综合性医院医学心理科会诊的回顾性分析

目的：探讨综合性医院医学心理科会诊情况。方法：2004年9月至2009年9月期间医学心理科会诊534例,分析其申请科室、申请理由以及精神障碍的诊断和处理。结果：综合性医院医学心理科会诊中最常见的精神科诊断是脑器质性精神障碍、躯体疾病所致精神障碍、神经症和心境障碍。结论：应在综合医院积极开展会诊-联络精神病学服务颇为重要。     

综合性医院精神科会诊210例分析

通过综合性医院精神科会诊２１０例分析，发现在综合性医院临床各科存在大量精神医学问题。会诊主要原因是躯体疾病出现精神障碍（５７．６％）及躯体化症状（２６．２％）要求诊断和处理；内科会诊占首位（６７．６％），其中神经内科最多（１９．５％），其次是心血管内科（１３．８％）和消化内科（１３．３％）；病种以器质性精神障碍最多见（４１．０％），其次是神经症（２１．４％），以焦虑症及抑郁性神经症为多见；躯体疾病心理反应（１３．０％）也不少，症状以情绪焦虑、抑郁为常见表现。作者认为，在综合性医院设置精神种，开展会诊一联络精神病学工作甚为必要。     

综合医院精神心理科会诊患者特点分析

目的 了解综合医院精神心理科联络会诊的原因、患者的科室分布、病种构成及处理情况,以更好地指导精神心理科医生的联络会诊工作,为进一步完善会诊精神医学在综合医院内的发展提供参考.方法 本研究采用回顾性方法复习综合医院住院患者的精神科会诊情况,分析在现代医学模式下综合医院的患者对精神卫生服务需求的特点,汇总2012年1月-2013年12月精神心理科联络会诊病历,资料完整者共612例,对一般人口资料、各科会诊人数及病种构成、会诊原因、诊断、处理构成等情况进行描述分析.结果 全部临床科室都有邀请精神心理科会诊,比例最高的科室前5位为：神经内科113例（18.5％）、心血管内科83例（13.6％）、消化内科69例（11.3％）、干部科56例（9.2％）、急诊科52例（8.5％）.病种主要为神经症性、应激相关的及躯体形式障碍151例（24.7％）,心境障碍139例（22.7％）,器质性精神障碍108例（17.6％）,伴有生理紊乱和躯体因素的行为综合征84例（13.7％）;精神科用药以SSRIs类药物、非典型抗精神病药物及苯二氮革类应用较多.结论 综合性医院各科存在较多的精神医学问题,住院患者伴发的精神障碍涉及各类疾病,综合医院就诊的患者精神心理障碍应引起重视,精神科会诊联络非常重要,可以提高临床各科医师对精神障碍的认识,减少或消除人们对精神科会诊的顾虑与不信任,提高会诊效率,治疗躯体疾病的同时应及时使用心理和药物等多种干预手段,使患者得到全面康复,从而提高患者的生命质量.     

综合性医院精神科会诊178例分析

作者对综合性医院精神科会诊178例分析发现，会诊的主要原因是躯体疾病伴发精神障碍(38.2%）及原患精神疾病又患躯体疾病(32．0％)要求诊断和处理，内科会诊占首位(34.3％)，以器质性精神障碍(36．5％)最多见；其次为神经症(18．8％)，以癌症为多见，随后为精神障碍(8．4％)；会诊后44．8％病人转精神科治疗，未转科者使用精神活性药物治疗者占17.9％，综台治疗占11．8％，心理治疗占8．5%。作者建议，在综台性医院设置精神科，开展会诊一联络精神病学(CLP)工作甚为必要。     

综合医院住院病人精神科会诊病例的临床分析

本文报告一综合医院一年度的精神科会诊情况，总会诊率１．８１％，会诊率无性别差异，＞６０岁年龄组会诊率最高（３．２％）。会诊科室以内科和传染科会诊率最高（分别为４．８％和３．２％）。会诊诊断以器质性精神障碍为主，占会诊病例的８５．７％，经精神科处理后，总有效率达７０％。     

综合综合精神科会诊185例分析

目的探讨会诊--联络精神病学在综合性医院的作用.方法回顾性的分析3年中综合性医院精神科向非精神科提供的185次会诊资料.结果在185次会诊中,男性72例(38.9%),女性113例(61.1%),男/女11.6,平均年龄(51±14.7)岁;急会诊40例(21.6%),一般会诊145例(78.4%);有自杀行为者29例(15.7%);会诊诊断脑器质性及躯体疾病所致精神障碍82例(44.3%),神经症61例(33.0%),精神分裂症和情感性精神障碍21例(11.4%),精神活性物质所致精神障碍13例(7.0%);会诊医嘱的总执行率达94.9%,治疗总有效率92.1%.结论综合医院内精神科会诊可及时发现和治疗各科患者的精神障碍,更好地落实医学模式的转变.     

综合性医院联络精神会诊291例分析

目的对综合性医院精神联络会诊进行分析研究．方法对一所综合性医院291例住院病人精神联络会诊资料进行回顾分析，以了解联络精神会诊于综合性医院的应用情况。结果邀请会诊的科室以内科最多(43．3％），会诊形式以普通会诊为主(69.4％)．躯体疾病伴发精神障碍要求协助诊治是会诊的主要原因(44．3％)。非精神科医生对精神疾病普遍认识不够，对精神障碍的实际诊断率和诊断符合率偏低，分别为51．9％和35，6％，能于会诊前使用精神药物仅22.7％。结论在综合性医院应大力开展联络精神会诊，这有利于提高精神科与非精神科医生业务水平，全方位提高医院诊治病人的能力。     

郑州市综合医院精神科院际会诊102例回顾分析

目的探讨郑州市综合医院开展精神科院际会诊的现状及临床特点。方法对2010-01—2011-12郑州市综合医院邀请郑州大学第一附属医院精神医学科或郑州市第八人民医院进行精神科院际会诊102例患者的一般情况、邀请会诊医院及科室分布、原发病、会诊原因、会诊后诊断及治疗情况进行回顾性调查、统计和分析。结果邀请精神科会诊的综合医院以二级医院居多,会诊科室中内、外科占前两位,最常见的精神科诊断依次是:抑郁症、神经症、器质性精神障碍、精神分裂症等。结论二级以上综合医院应开设精神、心理科以及时处理院内各科患者的精神、心理问题。未设置精神、心理科的综合医院,开展精神科院际会诊,既有利于临床各科各类精神障碍患者得到及时、准确的专科诊治,又有利于会诊—联络精神病学的发展,同时应加强综合医院各科医生精神、心理知识的教育培训。     

综合性医院住院病人的会诊精神病学

目的:探讨在综合医院设置精神科开放式病房后精神病学会诊的现状,方法:对我院近20年290例申请会诊的住院病人的科,地诊前后的论断对照,误诊情况及转科治疗情况进行分析.结果:总会诊率为1.38%,申请会诊的科室以内科最多138例(47.6%),会诊的精神科疾病中多见的是神经症84例(29.0%),躯体疾病致精神障碍60例20.7),器质性精神障碍50例(17.2%),精神分裂症37例(12.8%),误诊病例85例(29.3%),转科治疗64例(22.1%),结论:精神科会诊在综合医院呈增加趋势.综合设置精神科开放式病房既有利于精神科的发展,也有利于各类有精神障碍的患者得到及时妥善的治疗.     

内科住院病人精神科会诊213例分析

目的：探讨综合医院内科住院病人精神科会诊的现状。方法：对我院近3年来213例内科住院病人申请科学会诊的临床资料进行回顾性分析。结果：近3年来内科申请精神科会诊的 病例数逐年上升。申请会诊的科室,以神经内科最多,其次为心血管内科、呼吸内科、内分泌科和消化内科,会诊后精神科疾病以器质性精神障碍居多（46．4％）,其次为神经症（32．4％）及精神分裂症（7．0％）。申请会诊的病人中40例（18．8％）转入精神科治疗。结论：内科住院病人常伴发精神障碍,并有逐年增加的趋势,对普通内科医师加强精神科专业知识的培训,将有利于患有各类精神障碍的病人得到及时妥善的治疗。     

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.     

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.     

雷公藤内酯对癫痫大鼠神经元P13K／Akt／mTOR蛋白的影响

目的通过检测癫痫大鼠海马神经元P13K、Akt和mTOR蛋白表达,探讨雷公藤内酯抑制癫痫大鼠神经元凋亡的分子机制。方法30只大鼠随机分为对照组、海人酸组、雷公藤内酯干预组,免疫组化法检测各组大鼠海马神经元P13K、Akt和mTOR蛋白的表达情况。结果海人酸组神经元胞体皱缩,形态不规则,数量减少,而雷公藤内酯干预组神经元的数量和形态与对照组相似,海人酸组海马神经元P13K、Akt、ITITOR蛋白表达与对照组比较均减少,而雷公藤内酯干预组海马神经元的P13K、Akt、mTOR蛋白表达均较海人酸组增加,差异均有统计学意义（P〈0．05）。结论雷公藤内酯可能通过上调P13K／Akt／mTOR信号通路蛋白表达对癫痫大鼠海马神经元发挥保护作用。     

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.     

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。     

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.     

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.