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Although there are evident differences in the etiology, induction, and probably also maintenance between EAE and human inflammatory demyelinating diseases, there is a striking similarity between both conditions regarding the structural features and the evolution of the lesions in the central nervous system. These similarities make possible the conclusion that immunopathological mechanisms play a key role in the pathogenesis of human inflammatory demyelinating diseases. Thus our knowledge of the pathogenetic mechanisms involved in the animal model may be relevant for the understanding of the human diseases. There is a large number of original studies and reviews dealing with this topic available (Frick 1979; Lisak 1980; Wisniewski et al. 1982). For this reason only a few aspects will be discussed in the following chapters; these seem to be the most relevant for an understanding of the pathohistology of inflammatory demyelinating lesions.