脑梗死后认知障碍与血清视锥蛋白样蛋白-1水平及神经功能缺损关系的研究

目的探讨脑梗死后认知障碍与血清视锥蛋白样蛋白-1(VILIP-1)水平及神经功能缺损的相关性。方法收集120例急性脑梗死患者,根据蒙特利尔认知评估量表(Mo CA)测评结果分为认知障碍组和认知正常组,比较两组患者入院时和发病1年时血清VILIP-1水平、美国国立卫生研究院卒中量表(NIHSS)评分、Barthel指数(BI)评分,分析Mo CA分值与血清VILIP-1水平、NIHSS评分和BI评分的相关性。结果两组患者发病1年时NIHSS评分均低于入院时(P0.01);BI评分均高于入院时(P0.01)。认知障碍组入院时及发病1年时血清VILIP-1水平高于认知正常组(P0.01);NIHSS评分高于认知正常组(P0.01);BI评分低于认知正常组(P0.01)。入院时及发病1年时所有患者Mo CA分值与血清VILIP-1水平呈负相关(r=-0.736,P=0.000;r=-0.450,P=0.000);与NIHSS评分呈负相关(r=-0.575,P=0.000;r=-0.377,P=0.001);与BI评分呈正相关(r=0.431,P=0.000;r=0.483,P=0.000)。结论脑梗死后认知障碍与血清VILIP-1水平及神经功能的康复有重要相关性。     

脑梗死患者血清VILIP-1、IGF-1水平与卒中后认知障碍的关系

目的探讨血清VILIP-1、IGF-1浓度与缺血性卒中患者认知障碍的关系。方法收集2012年6月1日²012年12月31日在我院神经内科卒中单元住院治疗的急性脑梗死患者124例及健康志愿者96例。全面收集病例组及对照组的临床资料及数据,采用ELISA法测定血清VILIP-1、IGF-1浓度并比较各组血清VILIP-1、IGF-1浓度的差异,分析血清VILIP-1、IGF-1浓度与缺血性卒中后认知障碍的关系。结果血清IGF-1浓度认知功能障碍组(96.50±17.88 ng/ml)明显低于认知功能正常组(114.62±14.01 ng/ml),P<0.01;血清VILIP-1浓度认知功能障碍组(669.69±103.84 ng/ml)显著高于认知功能正常组(503.29±142.39 ng/ml),P<0.01。结论急性脑梗死患者高血清VILIP-1浓度、低血清IGF-1浓度,与卒中后认知障碍的发生存在相关性,且IGF-1可作为缺血性卒中后认知障碍的新的治疗靶点。     

水通道蛋白4与卒中后认知障碍的关系研究进展

卒中后认知障碍是卒中的重要后遗症之一,从病理上可以分为血管性、退变性及混合性认知障碍。水通道蛋白4广泛分布于中枢神经系统,参与多种神经系统疾病和认知障碍的病理过程,但其参与卒中后认知障碍的具体机制目前尚未明确。本文综述水通道蛋白4通过参与调节神经炎症、突触可塑性以及β-淀粉样蛋白的积聚和清除过程在卒中后认知障碍中发挥的可能作用。     

卒中患者血压水平与卒中后认知障碍关系的研究进展

卒中后认知障碍为卒中的常见并发症之一,可严重影响卒中患者的生活质量及预后。目前认为血压与卒中后认知障碍密切相关,血压可能对卒中后认知障碍的主要病理生理过程产生潜在影响,并且控制血压可能有助于卒中后认知障碍的改善或预防。血压与卒中后认知障碍之间的相关性较为复杂,可能取决于特定的血压参数和卒中的不同阶段。目前卒中后的最佳血压控制水平尚不统一。本文对卒中后认知障碍的流行病学,血压与卒中后认知障碍的相关性,血压影响卒中后认知障碍的相关机制,以及控制血压的作用进行综述,为进一步阐明卒中后认知障碍的病理生理过程提供重要依据,以期有助于指导临床治疗,从而改善卒中患者的预后。     

卒中后认知障碍管理专家共识

正2016年《中国脑卒中防治报告》报道:我国现有卒中患者7000万人,不同地区卒中年龄标准化患病率约260~719/10万人,每年新发卒中200万人,即每12 s新发1例卒中;而每年因卒中致死达165万人,即每21 s就有一人死于卒中,每年因卒中致死者占所有死亡原因的22.45%~[1]。2016年5月中国脑卒中大会的报告显示:卒中导     

视锥蛋白样蛋白:一种新兴的脑损伤生物标志物

视锥蛋白样蛋白(VILIPs)是神经钙传感蛋白的一个亚家族,研究表明该蛋白家族具有较高的神经系统特异性,对缺血性卒中、阿尔茨海默病等中枢神经系统疾病的诊断有较高的特异度和敏感度,有望成为重要的脑损伤标志物。本文结合国内外最新研究,就VILIPs在不同中枢神经系统疾病所致脑损伤中的作用机制及临床意义予以阐述。     

青年卒中后认知障碍的危险因素分析

目的 探讨青年卒中后认知障碍（post-stroke cognitive impairment,PSCI）的危险因素。      

后循环缺血性卒中与认知障碍相关性研究

目的 探究后循环缺血性卒中与认知障碍发生的关系。 方法 连续选取2013年11月至2014年11月浙江大学医学院附属第一医院及嘉兴市第二医院收治的急 性后循环缺血性卒中患者67例,收集患者人口学、影像学及认知功能评价资料,并通过磁共振成像 统计梗死部位;通过简明精神状态量表、阿尔兹海默病评定量表认知分量表、临床痴呆量表评估认 知功能;根据认知诊断标准同时结合认知功能评价结果,将患者分为认知功能正常组、血管性轻度 认知障碍组、血管性痴呆组。 结果 67例患者中,认知功能正常32例（47.8%）、血管性轻度认知障碍20例（29.9%）,血 管性痴呆15例（2 2.4%）。通过校正年龄、性别、汉密尔顿抑郁评分等因素后,多因素回归分 析显示：颞枕叶缺血性卒中［比值比（odd ratio,OR）75.89,95%可信区间（confidence interval, C I ）3.92～1 470.06）］增加认知障碍发生风险,脑桥缺血性卒中患者发生认知障碍的风险比 非脑桥缺血性卒中降低90%（OR 0.10,95%CI 0.02～0.60）;进一步分析显示,颞枕叶缺血性卒 中（OR 542.24,95%CI 7.85～37 481.44）增加轻度认知障碍发生风险;小脑缺血性卒中（OR 12.49, 95%CI 1.03～151.58）增加血管性痴呆发生风险。 结论 50%以上后循环缺血性卒中患者发生认知障碍;其中颞枕叶及小脑缺血性卒中增加认知障碍 发生风险,脑桥缺血性卒中与认知障碍发生无显著相关性。     

轻度认知障碍与卒中后抑郁关系的研究进展

轻度认知障碍（mild cognitive impairment,MCI）是认知正常和痴呆之间的过渡状态,MCI与 卒中后抑郁（post-stroke depression,PSD）关系密切。MCI常伴发抑郁,而PSD亦被认为是MCI向痴呆进展 的重要危险因素。本文就MCI与PSD关系的研究进展进行综述,着重介绍MCI和PSD关系的新进展,包 括流行病学、相关机制及治疗。     

卒中后认知障碍管理专家共识2021

2020年发布的《中国卒中报告》显示:我国卒中患病率为1114.8/10万,年发病率为246.8/10万,死亡率为149.49/10万[1-2]。在全球范围内,我国已经成为卒中终身风险最高和疾病负担最重的国家[3]。其中,约1/3的卒中患者会经历卒中后认知障碍(post-stroke cognitive impairment,PSCI)[4],生活质量及生存时间受到严重影响,是目前卒中疾病负担的重要原因,并成为当下国际卒中研究的热点和临床干预的重点。     

增强型体外反搏对缺血性脑卒中患者超敏C反应蛋白和内皮素1的影响

目的探讨增强型体外反搏治疗(enhanced external counterpulsation,EECP)对缺血性脑卒中患者超敏C反应蛋白(hs-CRP)和内皮素1(ET-1)的影响,为缺血性脑卒中的二级预防提供进一步的临床证据。方法选取缺血性脑卒中住院患者共187例,EECP治疗组95例,对照组92例,治疗组予常规治疗加上36 h的EECP治疗,对照组予常规治疗,分别比较两组在EECP治疗前、治疗36 h后、治疗后1个月hs-CRP及ET-1的差别。结果与治疗前相比,治疗组hs-CRP、ET-1的血清浓度在EECP治疗后均显著减低,(hs-CRP下降60.1%、ET-1下降40.9%),P值均小于0.05。与对照组比较,治疗组在EECP治疗后hs-CRP、ET-1的浓度均显著减低,(hs-CRP下降41.3%、ET-1下降24.3%),P值均小于0.05。治疗后1个月,与对照组比较,治疗组ET-1的浓度明显减低,(43.8%vs 31.8%),P0.05。治疗后1个月,治疗组hs-CRP的浓度与对照组比较无明显差异,P0.05,无统计学意义。结论通过EECP治疗,缺血性脑卒中患者的hs-CRP及ET-1血清水平显著下降,且作用持久,EECP治疗可以抑制动脉粥样硬化进程。     

急性脑梗死患者认知障碍与梗死部位的相关研究

目的分析急性脑梗死患者不同病灶部位认知障碍的特点。方法采用中文版蒙特利尔认知评估量表(MoCA)对97例单发病灶急性脑梗死患者和20例无脑卒中对照者进行认知功能评估,探讨MoCA 7个分项目(视空间与执行功能EF、命名NAM、注意力ATT、语言功能包括复述与流畅性LANG、抽象概括能力ABS、记忆能力包括瞬时记忆及近记忆MEM、定向力ORT)的评估结果与患者头部MRI影像结果中所示梗死部位之间的关系。结果 (1)97例急性脑梗死患者中MoCA26分者共73例,血管性认知障碍(VCI)总的发生率约为75.26%。(2)额叶部位梗死患者EF与ATT损害明显;颞叶部位梗死患者MEM、EF与ORT损害明显;丘脑部位梗死可能与ATT、LANG、EF损害有关;顶叶部位梗死可能与ORT、EF损害有关;枕叶、基底节部位梗死可能与EF损害有关。小脑、脑桥部位梗死在MoCA总分及分测验中均未显示有统计学意义的变化(P0.05)。结论脑梗死后认知障碍的发生率高;急性脑梗死患者不同梗死部位认知功能损害特点不同。     

Prognostic value of admission C-reactive protein in stroke patients undergoing IV thrombolysis

Objective   To test the hypothesis that pre-treatment Creactive protein (CRP) predicts outcome in stroke patients undergoing intravenous thrombolysis (IVT) treatment. Methods   We analyzed the data of 111 consecutive patients with IVT within 6 hours of stroke onset for stroke involving the middle cerebral artery territory and admission CRP ≤ 6 mg/dl. Results   CRP levels were consistently, yet non-significantly lower in patients with unfavourable outcome definitions. Median (range) CRP levels were 0.3 (0–5.9) mg/dl vs. 0.4 (0–5.7) mg/dl (p = 0.13) in patients dependent or dead after 3 months (modified Rankin Scale score > 2; n = 59) vs. independent patients (n = 52); 0.2 (0.1–1.5) mg/dl vs. 0.4 (0–5.9) mg/dl (p = 0.28) in patients dead after 3 months (n = 14) versus survivors (n = 97); and 0.2 (0.1–0.7) mg/dl vs. 0.4 (0–5.9) mg/dl (p = 0.09) in patients with significant neurological deterioration within 24 hours (increase in ≥ 4 points on National Institute of Health Stroke scale; n = 9) vs. patients without early deterioration (n = 102). Independent predictors of dependency/death after 3 months, identified by multivariate logistic regression analyses, were baseline NIHSS score (OR = 1.31, 95 % CI 1.16–1.48, p < 0.001), time from onset to treatment (OR = 1.01, 95 % CI 1.0–1.02, p = 0.024), and presence of diabetes (OR = 8.16, 95 % CI 1.18–56.5, p = 0.033). Conclusion   Pre-treatment CRP clearly failed to predict outcome in stroke patients treated with IVT. Our findings contradict previously published work and highlight the need for further research on this topic.     

Subthreshold depression and cognitive impairment but not demented in stroke patients during their rehabilitation

Background –  Subthreshold depression (sD) and cognitive impairment but not demented (CIND) in stroke patients are associated with poorer rehabilitative outcomes. Their diagnosis can easily be operationalized using validated scales.
Aim –  The aim of the study was to ascertain the prevalence of depressive symptoms and cognitive impairment in stroke patients during three crucial stages of the rehabilitative process, viz. upon admission, upon planned discharges from rehabilitation hospitals and at 6 months post-stroke, using validated scales like the Geriatric Depression Scale and Abbreviated Mental Test (recommended by the British Geriatric Society). Their baseline risk factors were also ascertained.
Results –  On admission, the prevalence of depressive symptoms and cognitive impairment was 60% and 54% respectively. The prevalence upon planned discharges and 6 months post-stroke, respectively, of depressive symptoms was 38% and 34% and that of impaired cognition was 33% and 40%. Baseline independent correlates at 6 months post-stroke depressive symptoms were: recurrent stroke (OR 3.34); on admission cognitive impairment (OR 4.78) and ADL dependence (OR 5.28). And that of cognitive impairment were: increasing age (OR 8.07); post-stroke dysphagia (OR 4.58); on admission cognitive impairment (OR 23.95) and on admission depressive symptoms (OR 3.50).
Conclusions –  Continuous screening and appropriate intervention, especially at baseline, would significantly decrease the burden posed by stroke patients with such psychological impairments in the community.     

Vascular cognitive impairment in patients with late-onset seizures after an ischemic stroke

BACKGROUND: Cognitive impairment and seizures are both common conditions in patients with cerebrovascular disease. PURPOSE: The present study investigates whether the occurrence of late-onset seizures, following an ischemic stroke, contributes to vascular cognitive impairment. PATIENTS AND METHODS: The mean Mini-Mental State Examination (MMSE) and the median modified Rankin (mR) scores were compared between 125 patients who developed late-onset seizures (66 with a single seizure and 59 with repeated seizures or epilepsy) following an ischemic stroke and 125 patients who did not during, at least, a 2-year follow-up. RESULTS: There were no differences in age, gender, etiology and degree of neurological impairment on admission for their stroke between the groups with and without seizures. Although the mean MMSE score was similar between both groups the median mR score was significantly higher in the seizure patients. Comparing the patients with a single seizure to the non-seizure ones showed the same results. On the other hand, comparison of the patients with epilepsy to the non-seizure group revealed, in addition to the higher median mR score, a significantly lower mean MMSE score in the former group. CONCLUSION: Repeated seizures following an ischemic stroke promote vascular cognitive impairment.     

Association between oxidized low‐density lipoprotein and cognitive impairment in patients with ischemic stroke

Background and purpose

The association between oxidized low‐density lipoprotein (oxLDL) and cognitive impairment is unclear. This study aimed to investigate the potential association between oxLDL and cognitive impairment among patients with acute ischemic stroke.

Methods

We measured the levels of oxLDL and recorded the Mini‐Mental State Examination (MMSE) score in patients with acute ischemic stroke who were recruited from the Study of Oxidative Stress in Patients with Acute Ischemic Stroke. Cognitive impairment was defined as an MMSE score of <24. The association between oxLDL and cognitive impairment was assessed by multivariate logistic or linear regression analysis. Other clinical variables of interest were also studied.

Results

A total of 3726 patients [1287 (34.54%) female] were included in this study, with a mean age of 63.62 ± 11.96 years. After adjusting for potential confounders in our logistic regression model, each SD increase in oxLDL was associated with a 26% increase in the prevalence of cognitive impairment (odds radio, 1.26; 95% confidence interval, 1.13–1.39; P < 0.0001). Similarly, higher oxLDL was associated with lower MMSE scores, with a 0.56‐point decrease in MMSE score for every SD increase in oxLDL in a linear regression analysis (β = ?0.56; 95% confidence interval, ?0.81 to ?0.32; P < 0.0001). There were no significant interactions between oxLDL and age, sex or education levels for cognitive impairment (all interactions, P > 0.05).

Conclusions

Elevated levels of oxLDL were associated with a higher prevalence of cognitive impairment in patients with ischemic stroke.     

缺血性脑卒中患者血清SIRT1水平与早期神经功能恶化的相关性研究

目的 探讨缺血性脑卒中患者血清沉默信息调节因子1(Silent information regulator 1,SIRT1)水平与早期神经功能恶化(Early neurological deterioration,END)的相关性。方法 选取2020年1月-2021年6月于本院就诊的缺血性脑卒中患者136例,根据患者入院72 h内是否出现END,将其分为合并END组(41例)和非END组(95例),检测并比较2组血清SIRT1水平,采用Logistic回归法分析END发生的影响因素,采用受试者工作特征曲线(Receiver operating characteristic curve,ROC)分析SIRT1诊断END发生的临床价值。结果 2组患者年龄、糖尿病占比、冠心病占比、基线美国国立卫生院卒中量表(National institute of health stroke scale,NIHSS)评分比较差异显著(P<0.05); 与非END组比较,合并END组患者血清SIRT1水平较低,超敏C反应蛋白(High sensitivity C-reactive protein,hs-CRP)水平较高(P<0.05); 糖尿病史、年龄、hs-CRP水平及SIRT1水平是缺血性脑卒中患者发生END的独立危险因素(P<0.05); SIRT1预测缺血性脑卒中患者发生END的曲线下面积为0.753[95%CI=0.559～0.903,P<0.05],诊断特异度为81.49%,敏感度为89.15%。结论 SIRT1在缺血性脑卒中早期神经功能恶化患者血清中呈低表达,且其表达水平与缺血性脑卒中患者发生END有关。     

缺血性脑卒中后非痴呆认知功能障碍的危险因素

目的 探讨缺血性脑卒中后非痴呆认知功能障碍(cognitive impairment no dementia,CIND)的危险因素.方法 以19～80岁汉族初发缺血性脑卒中患者为研究对象,起病后3个月采用简易智能量表和美国精神疾病统计和诊断于册第4版修订本进行认知测定,利用单因素和多元Logistic回归分析研究CIND患者的危险因素.结果 185例研究对象纳入统计分析,42例诊断为CIND,占22.7%.多因素Logistic回归分析发现,大面积和中等面积梗死(OR:4.687,P＜0.05;OR:4.734,P＜0.05)、糖尿病(OR:2.887,P＜0.05)是缺血性卒中后CIND的独立危险因素.结论 糖尿病、梗死面积是缺血性脑卒中后CIND的独立危险因素.     

sPECAM-1 in serum and CSF of acute ischaemic stroke patients

OBJECTIVES: As platelet endothelial cell adhesion molecule-1 (PECAM-1) is one of key mediators of transendothelial migration of leucocytes during inflammation, and inflammatory reaction is observed in cerebral ischaemia, we decided to determine the levels of soluble PECAM-1 (sPECAM-1) in serum and cerebrospinal fluid (CSF) of patients with acute stroke. MATERIAL AND METHODS: Twenty-three patients with first-ever in a lifetime completed ischaemic stroke have been studied. CSF and blood samples were obtained within 24 h of the onset of stroke and the levels of sPECAM-1 in serum and CSF were quantified by ELISA. RESULTS: Stroke patients displayed statistically significant higher levels of sPECAM-1 in sera and CSF in comparison with control group. The levels were significantly higher in serum than in CSF, correlated between each other, and CSF sPECAM-1 fraction was blood-derived. CONCLUSION: Our results indirectly suggest that PECAM-1 may play a role in the pathophysiological events during early phase of ischaemic stroke.