亚综合征性抑郁患者认知功能初探

目的：探讨亚综合征性抑郁（SSD）患者的认知功能。方法：45例SSD患者,以31例抑郁症患者和28名正常人作为对照。SSD组和抑郁症组均使用抗抑郁剂治疗12个月以上。采用韦氏成人智力量表、临床记忆量表、威斯康星卡片分类测验（WCST）于治疗前后分别评定3组患者的认知状况;采用抑郁自评量表（SDS）评定抑郁症状的严重度。结果：治疗3个月,SSD组和抑郁症组的言语智商、操作智商、总智商、记忆商数均较治疗前明显提高（P〈0.05或P〈0.01）;WCST总应答数显著减少,分类数显著提高（P〈0.01）;两组SDS评分较治疗前显著下降（P〈0.01）。治疗12个月,两组上述认知指标进一步显著改善,SDS评分与对照组相比差异无显著性（P〉0.05）;但两组指向记忆、联想学习、WCST正确百分数、随机错误数与对照组相比仍未恢复正常（P〈0.01）。结论：SSD患者存在认知功能障碍,治疗后症状虽有缓解,但部分认知功能仍不能完全恢复。     

亚综合征性抑郁30例认知功能临床分析

目的探讨亚综合征性抑郁（subsyndromal sympdomalic depression,SSD）认知功能状况及临床特征。方法 30例符合SSD诊断标准的初诊患者作为观察组,30例符合CCMD-3抑郁症诊断标准的初次住院患者作为对照组,运用抑郁自评量表（SDS）、中国科学院心理研究所等编制的临床记忆量表甲套测验、中国修订的韦氏成人智力量表（WAIS-RC）,对2组患者治疗前进行测试比较,治疗用药均为氟西汀,观察期均为3个月,治疗结束再进行SDS测评。结果 SDS测试结果：2组治疗前均存在抑郁症状,对照组抑郁症状严重程度高于观察组,2组比较差异有统计学意义（P〈0.05）;2组治疗后抑郁症状明显改善,差异有统计学意义,提示观察组疗效优于对照组。临床记忆量表测试结果：除指向记忆、人像特点联想回忆外,2组比较差异无统计学意义,提示2组均存在记忆障碍,而对照组记忆障碍程度较严重。WAIS-RC测试结果：2组总分比较差异有统计学意义（P〈0.05）,各分测验除领悟、数字广度、图片排列、图形拼揍外,其余各项比较差异无统计学意义（P〉0.05）,提示2组均存在智力障碍,而对照组程度较严重。结论 SSD与抑郁症同样存在明显的认知功能缺损,但抑郁症认知损害程度及范围较SSD明显,认为SSD与抑郁症具有共同的特殊生物学基础。SSD可能是抑郁症的一个临床亚型,常规抗抑郁药物结合心理干预治疗效果较好。     

乙醇对中枢神经系统γ-氨基丁酸受体和转运体的作用

γ-氨基丁酸(GABA)是中枢神经系统一种重要的抑制性神经递质,中枢GABA能突触传递改变与乙醇的神经毒性作用有关,本文着重介绍乙醇对GABA受体各亚型亚单位的表达、功能及GABA转运体功能的影响,以了解其在乙醇毒性作用中所起的作用,为预防及治疗乙醇中毒及乙醇依赖提供新思路.     

氯硝西泮预处理对癫痫大鼠海马区γ-氨基丁酸A受体γ2亚单位表达的影响

目的 探讨氯硝西泮预处理对癫痫大鼠海马区γ-氨基丁酸A受体γ2亚单位(GABAARγ2)表达的影响.方法 60只健康雄性SD大鼠随机分为假手术组、癫痫组和氯硝西泮预处理组;癫痫组再分为6h、12 h、1 d、3d、7d、15 d和30 d7个亚组;药物预处理组再分为假预处理组、预处理6h、12h和ld亚组.药物预处理组给予氯硝西泮6 mg/(kg·d)分2次灌胃,连续5d;然后癫痫组和预处理组通过向大鼠海马C3区注射海人酸建立颞叶癫痫模型;采用免疫组化法在相应时点检测各组大鼠海马区GABAARγ2的表达.结果 与假手术组比较,癫痫组CA1区癫痫发作ld后、CA3区癫痫发作后各时间点GABAARγ2表达明显下降(P＜0.05 ～0.01).与癫痫组相应亚组比较,预处理6h、12 h亚组海马CA3区及预处理ld亚组海马CA1区及CA3区GABAARγ2的表达明显增高(P＜0.05～0.01).结论 氯硝西泮预处理可上调癫痫大鼠海马区GABAARγ2的表达.     

亚综合征抑郁研究进展

对亚综合征抑郁的研究进行综述。     

γ-氨基丁酸与脑缺血损伤

近年来研究发现,脑缺血损伤中除能量耗竭等机制外,谷氨酸过量释放引起的神经兴奋毒性是导致神经元死亡的主要原因。而γ-氨基丁酸是哺乳动物中枢神经系统抑制性递质,具有突触后抑制作用,减轻细胞损伤,并能通过突触前抑制,减少谷氨酸的释放,共同拮抗谷氨酸的毒性作用。动物实验证明,γ-氨基丁酸受体激动剂有确切的脑保护作用。此类药物可能为临床防治缺血性脑血管病提出一条新的出路。     

γ-氨基丁酸和脑缺血

γ-氨基丁酸(GABA)作为中枢神经系统内的最重要的抑制性神经递质,在脑缺血诱发的神经元死亡中的作用开始受到重视,GABA能药物在许多动物脑缺血模型中均显示良好的神经保护作用。本文重点在于阐述GABA神经传递在脑缺血诱发的神经元死亡中的作用,并提供缺血诱发的神经元死亡与     

精神分裂症与γ-氨基丁酸信号转导系统的研究进展

本文是对精神分裂症与γ-氨基丁酸信号转导系统的研究进展做一综述。     

精神分裂症与γ-氨基丁酸系统关系的研究进展

近年来有研究开始关注γ-氨基丁酸(γ-aminobutyric acid,GABA)系统,认为该系统在精神分裂症发病中起重要作用[1].脑内GABA由脑内含量最高的氨基酸-谷氨酸在谷氨酸脱羧酶(glutamic acid decarboxylase,GAD)的催化作用下脱羧而成.     

γ-氨基丁酸能神经元在丙泊酚缓解抑郁模型大鼠电休克后脑损伤中的作用

目的探讨γ-氨基丁酸(γ-aminobutyric acid,GABA)能神经元在丙泊酚缓解抑郁大鼠电休克(electroconvulsive shock,ECS)后学习记忆损伤中的作用。方法将慢性温和不可预见性应激(chronic unpredictable mild stress,CUMS)法建模成功的36只抑郁症模型大鼠随机分为丙泊酚+电休克组、电休克组和抑郁组,另设同批次未建模的12只健康大鼠为对照组。丙泊酚+电休克组用丙泊酚联合电休克治疗,电休克组行电休克治疗,抑郁组与对照组行伪电休克处理。治疗完毕行Morris水迷宫实验评估大鼠空间学习记忆能力;ELISA法检测海马GABA浓度;免疫组化法和Western-blot检测海马GABAARα5的蛋白表达。结果Morris水迷宫实验结果提示,电休克组逃避潜伏期最长,空间探索时间最短(P<0.05);电休克组和丙泊酚+电休克组比抑郁组逃避潜伏期延长,空间探索时间缩短(P<0.05);与对照组比较,其余各组逃避潜伏期缩短,空间探索时间延长(P<0.05)。蛋白表达方面,与对照组相比,抑郁组GABA含量下降,GABAARα5表达水平降低(P<0.05),电休克组和丙泊酚+电休克组GABA含量和GABAARα5蛋白表达升高(P<0.05);与电休克组相比,丙泊酚+电休克组GABA含量下降,GABAARα5蛋白表达升高(P<0.05)。结论丙泊酚在电休克过程中具有脑保护作用,其机制可能与上调海马GABA能神经系统相关递质和受体的表达有关。     

Subsyndromal symptomatic depression: a new concept

Although DSM-IV acknowledged the clinical significance of some subthreshold forms of unipolar depression, such as minor depression (MinD) and recurrent brief depression (RBD), clinicians continued to struggle with the concept of "subthreshold" depression. A substantial number of patients continued to present with depressive symptoms that still did not satisfy any DSM-IV diagnosis. Generally, these patients failed to complain of anhedonia and depressed mood, a criterion that DSM-IV mandates for any diagnosis of depression. Therefore, researchers reexamined the question of whether this cluster of depressive symptoms, in the absence of anhedonia and depressed mood, was clinically significant. Some researchers labeled this cluster of symptoms, "subsyndromal symptomatic depression" (SSD). Specifically, SSD is defined as a depressive state having two or more symptoms of depression of the same quality as in major depression (MD), excluding depressed mood and anhedonia. The symptoms must be present for more than 2 weeks and be associated with social dysfunction. Using Medline Search, the authors reviewed the literature on the epidemiology, demographics, clinical characteristics, and psychosocial impairment of SSD. SSD is found to be comparable in demographics and clinical characteristics to MD, MinD, and dysthymia. SSD is also associated with significant psychosocial dysfunction as compared with healthy subjects. Further; it has significant risk for suicide and future MD. Few studies have been conducted on the treatment of SSD. The high prevalence of SSD, the significant psychosocial impairment associated with it, and the chronicity of its course make subsyndromal symptomatic depression a matter for serious consideration by clinicians and researchers.     

丝裂原活化蛋白激酶/胞外信号调节蛋白激酶的激酶基因多态性与亚综合征抑郁的关联性分析

目的:探讨丝裂原活化蛋白激酶/胞外信号调节蛋白激酶的激酶(MEK)基因多态性与亚综合征抑郁(SSD)的关系。方法:收集SSD患者(SSD组)143例和正常对照200名(正常对照组)的外周静脉血,提取基因组DNA。采用TaqMan探针SNP基因分型技术,检测两组受试者MEK1基因(rs1549854与rs4255740)和MEK2基因(rs7258366与rs12459484)共4个SNP位点的基因型,并分析基因多态性与SSD的关系。结果:SSD组和正常对照组MEK基因的4个位点的基因型和等位基因频率比较,差异均无统计学意义(P均>0.05)。结论:MEK基因rs1549854、rs4255740、rs7258366及rs12459484其4个位点的基因型及等位基因频率与SSD的发生可能无关。     

Effect of concurrent anxiety on response to sertraline and imipramine in patients with chronic depression

Anxiety commonly complicates the clinical presentation of depression and has been associated with poorer long-term outcome, but little information is available on the clinical correlates, and comparative effect on treatment response, of subsyndromic or secondary anxiety. Patients diagnosed with chronic major or double depression were randomized to 12 weeks of double-blind treatment with either sertraline or imipramine in a 2:1 ratio. A high anxiety subgroup was operationally defined by a HAM-D anxiety/somatization factor score > or = 7. The effect of study treatment was measured utilizing the HAM-D, CGI, HAM-D anxiety/somatization factor, as well as a quality of life measure (Q-LES-Q) and a measure of psychosocial functioning (the MOS-SF-36). Two hundred nine patients were treated with imipramine and 426 patients were treated with sertraline. Thirty-six percent of the total met criteria for the high anxiety subgroup. According to Kaplan-Meier probability estimates, patients with significant concurrent anxiety symptoms were more likely to respond by 12 weeks (66.4%) than those without significant anxiety symptoms (54.2%). There was no significant difference in response rates for sertraline vs. imipramine. Both drugs were effective at treating high baseline levels of anxiety, with 60% of sertraline patients and 58% of imipramine patients having 50% or greater reduction from baseline in HAM-D anxiety/somatization factor scores, and only 4.6% and 9.9%, respectively, reporting treatment-emergent worsening in anxiety at study endpoint. Despite the chronicity of depressive illness, acute treatment with both sertraline and imipramine significantly improved psychosocial and quality of life measures. High baseline levels of anxiety did not reduce overall antidepressant response but did somewhat delay the onset of response to sertraline or imipramine in patients with chronic depression.     

文拉法辛与舍曲林治疗抑郁症对照研究

目的：比较文拉法辛与舍曲林治疗抑郁症的临床疗效和安全性。方法：将76例抑郁症患者随机分为文拉法辛组（38例）和舍曲林组（38例）,疗程6周。采用汉密尔顿抑郁量表17项（HAMD）评定疗效,治疗中出现的症状量表（TESS）评定不良反应和安全性。结果：文拉法辛组治疗1周起效;疗程结束时,两组疗效和HAMD评分差异无显著性,不良反应少而轻。结论：文拉法辛与舍曲林治疗抑郁症疗效相似,文拉法辛起效较快。     

艾司西酞普兰治疗老年抑郁症的疗效

目的：探讨艾司西酞普兰治疗老年期抑郁症的疗效与安全性。方法：61例老年期抑郁症患者随机分为艾司西酞普兰组31例和舍曲林组30例治疗6周,采用汉密尔顿抑郁量表（HAMD）,临床大体印象量表（CGI）,治疗中出现的症状量表（TESS）评定疗效及不良反应。结果：治疗6周,两组各量表评分均较治疗前有显著改善（P〈0.01）,艾司西酞普兰组治疗1周比舍曲林组改善显著（P〈0.05）,提示西酞普兰组起效快,有效率93.5%,舍曲林组为90%,两组疗效相当（P〉0.05）,两组不良反应轻微,无需特殊处理。结论：艾司西酞普兰治疗老年期抑郁症疗效显著,安全性高,起效快,耐受性好。     

Sertraline treatment of elderly patients with depression and cognitive impairment

BACKGROUND: There is little information on the efficacy and side effects of antidepressant treatment in elderly patients with combined depression and cognitive impairment without dementia (DEP-MCI), and it is unclear if cognitive performance improves with antidepressant response in these patients. METHODS: In 39 elderly DEP-MCI patients, changes in depression and cognitive impairment were evaluated with open sertraline treatment up to 200 mg/day for 12 weeks. RESULTS: Of the 26 completers, 17 were responders and nine were non-responders. Diagnostic subtype of depression was unrelated to response. ANCOVA on WAIS-R digit symbol percent change scores revealed a significant effect for responder status (F = 5.59, p < 0.03), and age (F = 0.24, p < 0.64) and education (F = 1.64, p < 0.22) were not significant covariates. From pre-trial to post-trial, responders improved in WAIS-R digit symbol percent change scores (Mean -10% SD 24) while non-responders declined (Mean 14% SD 18; t = 2.60, p < 0.02). Other neuropsychological measures were unrelated to response. Percent change in HRSD scores showed significant inverse correlations with percent change in several cognitive measures. CONCLUSIONS: DEP-MCI patients showed moderate clinical response to sertraline treatment. When responders were compared to non-responders, cognitive improvement was limited to one measure of attention and executive function. Overall, there was little cognitive improvement with antidepressant treatment. The findings indirectly suggest that lack of improvement in cognition following treatment of depression in DEP-MCI patients may be associated with increased risk of meeting diagnostic criteria for dementia during follow-up.