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March 1950

EXPERIMENTAL DEMYELINATION BY MEANS OF ENZYMES, ESPECIALLY THE ALPHA TOXIN OF CLOSTRIDIUM WELCHII

Author Affiliations

BOSTON

From the Departments of Neuropathology of the Harvard Medical School and the Massachusetts General Hospital and from the Medical Laboratories of the Collis P. Huntington Memorial Hospital of Harvard University, located at the Massachusetts General Hospital.

Arch NeurPsych. 1950;63(3):367-381. doi:10.1001/archneurpsyc.1950.02310210013002
Abstract

DEMYELINATING diseases still constitute one of the major problems of neurology, and the lack of knowledge concerning their etiology is a constant handicap to rational therapy. The various manifestations of myelin degradation, as observed in the different demyelinating diseases, have been explained by divers causes: mechanical, chemical, infectious, immunologic and hereditary. The variety of mechanisms underlying the breakdown of myelin apparently is so great that one wonders with Hurst1 whether demyelination is not a "type of response" of the nervous system to noxious stimuli of multiple causation. On the other hand, it may be that "demyelination" itself is not always precisely the same thing. The order of events and the extent of degradation may not always be identical in the demyelinating process, and the implications of these variations may be significant.

It was shown in 19312 that experimental venous thrombosis might act as a contributory cause of demyelination.

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