大脑中动脉狭窄脑深部小梗死发病机制的研究

目的 研究大脑中动脉粥样硬化性狭窄患者脑深部小梗死的发生频率和发病机制。方法86例发病时间〈1周的急件脑梗死患者，行经颅多普勒超声、彩色超声、磁共振血管造影及功能磁共振成像等检查方法被明确诊断为症状性大脑中动脉粥样硬化性狭窄，并排除颈内动脉病变、心源性栓塞以及非动脉粥样硬化性狭窄。利用磁共振扩散加权成像观察梗死灶的形态学表现及特点，分析其发病机制。结果37例（43．02％）症状性大脑中动脉粥样硬化性狭窄患者存在深部小梗死，多呈孤立性单发病灶。其中内囊纹状体梗死及巨大腔隙者18例（20．93％），梗死灶体积多超过两个层面，少数病灶呈多灶分布的特点；直径较小的腔隙性梗死19例（22．09％），梗死灶体积〈15mm，多位于一个层面内。伴有大脑中动脉粥样硬化性狭窄的深部小梗死的患者，病情多不稳定，预后较差。所有脑深部小梗死患者均伴有大脑中动脉主干支狭窄，且梗死灶体积与大脑中动脉粥样硬化性狭窄程度有关，内囊纹状体梗死多见于大脑中动脉重度狭窄者。结论约50％大脑中动脉粥样硬化性狭窄患者存在脑深部小梗死，其发病机制与大脑中动脉粥样硬化斑块或斑块残端血栓蔓延堵塞深穿支动脉入口有关。对此类患者的治疗不同于经典的腔隙性脑梗死。

The pathogenic mechanism of deep small infarction in middle cerebral artery stenosis

Objective To investigate the morbidity rate and pathogenic mechanism of deep small infarction in patients with middle cerebral artery stenosis (MCAS). Methods A total of 86 symptomatic MCAS patients (onset within 1 week) were diagnosed through transcranial Doppler ultrasonography, color ultrasonography, magnetic resonance angiography (MRA) and function MRI. The patients with internal carotid disease, cardiac emboli and nonartherosclerotic stenosis were excluded through neck vascular color ultrasonography and MRA. Then, the morphological characteristics of deep small infarction on DWI were studied. Results Thirty seven cases (43.02%) of deep small infarction were found by DWI in symptomatic MCAS patients, including striatocapsular infarction and macrolacuna (n=18, 20.93%) and smaller diameter lacunar infarction (n=19, 22.09%). Most patients with deep small infarction (< 15 mm) characterized as single lesion and only a few patients showed multiple lesions on DWI. Patients of deep small infarction with middle cerebral artery stenosis were unfavourable prognosis. All small deep infarctions were associated with middle cerebral artery (MCA) truncal stenosis and the size of infarction was correlated with MCA atherosclerosis stenosis degree. Most cases of striatocapsular infarction were found in patients with more severe MCA truncal stenosis. Conclusion About 50 percent of MCAS patients have deep small infarction and the pathogenic mechanism is associated with the occlusion of lenticulostriate artery origin by thrombosis and/or artherosclerotic plaque, thus the treatment of deep small infarction with MCAS is different from that of classical lacunar cerebral infarction.