急性脑卒中患者血清神经元特异性烯醇化酶、S-100B蛋白、髓鞘碱性蛋白水平的变化

目的探讨急性脑卒中患者血清神经元特异性烯醇化酶(NSE)、S-100B蛋白、髓鞘碱性蛋白(MBP)水平变化及其临床意义。方法回顾性对照分析发病在48 h内的45例急性脑卒中患者(其中脑梗死组19例,脑出血组15例,短暂性脑缺血发作组11例)血清NSE、S-100B蛋白、MBP水平变化及其与脑梗死、脑出血患者神经功能缺损程度的相关性。结果脑梗死组和脑出血组患者血清NSE、S-100B蛋白、MBP水平均较对照组有不同程度增高(P<0.05),而短暂性脑缺血发作组与正常对照组比较均无明显变化。脑梗死组和脑出血组患者中神经功能缺损较重的中重型亚组患者血清NSE、S-100B蛋白、MBP水平较轻型亚组水平高(P<0.05)。结论血清NSE、S-100B蛋白、MBP水平可作为急性脑卒中患者病情判断、预后评估的指标之一,对早期脑梗死与短暂性脑缺血发作也有鉴别诊断价值,尤其适用于无法进行影像学检查的脑卒中患者。     

脑卒中急性期血清神经元特异性烯醇化酶水平的变化及意义

目的 探讨脑卒中急性期血清神经元特异性烯醇化酶(NSE)与脑卒中病灶部位、体积、神经功能缺损程度及预后的关系.方法 应用ELISA方法检测96例急性期的脑卒中患者[58例脑梗死(CI)、27例脑出血(ICH)、11例蛛网膜下腔出血(SAH)]以及25名正常对照者血清NSE水平,分析其与不同卒中类型患者的中国卒中量表评分(CSS)、Barthel 指数(BI)、Glasgow-Pittsburgh昏迷量表评分及病灶部位和体积关系.结果 脑卒中患者急性期血清NSE水平显著高于正常对照组(均P<0.01);发病4 d内,CI组及ICH组中,较大病灶的患者血清NSE水平显著高于小病灶患者 (均P<0.01);ICH组、CI组血清NSE水平与CSS呈正相关(r=0.52,r=0.56;均P<0.01),SAH组、ICH组、CI组血清NSE水平与Glasgow-Pittsburgh昏迷量表评分呈负相关(r=-0.51,r=-0.43,r=-0.53;均P<0.01);不同病灶部位患者血清NSE水平差异无统计学意义.结论 脑卒中急性期血清NSE水平可客观地反映脑损伤程度;动态监测有助于判断病情和预后.     

高血压性基底节区脑出血患者血清S100钙结合蛋白B、神经特异性烯醇化酶水平对病情的评估及预后的预测价值

目的探讨高血压性基底节区脑出血患者血清S100钙结合蛋白B(S100B)、神经特异性烯醇化酶(NSE)水平对病情评估及预后的预测价值。方法检测60例高血压性基底节区脑出血患者及30名正常对照者的血清S100B、NSE水平。于脑出血后3个月采用m RS评分评价患者的预后。结果脑出血组及脑出血轻度、中度、重度亚组患者各时间点间血清S100B及NSE水平差异有统计学意义(均P<0.05)。LSD多重比较显示,脑出血组及脑出血轻度、中度、重度亚组间各时间点血清S100B及NSE水平差异有统计学意义(均P<0.05)。脑出血组轻度、中度、重度亚组及正常对照组间第1 d、第7 d血清S100B(F=350.425,F=109.170;均P<0.05)及NSE水平(F=103.296,F=63.300;均P<0.05)差异有统计学意义,第90 d差异无统计学意义(F=0.347,P=0.791;F=1.470,P=0.233)。与正常对照组比较,脑出血组及脑出血轻度、中度、重度亚组第1 d、第7 d血清S100B及NSE水平差异有统计学意义(均P>0.05),第90 d差异无统计学意义(均P>0.05)。LSD多重比较分析显示,脑出血轻度亚组与中度、重度亚组及正常对照组第1 d、第7 d血清S100B及NSE差异有统计学意义(均P<0.05),第90 d差异无统计学意义(均P>0.05)。入院第1 d血清S100B及NES水平与颅内血肿量呈正相关(r=0.818,r=0.619;均P<0.01)。与预后不良亚组比较,预后良好亚组第1 d血清S100B及NSE水平显著降低(P=0.041,P=0.018),两组间第7 d及第90 d血清S100B(P=0.101,P=0.468)及NSE(P=0.077,P=0.980)差异无统计学意义。破入脑室亚组患者第1 d及第7 d血清S100B、NSE水平显著明显高于未破入脑室组(均P<0.05),两组第90 d血清S100B、NSE水平差异无统计学意义(均P>0.05)。结论血清S100B、NSE水平可以反映脑损伤的严重程度、预测颅内血肿量,对急性期高血压性基底节区脑出血患者的病情及预后方面具有一定的评估、预测价值。     

急性脑血管病神经元特异性烯醇化酶的测定及临床意义

目的 探讨急性脑血管病患者血清神经元特异性烯醇化酶(NSE) 浓度的变化及其临床意义.方法 应用放射免疫分析法测定50例急性脑血管病患者和30例正常人血清NSE浓度.病例组包括脑出血20例,脑梗死30例.应用直线相关分析方法分析NSE 浓度与病灶大小、病情严重程度以及预后的关系.结果 对照组的NSE 浓度为(9.14±4.39)μg/ L ,脑出血组NSE 浓度为(26.30±14.59)μg/ L,脑梗死组NSE 浓度为(24.95±12.88)μg/ L,病例组与对照组之间差异有统计学意义(P《0.01) , 患者组之间差异无统计学意义(P》0.05) .NSE 浓度与病变的大小、病情严重程度( GCS 评分) 和预后( GOS 评分) 之间存在相关性(P《0.01) .结论 急性脑血管病患者血清NSE 浓度明显增高, NSE 浓度的高低不仅为神经元损伤程度提供定量信息, 而且也是判断病情、评估预后的重要参数.     

脑梗死患者血清神经元特异性烯醇化酶的动态变化及临床意义

目的 探讨缺血性脑卒中患者急性期血清神经元特异性烯醇化酶(NSE)的动态变化及其临床意义。方法临床确诊的脑梗死患者75人,测量并计算脑梗死体积,采集其发病后不同时间的静脉血,凝固后立即3000r/s离心15min取血清,置-80℃保存,共248份标本;对照组为同年龄组健康成人,共30人,采集标本30份。采用神经元特异性烯醇化酶酶联免疫分析法测定血清中NSE浓度。数据用均数±标准差,各组间比较用方差分析和t检验及相关分析法。结果 (1)脑梗死组和对照组NSE浓度分别为(7.25±2.14)ng/ml和(3.97±1.12)ng/ml,具有明显差异,P<0.01;(2)血清NSE浓度与脑梗死体积呈正相关,梗死体积越大,NSE值越高,各组间均满足P<0.05;(3)脑梗死后NSE呈现动态变化,发病4小时内,变化不明显,6小时后 开始升高,24小时后明显升高,2天时大高峰,并可持续到5～7天,14天时基本恢复到正常;(4)血糖水平与NSE之间一定相关性,血糖水平高者,其NSE值亦高;(5)血清NSE水平与脑梗死患者的预后相关,NSE高的患者,其2周时的预后较差。结论 脑梗死后患者血清NSE升高并呈现一动态变化,它与脑梗死体积及患者的预后相关,且其变化早于影像学改变,可以作为判断脑梗死程度的依据之一,对确定临床治疗方案具有一定的指导意义。     

急性脑血管病患者血清钙、镁离子含量的变化及其临床意义

目的　观察急性脑血管病(ACVD)患者血清钙、镁离子(Ca2+、Mg2+)含量的变化及其与预后的 关系。方法　检测40例脑出血(ICH)及35例脑梗死(CI)患者发病早期血清Ca2+、Mg2+含量,并与30名健 康中老年人进行对照。结果　ACVD患者血清Ca2+、Mg2+含量显著低于对照组(P<0.01,P<0.05);ICH组 低于CI组(均P<0.05);ICH组中有意识障碍者明显低于无意识障碍者(均P<0.05);死亡者低于存活者(均 P<0.05)。大片梗死患者显著低于小片梗死者及对照组(均P<0.05),而小片梗死者与对照组差异无显著性 (均P>0.05)。结论　ACVD患者发病早期血清Ca2+、Mg2+含量均明显降低,与脑损害程度相关,可作为评估 其预后的指标之一。     

急性脑梗死患者甲状腺激素水平变化临床分析

目的探讨急性脑梗死患者甲状腺激素水平变化及其临床意义。方法动态观察60例急性脑梗死患者治疗前后甲状腺激素水平,同时检测40例健康对照者甲状腺激素水平,并对2组及治疗前后进行比较。结果与对照相比,治疗前脑梗死组血清FT3降低(P<0.01),TSH、FT4与对照组相比差异无统计学意义(P>0.05)。脑梗死组治疗前后相比,治疗前血清FT3水平低(P<0.05),TSH、FT4差异无统计学意义(P>0.05)。脑梗死治疗后FT3、FT4、TSH水平与对照组相比无统计学意义(P>0.05)。结论脑梗死患者急性期FT3下降,随着病情好转逐渐恢复;治疗前后甲状腺激素水平的变化的测定,对于监测治疗和判断预后有一定临床意义。     

病灶侧局部亚低温治疗急性脑出血临床研究

目的探讨及评估病灶侧局部亚低温治疗急性脑出血的有效性。方法根据入选及排除标准依住院号尾数单双号将收治的急性脑出血患者分为观察组(51例)及对照组(56例)。在常规治疗的基础上,观察组予病灶侧局部密贴式降温带治疗,对照组使用全头颅密贴式降温帽进行亚低温治疗。对2组急性脑出血患者的血清超敏C反应蛋白(hcCRP)及神经元特异性烯醇化酶(NSE)进行动态浓度监测,应用《美国国立卫生研究院卒中量表》(NIHSS)进行动态评分及并发症的发生率等指标进行综合分析。结果 2组患者在性别、年龄、出血量、发病时间、入院时NSE、hcCRP浓度及NIHSS评分比较差异无统计学意义(P>0.05),具可比性。亚低温治疗后2组血清NSE浓度在第3天、第7天比较差异无统计学意义(P>0.05);观察组在第14天明显低于对照组,差异有统计学意义(P<0.05)。而hcCRP浓度在第3天、第7天、第14天比较差异均无统计学意义(P>0.05);NIHSS神经功能评分观察组与对照组在入院时及第7天、第14天比较差异无统计学意义(P>0.05),第21天观察组低于对照组,差异有统计学意义(P<0.05)。2组均无出现明显心律失常、凝血功能障碍、低血压等并发症,无死亡病例。应激性溃疡出血、电解质紊乱发生率无差别(P>0.05);继发肺部感染发生率观察组为5.8%,对照组为19.6%,差异有统计学意义(P<0.05)。结论病灶侧局部亚低温治疗在达到理想的病变侧头部降温目的的,对健侧头部及全身影响和不良反应均较小,且复温无条件及时间的限制。而在减轻出血后神经元的损害、降低患者血清NSE水平、抑制炎症反应,从而达到降低神经功能损害程度、改善预后方面优于全头颅性亚低温治疗。     

急性脑梗死患者血清神经特异性烯醇化酶的含量变化及尼可林对其的影响

目的:探讨急性脑梗死患者血清神经特异性烯醇化酶(NSE)的含量变化及尼可林对其的影响。方法:观察急性脑梗死患者在发病3天内和治疗1周后血清NSE变化和神经功能缺损评分变化,并观察尼可林对其的影响。结果:急性脑梗死常规治疗组和尼可林组发病3天内血清NSE均高于对照组(P<0.01)。治疗1周后常规治疗组血清NSE含量仍高于对照组(p<0.05).而尼克林组与对照组之间无明显差异(P>0.05);尼克林组神经功能缺损评分与对照组相比有显著性差异(P<0.05)。结论:急性脑梗死患者血清NSE含量增高,而尼可林可显著降低血NSE的含量;尼克林的近期临床疗效也优予常规治疗组。表明尼可林对急性脑梗死患者具有脑保护作用。     

单唾液酸四己糖神经节苷脂对缺氧缺血性脑病患儿血清NSE S-100B的影响

目的探讨单唾液酸四己糖神经节苷脂(GM1)对缺氧缺血性脑病(HIE)患儿血清NSE、S-100B水平的影响及其作用机制。方法随机选择产科同期出生1d的健康足月新生儿20例作对照组,将40例HIE患儿随机分为常规治疗组(20例)和GM1治疗组(20例),GM1治疗组在常规治疗基础上于生后第2天加用GM1静滴,20mg/d,连续用药7d。常规治疗组进行常规治疗。3组新生儿均于生后第1天(治疗前)、第8天(治疗后)时采集血液标本,采用双抗体夹心ABC-ELISA法进行血清NSE、S-100B的检测。结果治疗前,2组HIE患儿血清中NSE、S-100B的水平高于正常新生儿(P<0.01);常规治疗组与GM1治疗组血清NSE、S-100B水平比较,差异无统计学意义(P>0.05)。2组第8天血清NSE、S-100B水平均低于第1天(P<0.01)。治疗后,HIE患儿血清中NSE、S-100B水平高于正常对照组(P<0.01)。GM1治疗组血清NSE、S-100B水平下降率大于常规治疗组(P<0.01)。结论 HIE患儿脑组织中神经元和神经胶质细胞均有不同程度的损伤,动态检测血清NSE、S-100B水平,可能有助于HIE的早期诊断和判断HIE脑损伤的修复程度,GM1对神经元及神经胶质细胞均有修复作用。     

脑出血患者血清NSE、S100β蛋白与认知功能障碍相关性研究

目的探讨脑出血患者血清神经元特异性烯醇化酶(NSE)、S100β蛋白浓度变化及其与出血量、神经功能缺损、认知功能障碍的相关性。方法收集脑出血患者56例,对照组30例。测定脑出血病人起病第1、3、7d血清NSE和S100β蛋白浓度,分析浓度的变化与出血量、美国国立卫生研究院卒中量表(NIHSS)评分、简易精神状态量表(MMSE)评分之间的关系。结果脑出血组血清NSE和S100β蛋白浓度均明显高于对照组(P<0.001),与出血量呈正相关(P<0.05);其浓度的变化与神经功能缺损及认知功能障碍相关,出血后NSE及S100β蛋白浓度越高,其神经功能缺损越严重(P<0.05);出血后认知功能障碍患者NSE及S100β蛋白浓度均明显升高(P<0.001)。结论脑出血病人血清NSE和S100β蛋白浓度变化能在一定程度上反映出血量;与神经功能缺损及卒中后认知功能障碍有密切的关系,可用于判断患者神经功能缺损及认知功能障碍的严重程度。     

急性脑梗死患者血浆内神经元特异性烯醇酶的变化：病例对照

BACKGROUND： The plasma level of neuron specific enolase （NSE） can be used to diagnose and evaluate neuronal injury and predict early prognosis.
OBJECTIVE： To observe the dynamic changes in plasma levels of NSE in patients with acute cerebral infarction, and to investigate its correlations with disease severity and prognosis.
DESIGN, TIME AND SETTING： This non-randomized, concurrent case-control experiment was performed at the Department of Neurology, First Hospital Affiliated to Heilongjiang University of Traditional Chinese Medicine between May and July 2007. PARTICIPANTS： Eighteen patients with acute cerebral infarction, who received treatment at the Department of Neurology, First Hospital Affiliated to Heilongjiang University of Traditional Chinese Medicine between May and July 2007, were recruited into the patient group. An additional 10 healthy individuals, who received health examinations simultaneously, were included as controls.
METHODS： Following admission （within 3 days） and at days 6, 12, and 30 subsequent to acute cerebral infarction attack, 3 mL venous blood was taken from each patient before the morning meal to determine the plasma level of NSE by enzyme-labeled immunosorbent assay. One-time blood extraction was performed in each healthy subject during the health examination for the same purpose as in patients. At 6 and 30 days following acute cerebral infarction attack, CT examination was performed for calculation of cerebral infarction volume according to the Tada formula. Following admission and at 30 days of disease invasion, all patients were scored by the National Institutes of Health Stroke Scale （NIHSS, 13 items）.
MAIN OUTCOME MEASURES： Comparison of NSE plasma level between acute cerebral infarction patients and healthy individuals; correlations of NSE plasma level in acute cerebral infarction patients with cerebral infarction volume, NIHSS score, and prognosis.
RESULTS： Following admission and at days 6 and 12 of disease invasion, the plasma level of NSE was significantly higher in the patient group than in the control group （P 〈 0.05）. Following admission and at day 30 of disease invasion, the NIHSS scores of the patient group were 17.706 and 11.222, respectively. Following admission and at day 6 of disease invasion, the plasma level of NSE was positively correlated with cerebral infarction volume （r = 0.503, 0.435, P 〈 0.05）, but it was negatively correlated with NIHSS score （r = -0.571, 0.368, P 〈 0.05）. The plasma level of NSE was mostly correlated with cerebral infarction volume, followed by NIHSS score, and lastly prognosis, with regression coefficients of 0.386, 0.343, and 0.340, respectively.
CONCLUSION： The plasma level of NSE is higher in patients with acute cerebral infarction than in the healthy population. It can reflect infarct severity and predict early prognosis of acute cerebral infarction.     

Prediction of early clinical severity and extent of neuronal damage in anterior-circulation infarction using the initial serum neuron-specific enolase level

CONTEXT: Prompt and precise measurement of neuronal damage in acute cerebral infarction is important to determine the prognosis of functional outcome. A feasible biochemical marker such as the neuron-specific enolase (NSE) level has been used to detect various diseases involving the central nervous system. OBJECTIVE: To determine whether the initial serum NSE level is a useful marker for predicting the severity of clinical neurological deficits and the extent of neuronal damage in acute anterior-circulation infarction. DESIGN: Case-control study with biochemical-clinicoradiological correlation. SETTING: Tertiary care center. PARTICIPANTS: Eighty-one patients and 77 age- and sex-matched control subjects. MAIN OUTCOME MEASURES: Patients with anterior-circulation infarction underwent intravenous serum NSE sampling within 24 hours after symptom onset. Recent infarction was confirmed by T2-weighted and diffusion-weighted magnetic resonance imaging of the brain about 1 week after the onset of stroke. Volumetric analysis of infarction was also performed. The National Institutes of Health Stroke Scale score was measured on admission to the hospital and 1 week after symptom onset. RESULTS: The patients' initial serum NSE levels were statistically significantly higher than the controls (P<.05). The initial serum NSE level highly correlated with the volume of infarction seen on T2-weighted magnetic resonance imaging of the brain (r = 0.62, P<.001) and with the National Institutes of Health Stroke Scale score obtained on hospital admission (r = 0.42, P =.002) and on the seventh day after the onset of stroke (r = 0.44, P<.001). CONCLUSION: The initial serum NSE level is a reliable predictor for the extent of neuronal damage and the severity of clinical neurological deficits in acute anterior-circulation infarction.     

脑出血急性期神经元特异性烯醇化酶的变化及临床研究

目的　探讨脑出血急性期血清神经元特异性烯醇化酶 (NSE)浓度变化及其与神经功能缺损和预后之间的关系。方法　用酶联免疫分析法分析测定 4 0例脑出血患者和 2 0例健康人血清 NSE浓度。神经功能缺损评定按 SSS标准 ,出血量以入院时 CT结果计算。结果　脑出血患者血清 NSE浓度明显高于正常对照组 (P<0 .0 5 ) ,与出血量呈明显正相关 (P<0 .0 5 ) ,与神经功能缺损程度呈正相关 (P<0 .0 5 ) ,与预后呈负相关 (P<0 .0 5 )。结论　脑出血急性期检测血清 NSE浓度 ,有助于判断神经功能缺损程度及预后。     

尼莫地平对高血压脑出血患者血浆NSE及预后的影响

目的：观察尼莫地平对高血压脑出血患血浆神经元特异性烯醇化酶(NSE)及预后的影响。方法：将85例高血压脑出血患随机分为对照组和尼莫地平治疗组，动态观察患的血浆NSE水平、血肿体积、神经功能缺损程度和总的生活能力评分。结果：两组患的血浆NSE水平存各个时间点上无明显差异，尼莫地平治疗组与对照组的临床神经功能缺损程度及生活能力评分在病程第14d时无显性差异，在第30、90d时治疗组的神经功能恢复优于对照组。结论：脑出血急性期静脉应用尼莫地平有可能改善患的预后。血浆NSE不宜做为临床评价脑出血药物疗效的指标。     

神经元特异性烯醇酶与急性脑梗死

目的：探讨急性脑梗死患者血清神经元特异性烯醇酶（NSE）的变化及其临床意义。方法：采集69例脑梗死患者起病3天内的血标本,用酶联免疫分析法测定血清NSE含量（其中35例2周时复测）。结果脑梗死3天内血清NSE明显高于对照组及2周时（P＜0．001）,血清NSE含量与梗死灶大小,神经功能缺损程度明显正相关（P＜0．001）,与意义障碍明显负相关（P＜0．001）,临床疗效赵差血清NSE含量越高（P＜0．001）。结论：脑梗死早期血清NSE明显升高,血清NSE含量与临床表现关系密切。     

115例脑卒中患者血清神经元特异性烯醇化酶测定及其意义

目的 研究脑卒中时血清神经元特异性烯醇化酶（NSE）的变化及与神经功能缺损的关系。方法 脑出血46例,脑梗死69例,正常对照21例,患者分别在起病3d内及2周时采集血标本。血清NSE测定采用酶联免疫分析方法,神经功能缺损评定按斯堪的纳维亚卒中量表（SSS）标准进行,结果 脑梗死,脑出血组3d内及起病2周时血清NSE明显高于正常对照组（均为P＜0．001）,并与SSS呈明显正相关（P＜0．001）,结论 脑卒中早期血清NSE明显升高,血清NSE与SSS之间有明显相关性。     

Intracerebral hemorrhage versus infarction: Stroke severity,risk factors,and prognosis

The purpose of this study was to compare stroke severity, risk factors, and prognosis in patients with intracerebral hemorrhage versus infarction. We prospectively studied 1,000 unselected patients with acute stroke of a verified type in the Copenhagen Stroke Study. Neurological deficits and functional disabilities were evaluated weekly from the time of acute admission throughout the rehabilitation period. Eighty-eight (9%) had intracerebral hemorrhage. The relative frequency of intracerebral hemorrhage rose exponentially with increasing stroke severity. In multivariate analyses, stroke type had no influence on mortality, neurological outcome, functional outcome, or the time course of recovery. Initial stroke severity was the all-important prognostic factor. The relative importance of hypertension and blood pressure on admission was not greater for intracerebral hemorrhage than for infarction. No preponderance was found between type of stroke and sex, age, and smoking. Diabetes, ischemic heart disease, and elevated serum total cholesterol level all favored cerebral infarction as opposed to intracerebral hemorrhage. We conclude that the type of stroke per se has no influence on stroke prognosis in general; the extent of the injury is decisive. The poorer prognosis in patients with intracerebral hemorrhage is due to the increase in frequency of intracerebral hemorrhage with increasing stroke severity. The likelihood of cerebral infarction occuring as opposed to intracerebral hemorrhage seems increased fivefold in stroke patients with diabetes. Hypertension and blood pressure on admission were not predictors of stroke type.