestion of the roots and dorsal root ganglia of the seventh lumbar and first sacral nerves were also present. Cortical evoked potentials revealed neurological abnormalities before the appearance of neurological signs and symptoms. Neurogenic claudication appeared to begin with venous congestion of the nerve root and dorsal root ganglion. With increasing compression, motor and sensory deficits occurred, as well as blockage of axoplasmic flow. Constriction of more than 50 per cent was the critical point that resulted in complete loss of cortical evoked potentials and in neurological deficits and histological abnormalities.