Spinal shock was defined by Franz1 as the "state of depression of spinal reflexes (hyporeflexia), generally transient in character, which occurs after transection in the bodily segments caudal to the lesion." Of several hypotheses,2,3 the most widely accepted is that of Sherrington: "Reflex depression is due to the sudden withdrawal of a continuous excitation (facilitation) which normally occurs from suprasegmental levels."4
Sherrington and Fulton observed that in monkeys spinal shock and the subsequent permanent disability are more severe and much longer lasting than in cats and dogs.5,6 In man it is well known that shock is even more severe and lasts longer than in monkey. Yet neither the intrinsic mechanism of the phenomenon nor its species variations are well understood.
Out of recent knowledge of the fusimotor (gamma efferent) system which functions to regulate the sensitivity of muscle stretch receptors, the idea has developed that the
HUNT RS, MELTZER GE, LANDAU WM. Fusimotor Function: Part I. Spinal Shock of the Cat and the Monkey. Arch Neurol. 1963;9(2):120–126. doi:10.1001/archneur.1963.00460080030003
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