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1.
神经性厌食的事件相关电位P300的实验研究   总被引:1,自引:0,他引:1  
目的研究神经性厌食(AN)患者的事件相关电位P300特点。方法应用Nicolet Bravo脑电生理仪,采用纯音"Oddball"刺激诱发模式,对43例AN患者和34名健康对照进行认知性电位P300检测。结果 AN组P300中靶P3的潜伏期[(297.8±29.3)ms]长于健康对照组[(285.6±19.7)ms],差异有统计学意义(t=2.19,P=0.03);AN组靶P3波幅为(6.5±3.4)μV,低于健康对照组(9.8±3.2)μV,差异有统计学意义(t=4.33,P〈0.01)。2组的靶P2、靶N2及非靶P2的潜伏期、波幅均无统计学差异。结论 AN患者的P300靶P3潜伏期延长、波幅降低。  相似文献   

2.
目的 探讨长期住院的男性精神分裂症患者认知功能的变化与事件相关电位P300的关系.方法入组长期住院男性精神分裂症患者82例和健康对照52人.采用美国Nicolet Viking Quste诱发电位仪记录事件相关电位P300的潜伏期和波幅.采用动物命名测验、范畴流畅性测验、数字划消测验、连线测验(TMT-A、TMT-B)、Stroop测验(单词、颜色、色词干扰测验)、木块图测验、WMS-Ⅲ空间广度测验评估认知功能.结果患者组各项认知功能测验成绩与对照组之间差异均有统计学意义(P<0.01).患者组事件相关电位P300潜伏期较对照组明显延长(t=22.990,P<0.01),波幅较对照组明显降低(t=-9.699,P<0.01).患者组事件相关电位P300潜伏期与数字划消测验及TMT-A呈正相关(r=0.481,P<0.01;r=0.245,P<0.05).事件相关电位P300波幅与数字划消测验呈负相关(r=-0.338,P<0.01).结论长期住院男性精神分裂症患者虽处于稳定期,但仍存在认知功能的损害.事件相关电位P300的潜伏期和波幅可能是精神分裂症认知功能的电生理指标,并与患者的认知量表评估结果之间存在相关性.  相似文献   

3.
目的探讨无抽搐电休克(MECT)治疗难治性抑郁症(TRD)前后患者的认知电位P300变化。方法入选30名正常对照和30例TRD患者,比较其P300及MECT治疗前后的P300变化。结果与正常对照比较,TRD患者P300中的靶指标N1和P3潜伏期延迟以及靶波幅P3降低(P均<0.01)。TRD患者经MECT治疗后,P300靶潜伏期N1和P3均有所恢复(P<0.05或P<0.01),但靶波幅P3显著下降(P<0.01)。结论 P300可作为MECT治疗TRD的监测指标。  相似文献   

4.
目的探讨老年慢性精神分裂症(SCS)和阿尔茨海默病(AD)患者的认知电位(CP)P300的特点。方法对38例SCS患者、32例AD患者及40例健康老人对照组(NC)进行P300检测。结果 SCS组、AD组和NC组在靶潜伏期(Oz脑区N2)、靶波幅(Oz脑区P3)、非靶波幅(Oz脑区P2)上均有显著差异(P<0.01)。AD组表现为主成分N2延迟,与NC组和SCS组有极显著差异(P<0.01)。SCS组和AD组的靶波幅P3和非靶波幅P2均见降低,与NC组比较有显著差异(P<0.05)。结论作为反映认知功能障碍的客观生理指标,P300有可能作为SCS和AD辅助诊断的一个脑电生理学标志。  相似文献   

5.
目的观察焦虑症患者事件相关电位P300的变化特点.方法对22例焦虑症患者和22例健康成年人,应用Nicolet Bravo脑诱发电位做事件相关电位P300检测.结果与正常组相比,焦虑症组靶N2潜伏期延长(P<0.05),靶P2波幅低(P<0.01),靶P3潜伏期长且波幅低(P<0.01),非靶P2波幅低(P<0.01).P300各指标在男女性别之间的差异无统计学意义(P>0.05).结论焦虑症患者P300有多项指标变化,值得进一步随访.  相似文献   

6.
目的探讨血管性痴呆(Vascular dementia,VD)的事件相关电位(Event-related potentials,ERP)P300的变化特点.方法应用Nicolet Bravo脑诱发电位仪对18例VD患者和20例正常老年人进行P300检测.结果与正常老年组相比,VD组的P300表现为靶N2、P3潜伏期延长,靶P3、非靶P2波幅下降,有显著性差异(P<0.05-0.01).结论P300可反映VD认知功能的变化,尤其是靶P3的潜伏期和波幅,有助于评估VD的认知功能状态.  相似文献   

7.
目的探讨轻度认知功能障碍老年人(MCI)和阿尔茨海默病(AD)在事件相关电位(ERP)P300检测中的不同表现.方法收集符合ICD-10诊断标准的36例MCI患者和30例AD,并以45例健康老人作对照组(NC).使用美国仪器以及"听觉靶-非靶刺激序列"为诱发事件,完成P300检测.结果 (1)3组和NC组在靶潜伏期Fz脑区N2以及在靶波幅Fz脑区P2P3和非靶波幅Fz脑区P2上均有显著差异(P<0.01).(2)AD主成分N2表现为延迟,与NC组和MCI组有极显著性差异(P<0.01).(3)MCI组和AD组靶波幅P3和非靶波幅P2均见降低,与NC组比较也有显著性差异(P<0.05~<0.01).结论提示作为反映MCI和AD认知功能障碍的客观生理指标,P300有可能作为MCI和AD辅助诊断的一个脑电生理学标志.P300检查可作为老年精神科的必查项目.  相似文献   

8.
目的探讨Alzheimer病(AD)患者与正常老年人在事件相关电位(Event-relatedpotentim,ERP)P300检测中的不同特点。方法应用国产WOND2000C脑诱发电位仪对32例AD患者和39例正常老年人进行P300检测。结果与正常老年组相比,AD组的P300表现为靶N2、P3潜伏期延长,靶P3、非靶P2波幅下降,有显著性差异(P〈0.05-0.01)。结论P300可反映AD认知功能的变化,靶P3的潜伏期和波幅,有助于评估AD的认知功能状态。  相似文献   

9.
焦虑症和抑郁症患者认知电位P300对照研究   总被引:2,自引:0,他引:2  
目的探讨焦虑症(AD)和抑郁症(CD)在事件相关电位(ERP)P300检测中的不同表现。方法收集符合CCMD-3诊断标准的37例焦虑症患者和32例抑郁症患者以及36例健康成人对照组(NC),使用美国仪器以及“听觉靶-非靶刺激序列”为诱发事件,完成P300检测。结果(1)AD组、CD组和NC组在靶潜伏期Pz脑区P3以及在靶波幅Pz脑区P2、P3和非靶波幅Pz脑区P2上均有显著差异(P<0.01)。(2)AD组主要成分P3表现为延迟,与NC组和CD组有极显著性差异(P<0.01)。(3)AD组和CD组靶波幅P3和非靶波幅P2均见降低,与NC组比较也有显著性差异(P<0.05)。结论P300有可能作为AD组和CD组辅助诊断的一个脑电生理学标志。  相似文献   

10.
目的 探讨焦虑障碍听觉认知性电位P300的特点.方法 对32例焦虑障碍患者(AN组)和30名健康成年人(NC组),应用美国脑诱发电位仪进行P300检测.结果 与NC组相比,AN组Oz点P3潜伏期后移[NC组(328±16)ms,AN组(340±18)ms,t=2.801,P<0.01],P3波幅降低[NC组(6.1±2.0)μV,AN组(4.6±2.2)μV,t=2.84,P<0.05],非靶P2波幅降低[NC组(3.1±0.8)μV,AN组 (1.9±0.9)μV,t=5.61,P<0.01].结论 焦虑障碍认知性电位P300变化诸特点值得进一步随访.  相似文献   

11.
抑郁症、焦虑症患者事件相关电位对照研究   总被引:2,自引:0,他引:2  
目的:探讨抑郁症、焦虑症患者脑诱发电位的变异特点及临床应用价值.方法:共有46例抑郁症患者(抑郁症组)、41例焦虑症患者(焦虑症组)及42名健康志愿者(正常组),使用美国Nicolet Bravo脑电生理仪进行事件相关电位P300(P300)和关联性负变化(CNV)的检测.并于治疗2个月时对两患者组进行相同项目的随访.结果:与治疗前比较,抑郁症组P300靶N2、P3潜伏期缩短(P<0.05),靶P3波幅升高(P<0.01),CNV潜伏期M1缩短(P<0.01),波幅M1、M2升高(P均<0.05).焦虑症组P300靶P3潜伏期缩短(P<0.05),CNV波幅M1下降(P<0.05),指令信号后负变化(PINV)的出现率下降(P<0.05).治疗后与正常组比较,抑郁症组P300非靶P2波幅偏低(P<0.01),P300的双峰P2波和CNV的PINV出现率均偏高(P<0.05~0.01);焦虑症组CNV的潜伏期M2缩短(P<0.01).抑郁症组与焦虑症组治疗后比较在P300非靶P2波幅、双峰P2波出现率,CNV潜伏期M2和PINV出现率等指标之间差异有显著性(P均<0.01).结论:抑郁症、焦虑症患者脑诱发电位有自己的变异特点,在诊断和鉴别诊断方面有一定的价值.  相似文献   

12.
目的探讨细胞色素P450酶(cytochromeP450enzymes,CYP)1A2、2C19基因多态性与难治性抑郁症的关联。方法应用聚合酶链反应(PCR)扩增技术及限制性片段长度多态性(RFLP)测定79例难治性抑郁症患者及107名正常对照者CYP1A2C163A、CYP2C19G681A基因多态性。结果两组间基因型及等位基因分布差异无显著性(χ2=3.605,P>0.05;χ2=3.154,P>0.05)。难治性抑郁症患者对照组间基因型及等位基因分布差异无显著性(χ2=0.853,P>0.05;χ2=0.568,P>0.05)。79名患者中46名接受氟西汀合并小剂量利培酮(0.5~2.0mg/d)治疗,将其分为治疗有效组和无效组,两组间CYP1A2C163A(χ2=0.785,P>0.05;χ2=7.142,P>0.05)CYP2C19G681A(χ2=3.008,P>0.05;χ2=2.722,P>0.05)基因型及等位基因分布差异均无显著性。根据CYP2C19G681A基因多态性将患者分为无突变组(G/G型)和突变组(G/A型和A/A型),两组患者CYP1A2C163A基因型及等位基因分布差异无显著性(χ2=0.252,P>0.05;χ2=0.682,P>0.05)。结论CYP1A2C163A和CYP2C19G681A基因多态性与难治性抑郁症无显著关联,不是影响利培酮对氟西汀增效作用的主要因素。  相似文献   

13.
BACKGROUND: Approximately 50% of patients diagnosed with major depressive disorder will experience a recurrent or chronic course of illness for which long-term treatment is recommended. Moreover, at least 20% of patients diagnosed with depression do not respond satisfactorily to several traditional antidepressant medication treatment trials. Very little is known about the health care costs of patients with treatment-resistant depression. METHOD: Based on medical claims data (MarketScan Research Database, The MEDSTAT Group, Cambridge, Mass.) from January 1, 1995, to June 30, 2000, a naturalistic, retrospective analysis was conducted to study the characteristics and health care utilization of patients with treatment-resistant depression. All patients having an International Classification of Diseases, Ninth Revision (ICD-9), diagnosis code for unipolar or bipolar depression with specified antidepressant dosing and treatment durations were initially selected. Patients were then classified as "treatment resistant" if either they switched from or augmented initial antidepressant medication with other antidepressants at least twice (outpatient treatment-resistant group) or they switched from or augmented their initial antidepressant medication and also had a claim for either a depression-related hospitalization or suicide attempt (hospitalized treatment-resistant group). Those meeting the initial medication and diagnosis selection criteria but not meeting the treatment-resistance criteria constituted the comparison group. Members of the comparison group had comparatively stable antidepressant medication use patterns, consistent with an acceptable response to treatment. Patients were followed for a minimum of 9 months. Resource utilization was calculated from index date to last available claims data point and then annualized. RESULTS: Treatment-resistant patients were more likely to be diagnosed with bipolar disorder or concurrent substance abuse or anxiety disorders than the comparison group (p <.001). Treatment-resistant patients were at least twice as likely to be hospitalized (general medical and depression related) and had at least 12% more outpatient visits (p <.02). Treatment resistance was also associated with use of 1.4 to 3 times more psychotropic medications (including antidepressants) (p <.001). Patients in the hospitalized treatment-resistant group had over 6 times the mean total medical costs of non-treatment-resistant depressed patients ($42,344 vs. $6512) (p <.001) and their total depression-related costs were 19 times greater than those of patients in the comparison group ($28,001 vs. $1455) (p <.001). CONCLUSION: Treatment-resistant depression is costly and associated with extensive use of depression-related and general medical services. These findings underscore the need for early identification and effective long-term maintenance treatment for treatment-resistant depression.  相似文献   

14.
There is a lack of knowledge about the effect of electroconvulsive therapy (ECT) on auditory event-related potentials (ERPs) in severe psychotic depression. The aim of this study was to investigate both the effect of ECT on attention-dependent ERP (P300) and the correlation of P300 values with depression level. We recorded the auditory ERPs of 23 patients expressing psychotic symptoms and fulfilling the DSM-III-R criteria for treatment-resistant severe major depressive episode before and a week after successful bitemporal ECT. The clinical status was assessed with Hamilton (Ham-D) and Montgomery and Asberg (MADRS) depression scales. ECT was clinically very effective with these scales. On the level of auditory processing, ECT increased P300 amplitude with no significant effect on latency. Small amplitudes over the left hemisphere before treatment were associated with bigger Ham-D-score decrement. ECT produces a significant increase in brain activity at the level of attention-dependent auditory processing in severe depression. The change in electrical responses seems to represent a largely independent variable from the clinical assessment scales, even if the recovery rate was remarkable, because the change in overall symptom scores did not correlate with the P300 changes.  相似文献   

15.
目的本研究探讨氟西汀合并奥氮平治疗难治性抑郁症的安全性和疗效。方法采用双盲对照研究,将52例诊断为难治性抑郁症的患者随机分为两组,一组采用氟西汀治疗,一组采用氟西汀合并奥氮平治疗,分别在治疗后第2、4、6、8周末,评定汉密顿抑郁量表(HAMD)和临床总体印象量表(CGI),同时采用Asberg抗抑郁剂副反应量表评定两组的药物副反应。结果氟西汀联合奥氮平治疗难治性抑郁症的疗效要明显优于单一应用氟西汀治疗(P<0.05),药物副反应两组间无明显差异(P>0.05)。结论氟西汀联合奥氮平治疗难治性抑郁症的疗效要明显优于单一应用氟西汀治疗(P<0.05),药物副反应两组间无明显差异(P>0.05)。  相似文献   

16.
17.
目的:比较单相与双相抑郁患者事件相关电位感觉门控P50及P300的电生理差异。方法:用配对听觉条件/测试刺激范式,对57例单相抑郁患者(单相组)、63例双相抑郁患者(双相组)进行事件相关电位P50,P300测定,测量其P50的波幅,P300的潜伏期及波幅。结果:双相组P50的S2波幅显著高于单相组,而且双相组P50的抑制率显著高于单相组。双相组N2,P3潜伏期长于单相组,同时N2,P3波幅低于单相组,差异均有统计学意义。结论:双相抑郁患者认知功能损害可能比抑郁症患者更严重,事件相关电位可以为鉴别单双相抑郁提供一种新的技术手段。  相似文献   

18.
5-羟色胺2A、2C受体基因多态性与难治性抑郁症的关联分析   总被引:3,自引:0,他引:3  
目的:探讨中国汉族人群难治性抑郁症患者5-羟色胺2C(5-HT2C)受体基因与5-HT2A受体基因之间的关联性。方法:应用聚合酶链式反应(PCR)扩增技术及限制性片段长度多态性(RFLP)分别测定77例难治性抑郁症患者及90名正常人5-HT2C受体基因和5-HT2A受体基因的基因型和等位基因。结果:难治性抑郁症组-759野生型频率明显低于对照组。-759野生型/-697野生型频率也显著低于正常;患者组5-HT2A受体基因型杂合子组的-759野生型、-697野生型以及-759野生型/-697野生型均明显高于纯合子组。结论:-759野生型可能与难治性抑郁症的发病存在一定的相关性;5-HT2A受体基因与5-HT2C受体基因相互之间对难治性抑郁症易患性可能存在一定的关系。  相似文献   

19.
Objective To compare the efficacy of venlafaxine combination of cognitive behavior therapy or lithium or olanzapine for treatment-resistant depression. Method A prospective stratified randomized controlled clinical trial were adopted to the patients with treatment-resistant depression. 69 cases were divided into three groups with random number table, each group including 23 cases. One group was with venlafaxine combination of cognitive behavior therapy, others with combination of lithium, or olanzapine, for 6 weeks to observe the efficacy. The major indexes for therapeutic effects was Hamilton Depression Scale (HAMD) reducing score rate. Results The differences were significant in HAMD reducing score rate between the group with combination of cognitive behavior therapy[(61±5) %] and the group with combination of lithium [( 54 ± 7 ) %] ( t = 8.90, P < 0. 05 ), or olanzapine [( 47 ± 6 ) %] ( t =3.46,P < 0.05 ), with no significant difference is between the group with combination of lithium and the group with combination of olanzapine. Conclusion The total efficacy of venlafaxine combination of cognitive behavior therapy is superior to venlafaxine combination of lithium or olanzapine for treatmet-resistant depression.  相似文献   

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