Abstract
Putnam and his co-workers1were the first to assign a primary role to vascular lesions in the pathogenesis of multiple sclerosis. They succeeded in producing patches of demyelination by the intravenous injection of various substances (e. g., tetanus toxin). The likeness of such lesions to the foci of multiple sclerosis indicated the possibility that the lesions of multiple sclerosis might be produced by a local circulatory disturbance, "apparently of the nature of an obstruction on the venous side." Dow and Berglund2analyzed a large number of lesions of multiple sclerosis. They found thrombi only fifteen times in sixty-five blocks carefully examined. Marburg3observed that "thrombosis occurs in acute foci of multiple sclerosis more frequently than is generally assumed.... Yet, there are many foci in which blood vessels exhibit no changes in their walls and no venous obstruction."3b The object of this paper is to present additional

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