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January 1947

RESULTS OF TREATMENT OF MULTIPLE SCLEROSIS WITH DICOUMARIN

Author Affiliations

NEW YORK

From the Department of Neurology, Columbia University College of Physicians and Surgeons, and the Neurological Institute of New York.

Arch NeurPsych. 1947;57(1):1-13. doi:10.1001/archneurpsyc.1947.02300240017001
Abstract

ETIOLOGY OF MULTIPLE SCLEROSIS  EVIDENCE has been accumulating over recent years which indicates that vascular destruction, or, more specifically, probably a thrombosis of venules, is an essential link in the chain of causation of multiple sclerosis and the related "encephalomyelitides."1 This evidence may be summarized as follows:1. Histologic pictures indistinguishable from the lesions of "encephalomyelitis" in the acute stage, and of multiple sclerosis when sufficient time has elapsed to permit gliosis to take place, have been produced experimentally in animals by the retrograde obstruction of cerebral venules2 and by the intravenous injection of various coagulants, especially organ extracts.32. Similar lesions are also often seen in pathologic material of human origin, following spontaneous thrombosis of veins of a certain size from any cause, or compression of a pial vein by a tumor.43. Thrombi, usually in venules and veins, have been observed in a large

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