110例精神发育迟滞调查分析

作者于１９９０年４月对兰州市某城镇和农村１５岁以上人口进行了精神发育迟滞的流行学调查，共查出精神发育迟滞患者１１０例，患病率２．５７‰，其中男性患病率２．８１‰，女性患病率２．２５‰，两者无显著差异（Ｐ＞０．０５）。城市患病率２．１９‰，农村患病率３．８４‰，以农村显著较高（Ｐ＜０．０１）。在各年龄组中以１５～２９岁组患者为最多。先天性因素所致者较多。家庭经济水平及文化程度低的人群中较多     

安徽阜阳市精神发育迟滞流行病学调查

目的：了解阜阳市城乡精神发育迟滞患病率及其发生的危险因素。方法：于2000年11月在阜阳市区和3县农村进行精神疾病流行病学调查，共调查≥15岁者33332人。以成人智残评定量表测定智力及进行残疾评定，以CCMD－2－R为诊断标准。结果：共检出中、重度精神发育迟滞患者91例，患病率及残疾率均为2．73‰。随年龄增加患病率有逐步降低趋势，男性患病率高于女性，农村高于城市，单身者占绝大多数。近亲婚配、地区经济落后，母亲文化均为较重要的危险因素。结论：应在经济欠发达的农村及边远地区，大力普及优生优良知识，并将精神发育迟滞为重点防治疾病之一。     

1 486例0～3岁精神发育迟滞的初步分析

精神发育迟滞是指智力明显低下和社会适应能力障碍、发病在18岁以前的一组疾病。我国10亿多人口中,14岁以下儿童占3亿多,3岁以下儿童9000多万。1981年南京地区在36776名14岁以下儿童中查得重度精神发育迟滞城、乡患病率为5.79‰。轻度更多于中、重度,男多于女,农村多于城镇。观察自1979～1988年的门诊患儿33533例。其中0～3岁共2231例,占门诊总数的6.65％,其中男     

中国七个地区精神发育迟滞流行病学调查

目的了解９０年代精神发育迟滞患病率的变化。方法于１９９３年在７个地区进行流行病学调查。在１９８２年调查方法的基础上，增加儿童用韦克斯勒智力量表对７～１４岁患儿进行智商测查和适应行为判定；用成人智残评定量表评定≥１５岁患者的智力残疾。结果在≥１５岁人口（１９２２３人）中精神发育迟滞的患病率为２．８４‰（６２例），较１９８２年（３．３３‰）有降低趋势（Ｐ＞０．０５）；成人智力残疾平均分为１１．２７分，６２例均为中度及其以上智力残疾。结论精神发育迟滞应列为精神疾病防治重点之一。     

河北省承德地区精神疾病流行病学调查

目的：了解河北省承德地区18岁及以上人群各类精神疾病的时点患病率和分布特点。方法：2004年10月至2004年11月采用多阶段分层整群随机抽样方法，抽取≥18岁者为调查对象。用一般健康问卷（CHQ-12）将调查对象分为高、中、低危险组，以美国精神障碍诊断与统计手册第4版（DSM-Ⅳ）轴Ⅰ用定式临床检查患者版进行调查，用DSM-Ⅳ对精神障碍进行诊断。结果：3025人完成调查，精神疾病总时点患病率为177．19‰，终生患病率为216．86‰。除精神发育迟滞和痴呆外，各类精神疾病时点患病率为175．86‰，终生患病率为215．54‰。时点患病率农村为（176．65‰），城市为（180．08‰）；女性（182．05‰）高于男性（171．94‰）。重性抑郁障碍患病率最高（51.57‰）。结论：本调查基本掌握了河北省承德地区18岁及以上人群各类精神障碍的患病水平和分布特点。     

宁夏同心县回族癫痫流行病学调查

目的调查宁夏回族人群癫痫患病率、发病率及治疗缺口,为回族人群癫痫的防治提供依据。方法通过随机、整群抽样,选取宁夏同心县豫海镇和石狮镇,分别作为城镇及农村代表地区进行调查;采用统一的癫痫流行病学调查表进行入户调查,对初步筛查的癫痫患者经由神经科医师再次确诊。结果实际调查11917例,确诊癫痫患者60例,癫痫患病率为5.03‰。其中城镇患病率为6.61‰,农村为3.37‰,城市和农村地区癫痫患病率存在显著性差异;回族男性与女性癫痫患病率无显著差异;回族儿童(≤14岁)癫痫患病率为8.43‰,高于其他年龄组;70%的患者癫痫的首次发作在儿童时期;癫痫患者的年龄在3月~51岁之间,其中儿童占40%(24/60),城镇癫痫患者的平均年龄为16.38±11.78岁,农村癫痫患者的平均年龄为30.05±14.63岁;在活动性癫痫患者中,正规接受抗癫痫治疗的患者为25.9%(15/58),治疗缺口为74.1%;在所有发作类型中,全面强直阵挛发作者46例,占75.0%;回族癫痫发病率为75.5/100000例。结论宁夏回族人群癫痫患病率城镇高于农村,儿童高于其他年龄组;回族癫痫发病率高于全国平均水平;回族癫痫患者治疗缺口大,需要对该地区进行政策支持并加强宣传,提高患者的就诊率,控制癫痫发作。     

潍坊市第三次精神障碍流行病学调查

目的了解和掌握潍坊市各类精神障碍患病率,城、乡患病率及其分布特征。方法采用分层、整群、随机抽样、抄户口入户,在18岁以上家庭成员中用随机数字表抽出1人作为调查对象。结果共调查了4763人,发现各类现症病人781例,既往病人30例,患病率170.27‰,排在前5位的分别是心境障碍(51.02‰),酒精使用障碍(50.18‰),焦虑障碍(47.66‰),精神分裂症(10.29‰)和精神发育迟滞(5.67‰)。城市患病率180.36‰,高于农村患病率166.95‰,但无显著性差异(P>0.05)。男、女性患病率无显著性差异(P>0.05)。结论潍坊市的各类精神障碍患病率均有非常显著增长,心境障碍增长迅速,和精神分裂症一起仍是目前防治重点。搞好精神卫生工作,有利于和谐社会的构建。     

农村社区精神卫生工作：四川新津的试点研究

一、四川省精神卫生工作概况1.精神病患病率 1987年抽样调查,各类精神病的总现患病率为4.66‰(不包括精神发育迟滞)。推算全省有精神病人48万左右。95％可信限为43.7万—52.3万,其中51.0 %为精神分裂症。各地区患病率:川西高原及西南山区、平原地区患病率高于盆周山区及盆地丘陵地区(U=7.9,p<0.01)。城市与农村患病率为3.67‰及4.74‰,两者无显著性差异(u=1.58,p>0.05)。     

116例精神发育迟滞司法精神医学鉴定分析

１１６例精神发育迟滞司法精神医学鉴定分析王增辉罗雪莲我院于１９８９～１９９２年期间接受司法精神医学鉴定２８９例，其中１１６例（４０．１％）被鉴定为精神发育迟滞。其中男７８例，女３８例。年龄１４～６５岁（平均３２．５岁）。已婚３１例，未婚８０例，离婚３...     

基诺族精神病,精神发育迟滞和癫痫的10年随访调查

对基诺族精神病、精神发育迟滞和癫痫进行１０年随访。精神病终身患病率前后为４．０３‰，３．８５‰，现患病率为２．８８‰，２．８８‰。精神病平均年发病率为９．６１／１０万人口。精神分裂症的现患病率前后为２．４２‰，２．４０‰，男性明显高于女性。随访表明，精神分裂症在自然状态下预后很差，社会性结局不好。精神发育迟滞现患病率前后为１．８４‰，２．９８‰，平均年发病率为１５．３８／１０万人口。癫痫（大发作）     

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.     

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。     

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.     

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.     

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.     

Dysfunctional autophagy in Alzheimer＇s disease： pathogenic roles and therapeutic implications

Neuronal autophagy is essential for neuronal survival and the maintenance of neuronal homeostasis. Increasing evidence has implicated autophagic dysfunction in the pathogenesis of Alzheimer＇s disease （AD）. The mechanisms underlying autophagic failure in AD involve several steps, from autophagosome formation to degradation. The effect of modulating autophagy is context-dependent. Stimulation of autophagy is not always beneficial. During the implementation of therapies that modulate autophagy, the nature of the autophagic defect, the timing of intervention, and the optimal level and duration of modulation should be fully considered.     

Oxidative stress in Alzheimer＇s disease

Oxidative stress plays a significant role in the pathogenesis of Alzheimer＇s disease （AD）, a devastating disease of the elderly. The brain is more vulnerable than other organs to oxidative stress, and most of the components of neurons （lipids, proteins, and nucleic acids） can be oxidized in AD due to mitochondrial dysfunction, increased metal levels, inflammation, and β-amyloid （Aβ） peptides. Oxidative stress participates in the development of AD by promoting Aβ deposition, tau hyperphosphorylation, and the subsequent loss of synapses and neurons. The relationship between oxidative stress and AD suggests that oxidative stress is an essential part of the pathological process, and antioxidants may be useful for AD treatment.     

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。