综合医院精神科联络会诊6年的变化

目的:比较2008年与2014年综合医院精神科联络会诊的变化。方法:回顾性分析、比较2008年及2014年武汉大学人民医院各科室邀请精神科会诊情况。结果:精神科会诊患者2008年257例,2014年为688例;两年的会诊率、会诊患者的年龄、性别分布差异无统计学意义。与2008年相比,2014年患者单次会诊比例显著增加(Z=4.20,P0.05);内科、妇产科、儿科、五官科、肿瘤科会诊比例显著增高,外科、感染科和老年科会诊比例显著降低(P均0.05);患者因不能解释的躯体症状和既往精神障碍史但目前无症状的会诊比例明显增高,而急性脑综合征和精神病性症状的比例明显降低(P均0.05)。结论:6年间综合医院住院患者对精神科联络会诊需求无明显变化;非精神科医生对患者精神问题的关注增高,但识别能力不足。     

综合医院精神科联络会诊分析

目的:探讨综合医院内精神科联络会诊的分布特征。方法:收集某综合医院1年内精神科联络会诊病例688例,完成自制调查问卷,使用SPSS统计软件进行描述性统计分析。结果:会诊病例最多分布在神经内科(19.3%),其次为心内科(9.7%)、骨科(9.3%)、消化内科(8.9%)、呼吸科(8.7%)以及脑外科(7.0%);患者年龄分布以40~69岁(53.2%)和20~29岁(13.5%)为多;会诊主要原因为急性脑病综合征(25.7%)、精神病性症状(22.8%)、不能解释的躯体症状(12.9%)和既往有精神障碍史而目前无明显症状者(13.8%);会诊诊断主要包括躯体疾病伴精神障碍(21.4%)、精神分裂症和其他精神病性障碍(20.9%)、脑器质性精神障碍(20.1%)等。结论:综合医院精神科联络会诊涉及各科室、各年龄段;主要会诊原因为急性脑病综合征和阳性精神病性症状,而抑郁、焦虑症状关注较少。     

综合医院会诊-联络精神病学10年间变化

目的：了解综合医院会诊-联络精神病学10年变化的情况。方法：对本院1991年和2001年临床各科住院病人邀请精神科会诊的数量、科室分布、精神科诊断与处理情况进行对比分析。结果：年会诊率1991年与2001年分别为0．45％与0．71％，呈上升趋势；会诊的科室以内、外科为主，会诊的疾病种类1991年与2001年前三种疾病仍分别是躯体疾病所致精神障碍、脑器质性疾病所致精神障碍及神经症。结论：综合医院住院病人精神医学问题呈上升趋势，应加强会诊-联络精神病学的研究与推广。     

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.     

综合医院围手术期精神科会诊——联络精神病学临床资料分析

<正>本研究通过回顾性调查综合医院围手术期患者精神科会诊——联络精神病学临床工作情况,旨在发现手术患者的精神状况及联络会诊精神病学工作对其干预的必要性。1对象和方法回顾我院2016年1月1日至2017年12月31日临床各科室申请精神科会诊共计4 369例,其中围手术期785例。收集围手术期会诊申请者的临床学资料,包括患者姓名、性     

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。     

综合医院老年精神科联络会诊：附131例分析

目的了解和探讨综合医院老年精神科联络会诊的特点。方法对申请精神科会诊的131例综合医院老年患者,通过精神检查依照ICD—10进行诊断,并电话随访疗效。结果患者年龄65～109岁,平均（77．62±9．09）岁;会诊请求中最困扰的精神问题为行为障碍（69．5％）,会诊诊断谵妄状态（42．0％）最为常见;会诊后疗效很好和有效的比例分别为36．6％、57．1％。结论综合医院老年精神科会诊有其特点,会诊有助于精神状态的判别和治疗。     

精神科与骨科联合会诊模式对高龄骨折患者术后谵妄识别率及住院时间影响

目的研究精神科与骨科联合会诊模式对高龄骨折患者术后谵妄识别率及住院时间影响。方法选择2015年1月至12月在我院接受治疗的高龄骨折患者180例,随机分为对照组和观察组,每组各90例。观察组在研究开始前由精神科医师对骨科医护人员进行精神卫生知识和谵妄评估量表的培训,为患者提供术前和术后心理咨询,每天采用CAM对患者进行评估,谵妄患者联络精神科医师协助诊疗。对照组接受骨科常规诊疗,出现精神症状后联络精神科医师会诊。结果观察组患者的会诊率为41.11%,而对照组患者的会诊率仅为17.78%,差异有统计学意义(P0.05),两组患者会诊后谵妄、焦虑障碍、抑郁发作等精神疾病的诊断率比较,差异无统计学意义(P0.05)。观察组患者谵妄的识别率为31.11%,对照组患者谵妄的识别率为11.11%,观察组患者的住院时间较短(P0.05)。结论精神科与骨科联合会诊模式可提高老年骨折患者术后谵妄的识别率,缩短住院时间。     

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。     

老年精神科住院患者综合医学会诊的研究

目的 探讨老年精神科住院患者综合医学会诊的临床状况,了解老年精神病患者的自身特征.方法 查阅2001～2003年、2008～2010年我院老年精神科住院患者的综合医学会诊记录共303例,并进行归纳分析.结果 老年精神科住院患者病程长,住院时间长.会诊患者诊断以器质性精神障碍、精神分裂症、心境障碍为多发病种.2001～2003年的器质性精神障碍患者总会诊人数高于2008～2010年,2001～2003年的精神分裂症患者的总会诊人数低于2008～2010年,差异均有统计学意义(P<0.01).2001～2003年的总会诊率低于2008～2010年,差异有统计学意义(P<0.01).会诊因为中,2001～2003年以原有躯体疾病为主,而2008～2010年以首发躯体疾病为主,两者差异有统计学意义(P<0.05).会诊科室以呼吸内科、神经内科、骨科最多.会诊处理中,要求转院和实际转院的人数2001～2003年低于2008～2010年,两者比较有统计学意义(P<0.05或P<0.01).死亡人数占总人数和占会诊人数的比例2001～2003年均大于2008～2010年,差异均有统计学意义(P<0.05).结论 我们需重视老年住院精神病患者的躯体情况,定期进行全面的身体检查,及早发现躯体疾病,及早治疗,应努力提高精神科医生综合医学知识水平.     

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.