By H. Lassmann
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 investigate in neu rology. The desire of decisive theoretical and useful development elevated whilst an experimental version featuring far-reaching conformity of structural and pathogenetic positive aspects used to be constructed, particularly power 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 entire review, completely fol lowing up his personal principles in several reviews of person facets. the recent danger of continuing and special research of the scientific, morphological and immunological features of temporal section series of autoimmune demyelination has resulted in many new findings, corrections offormer hypotheses, and, from correlated experiences of human a number of sclerosis, a sequence of vital information referring to, for instance, early manifestations of demyelination, the diversity of so-called acute mul tiple sclerosis and the prevalence of remyelination. in addition, Dr. Lass mann has analysed numerous distinct 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 anxious tissue. the result of those separate reviews additionally ended in a deeper figuring out of demyelinating tactics. This monograph integrates those experiences and summarizes their re sults.
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Additional info for Comparative Neuropathology of Chronic Experimental Allergic Encephalomyelitis and Multiple Sclerosis
Sample text
The above discussed studies have based the identification of active plaques in MS mainlyon the presence of sudanophilic myelin degradation products and did not document the presence of earlier stages of myelin degradation. From histochemical evidence in MS lesions, however, it is well known that the sudanophilic stage of myelin degradation is not a marker for initial lesions (Seitelberger 1960; Lumsden 1970; Adams 1975). Lumsden (1970) identified actively demyelinating plaques by the presence of the earliest stages of myelin debris.
14 a-d. Invasion of phagocytes into the myelin sheaths (myelin stripping) in acute multiple sclerosis. a Same lesion as described in Fig. 13; a phagocyte between the axon and the myelin sheath (arrow) Toluidine blue,x 1000. b,c21-year-old malewithsubacuteMS, leading to death 14 months after onset of the disease; relapsing disease course with rapid progression during the last 4 months; active lesion in the brain stem. b Phagocyte with debris, invaded between lamellae of the myelin sheath (arrow).
1967; Hochwald 1970). Some albumen leakage was found in old demyelinated plaques of chronic MS, but not in actively demyelinating lesions (Tavolato 1975). Albumen uptake together with IgG was observed in astrocytes, axons, and neurons in MS as well as in many other neurological diseases (Auff and Budka 1980). Neuroradiological studies of MS patients with the CT scanner in general showed areas of decreased density corresponding to the plaque extensions (Gyldensted 1976). In acute MS, however, cranial computed tomography revealed contrast enhanced lesions (Aita et al.