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May 1968

Demyelination and Muscle Spindle FunctionEffect of Diphtheritic Polyneuritis on Nerve Conduction and Muscle Spindle Function in the Cat

Author Affiliations

From the Neurological Unit, Boston City Hospital, and the Department of Neurology, Harvard Medical School, Boston. Dr. McDonald was a United Kingdom Medical Research Council Traveling Fellow, 1965 to 1966, and is now at the National Hospital, Queen Square, London.

Arch Neurol. 1968;18(5):508-519. doi:10.1001/archneur.1968.00470350066006

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,

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