Huang K, Wu L, Luo Y
Can J Neurol Sci. 1985 May;12(2):88-94. doi: 10.1017/s031716710004676x.
Since Binswanger's description of subcortical arteriosclerotic encephalopathy in 1894, numerous cases have been reported. Several authors doubt the validity of this malady, although the majority consider it to be a disease entity. We report seven cases with this type of pallor of myelin, only two of which are accompanied by a history of dementia. Among the seven cases, two had arteriosclerosis of penetrating arteries and arterioles in cerebral white matter. Electron microscopy showed splitting of myelin sheaths, probably the result of edema. In reviewing the blood supply of the cerebral white matter, we conclude that no pathological alterations of medullary branches of the cerebral arteries, the same vessels supplying the white matter, can give rise to such diffuse pallor of white matter and spare the arcuate fibres. This pallor can only be due to cerebral edema, most likely of hypoxic-ischemic, hypotensive, or acidotic origin. We also contend that arteriosclerosis can only cause dementia through multiple infarcts or lacunae, if it indeed leads to dementia.
自1894年宾斯万格描述皮质下动脉硬化性脑病以来，已有大量病例报道。尽管大多数人认为这是一种疾病实体，但有几位作者对这种病症的有效性表示怀疑。我们报告了7例这种类型的髓鞘苍白病例，其中只有2例伴有痴呆病史。在这7例病例中，2例脑白质的穿通动脉和小动脉硬化。电子显微镜显示髓鞘分裂，可能是水肿的结果。在回顾脑白质的血液供应时，我们得出结论，供应白质的大脑动脉髓质分支没有病理改变，而这些血管同样供应白质，却不会导致白质如此弥漫性的苍白而不累及弓状纤维。这种苍白只能归因于脑水肿，最有可能是缺氧缺血性、低血压性或酸中毒性的。我们还认为，动脉硬化如果确实导致痴呆，也只能通过多发性梗死或腔隙性梗死导致痴呆。
