卒中后认知障碍psci_卒中后睡眠障碍与认知障碍

  本文关键词：卒中后睡眠障碍与认知障碍，由笔耕文化传播整理发布。

        目的：本研究旨在研究脑卒中(Stroke)后睡眠障碍(Sleep Disorders)与认知障碍(Cognitive Impairment)及其相关因素，为临床诊治提供理论依据。方法：收集2013年5月至2014年1月在河北医科大学第四医院神经内科住院患者，均经头颅CT或头颅磁共振成像(Magnetic Resonance Imaging,MRI)检查，符合脑出血或脑梗死患者62例，诊断标准参考1995年中华医学会全国第四届脑血管病学术会议修订的诊断标准。年龄51～90岁，平均年龄68.61±9.75岁，其中男性41例，女性21例，合并高血压病46例，糖尿病32例，冠心病20例，出血性卒中12例，缺血性卒中50例，发病前无睡眠障碍及认知障碍史。患者均在入院2周内进行匹兹堡睡眠量表（PittsburghSleep Quality Index, PSQI）评分、多导睡眠图（Polysomnography, PSG）进行睡眠监测，分析脑卒中患者睡眠质量改变情况；用简易精神状态量表（Mini-mental State Examination, MMSE）、事件相关电位（Event-RelatedPotentials, ERP）P300对脑卒中患者进行认知功能评价，分析脑卒中后患者认知障碍情况。PSQI总分为2l分，0～6分表示正常，≥7分表示存在睡眠障碍。MMSE最高分为30分，认知障碍诊断标准经过受教育程度及年限校正：文盲≤17分，小学≤20分，中学及以上组≤24分。神经功能缺损程度评分采用脑卒中临床神经功能缺损程度评分量表（NDS），总分为45分，0～15分为轻度神经功能缺损，16～30分为中度神经功能缺损，31～45分为重度神经功能缺损。依据PSQI评分标准将全部患者分为：①睡眠障碍组22例，年龄52～90岁，平均年龄70.82±10.76岁，其中男性14例，女性8例；②非睡眠障碍组40例，年龄51～88岁，平均年龄67.40±9.07岁，其中男性27例，女性13例；依据MMSE诊断标准将全部患者分为：①认知障碍组20例，年龄53～88岁，平均年龄71.55±9.46岁，其中男性11例，女性9例；②非认知障碍组42例，年龄51～90岁，平均年龄67.21±9.69岁，其中男性30例，女性12例。分别对①②两组临床资料（性别、年龄、既往病史、卒中性质、卒中部位、神经功能缺损程度）、多导睡眠图（睡眠潜伏期、实际睡眠时间、睡眠效率、觉醒次数、非快速动眼睡眠1期比例、非快速动眼睡眠2期比例、非快速动眼睡眠3,4期比例、快速动眼睡眠期比例)及P300（潜伏期、波幅）进行对比分析。应用SPSS13.0统计学软件对资料进行统计学分析，计数资料以百分数表示，采用2检验，计量资料进行正态性检验，用x±s表示，采用t检验，P<0.05认为差异有统计学意义。结果：1卒中后睡眠障碍1.1一般资料对睡眠障碍组与非睡眠障碍组性别、年龄进行对比，睡眠障碍组22例，其中男性14例（63.64%），女性8例（36.36%），男女比例为1.75:1，年龄最大为90岁，最小为52岁，平均年龄70.82±10.76岁；非睡眠障碍组40例，其中男性27例（67.50%），女性13例（32.50%），男女比例为2.07:1，年龄最大为88岁，最小为51岁，平均年龄67.40±9.07岁。各年龄段中：≤60岁患者16例，有睡眠障碍者5例（5/16，31.25%），61～70岁患者18例，有睡眠障碍者6例（6/18，33.33%），71～80岁患者19例，有睡眠障碍者4例（4/19，21.05%），>80岁患者9例，有睡眠障碍者7例，（7/9，77.78%）。统计学分析显示：两组性别、平均年龄比较差异无统计学意义（P>0.05）。各年龄段睡眠障碍发生率比较差异有统计学意义（P<0.05）。1.2临床资料对睡眠障碍组与非睡眠障碍组既往病史（高血压病、糖尿病、冠心病）、卒中性质、卒中侧别、卒中部位、神经功能缺损程度进行比较显示：睡眠障碍组22例，其中合并高血压病20例（20/22，90.91%），糖尿病16例（16/22，72.73%），冠心病11例（11/22，50.00%）；非睡眠障碍组40例，其中合并高血压病26例（26/40，65.00%），糖尿病16例（16/40，40.00%），冠心病9例（9/40，22.50%），两组既往病史（高血压病、糖尿病、冠心病）进行比较差异有统计学意义（P<0.05）。对卒中性质进行比较：出血性卒中12例，出现睡眠障碍者5例(5/12，41.67%），缺血性卒中50例，出现睡眠障碍者17例（17/50，34.00%），两组比较差异无统计学意义（P>0.05）。对两组卒中侧别进行比较显示：左侧半球病变32例，出现睡眠障碍者17例（17/32，53.13%），右侧半球病变30例，出现睡眠障碍者5例（5/30，16.67%），两组比较差异有统计学意义（P<0.05）。对两组卒中部位进行比较显示：额叶病变4例，睡眠障碍者1例（1/4，25.00%）；颞叶病变3例，睡眠障碍者1例（1/3，33.33%）；顶叶病变2例，睡眠障碍者2例（2/2，100.00%）；枕叶病变3例，睡眠障碍者1例（1/3，33.33%）；基底节区病变28例，睡眠障碍者8例（8/28，28.57%）；脑干病变者14例，睡眠障碍8例（8/14，57.14%）；丘脑病变5例，睡眠障碍者1例（1/5，20.00%）。由于样本含量较少，两者无法进行统计学分析。对神经功能缺损程度进行比较：轻度神经功能缺损患者35例，存在睡眠障碍者7例（7/35，20.00%）；中度神经功能缺损患者19例，存在睡眠障碍者9例（9/19，47.37%）；重度神经功能缺损患者8例，存在睡眠障碍者6例（6/8，75.00%），统计学分析显示不同程度神经功能缺损组睡眠障碍发生率差别有统计学意义（P<0.05）。1.3多导睡眠图表现分别对卒中后睡眠障碍组与非睡眠障碍组PSG进行比较显示：睡眠障碍组睡眠潜伏期为52.86±13.85min，实际睡眠时间为387.59±31.96min，睡眠效率为80.75±6.66%，觉醒次数为6.05±2.01，非快速动眼睡眠1期比例22.22±6.47%，非快速动眼睡眠2期比例44.24±4.93%，非快速动眼睡眠3,4期比例11.97±4.36%，快速动眼睡眠期比例10.38±3.98%；非睡眠障碍组睡眠潜伏期为31.43±9.19min，实际睡眠时间为410.48±15.71min，睡眠效率85.72±3.29%，觉醒次数为4.45±2.18，非快速动眼睡眠1期比例14.91±5.18%，非快速动眼睡眠2期比例41.69±4.71%，非快速动眼睡眠3,4期比例15.05±4.58%，快速动眼睡眠期期比例13.34±4.24%。两组在睡眠潜伏期、实际睡眠时间、睡眠效率、觉醒次数、各期比例方面比较差异有统计学意义（P<0.05）。1.4P300对卒中后睡眠障碍组与非睡眠障碍组P300进行比较显示：睡眠障碍组P300潜伏期为386.95±68.75ms，波幅为6.45±1.83uV；非睡眠障碍组P300潜伏期为359.05±51.89ms，波幅为7.23±1.63uV。经统计学分析显示两组比较差异无统计学意义（P>0.05）。2卒中后认知障碍2.1一般资料对认知障碍组与非认知障碍组进行性别、年龄比较分析显示：认知障碍组20例，其中男性11例（11/20，55.00%），女性9例（9/29，45.00%），男女比例为1.22:1，年龄最大为88岁，最小为53岁，平均年龄71.55±9.46岁；非认知障碍组42例，其中男性30例（30/42，71.43%），女性12例（12/42，28.57%），男女比例为2.50:1，年龄最大为90岁，最小为51岁，平均年龄67.21±9.69岁。各年龄段中：≤60岁患者16例，有认知障碍者2例（2/16，12.50%），61～70岁患者18例，有认知障碍者5例（5/18，27.78%），71～80岁患者19例，有认知障碍者7例（7/19，36.84%），>80岁患者9例，有认知障碍者6例（6/9，66.67%）。统计学分析显示两组进行性别、平均年龄比较差异无统计学意义（P>0.05）。各年龄段认知障碍发生率比较差异有统计学意义（P<0.05）。2.2临床资料对认知障碍组与非认知障碍组既往病史（高血压病、糖尿病、冠心病）、卒中性质、卒中侧别、卒中部位、神经功能缺损程度进行比较显示：认知障碍组20例中合并高血压病19例（19/20，95.00%），糖尿病15例（15/20，75.00%），冠心病10例（10/20，50.00%）；非认知障碍组42例中合并高血压病27例（27/42，，64.29%），糖尿病17例（17/42，40.48%），冠心病10例（10/42，23.81%），两组既往病史（高血压病、糖尿病、冠心病）进行比较差异有统计学意义（P<0.05）。对卒中性质进行比较：出血性卒中12例，存在认知障碍者6例（6/12，50.00%）；缺血性卒中50例，存在认知障碍者14例（14/50，28.00%），两者比较差异无统计学意义（P>0.05）。对两组卒中侧别进行比较：左侧半球病变者32例，认知障碍者14例（14/32，43.75%）；右侧半球病变者30例，认知障碍者6例（6/30，20.00%），对卒中侧别进行比较差异有统计学意义（P<0.05）。对卒中部位进行比较：额叶病变4例，认知障碍者2例（2/4，50.00%）；颞叶病变3例，认知障碍2例（2/3，66.67%）；枕叶病变3例，认知障碍者1例（1/3，33.33%）；基底节区病变28例，认知障碍8例（8/28，28.57%）；脑干病变14例，认知障碍3例（3/14，21.43%）；小脑病变3例，认知障碍者1例（1/3，33.33%）；丘脑病变5例，认知障碍3例（3/5，60.00%）。由于本研究样本量较少，两者无法进行统计学分析。对神经功能缺损程度分析显示：轻度神经功能缺损患者35例，存在认知障碍者8例（8/35，22.86%）；中度神经功能缺损患者19例，存在认知障碍者6例（6/19，31.58%）；重度神经功能缺损患者8例，存在认知障碍者6例（6/8，75.00%），经统计学分析，不同程度神经功能缺损组认知障碍发生率差别有统计学意义（P<0.05）。2.3事件相关电位P300表现对认知障碍组与非认知障碍组P300潜伏期及波幅进行比较：认知障碍组P300潜伏期为437.90±40.08ms，波幅为6.42±1.24uV；非认知障碍组P300潜伏期为336.12±32.94ms，波幅为7.25±1.86uV，两组比较差异有统计学意义（P<0.05）。2.4PSG表现认知障碍组睡眠潜伏期为43.55±17.47min，实际睡眠时间为395.25±33.32min，睡眠效率为82.35±6.94%，觉醒次数为5.60±2.01，非快速动眼睡眠1期比例为20.93±7.90%，非快速动眼睡眠2期比例为43.76±5.02%，非快速动眼睡眠3,4期比例为13.65±4.21%，快速动眼睡眠期比例为10.69±3.87%；非认知障碍组睡眠潜伏期为36.88±13.48min，实际睡眠时间为405.74±19.71min，睡眠效率为84.53±4.11%，觉醒次数为4.83±2.38，非快速动眼睡眠1期比例为15.88±5.29%，非快速动眼睡眠2期比例为42.04±4.81%，非快速动眼睡眠3,4期比例为14.11±4.96%，快速动眼睡眠期比例为13.05±4.41%。两者在非快速动眼睡眠1期比例、快速动眼睡眠期比例方面差异有统计学意义（P<0.05）。睡眠潜伏期、实际睡眠时间、睡眠效率、觉醒次数、非快速动眼睡眠2期及非快速动眼睡眠3,4期比例比较差异无统计学意义（P>0.05）。结论：1卒中后睡眠障碍与既往病史（高血压病、糖尿病、冠心病）、卒中侧别及神经功能缺损程度有相关性。2卒中后睡眠障碍患者多导睡眠图表现为睡眠潜伏期延长，实际睡眠时间减少，睡眠效率降低，觉醒次数增加，非快速动眼睡眠1、2期比例增加，非快速动眼睡眠3,4期、快速动眼睡眠期比例减少。3卒中后认知障碍与既往病史（高血压病、糖尿病、冠心病）、卒中侧别及神经功能缺损程度有相关性。4卒中后认知障碍患者P300潜伏期延长，波幅降低，多导睡眠图表现为非快速动眼睡眠1期比例增加，快速动眼睡眠期比例减少。

    Objective:To investigate the clinical characteristics of sleep disordersand cognitive impairment after stroke.Methods:We screened a cohort of62patients diagnosed with strokeaccording to the revised diagnostic criteria of the Chinese society of the fourthsession of national cerebrovascular disease academic meeting in1995at theFourth Affiliated Hospital of Hebei Medical University from May2013toJanuary2014.This cohort included41males and21female, with a mean ageof68.61±9.75years(range,51-90years). Complications included hypertension(n=46), diabetes mellitus (n=32) and coronary heart disease (n=20). Thehemorrhagic cases were12and the ischemic cases were50. These patients hadneither sleep disorders nor cognitive impairment before the onset of stroke,and were examined with Pittsburgh Sleep Quality Index (PSQI), Mini-mentalState Examination(MMSE), Event-related potentials(P300) and monitored byPolysomnography(PSG)within two weeks after hospitalization. The totalglobal PSQI score was21. A PSQI global score greater than7was classifiedas the sleep disorder. The maximal point of MMSE was30, The raw scoremay also need to be corrected for educational attainment and age,illiteracy≤17points, primary school≤20points, above the middle school≤24points. The stroke clinical neurological deficit rating scale (NDS) score was45points,0-15points as mild neurological deficit,16-30as moderate neurologicaldeficit,31-45as severe neurological deficit. The patients were divided intotwo groups according to PSQI:①22cases in the sleep disorders group (14males,8females,52-90years of age, mean age70.82±10.76years),②40cases in the non-sleep disorders group (27males,13females,51-88years ofage, mean age67.40±9.07years). The patients were divided into two groupsaccording to MMSE.①20cases in the cognitive impairment group (11males,9females,53-88years of age, mean age71.55±9.46years),②42cases in the non-cognitive impairment group (30males,12females,51-90years of age,mean age67.21±9.69years).The clinical data (including gender, age,anamnesis, stroke type, stroke location, neurological deficit), PSG (the sleeplatency, actual sleep time, sleep efficiency, awake times, the ratio of non-rapideye movement1,2,3,4and rapid eye movement) and P300(The latency andamplitude) was analyzed, and SPSS13.0software was used for all analysis.The data is expressed as a percentage, and campared by chi-square test forcategorical variables, and2-sample t test depending on the distribution ofcontinuous variable. a P value <0.05was considered as statisticallysignificant.Results:1Sleep disorders1.1Common data: The sleep disorders patients (n=22) weremales(14/22,63.64%), females (8/22,36.36%) and the non-sleep disorderspatients(n=40) were males(27/40,67.50%),females (13/40,32.50%),The genderwas not statistically associated with the sleep disorders. The mean age was70.82±10.76years (range52-90years) in patients with sleep disorders and67.40±9.07years(range51-88years) without sleep disorders. It showed thatthere was no statistically significant (P>0.05) at the average age. Less than60years(5/16,31.25%),61～70years(6/18,33.33%),71～80years(4/19,21.05%),more than80years(7/9,77.78%),we found statistically significant(P<0.05) in all ages.1.2Clinical features: Compared the two groups for the anamnesis(hypertension, diabetes mellitus, coronary heart disease), stroke type, strokelocation and neurological deficit. In sleep disorders group, hypertension(20/22,90.91%),diabetes mellitus(16/22,72.73%),coronary heart disease(11/22,50.00%). In the non-sleep disorders group, hypertension(26/40,65.00%),diabetes mellitus (16/40,40.00%), coronary heart disease (9/40,22.50%).Prevalence of sleep disorders was significantly (P<0.05) related to theanamnesis (hypertension,diabetes mellitus,coronary heart disease). Theischemic stroke were50cases (17/50,34.00%) and hemorrhagic stroke were 12cases (5/12,41.67%), and there was no statistically significant (P>0.05).The left cerebral hemisphere32cases (17/32,53.13%), the right cerebralhemisphere30cases (5/30,16.67%), there was statistically significant (P<0.05)at the stroke side. The incidence of sleep disorders group for the frontal, thetemporal, the parietal, the occipital, the basal ganglia, the brainstem, and thethalamus stroke were (1/4,25.00%),(1/3,33.33%),(2/2,100%),(1/3,33.33%),(8/28,28.57%),(8/14,57.14%）,(1/5,20.00%),The data can not be statisticallyanalyzed because of the small sample content. The mild neurological deficitwere35(7/35,20.00%), the moderate neurological deficit were19(9/19,47.37%), the severe neurological deficit were8(6/8,75.00%), and there wasstatistically significant (P<0.05).1.3PSG the sleep latency were52.86±13.85min (the sleep disorders group),31.43±9.19min(the non-sleep disorders group) and the actual sleep time were387.59±31.96min versus410.48±15.71min. The sleep efficiency were80.75±6.66%versus85.72±3.29%. The awake times were6.05±2.01versus4.45±2.18. The ratio of NREM1,2,3,4and REM as follows:22.22±6.47%,44.24±4.93%,11.97±4.36%,10.38±3.98%(the sleep disordersgroup)and14.91±5.18%,41.69±4.71%,15.05±4.58%,13.34±4.24%(the non-sl-eep disorders group). We found statistically significant(P<0.05) between thetwo groups.1.4Event-related potentials (P300) The latency and the amplitude were386.95±68.75ms,6.45±1.83uV (the sleep disorders group)and359.05±51.89ms,7.23±1.63uV(the non-sleep disorders group). There was no statisticallysignificant (P>0.05).2Cognitive impairment2.1Common data The cognitive impairment group (n=20),11males(11/20,55.00%),9females (9/20,45.00%), mean age71.55±9.46years (range53-88years) and30males (30/42,71.43%),12females (12/42,28.57%), meanage67.21±9.69years (range51-90years) in the non-cognitive impairmentgroup. We found there was no statistically significant (P>0.05). In all ages:less than60years(2/16,12.50%),61～70years(5/18,27.78%),71～80years (7/19,36.84%), more than80years (6/9,66.67%) and there was statisticallysignificant (P<0.05)in all ages.2.2Clinical features Compared the two groups for the anamnesis(hypertension, diabetes mellitus, coronary heart disease), stroke type, strokelocation and neurological deficit. The cognitive impairment patients withhypertension(19/20,95.00%), diabetes mellitus(15/20,75.00%), coronary heartdisease (10/20,50.00%) and hypertension (27/42,64.29%), diabetes mellitus(17/42,40.48%), coronary heart disease (10/42,23.81%) in the non-cognitiveimpairment group, the anamnesis showed significant association withprevalence of cognitive impairment(P<0.05). The prevalence of cognitiveimpairment(14/50,28.00%)in ischemic stroke and (6/12,50.00%) inhemorrhagic stroke, and there was no statistically significant(P>0.05). The leftcerebral hemisphere were32(14/32,43.75%), the right cerebral hemispherewere30(6/30,20.00%）and there was statistically significant (P<0.05) at thestroke side. The incidence of the cognitive impairment group for the frontal,the temporal, the occipital, the basal ganglia, the brainstem, the cerebellumand the thalamus were(2/4,50.00%),(2/3,66.67%),(1/3,33.33%),(8/28,28.57%),(3/14,21.43%),(1/3,33.33%),(3/5,60.00%).The data can not be statisticallyanalyzed because of the small sample content. The mild neurological deficitwere35(8/35,22.86%), the moderate neurological deficit were19(6/19,31.58%), the severe neurological deficit were8(6/8,75.00%), andthere was statistically significant(P<0.05).2.3Event-related potentials (P300) The latency was437.90±40.08ms andthe amplitude was6.42±1.24uV (the cognitive impairment group) and336.12±32.94ms,7.25±1.86uV(the non-cognitive impairment group). Therewas statistically significant(P<0.05).2.4PSG The cognitive impairment group, the sleep latency43.55±17.47min,the actual sleep time395.25±33.32min, the sleep efficiency82.35±6.94%,awake times5.60±2.01, the ratio of NREM1,2,3,4and REM were20.93±7.90%,43.76±5.02%,13.65±4.21%,10.69±3.87%.The non-cognitive impairmentgroup were36.88±13.48min,405.74±19.71min,84.53±4.11%,4.83±2.38, 42.04±4.81%,14.11±4.96%,13.05±4.41%. We found statistically significant atthe ratio of NREM1and REM(P<0.05). The sleep latency, the actual sleeptime, the sleep efficiency, awake times and the ratio of NREM2, NREM3,4were no statistically significant(P>0.05).Conclusion:1The sleep disorders was associated with the anamnesis(hypertension,diabetes mellitus, coronary heart disease), stroke side and neurological deficit.2The sleep disorders showed the reduced actual sleep time, sleepefficiency, the ratio of NREM3,4, REM and prolonged sleep latency, awaketimes, the ratio of NREM1,2.3The cognitive impairment patients were related to the anamnesis(hypertension,diabetes mellitus,coronary heart disease),stroke side andneurological deficit.4The cognitive impairment patients had prolonged latency, reducedamplitude and increased ratio of NREM1, decreased ratio of REM.

卒中后睡眠障碍与认知障碍

摘要4-9ABSTRACT9-13前言14材料与方法14-16结果16-21附图21-26附表26-31讨论31-38结论38参考文献38-43综述 卒中后睡眠障碍与认知障碍43-53    参考文献48-53致谢53-54个人简历54

  本文关键词：卒中后睡眠障碍与认知障碍，由笔耕文化传播整理发布。