Prineas J W, Kwon E E, Cho E S, Sharer L R
Ann N Y Acad Sci. 1984;436:11-32. doi: 10.1111/j.1749-6632.1984.tb14773.x.
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.
通过对环氧树脂包埋组织的光学显微镜检查（5例）和电子显微镜检查（1例），研究了来自5例多发性硬化症患者的含有脂质巨噬细胞和含有未消化髓鞘碎片的巨噬细胞的斑块。电子显微镜确定的细胞计数显示，在开始髓鞘破坏的区域，少突胶质细胞数量减少。髓鞘破坏的主要机制是在极少数淋巴细胞和浆细胞存在的情况下，巨噬细胞对完整髓鞘的吞噬作用。当斑块定向以便检查整个髓鞘节间时，发现大多数病变，包括已知存在时间少于10个月的病变，都含有正在进行髓鞘再生的节间，有时数量足够多，足以形成影斑。得出的结论是，有时大量的髓鞘再生和活跃的脱髓鞘这两个过程经常共存于充满含脂质巨噬细胞的“脂肪性”亚急性斑块中，并且进行性病变边缘的髓鞘破坏包括正在进行髓鞘再生的节间的破坏。
