PTSD相关睡眠障碍的概述

创伤后应激障碍（PTSD）是突发威胁性或灾难性事件所致的延迟出现且长期存在的一组精神障碍，以再度体验创伤、回避行为和警觉性增高等为表现。创伤应激后常出现睡眠障碍，尤其那些发展为PTSD者。睡眠障碍是PTSD标志性症状之一，以梦魇和失眠最常见，不仅出现早，严重影响生活质量、健康和well—being，且预示PTSD的发生、程度和转归（Maher等，CNSDrugs，2006）。本文简述了PTSD相关睡眠障碍，现报道于后。     

瓦斯爆炸事件致创伤后应激障碍调查分析

创伤后应激障碍(posttraumatic stress disorder,PTSD)是由于受到威胁性、灾难性心理创伤,导致延长出现和长期持续的精神障碍[1].主要表现为再体验症状、回避症状、过度唤起症状、内疚、愤怒和失落感[2].我们对瓦斯爆炸事件中的相关人员进行调查,结果表明,这次爆炸事故是一次强烈的创伤性应激事件,受伤人员与其他相关人员均有符合第3版<中国精神障碍分类与诊断标准>中PTSD诊断标准[3]的病例,导致受伤者及相关人员广泛普遍的心理痛苦,PTSD发生率较高.     

心理治疗在创伤后应激障碍中的应用及机制 研究进展

创伤后应激障碍（PTSD）是一种严重的精神障碍,心理治疗是创伤后应激障碍常见的治疗 方法。已有研究证实心理治疗对于 PTSD 各种症状改善尤为重要,但目前对于每种心理治疗方法有何 差异,治疗机制、适应的症状有何不同研究较少。现回顾 PTSD 心理治疗的国内外研究,分别对各种心 理治疗适应症状及机制等方面进行综述。     

PTSD大鼠模型的实验研究

创伤后应激障碍(posttraumatic stress disorder,PTSD)是指受到亲身经历或目睹的异乎寻常的威胁性、灾难性事件所致的心理创伤,导致出现长期持续性精神障碍[1]。在竞争日益激烈的现代社会,应激事件日趋增多,PTSD的发生呈明显上升趋势,对PTSD的研究,可有效降低应激人群PTSD的发生,促进应激人群的身心健康。反复发生的闯入性体验的病     

创伤后应激障碍国内研究现状

创伤后应激障碍(Post traumatic stress disorder,PTSD),指在遭遇异乎寻常的威胁或灾难后延迟出现并长期持续的精神障碍。造成这种心灵创伤的应激通常指严重的自然灾害、残酷的战争经历、肉体酷刑或被强奸等。PTSD在《中国精神障碍分类与诊断标准第3版(CCMD-3)》中归在“应激相     

创伤后应激障碍患者下丘脑-垂体-肾上腺轴系统研究进展

创伤后应激障碍（Post-traumatic stress disorder,PTSD）是一种严重的应激相关障碍,是机体经历严重创伤事件后延迟出现的精神障碍,其临床表现以重复创伤性体验为特征,伴有情绪的易激惹和回避行为等,国外有调查显示其终身患病率约为7.8%[1].下丘脑-垂体-肾上腺（Hypothalamic pituitary adrenal,HPA）轴在调节人体功能中发挥着重要的作用,也通过负反馈抑制调节神经,内分泌,免疫系统功能.研究显示PTSD患者存在HPA轴功能异常,本文主要就PTSD患者HPA轴研究进展进行综述.     

创伤后应激障碍发病机制研究进展

创伤后应激障碍(post-traumatic stress disorder,PTSD)是一种发作与缓解交替出现的精神障碍。2019新型冠状病毒肺炎爆发,作为重大应激源,疫情过后人们容易罹患PTSD。本文就其发病机制涉及的遗传基因、神经内分泌、脑结构及功能研究现状作一综述。     

创伤后应激障碍的生物学机制研究

创伤后应激障碍 (posttraumaticstressdisorder,PTSD)是应激相关疾病中最为典型的一种[1] 。它以三组症状为特征 ,即对创伤的反复性体验、对创伤性提示物的持久性回避和长期的觉醒度增高 (根据美国精神障碍诊断与统计手册第 4版 )。PTSD诊断的确立需要一定的病程标准 ,而且其形成有深刻的生长发育史背景和现实背景[2 ] ,故PTSD可能是大脑功能和结构累积损害超过一定限度的结果 ,使创伤性记忆持久处于易化激活的状态[1 8] 。PTSD生物学机制框架是 :应激信息的传入导致了神经递质和激素的释放 ,继而作用于相应的受体引起快速反应。同时…     

外科全麻手术与创伤后应激障碍——读者来信

正编辑先生:根据《中国精神障碍分类与诊断标准》第3版的描述,创伤后应激障碍(PTSD)是由严重创伤所引起的,其创伤的严重程度应达到异乎寻常的威胁性或灾难性。据悉,国外有"外科全麻手术引起PTSD"的相关报道,这样的病例在我们的临床实践中几乎从未见过。请问专家:外科全麻手术怎么会成为"严重创伤"而引起PTSD的?     

新冠肺炎疫情期间的心理评估和创伤后应激障碍的预防

本文目的是为广大心理援助者介绍新冠肺炎疫情期间对大众进行心理评估的方法。目前心理援助者急需掌握对精神障碍诊断和风险评估的方法,故本文对心理评估中的关键点和侧重点进行了介绍。从评估情绪和行为的基本状态、是否患有某种精神障碍、是否有自杀风险、是否已发展为创伤后应激障碍(PTSD)以及如何预防发展为PTSD的具体方法进行了探讨。     

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.     

亚低温辅助治疗重型颅脑损伤的Meta分析

目的系统评价亚低温辅助治疗重型颅脑损伤的临床疗效。方法计算机检索Wanfang、CNKI、CBM、PubMed、Cochrane Central Register of Controlled Trials（CENTRAL）、EMBASE等数据库,筛选出符合要求的随机对照试验（RCT）,采用RevMan 5.1软件进行Meta分析。结果共纳入符合标准的18篇RCTs,共计1 916例患者。Meta结果显示亚低温组预后良好率（GOS 4~5分）显著高于对照组（OR=2.5,95%CI：2.06~3.02;P〈0.01）;亚低温组患者伤后24 h、3 d及7 d颅内压下降程度优于对照组（P〈0.05）。结论重型颅脑损伤患者在综合治疗的基础上早期行亚低温治疗具有明显的脑保护作用,能降低颅内压,改善患者预后。     

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.     

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.     

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.     

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.