In previous papers it has been shown that a series of histologic pictures resembling those of "postinfectious encephalomyelitis" may be produced in animals by a variety of agents, such as minute doses of tetanus toxin, carbon monoxide poisoning and certain types of embolism.1 The pathologic alterations ranged, sometimes in a single specimen, from mild perivascular infiltrations with glia and occasional lymphocytic cells through areas of damage to and loss of perivascular myelin to areas of softening and destruction of the axis-cylinders. In one instance, more than a year after the original injection of tetanus toxin, lesions were found which closely simulated those of multiple sclerosis,2 with plaques of loss of myelin, but with almost complete preservation of the axiscylinders and with local gliosis. Multiple sclerosis has been observed as a sequel of "postinfectious encephalomyelitis,"3 and the hypothesis that all of these conditions represent variants of the same