青少年生活事件应激的绘画特征

目的 探索青少年生活事件应激与房树人测验绘画特征的联系,为青少年生活事件应激评估研究提供新思路.方法 对937名青少年进行生活事件评定和房树人测验.对具有不同绘画特征的青少年生活事件总应激量及各因子应激量进行统计分析.结果 青少年生活事件应激相关的绘画特征有果实（β=-4.887）、房子大小（β=-2.378）、地平线（β=4.420）、人物涂黑（β=3.324）、尖锐部分（β=-3.135）、动物（β=4.605）、下雨雪花（β=-9.655）和画面简单（β=3.283）.结论 房树人测验对青少年生活事件应激评定具有一定的辅助参考价值.     

树木测验在青少年自尊水平调查中的应用

目的 探索青少年自尊水平与树木测验绘画特征的联系,为青少年自尊水平评估研究提供新思路。方法 对1053名青少年进行自尊水平评定和树木测验。结果 青少年自尊水平为（29．26±4．832）分,男生自尊水平高于女生,差异有统计学意义（t=2．929,P〈0．01）。青少年自尊水平相关绘画特征有果实（β=0．138）、重复线务（β=0．103）、太阳（β=0．098）、树根（β=0．091）、树冠凌乱（β=0．093）、树干强调（β=0．095）和鸟（β=0．088）。结论 树木测验对青少年自尊水平评定具有一定的辅助参考价值。     

苯丙胺类兴奋剂所致精神障碍首次发病患者认知功能的研究

目的:探讨首次发病住院苯丙胺类兴奋剂(ATS)所致精神障碍患者的认知功能特点及其影响因素。方法:采用韦氏记忆量表(WMS-RC)、连续操作测验(CPT)、威斯康星卡片分类测验(WCST)评定80例首发ATS所致精神障碍患者(研究组)和80名健康人(对照组)的认知功能;采用简明精神病量表(BPRS)评定患者病情严重程度。对影响神经心理学测验成绩与BPRS进行逐步多元回归分析。结果:研究组WCST中的总应答数、持续错误数、随机错误数显著高于对照组(F=10.87～68.78,P0.01或P0.001);正确应答数、完成分类数、记忆商数、数字累加、短时记忆、瞬时记忆、连续操作测验正确数均显著低于对照组(F=4.92～114.20,P0.05或P0.001)。研究组总应答数和持续错误数与BPRS总分呈正相关(β=0.26,P=0.01;β=0.20,P=0.02);随机错误数与敌对猜疑分呈正相关(β=0.23,P=0.02);正确应答数与思维障碍分呈负相关(β=-0.25,P=0.01);完成分类数与缺乏活力分呈负相关(β=-0.25;P=0.01);记忆商数和长时记忆与焦虑忧郁分呈负相关(β=-0.32,P=0.00;β=-0.25,P=0.00);短时记忆和瞬时记忆与缺乏活力分呈负相关(β=-0.36,P=0.00;β=-0.32,P=0.00);CPT正确数与BPRS总分呈负相关(β=-0.34,P=0.00)。结论:首发ATS所致精神障碍患者的记忆、注意和执行功能等明显减退,临床症状严重程度越大,认知功能损害越大。     

自我概念在应激性生活事件与抑郁、焦虑之间的调节效应分析

目的检验自我概念在青少年应激性生活事件与抑郁、焦虑情绪之间的调节效应。方法应用青少年生活事件量表、Wallace自我概念量表、Beck抑郁自评量表和Beck焦虑量表等对732名大学生进行测查,运用分层回归分析来检验调节效应。结果应激性生活事件、自我概念、抑郁和焦虑之间均两两显著相关。交互作用项"应激×自我概念"的回归系数在以抑郁和焦虑为因变量的回归方程中均达显著水平(β=-0.111,t=-3.377,P=0.001;β=-0.086,t=-2.489,P=0.013)。结论自我概念在应激和抑郁、焦虑情绪之间起调节效应,应激对自我概念差者的抑郁、焦虑情绪影响更大。     

中学生交往焦虑的相关因素分析

目的 研究中学生交往焦虑水平及其相关影响因素,为有针对性地采取干预措施提供依据.方法 采取分层整群随机抽样的方法,在长沙市抽取2 216名中学生,采用自制一般情况问卷、交往焦虑量表、青少年生活事件量表和自尊量表进行调查.结果 (1)中学生交往焦虑平均分为(41.46±8.299)分,主要体现在与异性交往、社交自信心、陌生社交环境等方面.(2)农村、非独生子女、单亲家庭中学生的交往焦虑显著高于城市、独生子女、非单亲家庭中学生,差异具有统计学意义(t=6.527,-3.760,3.806,P＜0.01).家庭经济条件越差、家庭关系越不和睦、父母要求越不严格、家庭暴力越频繁,中学生的交往焦虑越高,差异具有统计学意义(F=29.962,30.399,6.626,11.565,P＜0.01).(3)中学生交往焦虑与负性生活事件及自尊评分均显著正相关(r=0.347,0.397,P＜ 0.01).(4)中学生交往焦虑的相关危险因素有农村、非独生子女、单亲家庭、家庭经济条件差、家庭不和睦、父母要求不严格、家庭暴力、负性生活事件以及低自尊.结论 中学生交往焦虑的影响因素较多,应根据其影响开展针对性的心理健康教育及预防性干预.     

原发性失眠症患者认知功能的研究

目的:探讨原发性失眠症患者认知功能损害的特点。方法:采用神经心理测验包括韦氏记忆(数字累加、视觉再认、视觉再生、联想学习)、数字广度、数字划消、连线测验和威斯康辛卡片分类测验(WCST)分别对35例原发性失眠症患者(失眠组)和30名健康对照者(正常对照组)进行注意力、记忆力、执行功能等方面的测评;同时应用匹兹堡睡眠质量指数量表(PSQI)、抑郁自评量表(SDS)、焦虑自评量表(SAS)分别评定失眠及伴随的焦虑、抑郁症状的严重程度。结果:失眠组在数字累加、视觉再认、视觉再生、联想学习、数字广度测验的数字倒背、数字划消测验中的注意力失误率、连线测验B及BA完成时间和WCST测验的各项成绩(除正确应答数外)均明显差于正常对照组(F=4.646~28.224,P0.05或P0.01)。失眠组数字累加分与病程呈负相关(r=-0.558,P=0.001);联想学习分与PSQI评分呈负相关(r=-0.405,P=0.019);连线测验B-A时间与病程呈正相关(r=0.405,P=0.019);WCST持续错误百分比与SDS分呈正相关(r=0.309,P=0.045)。结论:原发性失眠症患者存在广泛认知功能损害,其病程、失眠程度以及伴随的焦虑抑郁情绪是导致认知功能损害的影响因素。     

青少年精神分裂症首次发病患者脑灰质体积与认知功能的相关性

目的:探讨首发青少年精神分裂症患者脑灰质体积与认知功能的关系。方法:33例首发青少年精神分裂症患者(患者组)和28名性别、年龄、右利手、受教育程度与之相匹配的正常对照组进行神经心理测评,包括连线测验、符号编码、词语流畅性测验、霍普金斯词语学习测验-修订版(HVLT-R)、简易视觉记忆测验-修订版(BVMT-R)、Stroop色词测验(ST-1、ST-2、ST-3)及迷宫测验和结构磁共振扫描(s MRI);用基于体素的形态学方法(VBM))分析比较两组脑灰质体积。结果:患者组除连线测验成绩显著高于正常对照组外(t=2.08,P0.05),符号编码(t=-4.36)、HVLT-R(t=-3.74)、BVMT-R(t=-4.83)、ST-1、ST-2、ST-3(t=-3.08,t=-3.85,t=-3.62)及迷宫测验(t=-3.14)成绩明显低于正常对照组(P0.01或P0.001)。患者组右侧颞上回及右侧颞中回脑灰质体积较正常对照组明显减小(t=-3.868,t=3.964;P均0.001)。Pearson相关分析显示,患者组符号编码(r=0.373,P=0.032)及迷宫测验评分(r=0.356,P=0.042)与右侧颞中回脑灰质体积正相关。结论:首发青少年精神分裂症患者存在脑灰质体积异常;这可能与认知功能广泛损害相关。     

首次发病的青少年精神分裂症患者执行功能的研究

目的:探讨首次发病的青少年精神分裂症患者执行功能及其与精神症状的关系. 方法:采用威斯康星卡片分类测验(WCST)及韦克斯勒记忆量表第3版(WMS-Ⅲ)空间广度测验测试75例首次发病的青少年精神分裂症患者(病例组)和80名健康对照者(对照组)的执行功能;病例组同时应用阳性和阴性症状量表(PANSS)评定病情. 结果:病例组WCST的错误总数、持续反应数和持续错误数显著高于对照组,正确总数显著低于对照组(P均＜0.01);WMS-Ⅲ总分和空间广度逆行分显著低于对照组(P均＜0.05).病例组PANSS阴性症状分与WMS-Ⅲ空间广度逆行分及总分负相关(r=-0.276,r=-0.230;P均＜0.05);阳性症状分与WCST完成分类数负相关(r=-0.258,P＜0.05);一般病理学总分与WMS-Ⅲ空间广度逆行分负相关(r=-0.244,P＜0.05). 结论:首次发病的青少年精神分裂症患者执行功能显著受损,并与病情有关.     

重庆市儿童青少年焦虑抑郁发生情况调查

目的 调查重庆市儿童青少年焦虑抑郁发生情况,为儿童青少年学生心理疏导提供参考.方法 通过整群抽样选取儿童青少年学生425名,年龄范围为7～16岁,采用儿童焦虑性情绪障碍筛查量表及儿童抑郁障碍自评量表对被试进行评估.结果 ①34.6％(147/425)的青少年存在焦虑情绪,9.9％(42/425)的青少年存在抑郁情绪;5.6％(24/425)同时存在焦虑抑郁情绪,33.2％(141/425)仅有焦虑或抑郁情绪,61.2％(260/425)无情绪问题.②男性、女性间焦虑抑郁情绪分布差异具有统计学意义(x 2=12.592,P＜0.05),男性中66.1％的无任何情绪问题,25.3％仅存在焦虑情绪,5.6％仅存在抑郁情绪,3.0％存在焦虑抑郁情绪;女性中55.2％的无任何情绪问题,33.3％仅存在焦虑情绪,2.6％仅存在抑郁情绪,8.9％存在焦虑抑郁情绪.不同性别间焦虑得分差异具有统计学意义(t=4.638,P＜0.05),抑郁情绪得分差异无统计学意义(t=0.672,P＞0.05).③年龄与焦虑(r=-0.42,P＞0.05)、抑郁情绪(r=0.071,P＞0.05)间相关关系无统计学意义,焦虑情绪与抑郁情绪评分之间存在相关关系(r=0.420,P＜0.001).结论 儿童青少年焦虑抑郁发生率较高,需要给予积极心理关注.     

抗抑郁剂疗效的预测因素分析

目的:探索影响抑郁症患者抗抑郁剂疗效的预测因素。方法:241例抑郁症患者给予抗抑郁药治疗6周,治疗前后进行汉密顿抑郁量表17项(HAMD)评分,采用减分率评定疗效。分析人口学因素、基线HAMD、明尼苏达多项人格测定(MMPI-2)、认知功能评分及脑源性神经营养因子(BDNF)、5-羟色胺转运体(5-HTTLPR)和糖皮质激素受体(GR)3种基因多态对疗效的预测。结果:基线HAMD评分(β=0.771,P0.001)、MMPI-2中偏执(Pa)分(β=-0.322,P=0.032,R2=0.451)、连线测验B评分(TMT-B)(β=-0.045,P=0.013)、汉诺塔总分(β=-0.067,P=0.026)、数字广度(倒序)分(β=-0.974,P=0.025)及GR BclI基因G-等位基因携带者(P=0.05)与抗抑郁剂HAMD减分率有关。整合模型回归分析显示,结合基线HAMD评分(β=0.894,P0.001)、MMPI-2-Pa分(β=-0.155,P=0.036)和TMT-B分(β=-0.038,P=0.034)3个预测因子可解释57.1%的变异。结论:基线HAMD评分、MMPI-2-Pa分和TMT-B分可预测抗抑郁剂的疗效。     

Edema and neuronal apoptosis in the hippocampus and cortex of elderly rats following transient cerebral ischemia/reperfusion injury

BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.     

Environmental factors in the development and progression of late-onset Alzheimer＇s disease

Late-onset Alzheimer＇s disease （LOAD） is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.     

Total saponins of Panax ginseng effects on proliferation and differentiation of human embryonic neural stem cells and in a Parkinson’s disease mouse model

BACKGROUND： Total saponins of Panax ginseng （TSPG） exhibits neuroprotection against Parkinson＇s disease in the substantia nigra. OBJECTIVE： To investigate the effects of TSPG on human embryonic neural stem cells （NSCs） proliferation and differentiation into dopaminergic neurons using in vitro studies, and to observe NSC differentiation in a mouse model of Parkinson＇s disease, as well as behavioral changes before and after transplantation. DESIGN, TIME AND SETTING： In vitro neural cell biology trial and in vivo randomized, controlled animal trial were performed at the Institute of Basic Medical Sciences, Chongqing Medical University between September 2004 and December 2007. MATERIALS： TSPG （purity 〉 95%） was isolated, extracted, and identified by Chongqing Academy of Chinese Materia Medica. Recombinant human basic fibroblast growth factor （bFGF） and recombinant human epidermal growth factor （EGF） were purchased from PeproTech, USA. A total of 25 C57/BL6J mice, aged 18-20 weeks were included. Twenty were used to establish a Parkinson＇s disease model with i.p. injection of MPTP （1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine） and TSPG alone or combined with interleukin-1 （IL-1）-treated NSCs prior to transplantation into the corpus striatum. The remaining five mice were pretreated for 3 days with TSPG prior to MPTP injection, serving as the TSPG prevention group. METHODS： Primary NSCs were isolated, cultured and purified from embryonic cerebral cortex. Immunocytochemistry was employed to detect specific antigen expression in the NSCs. In vitro experiment： （1） to induce proliferation, NSCs were treated with TSPG, EGF＋bFGF, or TSPG＋EGF＋bFGF, respectively; （2） to induce dopaminergic neuronal differentiation, NSCs were treated with TSPG, IL-1, or TSPG＋IL-1, respectively. MAIN OUTCOME MEASURES： In vitro experiment： the effects of TSPG on NSCs proliferation were evaluated with flow cytometry and MTT assay. Tyrosine hydroxylase expression was determined by immunocytochemistry assay to observe effects of TSPG on dopaminergic neuronal differentiation. In vivo experiment： differentiation of grafted NSCs in the mouse brain was determined by immunohistochemical staining. Behavioral changes were evaluated by spontaneous activity frequency, memory function, and score of paralysis agitans. RESULTS： （1） NSCs were cultured and passaged for more than three passages. Immunocytochemistry revealed positive nestin staining, as well as neurofilament protein and glial fibrillary acidic protein. （2） TSPG significantly increased NSC proliferation, in particular when combined with EGF and bFGF, which was twice as effective as FGF or bFGF alone. TSPG also induced dopaminergic differentiation in NSCs, in particular when TSPG was added together with IL-1, resulting in an effect five times greater than that of IL-1 alone. （3） At day 30 following transplantation, most NSCs in the TSPG prevention group differentiated into dopaminergic neurons, and the scores of paralysis agitans, spontaneous activity, and memory function were significantly increased compared with TSPG alone or TSPG＋IL-1 groups （P 〈 0.05）. CONCLUSION： TSPG stimulated NSC proliferation, in particular when combined with FGF and bFGF. TSPG significantly induced dopaminergic neuronal differentiation of NSCs, and the effect was greater when combined with IL-1. In addition, TSPG greatly improved behavior in the Parkinson＇s disease mouse model following NSC transplantation. Following NSC transplantation, TSPG pretreatment exhibited superior efficacy over either TSPG alone or TSPG in combination with IL-1, in terms of behavioral improvements in the Parkinson＇s disease mouse model.     

Targeting 13-secretase with RNAi in neural stem cells for Alzheimer＇s disease therapy

There are several major pathological changes in Alzheimer＇s disease, including apoptosis of cho- linergic neurons, overactivity or overexpression of 13-site amyloid precursor protein cleaving enzyme 1 （BACE1） and inflammation. In this study, we synthesized a 19-nt oligonucleotide targeting BACE1, the key enzyme in amyloid beta protein （AI3） production, and introduced it into the pSilenCircle vector to construct a short hairpin （shRNA） expression plasmid against the BACE1 gene. We transfected this vector into C17.2 neural stem cells and primary neural stem cells, resulting in downregulation of the BACE1 gene, which in turn induced a considerable reduction in reducing AI3 protein production. We anticipate that this technique combining cell transplantation and gene ther- apy will open up novel therapeutic avenues for Alzheimer＇s disease, particularly because it can be used to simultaneously target several pathogenetic changes in the disease.     

Disrupted structural and functional brain connectomes in mild cognitive impairment and Alzheimer＇s disease

Alzheimer＇s disease （AD） is the most common type of dementia, comprising an estimated 60-80% of all dementia cases. It is clinically characterized by impairments of memory and other cognitive functions. Previous studies have demonstrated that these impairments are associated with abnormal structural and functional connections among brain regions, leading to a disconnection concept of AD. With the advent of a combination of non-invasive neuroimaging （structural magnetic resonance imaging （MRI）, diffusion MRI, and functional MRI） and neurophysiological techniques （electroencephalography and magnetoencephaJography） with graph theoretical analysis, recent studies have shown that patients with AD and mild cognitive impairment （MCI）, the prodromal stage of AD, exhibit disrupted topological organization in large-scale brain networks （i.e., connectomics） and that this disruption is significantly correlated with the decline of cognitive functions. In this review, we summarize the recent progress of brain connectomics in AD and MCI, focusing on the changes in the topological organization of large-scale structural and functional brain networks using graph theoretical approaches. Based on the two different perspectives of information segregation and integration, the literature reviewed here suggests that AD and MCI are associated with disrupted segregation and integration in brain networks. Thus, these connectomics studies open up a new window for understanding the pathophysiological mechanisms of AD and demonstrate the potential to uncover imaging biomarkers for clinical diagnosis and treatment evaluation for this disease.     

阿尔茨海默病治疗的研究进展

阿尔茨海默病（AD）是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5～10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。     

墨蝶呤还原酶基因与精神分裂症相关性的研究进展

墨蝶呤还原酶（SPR）催化四氢生物蝶呤（BH4）从头合成途径的最后一步反应。SPR基因遗传缺陷或突变可导致BH。的合成紊乱,影响单胺类神经递质（如多巴胺、5-羟色胺及谷氨酸等）的合成或释放,进而参与包括精神分裂症在内的多种神经精神系统疾病的发生发展过程。此外,SPR基因敲除小鼠表现出持续增强的自主活动等类精神分裂症症状,说明该基因在精神分裂症的发病中扮演重要的角色。进一步研究SPR基因及其单核苷酸多态性的功能,可为阐明精神分裂症的发病机制提供重要的线索,也为新一代抗精神病药物的研制及开发开拓新的视野。现对SPR基因与精神分裂症的相关研究做一综述。     

Wnt信号通路与骨髓间充质干细胞增殖及分化的关系

骨髓间充质干细胞（bonemarrow—derived mesenchymal stem cells,BMSCs）是骨髓中不同于造血干细胞的一类细胞,其来源丰富,取材简便,易分离、纯化、培养,在一定的条件下可以迅速体外扩增,具有多向分化潜能,可以通过不同的方法被诱导分化成骨细胞、软骨细胞、肌细胞、神经胶质细胞、神经元细胞等,而且它具有低免疫源性,向病变部位迁移的能力,     

癫痫与自杀

自杀而导致死亡被为是增加癫痫患者死亡率的最重要原因之一。国外许多研究报道都表明癫痫患者的自杀率比普通人群的自杀率高几倍到二十几倍。可能导致癫痫患者自杀的危险性因素是有多方面的,本文将从5-HT、抗癫痫药及癫痫手术治疗、精神病理等方面对癫痫患者可能存在自杀危险因素进行综述,并希望在癫痫的综合治疗中对这些危险因素能加以考虑。     

喹硫平与SSRIs治疗难治性抑郁症对照研究

目的 探讨喹硫平与SSRIs合用与SSRIs治疗难治性抑郁症的临床疗效及安全性.方法 将80例难治性抑郁症患者随机分为两组各40例,研究组口服喹硫平与SSRIs治疗,对照组口服SSRIs药物治疗.观察9个月,于治疗前及治疗1,3,6,9个月.束采用汉密尔顿抑郁量表和副反应量表评定临床疗效和不良反应,生存质量量表评定患者的生存质量.结果 治疗9个月末,研究组有效率90.0%,对照组为72.5%,研究组显著高于对照组（x2=4.02,P＜0.05）.结论 喹硫平对难治性抑郁症疗效肯定,能显著改善患者的生存质量.