炎症反应在术后认知功能障碍和阿尔兹海默病中的作用

背景术后认知功能障碍(postoperative cognitive dysfunction,POCD)是老年患者术后常见的中枢神经系统并发症,阿尔兹海默病(alzheimer's disease,AD)是一种年龄相关性神经退行性疾病,神经突触和神经细胞丢失、老年斑形成和神经原纤维缠结是其主要病理特征. 目的 现就炎症反应在POCD和AD中的研究进展作一综述,为防治POCD和AD发生发展提供新的途径.内容 研究表明炎症反应在POCD和AD的发病机制中均起着重要作用,抗炎治疗可减缓POCD和AD患者病程.趋向 深入研究炎症反应在POCD和AD中的作用机制,有效的阻断或降低炎症反应,为POCD和AD的防治提供新的思路.     

β淀粉样蛋白在认知功能障碍中作用的研究进展

随着社会老年化进程的发展,以阿尔茨海默病(alzheimer's disease,Ad)为代表的中枢神经退行性疾病和术后认知功能障碍(postoperative cognitive dysfunction,POCD)的发病率逐年升高.以往的研究已经证实β淀粉样蛋白(amyloid-βprotein,Aβ)异常代谢及沉积在AD发生、发展中起到重要的作用.最近研究发现Aβ也可能参与了POCD的发生.现就Aβ在AD和POCD中的作用一概述.     

术后认知功能障碍发病机制的研究进展

术后认知功能障碍(post-operative cognitive dysfunction,POCD)是术后常见的中枢神经系统并发症,目前POCD的发病机制尚不明确。本文就POCD的几种可能的发病机制进行综述,通过进一步的研究以阐明POCD的发病机制,在临床工作中对POCD进行早期预防、诊断和治疗,具有重要的医学、社会和经济意义。     

右美托咪定改善术后认知功能障碍的机制及进展

背景 术后认知功能障碍(postoperative cognitive dysfunction,POCD)是手术麻醉后出现的中枢神经系统并发症,常见于65岁以上的老年患者. 目的 分析总结右美托咪定(dexmedetomidine,Dex)改善老年患者POCD的可能机制及临床应用. 内容 简述POCD的流行病学资料及发病机制;详细分析Dex改善POCD的可能机制. 趋向 目前对于POCD的治疗还在探索之中,Dex能否改善POCD,需要进一步的研究和探索.     

大麻素在认知功能障碍中的作用

背景 术后认知功能障碍(postoperative cognitive dysfunction,POCD)是手术后常见并发症之一,不仅导致患者康复延迟,增加医疗费用,而且严重影响患者术后生活质量.研究显示POCD的发生可能是多种机制作用的结果,主要与中枢胆碱能系统、应激反应及炎症反应有关.近年来研究发现大麻素系统在认知功能障碍中也扮演着重要角色. 目的 综述大麻素在认知功能障碍中的作用研究进展. 内容 简介POCD以及大麻素系统,总结目前对于大麻素与认知功能关系的研究成果. 趋向 为研究者提供最新信息,期望对于POCD发病机制的研究提供帮助.     

术后认知功能障碍的炎症机制

背景 术后认知功能障碍(postoperative cognitive dysfunction,POCD)是老年患者手术后常见的中枢神经系统并发症.目前POCD的发病机制尚不清楚.POCD的发生影响了患者术后恢复,延长了住院时间,增加了术后并发症的发生率和死亡率;对家庭及社会造成严重的经济负担,POCD将成为一个严重的社会问题.目的 旨在推进POCD的研究,使得这一严重问题得到解决.内容 以往的研究表明,麻醉、手术可能是的POCD主要原因,而老龄则是惟一明确的危险应素,提示中枢神经系统退行性改变与POCD的发生可能有着重要联系,而麻醉和手术加重了这种退行性改变所致的认知功能衰退.趋向 较多研究表明炎症反应在与衰老有关的认知功能减退中起着重要作用,而手术创伤和应激引起的炎症反应是围术期发生的重要病理生理学改变.近年来炎症反应在POCD发生中的作用备受关注,现对POCD发生中炎症反应方面的研究进展进行综述.     

星状神经节阻滞对术后认知功能障碍的影响

背景术后认知功能障碍(postoperative cognitive dysfunction,POCD)的发生率已日趋升高.近年来,针对POCD已展开了许多研究,发现星状神经节阻滞(stellate ganglion block,SGB)对POCD有重要作用.目的综述SGB对POCD的影响,旨在为临床上研究POCD的防治提供可能的理论依据.内容SGB是临床较常用的一种阻滞技术,其治疗范围越来越广泛,治疗效果也越来越确切,不仅应用于疼痛性疾病的治疗,也日益广泛地用于神经性、内分泌性及免疫障碍性等非疼痛疾病的治疗,并取得相当显著的疗效,研究发现它对POCD有重要作用. 趋向尽管至今POCD的病因和发病机制仍不清楚,但SGB在防治老年患者POCD方面有较大的研究空间.     

异氟醚吸入全麻术后老年患者早期认知功能障碍的研究

目的 研究老年患者异氟醚吸入全麻术后早期认知功能障碍(postoperative cognitive dysfunction,POCD)的发生率及相关因素分析.方法 68例行全膝关节置换手术的老年患者(年龄≥65岁)给予异氟醚吸入全麻,手术前1d及术后第7天分别进行1次神经心理学测试,通过Z评分的方法诊断POCD,计算其发生率,同时记录可能的相关因素并对其进行相关性分析.结果 异氟醚吸入全麻关节置换术后POCD的发生率为48.5％,而POCD的发生与术中低血压、低氧血症等无明显相关性.结论 异氟醚吸入全麻术后老年患者早期POCD的发生率为48.5％.     

术后认知功能障碍分子机制与麻醉的潜在联系

背景 术后认知功能障碍(postoperative cognitive dysfunction,POCD)的发病机制多年来倍受关注,其中麻醉因素在POCD相关的多种分子生物学改变中起到了重要作用.目的 将POCD分子机制与麻醉间的潜在关系作一系统综述.内容 近年大量动物实验及体外研究发现,全身麻醉药能引起神经细胞相关蛋白退行性变、调节炎性因子表达、与中枢胆碱能受体相互作用并能在特异条件下产生神经毒性物质,均与POCD相关.趋向 麻醉在POCD中的作用机制尚不明确,需要进一步研究以找到其防治方向.     

加兰他敏对老年患者术后POCD的临床观察

目的:研究术后应用加兰他敏对老年患者全麻下早期POCD发生率的影响.方法:选择全麻下行择期手术且年龄>65岁的老年患者200(男105,女95)例,分成治疗组和对照组.结果:加兰他敏纽术后认知功能障碍(POCD)发生率15%,对照组为57%,两组间差异有统计学意义(p<0.05),阿托品对加兰他敏有一定的拮抗作用.结论:术后肌肉注射加兰他敏能降低老年患者非心脏手术的POCD发生率,并有待进一步的大样本临床实验验证.     

Do inhalational anesthetics cause cognitive dysfunction?

Increasing evidence indicates that inhalational anesthetics may cause or increase the risk of developing postoperative cognitive dysfunction (POCD), especially in the elderly population. POCD may exist as a transient or long-term complication of surgery and anesthesia and is associated with reduced quality of life. There remains great discrepancy between clinical studies investigating the prevalence of POCD and inhalational anesthetics as many fail to show an association. However, numerous animal studies have suggested that inhalational anesthetics may alter cognitive function via amyloid β accumulation, modified neurotransmission, synaptic changes and dysregulated calcium homeostasis. Other factors such as neuroinflammation and pro-inflammatory cytokines may also play a role. This paper reviews the role of inhalational anesthetics in the etiology and underlying mechanisms that result in POCD.     

围术期因素与阿尔茨海默病发病机制的可能关系

手术和麻醉后会引起认知功能障碍,尤其是老年人.阿尔茨海默病也表现为记忆减退和认知障碍.有报道称一些围术期因素,如低氧血症、低碳酸血症及有些麻醉药物的应用可能参与阿尔茨海默病的发病机制,可能是引起认知功能障碍的新的原因.故有必要研究围术期因素与阿尔茨海默病的关系.现就阿尔茨海默病的发病机制及相关的围术期因素的在动物实验中发现的可能关系作一综述.     

Cognitive decline in the elderly: is anaesthesia implicated?

Postoperative cognitive dysfunction (POCD) was originally thought to be associated with cardiac surgery, but has since been associated with non-cardiac surgery and even sedation for non-invasive procedures such as coronary angiography. The focus of POCD has thus shifted from the type of surgery or anaesthetic to patient susceptibility. The realisation that cognitive impairment, such as mild cognitive impairment (MCI - the prodrome for Alzheimer's disease (AD)), may already exist in many elderly patients who incidentally present for surgery beckons anaesthesia to align cognitive research with that of AD in order to draw valid parallels between the two disciplines. Long-term studies are required to understand if POCD is merely a transient phenomenon, or if it is the harbinger of long-term cognitive deterioration which may lead eventually to dementia. In this regard, the use of CSF analysis to diagnose AD many years before symptoms appear may identify susceptible individuals. Furthermore, animal studies indicate that volatile anaesthestics may augment the pathological processes of AD by affecting amyloid-beta processing. Identification of a link between surgery/anaesthesia, POCD, MCI, and AD would create a unique opportunity to fast-track the development of clinical or pharmacological preventive strategies that would benefit a significant proportion of the population.     

Postoperative cognitive dysfunction. Possible neuronal mechanisms and practical consequences for clinical routine

Postoperative cognitive dysfunction (POCD) presents as a long-lasting decline in cognitive function after a surgical procedure, predominantly occurring in elderly patients. The causes are most likely multifactorial with the exact mechanisms still unknown. Hypotheses of the causes of POCD are based on experimental evidence that anesthetics can impair mechanisms of learning and memory on a neuronal level and might lead to neurodegeneration. Additionally, surgery can result in neuroinflammation which could also underlie POCD. The most important strategy to avoid POCD is to maintain the patient's physiological homeostasis perioperatively. According to the presently available clinical studies recommendations in favor or against certain anesthesiological procedures cannot be given.     

术后认知功能障碍的炎症机制

背景 术后认知功能障碍(postoperative cognitive dysfunction,POCD)是老年患者手术后常见的中枢神经系统并发症.目前POCD的发病机制尚不清楚.POCD的发生影响了患者术后恢复,延长了住院时间,增加了术后并发症的发生率和死亡率;对家庭及社会造成严重的经济负担,POCD将成为一个严重的...     

全身麻醉药引发的内质网应激和线粒体功能障碍对阿尔茨海默病影响的研究

背景 阿尔茨海默病(Alzheimer's disease,AD)是一种常见的神经退行性病变,以大脑特定区域蛋白蓄积以及神经元缺失为特点.有研究证实全身麻醉药物可引发内质网应激(endoplasmic reticulum stress,ERS)和线粒体功能障碍,进而引起细胞凋亡,而AD的发病及进展与ERS和线粒体功能障碍密切相关. 目的 探究全身麻醉药引发的ERS和线粒体功能障碍对AD的影响. 内容 介绍ERS及其与线粒体功能障碍之间的联系以及全身麻醉药对AD发病及病程影响. 趋向 ERS、线粒体功能障碍及ERS-线粒体之间的联系近年来成为AD临床治疗的重要靶点,也为全身麻醉药物合理选择及配伍提供新思路.     

MAC expanded: AD50 and AD95 values of common inhalation anesthetics in man.

Two important measures may be derived from patient responses to a range of anesthetic doses. The AD50, corresponding to MAC, estimates the median anesthetic concentration--that dose where half the patients are anesthetized and half are not. The AD95 approaches the theoretical "minimum" anesthetic concentration by estimating the dose that anesthetizes 95 per cent of a patient population. The AD50 and AD95 are logical extensions of the MAC concept and can be evaluated with current experimental methodology. Recomputed from available data , the AD50's of nine inhaled anesthetics proved to be numerically identical to their MAC values. The AD95's of nine inhaled anesthetics proved to be numerically identical to their MAC values. The AD95's were 5 to 40 per cent greater than the AD50's.)Key workd: Potency, anesthetic, MAC, AD50, AD95; Pharmacology, dose-response curves.)     

New insights into the pathophysiology of postoperative cognitive dysfunction

There is evidence that postoperative cognitive dysfunction (POCD) is a significant problem after major surgery, but the pathophysiology has not been fully elucidated. The interpretation of available studies is difficult due to differences in neuropsychological test batteries as well as the lack of appropriate controls. Furthermore, there are no internationally accepted criteria for defining POCD. This article aims to provide an update of current knowledge of the pathogenesis of POCD with a focus on perioperative pathophysiology and possible benefits achieved from an enhanced postoperative recovery using a fast‐track methodology. It is concluded that the pathogenesis of POCD is multifactorial and future studies should focus on evaluating the role of postoperative sleep disturbances, inflammatory stress responses, pain and environmental factors. Potential prophylactic intervention may include minimal invasive surgery, multi‐modal non‐opioid pain management and pharmacological manipulation of the inflammatory response and sleep architecture.