Etiology and Pathogenesis of Monophasic and Relapsing Inflammatory Demyelination — Human and Experimental

Abstract

Experimental allergic encephalomyelitis (EAE) is an autoimmune disease resulting from injection of homogenates of central nervous system tissue. Acute variants of this disease have been extensively studied during the past decades and from the view of pathohistology can be regarded as suitable models for acute inflammatory demyelinating diseases in humans (acute perivenous leucoencephalomyelitis and acute hemorrhagic leucoencephalomyelitis; Alvord 1970, Levine 1974). More recently reproducible models of chronic progressive or chronic relapsing EAE have been introduced using various animal species (Stone and Lerner 1965, Wisniewski and Keith 1977, Massanari 1980, Lublin et al.1981) which pathohistologically differ from acute models by the large extent of demyelination in the lesions (Raine et al.1974, Wisniewski and Keith 1977, Lassmann and Wisniewski 1979, Lassmann 1983). A more extensive comparative neuro- pathological study of cr-EAE and MS lesions revealed a close similarity in the essential features of the demyelinated plaques (inflammation, demyelination and sclerosis) as well as in more variable aspects like lesional topography, patterns of plaque growth, oligodendroglia involvement and remyelination, vascular pathology, axonal and neuronal alterations and others (Lassmann 1983). Differences in pathohistology of the two diseases are rather found in quatitative than in qualitative aspects (e.g. in the size of the lesions, or in the degree of oligodendroglia involvement and remyelinating).