Abstract
Abstract Experimental allergic encephalomyelitis (EAE)3 is an immunologically mediated disease produced in genetically susceptible animals by the injection of central nervous system (CNS) tissue or myelin basic protein emulsified in complete Freund's adjuvant. Because of the demyelinating character of the CNS lesions, EAE has served as a useful working model for the human demyelinating diseases, in particular multiple sclerosis. One limitation of the experimental model has been that, unlike multiple sclerosis, it is primarily a monophasic illness. Although recurrences have been induced in EAE (1, 2), spontaneous relapses have been infrequent and unpredictable (3). During studies of the factors involved in the immunoregulatory mechanisms of EAE in the Lewis Rat (4) we observed that, by providing supportive care during the acute episode, the majority of rats rapidly recovered and approximately 1 week later developed a second clinical episode, albeit milder than the first. The frequency of the second episode was age related.
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