Mews I, Bergmann M, Bunkowski S, Gullotta F, Brück W
Department of Neuropathology, University of Gottingen, Germany.
Mult Scler. 1998 Apr;4(2):55-62. doi: 10.1177/135245859800400203.
Oligodendrocyte and axon pathology was studied in 11 autopsy cases of clinically silent multiple sclerosis. A total of 54 lesions, either demyelinated or late remyelinated, were distributed through the whole brain and spinal cord with 39% of the lesions located in periventricular areas. Determination of axon density revealed an average reduction of 64% and 59% in demyelinated and remyelinated lesions with an extreme variation between different plaques and cases. Oligodendrocytes were identified by immunocytochemistry for myelin oligodendrocyte glycoprotein (MOG) and in situ hybridization for proteolipid protein (PLP) mRNA. Oligodendrocytes were almost completely lost in demyelinated lesions; remyelinated lesions revealed preservation of a considerable number of oligodendrocytes within the lesions. At the border between plaques and the periplaque white matter, similar oligodendrocyte numbers as in remyelinated lesions were found. Different factors including lesion site, axonal preservation and remyelination may thus contribute to the clinical nonappearance of multiple sclerosis lesions.
在11例临床无症状的多发性硬化症尸检病例中研究了少突胶质细胞和轴突病理学。共有54个脱髓鞘或晚期再髓鞘化病变分布于全脑和脊髓,其中39%的病变位于脑室周围区域。轴突密度测定显示,脱髓鞘和再髓鞘化病变中的轴突密度平均降低了64%和59%,不同斑块和病例之间存在极大差异。通过免疫细胞化学检测髓鞘少突胶质细胞糖蛋白(MOG)和原位杂交检测蛋白脂蛋白(PLP)mRNA来鉴定少突胶质细胞。在脱髓鞘病变中,少突胶质细胞几乎完全消失;再髓鞘化病变显示病变内保留了相当数量的少突胶质细胞。在斑块与斑块周围白质的边界处,发现少突胶质细胞数量与再髓鞘化病变中的相似。因此,包括病变部位、轴突保留和再髓鞘化在内的不同因素可能导致多发性硬化症病变在临床上未出现。