Abstract
As early as 1863 Eduard Rindfleisch described and systematically studied the topographic relationship between multiple sclerosis (MS) plaques and brain tissue venules frequently found in the center of MS lesions (Rindfleisch 1863). In the 1930-ies and 40-ies Tracy Jackson Putnam took an interest in the relationship between MS plaques and the venous vasculature (Putnam 1933; Putnam and Adler 1937). By this time formation of venous thrombi in central venules of acute MS lesions had already been recognized. Putnam – as opposed to the fraction of researchers who explained these thrombi in plaque venules as an effect of a local “allergic reaction”—assumed an increased liability of MS patients to form cerebral venous thrombi, which he believed to be the cause of the inflammatory process. Based on this hypothesis he undertook a clinical trial on the effects of anticoagulation on the clinical course of MS with no convincing results (Putnam et al. 1947).
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