Fusimotor Function

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Abstract
Increased excitability of segmental reflex pathways is the traditional paradigm of positive symptoms resulting from loss of control by higher neural mechanisms. As yet no satisfactory explanation of this commonplace phenomenon has been given. It has been suggested that motoneurons deprived of a significant portion of presynaptic neural excitation become hyperexcitable in response to stimulation by surviving connections in accordance with Cannon's Law of Denervation.1 More recently it has been suggested that hyper-reflexia results from the sprouting of new excitatory synaptic connections from dorsal root neurons to the motoneuron pool.2 Either of these theories may be held to account for hyper-reflexia developing days or weeks after an acute lesion, but neither can account for the much earlier changes seen both clinically and in experimental studies. Thus the stretch reflex in the cat is sometimes increased in less than a minute following spinal cord transection,3 and in the

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