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During a study of the intrinsic vasculature of the lumbosacral spinal nerve roots in cadavers, a typical case of spinal stenosis was encountered. A review of the antemortem anamnesis revealed that this patient had had an intermittent claudication of the cauda equina. Investigation of the concomitant vascular and histopathological alterations of the affected nerve roots suggested that the claudication may have resulted from ectopic nerve impulse discharges elicited by rapid changes in the blood supply following exertion. The unexpectedly slight apparent neural deficit relative to observed root damage may be attributed to a neuronal plasticity within the spinal cord that permitted functional compensations to develop during the slow acquisition of the chronic nerve root pathology.