Localization of toxic encephalopathies near lesions of experimental allergic encephalomyelitis

Abstract

Bipiperidyl mustard and a neurotoxic triamine are known to cause edematous and/or necrotizing lesions in particular areas of hypothalamus and dorsal medulla but not in spinal cord. Experimental allergic encephalomyelitis (EAR) causes widespread inflammatory lesions that are especially numerous in spinal cord. When the chemical toxicants were administered to rats during the acute phase of EAE, mortality was increased. This was due to a specific interaction between EAE and chemical toxicants leading to the development of necrotizing vasculitis and parenchymal necrosis near EAE lesions in spinal cord or brain. The interaction decreased as the EAE lesions healed. Another neurotoxic chemical, dipiperidinoethane, did not produce this phenomenon. These effects of EAE are probably related to damage to the vessel walls and the blood-brain barrier. The present work may increase the versatility of EAE as a model for multiple sclerosis if the EAE lesions can be enlarged progressively by repeated exposures to the toxicant.