成都市综合医院门诊抑郁和焦虑障碍调查

目的:调查成都市综合医院门诊患者抑郁和焦虑障碍的患病率.方法:对成都市3所综合医院神经内科、消化科、心内科及妇科门诊的1 780例就诊者使用医院焦虑抑郁量表(HADS)进行筛查.HADS评分≥8分者使用国际神经精神科简式访谈问卷(MINI5.0.0)进行诊断评定,最后根据美国精神障碍诊断和统计手册第四版(DSM-IV)...     

综合医院与精神专科医院抑郁障碍患者的临床特征比较

目的 比较不同性质医疗机构精神科门诊抑郁障碍患者的临床特征和治疗情况.方法 使用一般情况调查表和简明国际神经精神访谈对综合医院和精神专科医院精神科门诊100例抑郁障碍患者进行调查,对不同性质医疗机构患者的临床特征和治疗情况进行比较分析.结果 综合医院精神科门诊抑郁障碍患者的年龄和首次抑郁发作的年龄都大于精神专科医院患者(P ＜ 0.01).综合医院患者抑郁发作时有不典型症状的比例高于精神专科医院(P ＜ 0.05),而精神专科医院患者中有焦虑症状(P ＜ 0.05)、复发性抑郁(P ＜ 0.01)和有精神病性症状(P ＜ 0.05)的比例均高于综合医院,自杀风险的等级也高于综合医院(P ＜ 0.05).综合医院精神科门诊抑郁障碍患者使用苯二氮类药物的比例较高(P ＜ 0.05),而精神专科医院心境稳定剂的使用比例较高(P ＜ 0.05).两类医院中抗精神病药物的使用和是否有精神病性症状的内部一致性均不高(Kappa ＜ 0.4).结论 综合医院的抑郁障碍患者的临床表现更多不典型的特征,抑郁障碍的药物治疗情况也与专科医院不同,值得临床注意和深入分析.     

北京地区综合医院患者抑郁障碍的患病率

目的了解综合医院患者抑郁障碍(目前为抑郁发作的心境障碍)的患病率。方法由精神科护士采用抑郁症诊断筛查量表对分层抽样的北京50家综合医院顺序就诊的2877例门诊患者和2925例住院患者进行筛查,然后由精神科医师在盲法下采用美国《精神障碍诊断与统计手册》第4版(DSM-IV)配套的轴Ⅰ障碍用临床定式检查患者版(SCID-I/P)》对筛查阳性和10%筛查阴性者进行半定式精神科检查,以确定最后诊断。结果综合医院患者抑郁障碍的现患率、年患病率和终生患病率分别为5.23%、5.72%和8.22%;其中重性抑郁障碍的相应患病率分别为2.94%、3.46%和5.32%。结论北京地区综合医院患者抑郁障碍总的现患率并不显著高于我国普通人群。     

上海某综合性医院内科门诊患者焦虑与抑郁症状调查

目的调查综合性医院内科门诊患者的焦虑和抑郁症状的发生率及不同性别、年龄、文化程度和职业间的差异。方法采用综合性医院焦虑抑郁量表（HADS）在上海某三级综合性医院4个普通内科门诊按10∶1随机调查6117例患者,有效回收完整量表6104例。HADS每个亚量表评分大于等于8分即表示存在焦虑或抑郁症状。结果调查对象中焦虑和抑郁的检出率分别为9.5%（95%CI=8.8%～10.2%）和23.0%（21.9%～24.1%）。其中30岁以下、文化程度高、职业为学生或无业者的人群,焦虑检出率较高;男性、60岁及以上、文化程度低、职业为农民或学生的人群抑郁检出率较高。结论上海三级综合性医院内科门诊患者焦虑和抑郁的发生率较高,应提高识别率,给予有效的预防和干预。     

继续教育思考题

1.不同性质医疗机构精神科门诊抑郁障碍患者的说法正确的是()A.综合医院患者年龄小于精神专科医院患者B.综合医院患者抑郁发作时有不典型症状的比例高于精神专科医院C.精神专科医院患者中焦虑症状低于综合医院D.精神专科医院患者中自杀风险的等级高于综合医院     

综合医院不同科室门诊多躯体症状患者抑郁、焦虑障碍的检出率及症状分布特点——一项多中心横断面研究

目的:描述综合医院不同科室门诊中多躯体症状患者的躯体、抑郁和焦虑症状分布特点及抑郁障碍、焦虑障碍检出率。方法:对国内6个综合医院中医科、西医内科和精神/心理科门诊候诊患者连续筛查,并完成简明国际神经精神障碍访谈(MINI)。结果:本研究共纳入491例受试者,其中多躯体症状组(SOM+)237例(48.3%)。SOM+患者最常受困扰的抑郁症状为疲劳和睡眠问题等;其抑郁或焦虑障碍的检出率为50.4%。此外,尽管躯体症状严重程度相似,在心理科就诊的SOM+患者抑郁或焦虑障碍的检出率更高(34.6%,43.9%,76.2%;χ~2=17.1,P0.01)。结论:综合医院门诊多躯体症状患者中抑郁或焦虑障碍的检出率较高;疲劳和睡眠问题是多躯体症状患者中最常见症状。     

综合医院门诊患者焦虑抑郁症状的筛查研究

目的 了解综合性医疗机构门诊就诊患者的焦虑和抑郁症状。方法 采用非概率抽样方 法对中国12 个城市的19 家三级甲等医院门诊患者进行调查研究。研究时间为2017 年3— 8 月。门诊患 者使用手机接入医院免费的无线网络时收到推送的调查问卷,匿名填写患者健康问卷-9（PHQ-9）和广 泛性焦虑障碍问卷（GAD-7）。结果 32 631 例门诊患者完成PHQ-9 和GAD-7 填写。8 945 例抑郁症状筛 查阳性,阳性率为27.41%,其中70.30% 的患者同时伴有中度以上的焦虑症状。焦虑症状筛查阳性率为 38.29%,6 285 例患者抑郁症状和焦虑症状均筛查阳性,共病率达19.26%,女性筛查阳性率均略高于男 性。结论 三级甲等综合医院门诊患者抑郁、焦虑症状筛查阳性率较高,且共病情况较严重。     

神经内科门诊患者焦虑与抑郁症状的调查研究

目的 探讨综合医院神经内科门诊患者焦虑与抑郁症状的特征及影响因素.方法 调查河南省人民医院神经内科门诊患者,采用综合医院焦虑抑郁量表(HADS)和自制问卷.从年龄、性别、文化程度、职业和健康状况等多因素进行调查.结果 神经内科门诊患者焦虑症状阳性者占所有就诊患者的34.8%,抑郁症状阳性者占39.8%;伴发神经内科疾病组的焦虑/抑郁分和阳性率均高于无神经内科疾病组;焦虑和抑郁症状的发生与患者的年龄、性别、文化程度有密切关系.结论 神经内科门诊患者焦虑与抑郁症状是一种普遍现象,女性多于男性,随着年龄的增大其发生率呈增加趋势,高学历人群更易患焦虑与抑郁症状.     

以躯体不适为主要症状的抑郁症误诊分析

目的分析综合医院中伴有躯体不适的抑郁症误诊情况,提高早期诊治率.方法将各科以躯体不适就诊经多方治疗无效而转来我院精神科门诊的患者,进行汉密顿抑郁量表(HAMD)评分,分值≥18分,且符合CCMD-2-R抑郁症诊断标准者80例,给予氟西汀治疗8周,进行疗效评定.结果80例患者中,轻、中度抑郁占82.5%,重度抑郁占17.5%.有77.5%的初诊患者的第一主诉是躯体不适和睡眠障碍,而不是抑郁症状.氟西汀治疗8周后,HAMD评分明显下降.结论对综合医院抑郁症患者及时识别、诊断,适当应用抗抑郁剂可有效缓解抑郁症状和躯体症状,减少不必要的检查和治疗,有利于患者的早日康复.     

三甲综合医院心血管内科门诊原发性高血压患者抑郁障碍的现患率及相关因素

目的调查三级甲等综合医院心血管内科门诊原发性高血压患者抑郁障碍的现患率及其相关因素。方法 5名精神科专业人员对876例心血管内科门诊原发性高血压患者采用《美国精神疾病诊断与统计手册第四版》轴I精神障碍临床定式访谈中文版进行抑郁障碍的评估,并收集其社会人口学资料和临床特征因素。结果三甲医院门诊原发性高血压患者抑郁障碍的现患率为16.6%(145/876),高血压患者抑郁障碍的危险因素为女性(OR=2.817,95%CI:1.161~6.885)、年龄65岁及以上[以35~49岁为参照(OR=1.747,95%CI:1.118~2.688)]、无婚姻关系(OR=2.023,95%CI:1.203~3.398)、三级高血压[以一级为参照(OR=1.776,95%CI:1.226~2.333)]和冠心病(OR=2.018,95%CI:1.427~2.587)。结论三甲医院心血管内科门诊原发性高血压患者抑郁障碍患病率高,临床上需要予以重视。     

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.     

大学生生活事件、应对方式和睡眠质量的关系

目的 探讨生活事件、应对方式与大学生睡眠质量的关系,为学校心理健康教育及临床治疗提供依据.方法 采取整群随机抽样方法,抽取某师范院校大学生180名(均为住校生)为研究对象,采用匹兹堡睡眠质量指教(PSQI)、青少年生活事件量表(ASLEC)及简易应对方式问卷对大学生进行测量.结果 (1)大学生睡眠问题检出率为17.2％；(2)大学生的生活事件与睡眠质量呈显著正相关(r=0.320,P＜0.01)；消极应对方式与睡眠质量呈显著正相关(r=0.247,P＜0.01).PSQI总分高低分组在生活事件及消极应对方式使用上均存在显著差异；(3)生活事件对睡眠质量有显著预测作用,消极应对方式在社交焦虑对睡眠质量的预测中起部分中介作用.积极应对方式没有中介效应.结论 生活事件对大学生睡眠质量有显著预测作用,消极应对方式具有显著中介作用.     

过度觉醒与失眠

原发性失眠或者心理生理性失眠的症状主要包括入睡困难、睡眠维持难或者再入睡困难,并伴随有日间功能障碍.近年来的研究表明原发性失眠患者在自主神经活动、神经内分泌、神经免疫、神经电生理和神经影像学等方面与正常睡眠者相比存在着过度唤醒现象.提高正常睡眠者的生理觉醒水平1周后就会产生失眠患者的继发症状,而正常睡眠者即使给予睡眠干扰也不会产生典型的失眠症状.这些证据表明了提高生理性觉醒水平就会产生失眠和其他伴随症状.因此,降低失眠患者的觉醒水平有望成为治疗失眠患者的新策略.     

睡眠紊乱与躁狂发作

睡眠紊乱作为情感障碍的常见症状已成为共识,在DSM-IV躁狂的诊断标准中[1],睡眠需求减少是七条诊断条目之一,对多导睡眠图的研究表明,睡眠减少的躁狂患者REM潜伏期缩短-而REM与情感功能密切相关[2].近年来许多证据表明睡眠紊乱会导致躁狂发作同时也可以作为躁狂发作的预测指标,同样,在躁狂治疗时改善睡眠质量也是重要的治疗手段,本文就近年来有关双相躁狂睡眠障碍的研究综述如下.     

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.     

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.     

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。