Background and Study Aims Antiepileptic drugs are the first choice of treatment for patients with epilepsy. However, the withdrawal of antiepileptic drugs after seizure-free remains a significant focus for the majority of patients with epilepsy and their families. In this study, we evaluated the risk factors associated with relapse after drug withdrawal in patients with seizure free for 2 years. We aimed to guide patients in seizure-free to assess the risk of drug withdrawal. Patients and Methods Through screening, 452 patients with epilepsy were included in the study.Patients were followed up for at least 2 years or more. Analyzed their clinical data by applying the χ2-test, Kaplan-Meier survival analysis and multivariate Cox regression analysis. Results 423 patients completed follow-up, of which 304 cases recurred (71.9%).Related recurrence factors include age of onset, type of seizure, number of AEDs, seizure-free time before withdrawal, and electroencephalogram (EEG) results before drug withdrawal (P<0.05). The results of correlation analysis showed that age of onset, seizure frequency, seizure type, number of AEDs, the period from AEDs treatment to a seizure-free status, EEG results before drug withdrawal, and pre-medication course, were all significantly related to the recurrence of seizures after drug reduction and withdrawal (P<0.05). We identified a range of independent risk factors, including onset age, seizure frequency, Multiple AEDs and the period from AEDs treatment to a seizure-free status. Conclusion The overall recurrence rate of epilepsy in our patient cohort was high, and the peak recurrence period was within one-year of drug withdrawal. Patients with partial seizures, a short seizure-free time before withdrawal, severe EEG abnormalities before drug reduction, and a long course of the disease, are prone to relapse. Patients with an older age at onset and a high frequency of attack, those taking multi-drug combination therapy, and those that take a long time to gain control, should be managed carefully to AEDs withdrawal.

Increasing evidence reveals that delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) results from the combined effects of environmental and genetic factors. The main pathological feature of DEACMP was generalized demyelination of cerebral white matter. Myelin basic protein (MBP) levels in cerebrospinal fluid (CSF) and serum samples from DEACMP patients were elevated. This study investigated the association of MBP single nucleotide polymorphisms(SNPs) (rs470555, rs470724, rs4890785, rs595997, rs76452994, and rs921336) with DEACMP. We genotyped 416 DEACMP patients and 785 age, educational level, and sex-matched ACMP patients for rs470555, rs470724, rs4890785, rs595997, rs76452994, and rs921336 SNPs using the Agena MassArray. There were no significant differences in the allele frequency distribution, four genetic models, and genotype distributions between the DEACMP and ACMP groups for rs470555, rs470724, rs4890785, and rs595997. However, significant differences were observed for rs76452994 and rs921336. This study revealed that the MBP polymorphisms, rs470555, rs470724, rs4890785, and rs595997, were not associated with DEACMP. Based on the codominant, dominant, and overdominant genetic inheritability patterns, the MBP rs76452994 and rs921366 polymorphisms were associated with DEACMP. Furthermore, the G allele of rs76452994 and T allele of rs921336 could lead to higher DEACMP risk.

Objective. The purpose of this study was to analyze the relationship between cadherin gene single-nucleotide polymorphisms (SNPs) and the risk of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Materials and Methods. A total of 416 patients with DEACMP and 754 patients with acute carbon monoxide poisoning (ACMP) were recruited. We used the Sequenom MassARRAY® system to detect cadherin gene SNPs related to DEACMP. Using different genetic analysis models, we evaluated the relationship between the cadherin gene polymorphisms and risk of DEACMP. Results. We found that rs1944294 in the N-cadherin (CDH2) gene showed significant differences in genotype frequencies between the two groups under codominant and dominant inheritance models. Similarly, rs2513796 in the cadherin-17 (CDH17) gene showed significant differences under the codominant, dominant, and overdominant genetic models. And the T allele frequency of rs1944294 in the DEACMP group was significantly higher than that in the ACMP group (P=0.023). Conclusions. Cadherin gene SNPs (rs1944294, rs2513796) are associated with an increased risk of DEACMP in the Chinese population.

目的 检测老年癫痫患者急性发作后血浆外泌体中长链非编码RNA(LncRNA)MIR155HG表达水平,并探讨其对老年患者预后的意义.方法 159例老年癫痫患者,根据随访期间是否发生预后不良将患者分为预后不良组和预后良好组.采用实时荧光定量-聚合酶链反应(qRT-PCR)检测患者血浆外泌体中LncRNA MIR155HG表达水平;分析预后不良组老年癫痫患者血浆外泌体LncRNA MIR155HG与血浆细胞因子水平相关性;分析血浆外泌体LncRNA MIR155HG水平对老年癫痫患者预后不良的预测价值;分析影响老年癫痫患者预后不良的因素.结果 预后不良组血浆外泌体LncRNA MIR155HG及血浆白细胞介素(IL)-2、IL-6、IL-8、IL-1β、肿瘤坏死因子(TNF)-α水平显著高于预后良好组(P<0.05);预后不良组老年癫痫患者血浆外泌体LncRNA MIR155HG与血浆IL-2、IL-6、IL-8、IL-1β、TNF-α 水平呈正相关(P<0.05);血浆外泌体LncRNA MIR155HG水平预测老年癫痫患者预后不良的曲线下面积(AUC)为0.852,截断值为1.171,特异性为79.5％,敏感度为85.5％;LncRNA MIR155HG、TNF-α是影响老年癫痫患者预后不良的独立危险因素.结论 老年癫痫患者血浆外泌体Ln-cRNA MIR155HG水平的变化与病情发展及预后密切相关.

目的 探讨微小RNA(miR)-134调节环腺苷酸应答元件结合蛋白(CREB)/脑源性神经营养因子(BDNF)通路参与脑卒中后抑郁(PSD)的作用机制.方法 32只SD大鼠按照随机数字表法分为假手术组、模型组、antagomir NC组、miR-134 antagomir组,每组8只;除假手术组外,其余各组行大脑中动脉阻塞(MCAO)术,然后采用慢性不可预见温和应激(CUMS)诱导建立PSD模型,假手术组除不插入线栓外其他操作相同.MCAO术后CUMS前antagomir NC组、miR-134 antagomir组分别于大脑双侧海马区注射5μL antagomir NC、miR-134 antagomir(1μmol/L),5 d注射1次,连续5次.假手术组、模型组注射等体积生理盐水.CUMS应激前,应激第7、14、21天对大鼠称体质量,动物敞箱实验评价大鼠运动行为改变、蔗糖偏爱实验评价大鼠快感缺乏行为改变.实验结束后处死大鼠,分离海马CA1区,实时荧光定量PCR(qPCR)检测miR-134、CREB、BDNF mRNA表达,免疫组化染色检测CREB、BDNF蛋白表达情况.双荧光素酶报告基因实验鉴定CREB与miR-134的靶向关系.结果 与假手术组相比,模型组大鼠体质量、水平和垂直活动得分、糖水饮用比例降低(P<0.05);与模型组、antagomir NC组相比,miR-134 antagomir组大鼠体质量、水平和垂直活动得分、糖水饮用比例升高(P<0.05),随着应激时间的延长,该效应逐渐明显.与假手术组相比,模型组海马CA1区miR-134水平升高(P<0.05),CREB、BDNF mRNA表达和阳性细胞数减少(P<0.05);与模型组、antagomir NC组相比,miR-134 antagomir组海马CA1区miR-134水平降低(P<0.05),CREB、BDNF mRNA表达和阳性细胞数增多(P<0.05).与miR-134 mimic NC+CREB-WT相比,miR-134 mimic+CREB-WT共转染细胞荧光素酶相对活性下降(P<0.05),证明CREB序列上存在miR-134特异结合位点.结论 降低miR-134可促进CREB/BDNF通路蛋白的表达,进而改善抑郁状态,实现对PSD大鼠的保护.

目的 探讨托吡酯与卡马西平单药治疗癫痫部分性发作的疗效和安全性.方法 计算机检索PubMed、Cochrane、Embase、中国知网、万方数据库和中国生物医学文献数据库中,建库—2019年01月31日关于托吡酯与卡马西平单药治疗癫痫部分性发作患者的临床对照试验文章.对其进行文献筛选,数据提取,文献质量及风险偏倚评估,并交叉核对,使用Meta分析专用软件Revman 5.3进行数据分析.结果 初检文献459篇,最终纳入文献12篇,共2348例患者,其中托吡酯组1075例,卡马西平组1273例.其中高质量文献3篇,低质量文献9篇.Meta分析结果显示:托吡酯组完全控制540例,占52.38％(540/1031);卡马西平组完全控制546例,占45.73％(546/1194),两组差异有统计学意义[OR=1.53,95％CI(1.05,2.24),P<0.05].托吡酯组有效204例,占37.02％(204/551);卡马西平组有效326例,占47.52％(326/686),两组差异无统计学意义[OR=0.91,95％CI(0.70,1.19),P>0.05].托吡酯组出现不良反应372例,占39.45％(372/943);卡马西平组出现不良反应466例,占44.72％(466/1042),两组差异有统计学意义[OR=0.75,95％CI(0.56,1.00),P<0.05].结论 托吡酯单药治疗癫痫部分性发作的疗效及安全性优于卡马西平.

目的 探讨环状RNA小脑变性相关蛋白1反义转录物(CDR1as)与微小RNA-7(miR-7)在癫痫患者血浆中的表达及与脑电图异常的关系.方法 选取2016年12月—2019年12月在新乡医学院第二附属医院门诊及住院的癫痫患者87例为观察组,并根据脑电图结果分为正常组(6例)、轻度异常组(18例)、中度异常组(37例)及重度异常组(26例);选取同期健康体检者90例为对照组.实时荧光定量PCR(qPCR)法检测血浆CDR1as、miR-7水平,酶联免疫吸附测定(ELISA)法检测血浆白细胞介素(IL)-2、肿瘤坏死因子(TNF)-α和IL-1β水平;Pearson法分析癫痫患者血浆CDR1as、miR-7水平与IL-2、TNF-α和IL-1β水平的相关性.结果 对照组、正常组、轻度异常组、中度异常组、重度异常组血浆CDR1as、IL-2、TNF-α和IL-1β水平总体呈升高变化,miR-7水平总体呈降低变化,差异均有统计学意义(P<0.05).癫痫患者血浆CDR1as水平与IL-2、TNF-α和IL-1β水平呈正相关(P<0.05),miR-7水平与IL-2、TNF-α和IL-1β水平呈负相关(P<0.05).结论 CDR1as、miR-7在癫痫患者血浆中分别呈高表达、低表达,与炎症因子水平、脑电图异常程度密切相关,可能通过影响炎症反应引起脑部异常放电.

Objective: To investigate the association of WWP2 single nucleotide polymorphism (rs3790088, rs4247109) with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) , and explore the influences of DEACMP genetic predisposition. Methods: From November 2006 to December 2017, 235 DEACMP cases and 429 acute carbon monoxide poisoning (ACMP) cases were selected. All ACMP patients were followed up for more than 90 days without DEACMP. The DNA in all blood samples were extracted with the blood Genome DNA Extraction Kit. The method of Sequenom Mass Array SNP technique was used to detect the genotype and allele of WWP2. All DEACMP patients were assessed every 3 days after hospitalization by the Hasegawa Dementia Scale (HDS) and Activity of Daily Living Scale (ADL) . The distribution of genotypes in conformty with Hardy-Weinderg law was analyzed by goodness-of-fit χ(2) test, and χ(2) test was used for association analysis. Results: For rs3790088, there were 226 DEACMP cases and 414 ACMP cases. For rs4247109, there were 234 DEACMP cases and 428 ACMP cases. For rs3790088 and rs4247109 in WWP2 gene: there were not significant differences in the gene genotype distribution and allele frequency of both DEACMP group and ACMP group (P>0.05) . According to gender, there were not significant differences in WWP2 gene genotype distribution and allele frequency between two female groups and two male groups (P>0.05) . After analysis by genetic model, the genotype distributions in both DEACMP group and ACMP group were not significantly differences in three genetic models (codominant genetic model, recessive genetic model and dominant genetic model, P>0.05) . Conclusion: It has not confirmed the genetic correlation between the two gene single nucleotide polymorphisms (rs3790088, rs4247109) of WWP2 gene and the incidence of DEACMP.

Objective. The aim of this study is to explore the relationship between neuron-specific enolase (NSE) gene polymorphism and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) and provide a theoretical basis for DEACMP pathogenesis, diagnosis, and prognosis. Methods. To investigate this relationship, we screened 6 NSE single nucleotide polymorphisms (SNPs), based on the results of the previous genome-wide association studies (GWAS). A total of 1,201 patients, including 416 in the DEACMP group and 785 in the acute carbon monoxide poisoning (ACMP) group, were detected by the Sequenom MassARRAY® method. The genotype frequencies and alleles of the 6 NSE SNPs (rs2071074, rs2071417, rs2071419, rs11064464, rs11064465, and rs3213434) were compared using different genetic models. Results. In the SNPs rs2071419 and rs3213434, we found that the genotypes and allele frequencies in the two groups significantly correlated with the grouping of patients ( χ 2 = 6.596 , p = 0.037 ; χ 2 = 8.769 , p = 0.012 ). The haplotypes GGTTTC and CCTTTC of ACMP and DEACMP were different ( χ 2 = 6.563 , p = 0.010 ; χ 2 = 4.151 , p = 0.042 ). We also observed that rs2071419 and rs3213434 significantly correlated with DEACMP-increased risk in the dominant, codominant, and overdominant genetic models. In addition, we speculated that the C allele of the rs2071419 polymorphism and the T allele of the rs3213434 polymorphism in NSE may increase the DEACMP risk ( p = 0.011 , p = 0.006 ). Conclusions. The results show that rs2071419 and rs3213434 are susceptible sites of DEACMP. The NSE C allele of rs2071419 and T allele of rs3213434 and the haplotypes GGTTTC and CCTTTC may be risk factors for DEACMP.

目的 探讨豫北地区首次急性脑梗死患者卒中后抑郁(PSD)的危险因素.方法 选择2015年1月至2018年9月新乡医学院第二附属医院神经内科收治的首次发病急性脑梗死患者387例为研究对象.收集患者的人口学资料和临床资料,采用单因素分析PSD危险因素,将单因素分析结果 中差异有统计学意义的指标进一步行单因素和多因素logistic回归分析,筛选PSD的独立危险因素.结果 急性脑梗死患者在发病14 d至6个月PSD的患病率为47.0％(182/387).单因素分析结果 显示,患者的职业类型、性格、病灶部位、失语、脑梗死体积、美国国立卫生研究院卒中量表(NIHSS)评分、日常生活活动能力量表(ADL)评分与PSD有关(P<0.05);患者的年龄、性别、婚姻状况、文化程度、家庭收入、近期负性事件,高血压病、糖尿病、吸烟、饮酒、卒中家族史、颈动脉斑块与PSD无关(P>0.05).单因素logistic回归分析结果 显示,病灶部位、入院时NIHSS评分、性格、职业类型、失语是急性脑梗死发生PSD的危险因素(P<0.05);多因素logistic回归分析结果 显示,患者入院时NIHSS评分、性格、病灶部位和失语是急性脑梗死发生PSD的独立危险因素(P<0.05).结论 豫北地区首次急性脑梗死后患者PSD发生率较高,患者入院时NIHSS评分、性格、病灶部位和失语是PSD发生的独立危险因素.

目的 探讨事件相关电位P300、血清神经元PAS结构域蛋白4(NPAS4)水平与脑小血管病(CSVD)患者认知功能障碍的相关性.方法 选择2017年2月至2019年6月新乡医学院第二附属医院收治的98例CSVD患者为研究对象.采用简明精神状态量表(MMSE)评分评估患者认知功能,根据MMSE评分将患者分为轻度组(n=52,MMSE评分21～26分)和中重度组(n=46,MMSE评分<21分),同期选择健康体检者50例作为对照组(MMSE评分27～30分).采用诱发电位仪检测3组受试者P300潜伏期和波幅,采用酶联免疫吸附法检测3组受试者血清NPAS4水平,采用Spearman相关分析患者P300电位、NPAS4水平与MMSE评分的相关性.结果 中重度组患者血清NPAS4水平高于对照组和轻度组(P<0.05);轻度组患者血清NPAS4水平高于对照组(P<0.05).轻度组和中重度组患者P300潜伏期长于对照组,P300波幅低于对照组(P<0.05);中重度组患者P300潜伏期长于轻度组,P300波幅低于轻度组(P<0.05).MMSE评分与P300潜伏期、NPAS4水平呈负相关(r=-0.706、-0.425,P<0.05),与P300波幅呈正相关(r=0.758,P<0.05).结论 P300电位、血清NPAS4水平变化与CSVD患者认知障碍严重程度有关,P300电位和血清NPAS4水平可用于CSVD患者认知功能的早期评估.

目的 探讨白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)基因多态性与急性脑梗死的相关性.方法 选择2016年4月至2017年8月新乡医学院第二附属医院神经内科收治的86例脑梗死患者为研究对象(脑梗死组),另选择同期健康体检者92例为对照组.采用序列特异性引物和聚合酶链式反应(PCR)、限制性内切酶酶切技术检测2组受试者血液中IL-1β(-511)C/T、TNF-α(-238)G/A基因多态性.结果 2组受试者IL-1β(-511)位点基因型频率和TNF-α(-238)位点基因型频率均符合Hardy-Weinberg遗传平衡定律(P＞0.05).脑梗死组患者IL-1β(-511)位点Tt基因型频率高于对照组(OR=2.059,95％可信区间:1.087～3.899,P＜0.05);脑梗死组患者IL-1β(-511)位点C等位基因频率低于对照组(OR=0.486,95％可信区间:0.256 ～0.920,P＜0.05).2组受试者TNF-α(-238)位点基因型频率和等位基因频率比较差异无统计学意义(P＞0.05).其中AA基因型在全部研究对象中未检出,G等位基因见于全部研究对象.结论 IL-1β(-511)C/T多态性可能与脑梗死有关,TNF-α(-238)G/A多态性可能与脑梗死无关.

Abstract Background We explored the association of leucine-rich repeats and calponin homology domain containing 1 (LRCH1) gene polymorphisms with genetic susceptibility to delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), which might provide a theoretical basis for the pathogenesis, diagnosis, and prognosis research of DEACMP. Methods Four single nucleotide polymorphisms, rs1539177 (G/A), rs17068697 (G/A), rs9534475 (A/C), and rs2236592 (T/C), of LRCH1, selected as candidate genes through genome-wide association analysis, were genotyped in 661 patients (DEACMP group: 235 cases; ACMP group: 426 cases) using Sequenom Massarray®. The association analysis of four SNPs and LRCH1 was performed under different genetic models. Results LRCH1 polymorphisms (rs1539177, rs17068697, rs9534475) under additive and dominant genetic models were significantly associated with an increased risk of DEACMP, but no significant association under allele and recessive models was found. The LRCH1 rs2236592 polymorphism was susceptible to DEACMP only under the dominant model (TT/TC + CC, OR = 1.616, 95% CI: 1.092–2.390, P = 0.015784). In addition, the A allele gene of rs9534475 polymorphism in LRCH1 might increase the risk for DEACMP (OR = 1.273, 95% CI: 1.013–1.601, P = 0.038445). Conclusions We found a significant association between the four LRCH1 polymorphisms and DEACMP. The allelic A of rs9534475 polymorphism in LRCH1 might be a risk factor for DEACMP.

目的 验证急性一氧化碳中毒后迟发性脑病(DEACMP)预测概率方程的可靠程度,评价其对该病的临床预测价值.方法 以2001年1月至2014年12月豫北地区3座城市12家医院符合急性一氧化碳中毒(AGMP)诊断标准的752例住院患者为研究对象,采集患者基本信息并随访至清醒后90 d.应用秦洁等1987年10月至1990年3月从中国人民解放军海军总医院收集的被诊断为ACMP的223例患者随访结果分析中所得出的预测发生DEACMP的概率logistic回归方程,计算ACMP患者发生DEACMP的概率.预测结果与实际DEACMP发病率相比较,分析该方程的符合率及临床预测价值.结果 752例ACMP患者在随访期内实际有127例发生DEACMP,发生率16.9％,预测概率≥50％时,实际发生DEACMP者19例,明显低于理论推测发病数49例(x2=20.27,P＜0.05);预测概率分别≥60.0％、≥80.0％、≥90.0％时,实际发生DEACMP者分别为13、3、2例,明显低于理论推测发病数37、21、8例(x2=19.30、25.07、8.10,P＜0.05).随着预测概率的增加,实际发生DEACMP的比率逐渐降低.预测概率越大,患者发生DEACMP假阴性率越大,灵敏度越低,假阳性率越小,特异度越高,诊断符合率越小.结论 应用DEACMP预测概率方程预测本研究752例ACMP患者发生DEACMP的概率与实际发病情况符合率很低.

Objective To investigate the clinical and molecular genetic features of idiopathic basal ganglia calcification ( IBGC) with acute cerebral infarction. Methods Clinical data of 1 patient with IBGC and his family were analyzed retrospectively. Results There were 9 patients in 3 generations family. The proband presented paralysis of left limbs, craniocerebral CT showed bilateral basal ganglia calcification and craniocerebral MRI discovered acute infarction of the right basal ganglia besides bilateral basal ganglia calcification. Until now, no obvious clinical symptom was found in the other patients except facial pigmentation. Bilateral basal ganglia calcification was found in all the patients. Karyotype analysis and electroencephalogram were normal. No mutation of SLC20A2 was found in the proband. Conclusions Besides typical the characters of craniocerebral imaging, IBGC can be accompanied with acute infarction and skin pigmentation. This family was not caused by SLC20A2 gene, which suggested genetic heterogeneity of IBGC.

Objective To study and analyze the relation between cognitive impairment and apolipoprotein E(ApoE) gene polymorphism in post-stroke depression patients(PSD).Methods The patients were divided into PSD group(83 cases) and brain stroke group(96 cases) by using the 24-item Hamilton Depression Rating Scale (HAMD-24),and healthy volunteers were selected as a control group(53 cases).Cognitive function was evaluated by using the event-related potential (ERP) P300 and single nucleotide polymorphisms of ApoE exon 4 of 112 (rs429358) and 158 (rs7412) were determined by using gene sequencing method.Results 1.Compared with the brain stroke group and the control group,latency in ERP including N2 and P3 of PSD group was significantly prolonged (P＜ 0.05 ),while the amplitude of P3 in PSD was significantly lower(P＜ 0.05 ).2.e3/ε4 genotype frequency in PSD group(24 cases) was significantly higher than that in the control group(7 cases) (P＜0.05).The e4/4 genotype fiequency in PSD group (8 cases) was significantly higher than that in brain stroke group (2 cases) (P ＜ 0.05 ).The e4 allele rate in PSD group ( 24.7％ ) was significantly higher than that in both brain stroke group (16.1％) and contro] group(9.4％ ) (all P＜0.05).3.The PSD patients with ε4 allele had significantly higher score of HAMD-24 and prolonged latency of N2 and P3 than those without e4 allele (P ＜ 0.05 ).Conclusion There is cognitive impairment in PSD patients.The ApoE ε4 allele may associate with the cognitive impairment and depression in PSD patients.

目的 观察美金刚联合小剂量奥氮平治疗伴有行为和精神症状的阿尔兹海默病(AD)患者的疗效及对患者认知功能的影响.方法 将87例AD伴行为和精神症状患者随机分为美金刚单药治疗组(单药治疗组)和联合奥氮平治疗组(联合治疗组),对所有入组患者在治疗前及治疗4、12周末均行AD病理行为(Behave-AD)评分、简易智力状态检查(MMSE)评定,并对评定结果进行比较.结果 2组患者治疗前Behave-AD和MMSE评分比较差异均无统计学意义(t =0.47、0.33,P＞0.05).治疗第4周末2组患者Behave-AD评分均较治疗前显著下降(t=7.02、9.79,P＜0.05),且联合治疗组较单药治疗组下降更显著(t=2.35,P＜0.05);2组患者MMSE评分均较治疗前显著升高(t =8.15、5.82,P＜0.05),但2组患者之间MMSE评分比较差异无统计学意义(t=0.16,P＞0.05).治疗第12周末2组患者Behave-AD评分均较治疗前显著下降(t=10.94、12.64,P＜0.05);2组患者MMSE评分均较治疗前显著升高(t=14.21、14.82,P＜0.05),但2组患者之间MMSE评分比较差异无统计学意义(t=0.24,P＞0.05).治疗第12周末2组患者Behave-AD评分均较治疗第4周末显著下降(t=3.93,3.99,P＜0.05),且联合治疗组较单药治疗组下降更显著(t=2.12,P＜0.05);2组患者MMSE评分均较治疗第4周末显著升高(t=5.49、5.05,P＜0.05),但2组患者之间MMSE评分比较差异无统计学意义(t=14.82,P＜0.05).结论 美金刚联合小剂量奥氮平治疗AD伴行为和精神症状患者较美金刚单药治疗更能减轻其精神行为症状,但对认知功能改善二者效果相当.

目的 探讨急性脑梗死患者颈动脉粥样硬化斑块稳定性与血清YKL-40水平之间的相关性,为颈动脉粥样硬化及脑梗死的早期诊治提供临床依据.方法 选取95例急性脑梗死患者为研究对象,按照颈动脉彩超检查结果将脑梗死组分为不稳定斑块组、稳定斑块组和无斑块组.选取同期健康体检人员50例为对照组.采用双抗体夹心酶联免疫法检测急性脑梗死患者入院48 h、入院14 d及对照组血清YKL-40水平,比较不同时期不同性质颈动脉斑块血清YKL-40的差异.结果 脑梗死组患者血清YKL-40水平明显高于正常对照组,且不稳定斑块组血清YKL-40的水平＞稳定斑块组＞无斑块组,差异均具有统计学意义(P＜0.05),脑梗死各亚组入院14 d血清YKL-40水平均低于入院48 h血清值,差异有统计学意义(P＜0.05).YKL-40的水平与梗死面积、NIHSS、胆固醇、血压、GLU、LDL-C、TG呈正相关(P＜0.05).结论 血清YKL-40是AS形成的重要标志物,与动脉粥样硬化斑块的稳定性相关.血清YKL-40可以监测动脉粥样硬化的程度,从一定程度上预测脑梗死发生的风险.

目的 研究卒中后抑郁患者(post-stroke depression,PSD)抑郁情绪与ApoE基因多态性之间的相关性.方法 采用24项汉密尔顿抑郁量表(HAMD-24)将病例分为PSD组(83例)和卒中组(96例),选取健康志愿者(53例)作为对照组.采用基因测序法测定载脂蛋白E基因第四外显子112位(rs429358)和158位(rs7412)单核苷酸位点多态性.结果 (1)PSD组ε3/ε4基因型频数(24例)高于对照组(7例),ε4/4基因频数(8例)高于卒中组(2例),差异有统计学意义(P ＜0.05);ε4等位基因频率(24.7％)高于对照组(9.4％)和卒中组(16.1％),差异有统计学意义(P＜0.05).(2)卒中组ε2基因型频率(13.5％)大于PSD组(4.8％),差异有统计学意义(x2=5.563,P=0.018).(3)PSD组携带ε4等位基因的HAMD-24评分高于非携带ε4等位基因组,差异有统计学意义(P＜0.05).结论 ApoE基因多态性与PSD存在相关性,ε4等位基因可能是PSD的危险因子,而ε2等位基因是PSD的保护因子.

目的：观察分析前列地尔脂微球载体制剂联合葛根素治疗椎基底动脉供血不足的疗效及安全性。方法将椎基底动脉供血不足患者90例随机分为治疗组44例和对照组46例，治疗组给予前列地尔脂微球载体制剂及葛根素联合治疗，对照组单用葛根素注射液治疗，比较2组临床疗效。结果治疗组总有效率97.8％，对照组为76.2％，治疗组明显优于对照组，差异有统计学意义（ P＜0.05）。结论前列地尔脂微球载体制剂联合葛根素治疗椎基底动脉供血不足疗效显著，且安全性好。