Etiology and pathogenesis of monophasic and relapsing inflammatory demyelination - human and experimental.

The close similarity of the CNS lesions in cr-EAE and MS renders this model especially valuable for the study of pathogenetic factors, leading to the formation of inflammatory demyelinated plaques. Recent evidence indicates, that various immune reactions, directed against different CNS antigens cooperate in the formation of the plaques. Furthermore it is discussed, that a combination of virus infection and autoimmunity may result in similarity structured lesions. It is thus propose that multiple different etiologic factors (autoimmune as well as exogenous events) may lead to the clinical pathohistological syndrome of multiple sclerosis.