Multiple nicht eitrige Encephalomyelitis und multiple Sklerose

Neuroglia and the myelin-bearing cell: a symposium. Pathogenesis of multiple sclerosis.

“…A fundamental feature in its pathogenesis was early and marked hypertrophy of astrocytes. The same had been reported by Charcot (1876), Muller (1904), Anton andWohlwill (1912), andJakob (1967) to be the earliest change in multiple sclerosis. The hypothesis might be put forward that the pathogenetic mechanism at work in kuru, scrapie, and Jacob-Creutzfeldt disease which leads to marked astroglial hypertrophy (with the character of a benign neoplasia) was also operative in multiple sclerosis.…”

Axonal Pathology in Multiple Sclerosis. A Historical Note

“…By 1915, not only had the presence of axonal degeneration in the lesions of MS been well established, but also the changes axons undergo during different stages of the disease had been described: axonal swellings (2, 7-10, 15, 21-23, 28, 30, 35, 41, 46, 50), alternating constrictions and dilatations (2,9,22,35,41) and transections (2,22,28,35,46) in actively demyelinating lesions ("Körnchenzellen," myelin debris containing macrophages were defined as a characteristic of "fresh" lesions; reviewed by Siemerling and Raecke (52)) as well as decrease of the axonal diameter in chronic plaques (23,41,47) (Figure 1). Thus, it was generally accepted that the bulk of acute axonal injury appeared in the early stage of the disease.…”

“…Most authors agreed that some axons were definitively lost in the early stage of the disease (15,22,23,27,30,52), and that axonal degeneration proceeded with disease duration, leading to pronounced axonal loss in old plaques (2,4,21,26,27,41,45,50,52) and sometimes even to severe atrophy (9,10,21). Few authors claimed that axons remained "nearly complete or relative as the case may be in each instance (Lumsden (40))" preserved (33,43,53,58), although with morphological changes (33,58).…”

“…Review of early literature suggests that axonal damage, including axonal pathologic changes such as axonal swellings (2, 7-10, 15, 21-23, 28, 30, 35, 41, 50) and transections (2,22,28,35,46), had already been recognized and described in detail at the turn of the century (Figure 1). At the time of their publication, the first descriptions of axonal pathology in MS were an intensely discussed and controversial subject (9,10,13,52,55).…”

Transmission experiments with multiple sclerosis: an interim report.

“…Pathologically, too, they show little similarity at first sight, though both present a remarkable overgrowth of astroglial cells (Muller, 1904 ;Anton and Wohlwill, 1912 ;Chandler, 1961 ;Pattison, 1965), a feature apparently shared with kuru. The possible implications of this have been briefly discussed elsewhere (Field, 1966).…”