Comparative Neuropathology of Chronic Experimental Allergic by H. Lassmann

By H. Lassmann

For numerous a long time the unsolved etiogenetic and healing difficulties of a number of sclerosis have provided the most powerful problem to analyze in neu rology. The desire of decisive theoretical and sensible growth elevated whilst an experimental version featuring far-reaching conformity of structural and pathogenetic beneficial properties used to be built, specifically continual re lapsing experimental allergic encephalomyelitis (CREAE). up to now years, Dr. Lassmann has contributed considerably to the difference of this version with the purpose of finished assessment, completely fol lowing up his personal rules in several stories of person facets. the recent threat of continuing and distinctive research of the medical, morphological and immunological features of temporal part series of autoimmune demyelination has resulted in many new findings, corrections offormer hypotheses, and, from correlated experiences of human a number of sclerosis, a chain of significant information bearing on, for instance, early manifestations of demyelination, the variety of so-called acute mul tiple sclerosis and the prevalence of remyelination. additionally, Dr. Lass mann has analysed a number of distinctive difficulties which turned definable during his personal reports or in collaboration with different teams, in cluding the preliminary distribution of demyelinated foci, the cerebrospinal fluid phenomena and immunological findings within the fearful tissue. the result of those separate experiences additionally resulted in a deeper knowing of demyelinating strategies. 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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1977; Tourtellotte and Ma 1978; Tourtellotte 1970). No clear-cut correlation between the clinical stage of MS (active versus inactive) and BBB function were found (Eichhoff et al. 1977). These data indicate that the BBB is normal in more than 70 % of the chronic MS cases. On the basis of our data in chronic relapsing EAE, however, the leakage of serum proteins in one or a few active focal lesions is not necessarily reflected in an overall change of BBB function in the CSF or brain extracts. On the contrary large active lesions in silent regions of the brain may reflect BBB damage in the CSF in cases with clinically remitting disease.

B Detail of a; so-called activated microglia in the cerebellar cortex adjacent to the lesion. x400. c "Activated microglia" and normal oligodendrologia in the periplaque area. x400

This view seems to be partly due to difficulties in the identification of remyelination in tissue obtained from autopsy, performed several hours after death. Furthermore, little is known about the time course of remyelination in human demyelinating diseases. Thus the study of the dynamics of remyelination in chronic relapsing EAE may help us to understand the factors regulating the extent of remyelination, not only in the experimental model but also in the human disease. 1 Remyelination in Acute and Chronic EAE The presence of remyelination in EAE has been well established since the earliest descriptions by Lapert (1965, 1967).

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