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L. RAYMOND MORRISON, M.D.; PAUL C. ZAMECNIK, M.D.

Arch Neurol Psychiatry. 1950;63(3):367-381.

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

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. . . . [Full Text PDF of this Article]

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.

Footnotes
This work was aided by a grant from The Commonwealth Fund and is publication no. 109 of the Robert W. Lovett Memorial Foundation for the Study of Crippling Disease and publication no. 690 of the Harvard Cancer Commission.