By H. Lassmann
ISBN-10: 3642455581
ISBN-13: 9783642455582
ISBN-10: 3642455603
ISBN-13: 9783642455605
For a number of 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 useful development elevated whilst an experimental version proposing far-reaching conformity of structural and pathogenetic positive factors was once constructed, particularly continual re lapsing experimental allergic encephalomyelitis (CREAE). in the past years, Dr. Lassmann has contributed considerably to the difference of this version with the purpose of complete overview, completely fol lowing up his personal rules in different reports of person features. the recent hazard of constant and targeted research of the scientific, morphological and immunological features of temporal part series of autoimmune demyelination has ended in many new findings, corrections offormer hypotheses, and, from correlated experiences of human a number of sclerosis, a chain of significant facts referring to, for instance, early manifestations of demyelination, the diversity of so-called acute mul tiple sclerosis and the occurrence of remyelination. in addition, Dr. Lass mann has analysed a number of designated difficulties which turned definable during his personal reviews 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 ended in a deeper realizing of demyelinating procedures. This monograph integrates those experiences and summarizes their re sults.
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Extra info for Comparative Neuropathology of Chronic Experimental Allergic Encephalomyelitis and Multiple Sclerosis
Sample text
Cryostat section, x 15. c Detail of a. Focal blood-brain barrier leakage in the meninges. x 40. d, e Centrum semiovale and fornix lesion showing variable peroxidase leakage {arrows}. Cryostat section, x 20 24 25 As expected HRP leakage into the stroma of the choroid plexus in chronic relapsing EAE occurred in the presence as well as absence of inflammatory infiltrates (Fig. 7c). The number of vascular segments with increased permeability for HRP decreased with chronicity of the disease. This may be explained by the lower incidence of active lesions in the late chronic compared with the early chronic stage of the disease.
When such inactive lesions are studied, the degree of oligodendrocyte loss in chronic EAE lesions seems to be variable, depending mainly upon the time interval between sensitization and plaque formation (Lassmann et al. 1980b). In the acute, subacute, and early chronic stage of the disease (10-100 days after sensitization), cells resembling the light and electron microscopic features of oligodendrocytes can be found in high numbers in the lesions (Figs. 17, 18f, g), and remyelination may take place within 1-2 weeks after plaque formation (Lampert 1965; Lassmann et al.
Their precise origin (hematogenous or local) has so far not been clear. The perivenous and pericapillary accumulation of debris-containing cells, which, as discussed 46 above, may be an indicator for their hematogenous origin, varies from case to case and also within different plaques in the same case. As a general rule, however, pericapillary accumulation of debris-containing phagocytes is more pronounced in acute MS than in active lesions in chronic MS. However, in both acute and chronic MS, a minor fraction of the myelin debris can also be found in typical local cells of the CNS (Marburg 1906; Sluga 1979).
Comparative Neuropathology of Chronic Experimental Allergic Encephalomyelitis and Multiple Sclerosis by H. Lassmann
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