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  Vol. 18 No. 6, June 1968 TABLE OF CONTENTS
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Neuromuscular Changes With Alloxan Hyperglycemia

Electrophysiological, Biochemical, and Histological Study in Rats

J. Hildebrand, MD; A. Joffroy, MD; G. Graff, MD; C. Coërs, MD

Arch Neurol. 1968;18(6):633-641.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]


Author Affiliations

Brussels

From the Medical Biochemistry Department, Hôpital St. Pierre, Brussels University (Dr. Graff), the service de médecine interne et d'investigations cliniques, Institut Bordet (Dr. Hildebrand), and the Neurology Department (medical clinic), Hôpital Brugmann (Drs. Coërs and Joffroy), Brussels.


Footnotes

Submitted for publication Dec 19, 1967; accepted Jan 5, 1968.

Reprint requests to Département de Neurologie, Clinique Médicale, Hôpital Brugmann, Brussels (Dr. Coërs).



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