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。     

综合医院住院患者抑郁障碍患病率调查

目的调查综合医院住院患者抑郁障碍的现患率及其在不同科室的分布情况。方法首先采用抑郁自评量表（SDS）对2007年5月在某综合医院不同科室住院的863例患者进行调查,然后对筛选有抑郁者和20％的无抑郁者采用美国《精神障碍诊断与统计手册第四版》DSM—IV轴I障碍定式临床检查（SCID—I／P）作为金标准进行抑郁障碍的诊断。结果综合医院住院患者各种抑郁障碍现患率为39．24％,重性抑郁障碍现患率为4．78％、抑郁障碍者中以女性、年龄大者、经济状况差、文化程度低、住院时间长、既往有躯体疾病史及复发情况者居多（x2=37．932,12．447,22．490,19．670,37．932,12．447,22．490,19．670;P均〈0．01）。综合医院医生识别率仅为2．88％。结论综合医院住院患者抑郁障碍患病率高;医生识别率低;女性、年龄大者、经济状况差、文化程度低、住院时间长、既往有躯体疾病史及复发者是抑郁障碍患病的高危人群。     

保定市重性抑郁障碍流行病学调查

目的：了解保定市重性抑郁障碍的患病率、人口学特征和社会生活功能状况。方法：采用多阶段分层整群抽样方法随机抽取≥18岁的人群10073人，以一般键康问卷12项（GHQ-12）为筛选工具，以美国精神障碍诊断与统计手册第4版（DSM-Ⅳ）轴Ⅰ障碍定式临床检查病人版（SCID-I／P）为调查诊断工具。用功能大体评定量表（GAF）评价功能状况。结果：重性抑郁障碍的终生患病率为4．19％（95％CI：3．78％～4．60％）；时点患病率为2．64％（95％CI：2．31％～2．97％）。时点患病率女性3．26％明显高于男性2．00％（u=3．73，P〈0．01）；农村2．84％明显高于城市1．40％（u=2．76，P〈0．01）；50～69岁年龄段患病率较高；单次发作60．80％，复发39．20％；GAF平均为（50．74±6．73）分，社会和生活功能受损明显。结论：重性抑郁障碍的患病率相对较高，严重影响患者的社会生活功能。     

河北省精神障碍的现况调查

目的了解河北省≥18岁人群各类精神障碍的患病率和分布特点。方法2004年10月至2005年3月采用多阶段分层整群抽样方法随机抽取≥18岁人群，共24000名，以美国精神障碍诊断与统计手册第4版（DSM-Ⅳ）轴Ⅰ障碍定式临床检查患者版进行调查，用DSM，Ⅳ对各类精神障碍进行诊断。结果（1）患病率：20716人完成调查，精神障碍的时点患病率为162．43‰[95％可信区间（95％CI）为15．8％-16．7％]，排在前三位的是重性抑郁障碍（27．01‰）、未特定的焦虑障碍（25．09‰）和心境恶劣障碍（23．12‰）；终生患病率为185．12‰（95％CI为18．0％～19．0％），排在前三位的是重性抑郁障碍（47．47‰）、酒精依赖性和滥用性障碍（38．62‰）和未特定抑郁障碍（25．51‰）。（2）时点患病率：女性（167．95‰）高于男性（156．95‰），农村（165．63‰）高于城市（144．31‰），均P〈0．05～0．01；并随年龄的增长而不断上升，其中30～49岁为137．17‰～156．71‰，50-≥70岁为201．44‰～285．41‰。结论河北省精神疾病的患病率较高，其中女性和农村的患病率高；重性抑郁障碍是省内患病率最高的精神疾病。     

ZUNG氏抑郁自评量表（SDS）作为外科住院患者抑郁障碍常规筛查工具的可行性研究

目的探讨ZUNG氏抑郁自评量表（SDS）作为外科住院患者抑郁障碍筛查工具的可行性。方法首先对符合入组条件的293例外科住院患者进行SDS的初步筛查,然后采用美国《精神障碍诊断与统计手册第四版》DSM—Ⅳ轴Ⅰ障碍定式临床检查（Structured Clinical Interview for DSM—Ⅳ Axis Ⅰ Disorders,SCID）作为金标准进行诊断,将SDS筛查抑郁障碍的效能与SCⅡ）对抑郁障碍诊断的金标准进行比较。结果资料完整的266例患者用SDS筛查外科住院患者抑郁障碍发生率为30．8％,用SCID诊断抑郁障碍的发生率为37．18％。外科医师对抑郡障碍的识别率仅为2．53％。SDS筛选抑郁障碍与SCID诊断抑郁障碍的一致性好。结论综合医院外科住院患者抑郁发生率高,外科医师对抑郁障碍的识别率极低,SDS可作为外科住院患者抑郁障碍的常规筛查工具。     

喹硫平治疗心境障碍的作用机制

双相情感障碍，简称双相障碍（BPD），是针对单相情感障碍（重性抑郁）而言。DSM—Ⅳ和ICD-10将二者并列为两种主要心境障碍。顾名思义，双相兼有心境变高和变低两极性特点，是心境在正常，高涨（躁狂），低落（抑郁）之间往返摆动。DSM—Ⅳ将双相障碍又分为若干个亚型，这在诊断上是一个重要变更，突出表现在分出了双相Ⅰ型和双相Ⅱ型，基本区别是前者一般以躁狂发作严重；后者以抑郁发作严重，躁狂发作较轻，且家族史中阳性率高，发作次数多，对治疗反应差。流行病学资料显示，双相Ⅰ型发病率为0．5％～2．4％，双相Ⅱ型发病率为0．2％-5．0％。双相障碍是精神科常见病，多发病，具有较高同病率（焦虑障碍，酒依赖，药物依赖）与较高死亡率（特别是在抑郁相或者混合状态）特点。目前有关躁狂症状的治疗已有很大进展；而抑郁症状则被认为治疗困难，传统抗抑郁药物或心境稳定剂疗效均不佳。美国最近一项研究发现，喹硫平除对躁狂症状（单药或喹硫平＋锂盐／双丙戊酸钠）或精神分裂症疗效明确外，还能控制抑郁症状，从而提高患者生活质量。因此，喹硫平是目前唯一被FDA批准单药既可用于治疗双相躁狂急性发作，     

HCL-32在精神科门诊双相障碍诊断中的应用

目的 了解双相障碍的诊断现状及识别率.方法 将符合DSM-Ⅳ抑郁障碍诊断标准的36例门诊患者使用MDQ和HCL-32进行测评,然后按照DSM-Ⅳ诊断标准对所有完成测试的患者进行晤谈并做出诊断.结果 HCL-32的阳性筛检率（72％）高于MDQ（33％）,差异有统计学意义（x2=10.923,P=0.001）;DSM诊断系统晤谈诊断阳性率为47％与HCL-32的阳性率比较差异无统计学意义（x2=0.332,P=0.471）.结论 HCL-32筛查量表检测阳性率高,能够有效避免漏诊,可作为精神科门诊双相障碍诊断的初步筛查工具.     

保定市特殊恐怖症的流行病学调查

目的探讨保定市民特殊恐怖症的患病率和分布特点。方法2004年10月～2005年3月采用多阶段分层整群抽样方法随机抽取18周岁及以上的人群10073例,用扩展的一般健康问卷（GHQ—12）将调查对象分为高、中、低危险组,采用美国精神障碍诊断标准（DSM—Ⅳ）,以美国精神障碍诊断与统计手册第4版（DSM-Ⅳ）轴Ⅰ障碍定式临床检查病人版对调查对象进行特殊恐怖症的诊断。结果9021例完成调查,特殊恐怖症的终生患病率为0．74％,时点患病率为0．68％;各类型的终生及时点患病率分别为：动物型0．38％、0．36％,自然环境型0．31％、0．27％,其他型0．07％、0．03％;血液-注射-损伤型的终生和时点患病率均为0．09％,情景型仅终生患病率为0．01％。女性时点患病率高于男性;农村时点患病率高于城市;30-39岁的患病率最高,18～19岁的患病率最低。特殊恐怖症的精神科就诊率为2．5％。结论特殊恐怖症常见于年轻的女性,各类型患病率不同,且就诊率低。     

综合医院内精神科会诊的回顾性分析

目的探讨联络精神病学在综合医院中的作用。方法回顾性分析３年内综合医院精神科向非精神科３１０例患者提供的４１１次会诊。结果总会诊率０．６％，其中５９．０３％的患者来自内科；会诊后的诊断主要为器质性疾病所致精神障碍（３６．５％）、神经症（３２．９％）、精神分裂症和情感性精神障碍（共１０６％）；会诊医嘱执行率达９８．１％；精神科问题经会诊处理后的总有效率达８９．２％。结论综合医院内精神科会诊可及时发现和治疗精神障碍，并拓展精神病学业务     

内科住院患者情感性精神障碍的研究

目的了解综合医疗机构患者中情感性精神障碍的患病率。方法对综合医院内科４１７例住院患者进行调查，并以中国精神疾病分类与诊断标准第２版修订本和国际疾病分类第１０版诊断标准进行诊断。结果亚临床抑郁性障碍和焦虑性障碍的患病率分别为２３．７％和３４．８％，重性抑郁症、心境恶劣、惊恐障碍和躯体形式障碍的患病率分别为３．６％、２．４％、１．２％和１．０％；内科医师对情感性精神障碍的识别率仅为１０．５％。结论在综合医疗机构患者中情感性精神障碍的患病率较高，应重视对其研究，并提高综合科医师的识别和处理能力     

视频脑电图在小儿癫痫诊断中的应用

目的评价视频脑电图(video-EEG)在小儿癫诊断中的应用价值。方法对126例具有发作性症状的患儿进行连续8h的包括清醒、睡眠、诱发试验及必要的认知测验的视频脑电图监测。结果经发作期视频脑电图证实,39例初诊为癫性发作的患儿中14例(35%)为非癫性发作;15例其他症状发作中13例(86%)为非癫性发作。64例样放电患儿中51例(80%)确定发作类型,22例(34%)确定癫类型。视频脑电图可发现短暂轻微的癫发作及样放电引起的一过性认知损伤。结论视频脑电图在排除非癫性发作、确定癫性发作的类型、评价脑电-临床关系方面可提供准确可靠的证据,进一步提高癫的临床诊断水平。     

Storage of lipofuscin in neurons in mucopolysaccharidosis

Summary A histochemical and ultrastructural study was made on the brain of a 23-year-old man with Sanfilippo's syndrome. In accordance with previous reports the cortical nerve cells contained a PAS-positive lipid storage substance. This showed intense autofluorescence in UV-light and was positive with various stains for lipofuscin. The storage material appeared ultrastructurally as inclusion bodies composed of short lamellated membranes, granular material, and vacuoles. In addition, concentrically and transversely lamellated membranous cytoplasmic bodies were observed in the nerve cells. It is concluded that the PAS-positive lipid storage material in the neurons was composed partly of lipofuscin in addition to other lipids presumably glycosphingolipids.Supported by a grant from the Expressen Prenatal Research Foundation     

Neuroprotective properties of memantine in different in vitro and in vivo models of excitotoxicity

The pathogenesis of stroke, trauma and chronic degenerative diseases, such as Alzheimer's disease (AD), has been linked to excitotoxic processes due to inappropriate stimulation of the N-methyl-D-aspartate receptor (NMDA-R). Attempts to use potent competitive NMDA-R antagonists as neuroprotectants have shown serious side-effects in patients. As an alternative approach, we were interested in the anti-excitotoxic properties of memantine, a well-tolerated low affinity uncompetitive NMDA-R antagonist presently used as an anti-dementia agent. We explored in a series of models of increasing complexity, whether this voltage-dependent channel blocker had neuroprotective properties at clinically relevant concentrations. As expected, memantine protected neurons in organotypic hippocampal slices or dissociated cultures from direct NMDA-induced excitotoxicity. However, low concentrations of memantine were also effective in neuronal (cortical neurons and cerebellar granule cells) stress models dependent on endogenous glutamate stimulation and mitochondrial stress, i.e. exposure to hypoxia, the mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+) or a nitric oxide (NO) donor. Furthermore, memantine reduced lethality and brain damage in vivo in a model of neonatal hypoxia-ischemia (HI). Finally, we investigated functional rescue (neuronal capacity to migrate along radial glia) by memantine in cerebellar microexplant cultures exposed to the indirect excitotoxin 3-nitropropionic acid (3-NP). Potent NMDA-R antagonists, such as (+)MK-801, are known to block neuronal migration in microexplant cultures. Interestingly, memantine significantly restored the number of neurons able to migrate out of the stressed microexplants. These findings suggest that inhibition of the NMDA-R by memantine is sufficient to block excitotoxicity, while still allowing some degree of signalling.     

Role of vincristine in the inhibition of angiogenesis in glioblastoma

Objective: Vincristine, a microtubule-destabilizing drug, was found to exhibit anti-angiogenic effects and anti-tumoral activity. However, the precise mechanism by which vincristine inhibits angiogenesis in glioblastomas is not well understood. Our aim was to investigate whether vincristine affects vascular endothelial growth factor (VEGF) expression in glioblastoma cells and determine whether it is mediated by the downregulation of hypoxia-inducible factor-1α (HIF-1α).

Methods: We investigated the expression of HIF-1α in glioblastoma tissues resected from patients and in human glioblastoma cell lines using immunohistochemistry, Western blot analysis, and immunocytochemistry. In addition to an MTT assay assessing the effect of vincristine on cell proliferation and viability, the effects of vincristine on VEGF mRNA expression and HIF-1α protein were examined using real-time RT-PCR and Western blot analysis under 1% O₂ (hypoxia).

Results: HIF-1α was expressed in the majority of glioblastoma tissues and was detected mainly in the nucleus. Strong immunoreactivity for HIF- 1 α was found often in the hypercellular zones. Under hypoxic conditions, HIF-1α protein levels in the glioblastoma cell lines increased, primarily localizing into the nucleus similar to glioblastoma tissues. Exposure of glioblastoma cells to vincristine resulted in enrichment of the G₂-M fraction of the cell cycle, which suggests that vincristine-mediated growth inhibition of glioblastoma is correlated with mitotic inhibition. Using doses lower than those found to reduce the viability and proliferation of cells by 50% (IC₅₀), vincristine decreased both the expression of VEGF mRNA and the level of HIF-1α protein in hypoxic glioblastoma cells. In addition, following exposure to vincristine, the expression of VEGF mRNA was correlated with HIF-1α protein levels.

Conclusions: Our results suggest that the mechanism by which vincristine elicits an anti-angiogenic effect in glioblastomas under hypoxic conditions might be mediated, in part, by HIF-1α inhibition.     

脑电图预测痫性发作研究进展

癫痫(epilepsy)是由脑部神经元高度同步化异常放电所致的临床综合征,系神经系统的常见病,困扰着全世界约1%的人群.每次神经元的阵发性放电或短暂的脑功能异常称为痫性发作(seizures).     

Midazolam in treatment of various types of seizures in children

Midazolam is a recently developed water-soluble benzodiazepine that shares anxiolytic, muscle relaxant, hypnotic and anticonvulsant actions with other members of this class. There are limited studies that midazolam can be used successfully to treat seizures in adults and children. In this study, 0.2 mg/kg intramuscular (IM) midazolam was administered to 11 children (eight boys and three girls), aged 3 days to 4 years (mean age 1.8±1.4 years), with seizures of various types. In all but one child, seizures stopped in 15 s–5 min after injection. No side effects were observed. These results suggest that IM administration of midazolam may be useful in a variety of seizures during childhood, especially in case of intravenous (IV) line problem.     

Developmental effects of in vivo and in vitro inhibition of nitric oxide synthase in neurons

The diffusible chemical messenger nitric oxide (NO) is involved in neuronal plasticity and it is, therefore, supposed to play a role in brain development. A shortage of NO during the critical period of brain maturation may theoretically have long-lasting consequences on the organization of the adult brain. We have performed in neonatal rats a chronic inhibition of the enzyme responsible for NO production, nitric oxide synthase (NOS), from postnatal day 3 to postnatal day 23, through administration of the competitive antagonist N-nitro-L-arginine methylester (L-NAME). The calcium-dependent catalytic activity resulted almost completely inhibited throughout the period of treatment and it took more than 4 days after its suspension to get a full recovery. The expression of the neuronal isoform of the enzyme (nNOS), revealed by immunoblotting, was unchanged during the treatment and after it. The histochemical reaction for NADPH diaphorase was reduced at the end of the treatment and recovered in concomitance with the recovery of the catalytic NOS activity. No gross structural alterations were detected in brain morphology. The levels of three neurotransmitter-related and one astrocytic marker were unchanged in the cerebellum, hippocampus and cortex of 60-day-old rats which had been neonatally treated. A similar lack of significant effects on neurochemical brain maturation was also noticed in a parallel series of experiments, in which a short pulse of NOS inhibition was performed at a critical prenatal time of brain development, from gestational day 14 to gestational day 19. In vitro, chronic exposure of cerebellar granule cells to L-NAME (500 microM) resulted in slight decrease of surviving neurons after 8 days in culture and in better resistance to the challenge of stressful culture conditions. The present results suggest that the basic plan of brain organization can be achieved despite an almost complete NOS inhibition during the maturation period. In vitro, NOS inhibition may bring to more pronounced consequences on neuronal viability and function.     

The Burden of Agoraphobia in Worsening Quality of Life in a Community Survey in Italy

ObjectiveCurrent nosology redefined agoraphobia as an autonomous diagnosis distinct from panic disorder. We investigated the lifetime prevalence of agoraphobia, its association with other mental disorders, and its impact on the health-related quality of life (HR-QoL). MethodsCommunity survey in 2,338 randomly selected adult subjects. Participants were interviewed with the Advanced Neuropsychiatric Tools and Assessment Schedule (ANTAS), administered by clinicians. The diagnoses were based on the ICD-10 criteria. The Short-Form Health Survey (SF-12) was used to quantify HR-QoL. ResultsIn the sample, 35 subjects met the criteria for agoraphobia (1.5%), with greater prevalence among women (2.0%) than men (0.9%): odds ratio (OR) 2.23; 95% CI: 1.0-5–2. Agoraphobia was more often seen among those with (n=26; 1.1%) than without (n=9; 0.4%) panic disorder: OR=8.3; 2.9–24.4. Co-morbidity with other mental disorders was substantial. The mean score of SF-12 in people with agoraphobia was 35.2±7.8, with similar levels of HR-QoL in people with (35.3±7.9) or without (34.8±7.3) panic disorder: ANOVA: F(1;33)=0.0; p=1.00. ConclusionOne out of seventy people may suffer from agoraphobia in their lifetime. The attributable burden in terms of HR-QoL is substantial and comparable to the one observed for chronic mental disorders such as major depression, post-traumatic stress disorder, or obsessive-compulsive disorder.     

自噬参与帕金森病发病的研究进展

近年来,蛋白质的降解障碍被认为是帕金森病（Parkinson’Sdisease,PD）发病过程中的重要因素,人们已经公认泛素一蛋白酶体系统（ubiquitin--pro—teasomesystem,UPS）功能异常或衰竭能够导致细胞内异常蛋白蓄积、细胞功能障碍,甚至细胞凋亡。与此同时,蛋白降解的另一条途径——自噬-溶酶体途径（autophagy—lysosomepathway,ALP）也已成为了生命科学领域的研究热点,自噬与神经变性疾病,尤其是PD的关系日益受到人们的重视。