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目的:分析首发前循环急性缺血性脑卒中后认知障碍患者脑灌注水平的变化及与认知障碍的关系。方法:选取2018年3月至2020年3月于华北理工大学附属开滦总医院神经内科治疗并符合纳入、排除标准的70例首发前循环急性缺血性脑卒中患者进行回顾性分析。采用简易精神状态检查量表(mini-mental state examination，MMSE)分为卒中后认知障碍(post-stroke cognitive impairment，PSCI)组36例，卒中后无认知障碍组34例。全部入选患者行电子计算机断层扫描(computed tomography，CT)和磁共振弥散加权成像(diffusion-weighted MR imaging，MRI-DWI)确立诊断和明确病灶分布；应用磁共振血管造影(magnetic resonance angiography，MRA)检测脑供血动脉狭窄情况；应用三维准连续动脉自旋标记(3D pseudo-continuous arterial spin labeling，3D-pCASL)灌注成像技术，设置两个标记后延迟时间(post label delay，PLD)1.5、2.5 s检测脑血流量。结果:(1)两组间临床基本资料比较差异均无统计学意义(n P均>0.05)。(2)卒中后认知障碍组病灶侧存在大脑中动脉(middle cerebral artery，MCA)、大脑前动脉(anterior cerebral artery，ACA)、颈内动脉(internal carotid artery，ICA)≥1条或≥2条中重度狭窄/闭塞患者比例[91.67%(33/36)、33.33%(12/36)]高于卒中后无认知障碍组[23.53%(8/34)、8.82%(3/34)]；卒中后认知障碍组病灶侧分别存在MCA、ICA中、重度狭窄/闭塞患者比例[69.44%(25/36)、44.44%(16/36)]高于卒中后无认知障碍组[14.71%(5/34)、11.76%(4/34)]；差异均有统计学意义(χn 2值分别为33.455、6.239、21.394、9.150，n P均<0.05)。⑶卒中后认知障碍组同时存在≥2个脑区梗死病灶患者比例[61.1%(22/36)]及额叶梗死病灶构成比[38.03%(27/71)]高于卒中后无认知障碍组[20.6%(7/34)与19.05%(8/42)]，差异均有统计学意义(χn 2值分别为11.833、4.447，n P均<0.05)；PLD 2.5 s时，卒中后认知障碍组额叶梗死病灶CBF值[(31.516±8.333) mL/(100 g·min)]低于卒中后无认知障碍组[(45.442±8.281) mL/(100 g·min)]，差异有统计学意义(n t＝3.835，n P<0.05)；相关性分析发现，PLD 2.5 s额叶梗死病灶CBF值与MMSE评分呈正相关(n r＝0.738，n P<0.05)。⑷卒中后认知障碍组PLD 1.5、2.5 s病灶侧存在≥1个或≥2个低灌注脑区(额叶、颞叶、顶叶)患者比例[88.89%(32/36)、88.89%(32/36)、77.78%(28/36)、66.67%(24/36)]高于卒中后无认知障碍组[67.65%(23/34)、8.82%(3/34)、29.41%(10/34)、0]，差异有统计学意义(χn 2值分别为4.686、44.837、16.483、34.493，n P均<0.05)；PLD 1.5 s时，卒中后认知障碍组病灶侧低灌注脑区额叶、顶叶CBF值[(20.260±5.266) mL/(100 g·min)、(17.664±3.947) mL/(100 g·min)]低于卒中后无认知障碍组[(33.442±10.563) mL/(100 g·min)、(28.071±6.913) mL/(100 g·min)]，差异有统计学意义(n t＝3.392、6.225，n P均<0.05)；PLD 2.5 s时，卒中后认知障碍组病灶侧额叶、顶叶、颞叶低灌注代偿后CBF值[(37.732±8.355) mL/(100 g·min)、(32.942±6.459) mL/(100 g·min)、(39.282±7.443) mL/(100 g·min)]低于卒中后无认知障碍组[(57.189±9.965) mL/(100 g·min)、(52.415±7.017) mL/(100 g·min)、(49.258±8.912) mL/(100 g·min)]，差异均有统计学意义(n t值分别为5.443、10.227、2.950，n P均<0.05)；相关性分析发现，PLD 1.5 s病灶侧低灌注脑区额叶、顶叶CBF值及PLD 2.5 s低灌注脑区额叶、顶叶、颞叶低灌注代偿后的CBF值均与MMSE评分呈正相关(n r值分别为0.693、0.675、0.823、0.799、0.545，n P均0.05). (2) The proportion of patients with middle cerebral artery, anterior cerebral artery and internal carotid artery ≥1 or ≥2 moderate and severe stenosis / occlusion on the focal side in the post-stroke cognitive impairment group (91.67%(33/36), 33.33%(12/36)) was higher than that in the post-stroke non-cognitive impairment group (23.53%(8/34), 8.82%(3/34)); the proportion of patients with moderate and severe stenosis / occlusion of MCA and ICA on the focal side in the post-stroke cognitive impairment group (69.44%(25/36), 44.44%(16/36)) was higher than that in the post-stroke cognitive impairment group (14.71%(5/34), 11.76%(4/34)), and the difference was statistically significant(χn 2 values were 33.455, 6.239, 21.394, 9.150, all n P<0.05). (3) The proportion of patients with ≥ 2 cerebral infarction lesions in the post-stroke cognitive impairment group (61.1%(22/36))was higher than that in the post-stroke cognitive impairment group (38.03%(27/71))than that in the non-stroke group (20.6%(7/34), 19.05%(8/42)), and the difference was statistically significant(χn 2=11.833, 4.447, all n P<0.05). PLD 2.5 s, the CBF value of frontal lobe infarction in post-stroke cognitive impairment group((31.516±8.333) mL/(100 g·min)) was lower than that in post-stroke non-cognitive impairment group((45.442±8.281) mL/(100 g·min)), the difference was statistically significant(n t=3.835, n P<0.05). Correlation analysis showed that the CBF value of PLD 2.5 s frontal infarction lesion was positively correlated with MMSE score(n r=0.738, n P<0.05). (4) The proportion of patients with ≥ 1 or ≥ 2 hypoperfusion areas (frontal lobe, temporal lobe, parietal lobe) on the focal side of PLD 1.5 s and 2.5 s after stroke (88.89%(32/36), 88.89%(32/36), 77.78%(28/36), 66.67%(24/36)) were higher than those without cognitive impairment after stroke (67.65%(23/34), 8.82%(3/34), 29.41%(10/34), 0), the difference was statistically significant(χn 2 values were 4.686, 44.837, 16.483, 34.493, all n P<0.05). At PLD 1.5 s, CBF values of frontal lobe and parietal lobe in cerebral hypoperfusion area ((20.260±5.266) mL/(100 g·min), (17.664±3.947) mL/(100 g·min)) in patients with cognitive impairment after stroke were lower than those in patients without cognitive impairment ((33.442±10.563) mL/(100 g·min), (28.071±6.913) mL/(100 g·min)), the difference was statistically significant(n t values were 3.392, 6.225, all n P<0.05), at PLD 2.5 s, the CBF value after compensatory perfusion of frontal lobe, parietal lobe and temporal lobe in the post-stroke cognitive impairment group ((37.732±8.355) mL/(100 g·min), (32.942±6.459) mL/(100 g·min), (39.282±7.443) mL/(100 g·min)) was lower than that in the non cognitive impairment Group ((57.189±9.965) mL/(100 g·min), (52.415±7.017) mL/(100 g·min), (49.258±8.912) mL/(100 g·min)), the difference was statistically significant(n t values were 5.443, 10.227, 2.950, all n P<0.05). Correlation analysis found that the CBF value of the frontal lobe and parietal lobe of the PLD 1.5 s lesion area and the CBF value of the PLD 2.5 s hypoperfusion brain area after the perfusion of the frontal lobe, parietal lobe, and temporal lobe were positively correlated with the MMSE score(n r values were 0.693, 0.675, 0.823, 0.799, 0.545, all n P<0.05).n Conclusion:Patients with first anterior circulation acute ischemic post-stroke cognitive impairment often have extensive hypoperfusion in the peripheral cerebral region, the occurrence of cognitive impairment after the first anterior circulation acute ischemic post-stroke cognitive impairment is related to the decrease of the perfusion level of the infarct lesion and the brain area around the lesion.