Effect of induced localization on incidence and distribution of experimental allergic encephalomyelitis

Abstract

Severe cyanide encephalopathy was produced in rats by 3 consecutive hydrogen cyanide exposures during the incubation period of experimental allergic encephalomyelitis (EAE). Incidence of EAE in rats with cyanide lesions was greater than that in controls. The increased incidence was attributed to lowered threshold for EAE in and around areas damaged by cyanide. Despite extensive localization of EAE in and around cyanide lesions in the forebrain, it was not possible to demonstrate a significant degree of protection against EAE in the spinal cord. If the presumed noxious agent of EAE was absorbed in the forebrain lesions, the diversion was not of sufficient magnitude to spare the spinal cord.