Demyelination and Muscle Spindle Function

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Abstract
IT IS NOW well established that demyelination may produce slowing of conduction in peripheral nerve. In previous studies of acute experimental neuropathies a fairly good correlation has been found between the reduction in maximum conduction velocity of peripheral nerves and the severity of the clinical abnormalities of the experimental animals.1-3 However, some discrepancies have been observed; some severely ataxic animals have had normal maximum conduction velocities and, especially in chronic neuropathies,4 some clinically normal animals have had slowed conduction. Comparable anomalies are sometimes encountered in human cases of polyneuritis.5,6 We therefore decided to investigate further the relationship between conduction velocity and clinical disturbance in cats with acute experimental diphtheritic polyneuritis. The striking clinical feature of diphtheritic polyneuritis in the cat is ataxia,1 and so we were also interested to determine whether the function of muscle spindle receptors is abnormal in this condition and if so,