Neuromuscular Changes With Alloxan Hyperglycemia

Abstract

CHANGES in peripheral nerves occurring in diabetes have been extensively studied during the past few years by refined electrophysiological and histological methods. The most common functional change is a slowing in nerve conduction velocity¹ which may be present without clinical signs of motor or even sensory involvement, and therefore has proved to be the expression of a latent neuropathy.² It was later recognized that the reduction of conduction velocity was related to a segmental demyelination of the nerve fibers, and that the diabetic neuropathy was a prominently demyelinating condition, although axonal degeneration could occur as well.³ The histological study of intramuscular innervation and muscle tissue in diabetic patients disclosed a high incidence of subclinical changes and made it possible to describe the various steps of neuromuscular aggression.^4,5 An early reduction or an abnormal extension of the motor end plates are followed by collateral sprouting of