Iwamoto T, Sasaki A, Yanagawa K, Kubo H, Takasaki M
Department of Ceriatric Medicine, Tokyo Medical College.
Nihon Ronen Igakkai Zasshi. 1994 Sep;31(9):677-82. doi: 10.3143/geriatrics.31.677.
White matter changes, which are noted in Binswanger's disease and which may be due to ischemia, have previously been explained mainly on the basis of the hemodynamic mechanism. To elucidate the etiopathophysiology of Binswanger's disease from the hemorheology viewpoint, platelet activation in the cerebral circulation was studied in 30 patients with Binswanger's disease, who satisfied the diagnostic criteria of Binswanger's disease proposed by Bennett et al. Plasma beta-thromboglobulin concentration gradients (delta BTG) between the jugular vein and the antecubital vein, as indicators of platelet activation in the cerebral circulation, were determined in these patients (Binswanger's disease group) compared with those of different stroke subtypes groups (lacunar, atherothrombotic, cardioembolic) in the chronic phase and 25 patients with various diseases other than stroke (non-stroke group). Among these groups, the elevation of delta BTG levels in the Binswanger's disease group (4.55 +/- 6.95) were so frequent and prominent that differences were significant, especially in comparison to those of the cardioembolic group, and the non-stroke group. The enhanced platelet activation in the cerebral circulation observed in Binswanger's disease indicated not only the widespread development of underlying vascular lesions, but also accelerated release reaction of vasoactive substances from platelets into the blood stream, which could biochemically injure the vascular wall and neurons downstream, resulting in Binswanger's disease.
白质改变见于宾斯旺格病，可能由缺血引起，此前主要基于血液动力学机制进行解释。为从血液流变学角度阐明宾斯旺格病的病因病理生理学，对30例符合贝内特等人提出的宾斯旺格病诊断标准的宾斯旺格病患者的脑循环中的血小板活化情况进行了研究。测定了这些患者（宾斯旺格病组）颈静脉和肘前静脉之间的血浆β-血小板球蛋白浓度梯度（δBTG），作为脑循环中血小板活化的指标，并与不同卒中亚型组（腔隙性、动脉粥样硬化血栓形成性、心源性栓塞性）的慢性期患者以及25例非卒中的各种疾病患者（非卒中组）进行比较。在这些组中，宾斯旺格病组的δBTG水平升高（4.55±6.95）非常频繁且显著，差异具有统计学意义，尤其是与心源性栓塞组和非卒中组相比。在宾斯旺格病中观察到的脑循环中血小板活化增强不仅表明潜在血管病变广泛发展，还表明血管活性物质从血小板加速释放到血流中，这可能会对下游血管壁和神经元造成生化损伤，从而导致宾斯旺格病。
