脑卒中后认知功能障碍发生率及其危险因素分析

目的 探讨缺血性脑卒中后认知功能障碍(PSCI)的发生率,并筛查其发生的相关危险因素.方法 选择2016年1月至2018年9月西安交通大学医学院附属三二〇一医院急性缺血性脑卒中病人(7 d内)180例,随访观察6—12个月后,共入组148例,根据简易精神状态量表(MMSE)和蒙特利尔认知评估量表(MoCA)将病人分为卒中后认知功能正常组(NPSCI)70例和卒中后认知功能障碍组(PSCI)78例,采用不同认知域功能量表对病人认知功能进行评估,比较两组一般临床资料、认知功能损害域、放射影像学资料,采用logistic回归模型对随访6—12个月PSCI发生的危险因素进行筛查.结果 随访6—12个月,PSCI发生率为52.7％(78例),与PSNCI组比较,PSCI组年龄(61.5岁比64.0岁)、糖尿病患病率(15.7％比42.3％)、NIHSS评分(3分比4分)、前循环梗死部位(54.3％比71.8％)明显升高、受教育程度水平明显下降,差异有统计学意义(P<0.05);PSCI组整体认知功能及不同认知域(记忆功能、执行功能、语言功能、视空间功能)均明显下降(P<0.001);在脑组织急性非腔隙性梗死病灶中,PSCI组脑组织皮层(0.31±0.523)分比(0.58±0.750)分]或皮层下梗死病变(0.41±0.738)分比(0.69±0.852)分]及梗死数目(1.19±1.254)分比(1.78±1.618)分]明显升高;在慢性缺血脑组织改变中,PSCI组GCA评分明显下降(2.32±1.023)分比(1.93±0.892)分],颞叶萎缩(1.14±0.805)分比(1.64±0.816)分]、Fazekas评分(1.05±0.935)分比(1.28±0.822)分]、侧脑室周围高信号(PVH)(2.51±1.789)分比(3.51±1.051)分]明显升高;在慢性腔隙性脑梗死病灶中,PSCI组脑组织皮层(0.15±0.551)分比(0.58±1.111)分]及皮层下病变(0.28±0.721)分比(0.58±1.081)分]及梗死数目(0.84±1.682)分比(1.78±2.582)分]明显升高,差异有统计学意义(P<0.05);logistic回归分析示,年龄、受教育程度、糖尿病、急性非腔隙性脑梗死数目、PVH是PSCI发生的独立危险因素(P<0.01).结论 年龄、受教育程度、糖尿病、急性非腔隙性脑梗死数目、PVH与脑卒中后6-12个月认知功能障碍的发生密切相关,为临床早期识别和筛查PSCI的发生率及危险因素,提供了有力的临床证据.

Prospective study on incidence of cognitive dysfunction after stroke and its risk factors

Objective To investigate the incidence of post-stroke cognitive dysfunction (PSCI) in patients with ischemic stroke from 6 to 12 months, and to screen the related risk factors.Methods A total of 180 patients with acute ischemic stroke (within 7 days) whowere admitted to the Department of Neurology of 3201 Hospital Affiliated to Xi''an Jiaotong University School of Medicine from January2016 to September 2018 were selected, after follow-up observation for 6 to 12 months, 148 patients were enrolled, patients were assigned into 70 patients with normal poststroke cognitive function (NPSCI) and 78 patients with poststroke cognitive function (PSCI) according to the simple mental state scale (MMSE) and the Montreal cognitive assessment scale (MoCA). The cognitive function of the patients was evaluated with different cognitive domain function scales, and the general clinical data, cognitive impairment domain, and radiographic data of the patients in the two groups were compared, logistic regression model was used to screen risk factors of PSCI during 6-12 months of follow-up.Results After 6-12 months of follow-up, the incidence of PSCI was 52.7% (78 cases); compared with the PSNCI group, age (61.5 vs. 64.0), prevalence of diabetes (15.7% vs. 42.3%), NIHSS score (3 vs. 4) and anterior circulation infarct site (54.3% vs. 71.8%) were significantly increased, and education level was significantly decreased in the PSCI group, with statistically significant difference (P < 0.05). Overall cognitive function and different cognitive domains (memory function, executive function, language function and visuospatial function) decreased significantly in the PSCI group (P < 0.001). In the brain tissue acute non-lacunar infarction lesions, cerebral cortex (0.31±0.523) vs. (0.58±0.750)] or subcortical infarction lesions (0.41±0.738) vs. (0.69±0.852)] and the number of infarction (1.19±1.254) vs. (1.78±1.618)] significantly increased in the PSCI group. In the chronic ischemic brain tissuechanges, GCA score in the PSCI group decreased significantly (2.32±1.023) vs. (1.93±0.892)], temporal lobe atrophy (1.14±0.805) vs. (1.64±0.816)], Fazekas score (1.05±0.935) vs. (1.28±0.822)], and high signal around the lateral ventricle (PVH) (2.51±1.789) vs. (3.51±1.051)] increased significantly. In the chronic lacunar cerebral infarction lesions, the number of cortical (0.15±0.551) vs. (0.58±1.111)] and subcortical lesions (0.28±0.721) vs. (0.58±1.081)] and infarction (0.84±1.682) vs. (1.78±2.582)] in the PSCI group increased significantly, with statistically significant differences (P < 0.05). Logistic regression analysis showed that age, education, diabetes, number of acute non-lacunar cerebral infarction and PVH were independent risk factors for PSCI (P < 0.01).Conclusion Age, education level, diabetes, number of acute non-segmental cerebral infarction and PVH are closely related to the occurrence of cognitive dysfunction 6-12 months after stroke, which provides strong clinical evidence for early clinical identification and screening of high riskincidence and risk factors of PSCI.