The depression of neural activity which takes place in the distal spinal cord abruptly separated from rostral control is the classical model for interpreting the transient disturbances of neural function that follow acute lesions of the nervous system. The behavior of isolated spinal cord has been relatively easy to analyze because its afferent and efferent pathways are so accessible. Modern neurological thinking is firmly based upon the observations of spinal cord behavior made in animals by Sherrington and in man by many clinicians of his generation. The riddle of spinal shock and the even more puzzling recovery to a hyperactive state which evolves out of it are little nearer solution now than when originally described. The most widely accepted explanation of shock is that the cord's internuncial pool and final common path are depressed below normal levels of excitability by the sudden transection of descending, largely excitatory pathways.1 Some