特发性脑动脉夹层28例致缺血性卒中机制分析

目的通过回顾分析特发性脑动脉夹层(cerebral artery dissection,CAD)患者影像学和血管学资料研究其缺血性卒中机制,为治疗策略提供依据。方法选取28例特发性CAD所致急性缺血性卒中患者,根据缺血性卒中病灶形态和分布来确定CAD致缺血性卒中机制;根据夹层病变的位置分为颅内组和颅外组,对两组患者夹层致缺血性卒中机制进行比较。结果共28例患者纳入研究,男19例,女9例。颅外组17例,其中颈内动脉央层15例,椎动脉V1段夹层2例。颅内组11例,其中大脑中动脉M1段夹层3例,基底动脉夹层2例,椎动脉V4段央层6例。颅内组高血压和糖尿病患者分别为7例(63.6%)和5例(45.5%),颅外组均为1例(5.9%),颅内组高血压和糖尿病患病比例多于颅外组(P=0.002,0.022)。颅外组和颅内组单纯栓塞性缺血性卒中分别有12例(70.6%)和2例(18.2%),两组比较差异有统计学意义(P=0.018)。颅内组由夹层病变闭塞局部穿支动脉所致缺血性卒中7例(63.6%),由夹层闭塞穿支合并血流动力学机制所致1例(9.1%),单纯血流动力学机制所致1例(9.1%)。结论颅外CAD致缺血性卒中机制与颅内CAD有所不同,前者主要导致栓塞性缺血性卒中,而后者致缺血性卒中机制主要为夹层病变闭塞局部穿支动脉。

Mechanism of Ischemic Infarct in Spontaneous Cerebral Arteries Dissection: 28 Cases Report

Objective This study investigated the mechanism ofischemic stroke induced by cerebral arteries dissection through brain imaging and cerebrovascular findings, and provided evidences for the relative strategies of therapy. Methods Twenty-eight patients with acute ischemic infarct induced by cerebral arteries dissection confirmed by clinical and neuroradiological data were recruited. Mechanisms of ischemic infarct were determined by the infarct lesion morphous and distribution. All patients were divided into the extracranial group and the intracranial group according to the location of vessel lesions, and the mechanisms of the two groups were compared. Results Twenty-eight patients （19 males and 9 females） were recruited. There were 17 patients with extracranial dissection, 15 patients with extracranial internal carotid artery dissection and 2 patients with V1 segment dissection of vertebral artery. There were 11 patients with intracranial dissection, 3 patients with M1 segment dissection of middle cerebral artery and 6 patients with V4 segment dissection of vertebral artery and 2 patients with basilar artery dissection. There were 7 patients （63.6%） with hypertension and 5 patients （45.5%） with diabetes in the intracranial group, and one patient （5.9%） and one patient （5.9%） respectively in the extracranial group （P values were 0.002 and 0.022）. There were 12 patients （70.6%） with only thromboembolism infarction in the extracranial group, 2 patients （18.2%） in the intracranial group （P~0.020）. In the intracranial group, there were 7 patients （63.6%） with infarction resulted in obstruction of perforating branches caused by dissection lesion, and one patient （9.1%） with infarction caused by obstruction of perforating branches and hemodynamic mechanism. Conclusion The mechanisms of ischemic infarct induced by extracranial and intracranial dissection were different. Thromboembolism was the main mechanism of infarct induced by extracranial dissection, and obstruction of perforating branches caused by dissection lesion was the main mechanism of infarct induced by intracranial dissection.