Gray F, Dubas F, Roullet E, Escourolle R
Ann Neurol. 1985 Jul;18(1):54-9. doi: 10.1002/ana.410180110.
We have studied 12 patients with diffuse hemorrhagic cerebral amyloid angiopathy clinically and at postmortem examination. The brains in 8 patients had diffuse bilateral loss of myelin in the hemispheric white matter sparing the U fibers, corpus callosum, and internal capsules. The periventricular areas were predominantly affected. Microscopic examination of the white matter showed an association with subacute or chronic edematous lesions: spongiosis, swollen oligodendroglia, widening of the perivascular spaces with edema fluid or siderophages, hyalinization of the blood vessel walls, incomplete myelin loss, and astrocytic gliosis. Three of 8 autopsied patients had undergone computed tomographic examination, which showed bilateral hypodensity of the hemispheric white matter. The brains of 4 patients with illnesses of shorter duration showed only discrete but similar lesions in the centrum semiovale. These white matter changes are similar to those observed in Binswanger's subcortical encephalopathy. We suggest that a common mechanism of hypoperfusion of the distal white matter causes the leukoencephalopathy.
我们对12例弥漫性出血性脑淀粉样血管病患者进行了临床研究和尸检。8例患者的大脑半球白质出现弥漫性双侧髓鞘脱失,U形纤维、胼胝体和内囊未受影响。脑室周围区域受影响最为明显。白质的显微镜检查显示与亚急性或慢性水肿性病变有关:海绵状变性、少突胶质细胞肿胀、血管周围间隙因水肿液或含铁血黄素吞噬细胞而增宽、血管壁玻璃样变、髓鞘部分脱失以及星形细胞增生。8例接受尸检的患者中有3例进行了计算机断层扫描检查,结果显示半球白质双侧低密度。4例病程较短的患者大脑仅在半卵圆中心出现散在但类似的病变。这些白质变化与宾斯旺格皮质下脑病中观察到的变化相似。我们认为,远端白质灌注不足的共同机制导致了白质脑病。