Tanoi Y, Okeda R, Budka H
Department of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Japan.
Acta Neuropathol. 2000 Oct;100(4):347-55. doi: 10.1007/s004010000203.
To identify arterial changes that are characteristic of Binswanger's encephalopathy (BE), we analyzed cerebral subarachnoid and medullary arteries of seven BE autopsy specimens by reconstruction of stained serial sections. We also noted the frequency of intimal fibrosis with or without atheroma of the subarachnoid arteries, and determined the medial thickness of the subarachnoid and medullary arteries. The results for the BE specimens were compared with those of six hypertensive brain hemorrhage (HH) specimens and six normotensive (NT) specimens from patients without cerebral abnormalities. In medullary arteries of BE in comparison with HH, we observed nonspecific but significantly more widespread intimal fibrosis with or without atheroma, as well as segmental loss of the medial smooth muscle cells (SMCs), which was sometimes associated with intimal plasma exudation or microaneurysm. A few medullary arteries in BE were completely occluded by fibrous connective tissue. Intimal fibrosis of the subarachnoid arteries was significantly more widespread in BE than in HH and NT. The media of the subarachnoid and medullary arteries was significantly thicker in BE and HH than in NT, and tended to be thicker in BE than in HH. In NT specimens the medullary arteries tended to be thinner in medial thickness than the subarachnoid arteries. These findings suggest that dysfunction of blood flow regulation due to increased arterial stiffness caused by hypertension-induced intimal fibrosis and loss of medial SMCs is an essential mechanism resulting in diffuse myelin loss of the cerebral white matter in BE, whereas luminal stenosis or occlusion and adventitial fibrosis are secondary. Moreover, selective and severe involvement of the cerebral medullary arteries compared with the subarachnoid arteries may be explained by the following two factors, (1) that many medullary arteries have normally dilated segments, and (2) that their media is thinner compared with that of the subarachnoid arteries of the corresponding diameter.
为了确定宾斯旺格脑病（BE）的特征性动脉变化，我们通过对七个BE尸检标本的染色连续切片进行重建，分析了脑蛛网膜下腔和髓质动脉。我们还记录了蛛网膜下腔动脉内膜纤维化伴或不伴动脉粥样硬化的频率，并测定了蛛网膜下腔和髓质动脉的中膜厚度。将BE标本的结果与六个高血压脑出血（HH）标本和六个无脑部异常患者的正常血压（NT）标本的结果进行比较。与HH相比，在BE的髓质动脉中，我们观察到内膜纤维化伴或不伴动脉粥样硬化非特异性但明显更广泛，以及中膜平滑肌细胞（SMC）节段性缺失，有时伴有内膜血浆渗出或微动脉瘤。BE中的一些髓质动脉被纤维结缔组织完全阻塞。BE中蛛网膜下腔动脉的内膜纤维化比HH和NT明显更广泛。BE和HH中蛛网膜下腔和髓质动脉的中膜明显比NT厚，并且BE中往往比HH厚。在NT标本中，髓质动脉的中膜厚度往往比蛛网膜下腔动脉薄。这些发现表明，高血压诱导的内膜纤维化和中膜SMC丢失导致动脉僵硬度增加，进而引起血流调节功能障碍，是BE中脑白质弥漫性髓鞘脱失的重要机制，而管腔狭窄或闭塞以及外膜纤维化是次要的。此外，与蛛网膜下腔动脉相比，脑髓质动脉的选择性和严重受累可能由以下两个因素解释：（1）许多髓质动脉通常有扩张段；（2）与相应直径的蛛网膜下腔动脉相比，它们的中膜更薄。
