Recent studies have shown that lesions closely resembling those of "encephalomyelitis" (and at a later stage of development those of multiple sclerosis) may be produced by experimental obstruction of cerebral venules1 and may be observed in human pathologic material after thrombosis or sclerosis of small veins or, less often, of arteries under certain conditions.2 Thrombi are common in the early stages of "encephalomyelitis" of certain types (e. g., those following measles and vaccinia).3 The onset of such "encephalomyelitides" usually corresponds closely with the first establishment of an immunity to the antecedent disease.4 An abnormal lability of the coagulation mechanism may be demonstrated in many cases of multiple sclerosis.5
It is reasonable to suppose, therefore, that experimentally produced hypercoagulability of the blood might in some instances result in thrombosis of cerebral vessels, and in parenchymal lesions of an "encephalitic" type. The present study was undertaken to