Download e-book for iPad: Comparative Neuropathology of Chronic Experimental Allergic by H. Lassmann

By H. Lassmann

ISBN-10: 3642455581

ISBN-13: 9783642455582

ISBN-10: 3642455603

ISBN-13: 9783642455605

For numerous a long time the unsolved etiogenetic and healing difficulties of a number of sclerosis have provided the most powerful problem to investigate in neu rology. The wish of decisive theoretical and sensible growth elevated while an experimental version providing far-reaching conformity of structural and pathogenetic beneficial properties was once built, specifically persistent re lapsing experimental allergic encephalomyelitis (CREAE). in past times years, Dr. Lassmann has contributed considerably to the variation of this version with the purpose of accomplished review, completely fol lowing up his personal principles in different stories of person points. the recent probability of continuing and particular research of the medical, morphological and immunological features of temporal section series of autoimmune demyelination has resulted in many new findings, corrections offormer hypotheses, and, from correlated reports of human a number of sclerosis, a chain of vital information touching on, for instance, early manifestations of demyelination, the variety of so-called acute mul tiple sclerosis and the occurrence of remyelination. in addition, Dr. Lass mann has analysed a number of distinctive difficulties which turned definable during his personal stories or in collaboration with different teams, in cluding the preliminary distribution of demyelinated foci, the cerebrospinal fluid phenomena and immunological findings within the apprehensive tissue. the result of those separate reports additionally resulted in a deeper knowing of demyelinating techniques. This monograph integrates those experiences and summarizes their re sults.

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Extra resources for Comparative Neuropathology of Chronic Experimental Allergic Encephalomyelitis and Multiple Sclerosis

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EM, x I> I> 15000 55 56 57 interval between sensitization and plaque formation. Thus in late chronic lesions less oligodendrocytes are available for remyelination in the lesions than in early chronic plaques. The availability of oligodendrocytes seems to be one of the most important limiting factors regulating the degree of remyelination, at least in cuprizone-induced demyelinated lesions (Ludwin 1980). Also gliosis is more pronounced in late chronic, compared with early chronic lesions. Some evidence from in vitro studies suggests that gliosis may also have an inhibiting effect on remyelination in vitro (Raine and Bomstein 1970b) although in vivo the degree of gliosis did not influence the extent ofremyelination (Ludwin 1980).

In these lesions central (oligodendroglial) remyelination is sparse, mainly located at the lesional borders, and only found late after plaque formation, with an interval of demyelination and remyelination of up to several months. Thus in general in these lesions the simultaneous presence of phagocytes with myelin degradation products and remyelinated nerve fibers was not observed, and the classical lesion in this stage is the demyelinated sclerotic plaque. Furthermore, invasion of Schwann cells into demyelinated plaques of the spinal cord and partial peripheral remyelination is a common observation in lesions formed during the late chronic stage of the disease (Fig.

1972). These changes are best interpreted as reactive alterations due to edema. Also the absence of oligodendrocytes from the center of old sclerotic lesions has been described (Sluga 1969). More recently Raine et al. (l981a, b) confirmed the relative preservation of interfascicular oligodendrocytes at the borders of active MS lesions. In an immunohistochemical study of the distribution of myelin basic protein and myelin-associated glycoprotein in MS lesions, Itoyama et al. (1980) suggested that the formation of MS lesions is due to a primary defect of oligodendrocytes.

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Comparative Neuropathology of Chronic Experimental Allergic Encephalomyelitis and Multiple Sclerosis by H. Lassmann

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