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。     

会诊联络精神病学在综合医院的现状分析

目的对综合医院精神病学会诊现状进行分析研究。方法2007年度申请精神科会诊的病例279例,分析其申请科室、原发病、申请理由及精神科诊断处理。结果综合医院精神病学会诊中最常见的精神科诊断是脑器质性精神障碍、躯体疾病伴发精神障碍、焦虑障碍和抑郁障碍。结论应在综合医院积极开展会诊联络精神病学服务及对综合科医生加强精神病学知识教育。     

某综合医院168例老年住院患者精神科会诊-联络资料分析

目的 了解综合医院老年患者精神(心理)服务需求的特点.方法 选取2010年1月～2012年12月某综合医院老年精神科会诊的168例患者,对其社会人口学资料、会诊科室、会诊原因、精神科诊断及治疗等进行分析.结果 在申请会诊的各科室中,前三位分别为神经内科(34.5％)、呼吸内科(19.1％)、高干病房(10.1％);常见会诊原因依次为以谵妄为主的意识障碍(20.8％)、躯体不适(19.6％)、焦虑抑郁(17.9％)、睡眠障碍(11.9％);会诊常见诊断主要为脑器质性精神障碍(34.5％);处理方式主要包括药物治疗及心理治疗等.结论 综合医院老年患者对精神(心理)服务需求大,精神科会诊联络服务有助于住院老年患者全面诊断和治疗.     

四川省成都市三级综合医院门诊就诊者睡眠障碍的现况调查

目的 通过流行病学调查,以研究成都市三级综合性医疗机构门诊就诊者睡眠障碍的现况和医务人员的识别及处治现状.方法 随机抽取综合医院四个门诊科室的调查日期,使用焦虑抑郁量表(HADS)和病人15项健康状况量表(PHQ-15)对门诊就诊者睡眠情况以及躯体症状进行评估,所有HADS评分(抑郁和/或焦虑)≥8分的就诊者由精神科医师用国际神经精神科简式访谈问卷(MINI)进行检查确定诊断.结果 三级综合医院门诊中有56%就诊者存在睡眠障碍,发病年龄集中在30～45岁,主诉最多为头昏、头痛,占17%;其次为腹痛,为13.1%;神经内科门诊就诊者中睡眠障碍现患率最高,为63%;有睡眠障碍的患者检出抑郁或(和)焦虑的比例为25%;门诊非精神科医师对患者精神系统疾病的认识率普遍偏低,仅有9.1%;患者愿意到精神科接受治疗仅占42.6%.结论 三级综合性医疗机构门诊就诊者睡眠障碍发生率较高,而非精神科医师对患者精神系统疾病的认识率普遍偏低.     

非精神科医师对精神障碍处理现状调查

目的：了解上海市非精神科医师对精神障碍处理的能力和方式。方法：对上海市7家医院的1016名非精神科临床医师进行了自制问卷调查。结果：非精神科医师在临床工作中对患者的精神状况或情绪的关注存在较大差距;对可能有精神障碍的患者大多数医师会选择请精神科人员进行会诊;有近三分之一的医师对精神卫生知识培训存在消极态度。结论：非精神科医师对精神障碍识别和处理能力需要进一步提高。     

重视综合性医院双相障碍的诊断问题

双相障碍是指既有符合症状学诊断标准的躁狂或轻躁狂发作,又有抑郁发作的一类心境障碍.双相障碍一般呈发作性病程,躁狂和抑郁常反复循环或交替出现,但也可以混合方式存在,是一种高致残、高负担的重性精神障碍,对患者的社会功能产生不良影响.综合医院和基层医疗机构通常是双相障碍患者首次就诊机构.据估计,在综合医院所有就诊人群中,双相障碍的比例约为10％左右,而在精神科门诊可达20～30％[1-4].在发达国家,双相障碍往往首诊于全科医师执业的基层医疗机构,所以他们强调要重视在基层医疗机构的双相障碍的正确诊断问题.在我国,全科医学正在起步,患者常在综合医院的非精神科就诊,因此,更要强调综合医院中双相障碍的误诊和漏诊.     

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     

综合医院住院患者对会诊联络服务的需求

目的：调查综合医院住院患者对精神科会诊联络服务（CLS）的需求。方法：对我院临床各科申请精神科会诊的住院患者,共131例,进行精神科会谈,得出精神障碍的诊断及治疗建议;并对患者进行综合医院焦虑抑郁量表（HADS）及综合医院住院患者精神科会诊联络服务需求临床调查表评估和调查。结果：①精神科会诊率为1．37％（95％可信区间：1．14％-1．59％）,精神科会诊后精神障碍的诊断：神经症性、应激相关以及躯体形式障碍为30．5％（n=40）,器质性精神障碍22．2％（n=29）,心境障碍16．0％（n=21）,与生理紊乱和躯体因素有关障碍12．2％（n=16）,精神分裂症,分裂性障碍和妄想性障碍9．9％（n=13）。②综合医院焦虑抑郁量表评分：焦虑症状检出比例为37．9％（39／103）,抑郁症状检出比例为61．2％（63／103）。③对精神科治疗的需求：72．8％患者对精神药物治疗表示兴趣;57．3％对心理社会治疗有兴趣。④需求相关因素：患者对精神药物治疗需求与3个因素有关：是否有焦虑症状（P：0．001）,既往是否接受过精神科药物治疗（P=0．005）,以及患者最近一段时间（至少1周以内）的睡眠状况（P=0．014）。心理社会支持需求与2个因素有关：是否有焦虑症状（P=0．006）,是否患者自己提出会诊申请（P=0．038）。结论：综合医院住院患者伴发心理社会问题及精神障碍时,对精神药物及心理社会治疗的需求均相当高。     

评《综合医院精神卫生》

由同济大学附属同济医院吴文源教授和复旦大学附属中山医院季建林教授主编、7位青年专家同道撰写的《综合医院精神卫生》一书 ,已于 2 0 0 1年 8月由上海科学技术文献出版社出版。该书系统地阐述了在综合医院中的精神卫生问题 ,内容充实、全面 ,载有大量的新知识信息 ,对在综合医院中开展精神卫生工作有着现实的指导意义。该书共计 2 8万字 ,分为 14章 :脑器质性精神障碍、抑郁障碍、焦虑障碍、躯体形式障碍、心理生理障碍、躯体疾病伴发的精神障碍、临床各科患者的心理问题、精神活性物质所致精神问题、特殊问题、精神分裂症、精神科会诊原…     

病人健康问卷抑郁自评量表（PHQ-9）的临床应用

病人健康问卷（Patient Health Questionnaire-9,PHQ-9）是一个简便、有效的抑郁障碍自评量表,在抑郁症诊断的辅助和症状严重程度评估方面,均具有良好的信度和效度.在基于评估的治疗策略中,PHQ-9可以作为制订治疗方案的参考,以及治疗过程中对疗效的评估工具.PHQ-9的衍生版本PHQ-8,PHQ-2和他评量表PHQ-9-OV,针对不同研究对象,有着相应的临床应用效果.现就PHQ-9在临床的应用及优势进行论述.     

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.     

高血压脑出血的显微外科治疗进展

高血压脑出血（Hypertensive intrac-rebral hemorrhage,HICH）是具有高发病率、高病死率、高致残率的急性脑血管疾病,占所有脑卒中患者的10%-20%,早期病死率可高达49.4%。随着人口老龄化,其发病率逐年提高;而外科手术的干预,使其病死率有所下降,但致残率居高不下。如何提高手术疗效和患者生存质量,一直是神经外科医师努力的方向。微侵袭血肿清除术因其手术创伤小,恢复快,是目前国内治疗高血压脑出血的重要手段。     

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.     

神经内镜联合亚低温治疗高血压基底节区脑出血

目的 探讨神经内镜联合亚低温在治疗高血压基底节区脑出血中的临床应用价值.方法 回顾性分析我院神经内镜治疗高血压基底节区脑出血患者40例的临床资料,并对治疗结果进行分析.结果 神经内镜治疗组22例(甲组),神经内镜联合亚低温治疗组18例(乙组),术后3个月根据GCS评分,甲组恢复良好1例,中残4例,重残6例,植物生存6例,死亡5例;乙组恢复良好4例,中残8例,重残3例,植物生存1例,死亡2例,两组比较差异有统计学意义(P＜0.05).两组颅内压比较第1天两者差异不明显,但第2、3天亚低温组颅内压明显降低.结论 神经内镜是治疗高血压基底节区脑出血较为有效的手术方式,联合亚低温治疗能有效降低颅内压,改善术后神经功能恢复,具有较好的临床应用价值.     

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.     

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.     

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。