大脑中动脉狭窄患者皮质下梗死发病机制的研究

目的 旨在研究大脑中动脉粥样硬化性狭窄患者皮质下梗死的发病机制。 方法 利用磁共振弥散加权成像,研究86例症状性大脑中动脉粥样硬化性狭窄患者皮质下梗死的形态学表现,以及与经颅多普勒超声(TCD)监测微栓子的相关性。 结果 86例大脑中动脉粥样硬化性狭窄皮质下梗死的患者,63例(73.3％)呈多发性病灶,主要累及内交界区及半卵圆中心。TCD监测到14例(29.8％)皮质下梗死患者的微栓子,其中13例为多发性病灶,多表现为半卵圆中心梗死(P<0.001)、皮质播散性小梗死(P<0.001)以及多发性脑梗死(P<0.02)。结论 动脉-动脉栓塞与血流动力学低灌注的共同作用是大脑中动脉粥样硬化性狭窄患者皮质下多发性脑梗死的发病机制。内交界区梗死、半卵圆中心梗死为不同发病机制的两种梗死类型,后者与栓塞机制关系更为密切。

The pathogenesis of subcortical infarction in patients with MCA atherosclerotic stenosis

Objective To investigate the pathogenesis of subcortical infarction in patients with MCA atherosclerotic stenosis (MCAAS) . Methods Diffusion-weighted magnetic resonance imaging (DWI) and transcranial Doppler (TCD)were used to study the relationship between infarct pattern and the microemboli signals. Results DWI showed that 63(73. 3% ) patients had acute multiple infarction, which mainly involved internal border zone(70. 2%), centrum semiovale infarction (29. 1% ) . 14 patients were detected microembolic signal, among of them, 13 patients were multiple infarction. Microembolic signal were associated with multiple infarction ( P < 0. 02), centrum semiovale ( P < 0. 001) and cortical small infarction ( P < 0. 001). Conclusion Our study suggests that subcortical infarction with MCAAS is characterized as multiple lesion and combination of artery-artery embolism and homodynamic low-flow is the main pathogenesis of subcortical multiple infarction. Artery-artery embolic make a greater contribution to centrum semiovale infarction than IBZ infarction in MCAAS patients.