Continual breakdown and regeneration of myelin in progressive multiple sclerosis plaques.
Plaques with lipid macrophages and macrophages containing undigested myelin fragments from five multiple sclerosis patients were studied by light microscopy of epoxy-embedded tissue (five cases) and electron microscopy (one case). Cell counts determined electron microscopically revealed that oligodendrocytes were reduced in number in areas of commencing myelin breakdown. The major mechanism of myelin destruction was phagocytosis by macrophages of intact myelin sheaths in the presence of very small numbers of lymphocytes and plasma cells. When plaques were orientated to allow examination of whole myelin internodes, it was found that most lesions, including lesions known to have been present for less than ten months, contained remyelinating internodes, sometimes in numbers large enough to form shadow plaques. It is concluded that the two processes of sometimes massive remyelination and active demyelination frequently coexist in "fatty" subacute plaques filled with lipid-containing macrophages, and that myelin breakdown at the edges of progressive lesions includes destruction of remyelinating internodes.
D000328:Adult; D001921:Brain / Q000378:metabolism / Q000648:ultrastructure; D002531:Cerebellum / Q000378:metabolism / Q000648:ultrastructure; D002908:Chronic Disease; D005260:Female; D006651:Histocytochemistry; D006801:Humans; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000378:metabolism* / Q000473:pathology; D009186:Myelin Sheath / Q000378:metabolism* / Q000648:ultrastructure; D013116:Spinal Cord / Q000378:metabolism / Q000648:ultrastructure