神经胶质细胞活化在神经病理性疼痛中的作用研究进展

神经病理性疼痛(neuropathic pain,NP)是一种慢性顽固性疼痛综合征,发病率高,其持续存在严重影响病人的生活质量。目前NP的病理机制尚不完全明确,对神经元-神经胶质细胞的交互作用的基础研究日益受到重视。本文详述了神经胶质细胞的活化在调节NP中的可能机制,并总结了神经元与神经胶质细胞间的信息交流,以及具有痛觉调制作用的神经趋化因子、促肾上腺皮质激素释放激素以及肿瘤坏死因子-α在NP过程中的作用。总之,本文既能加深我们对NP病理发生机制的认识,也能为临床诊治NP寻找到新的干预靶点提供理论指导。     

神经-免疫通信在疼痛中的作用研究进展

疼痛是临床最常见的综合征之一,其发生机制复杂,严重影响病人生活质量。近年来,研究发现疼痛的产生与免疫细胞释放的炎性物质,以及外周和中枢神经元敏化密切相关。进一步的研究表明,神经系统与免疫系统之间密切关联、相互作用,形成了对疼痛的感知与调节环路,共同参与疼痛的发生发展。本文旨在对疼痛中免疫细胞和伤害性感受神经元之间的双向调控进行综述,以期揭示疼痛背后的神经-免疫机制,并为探索防治疼痛的新型靶点提供理论依据。     

神经元-小胶质细胞信号在神经病理性疼痛中的作用机制

脊神经慢性压迫性损伤引起的神经病理性疼痛是临床常见、多发病,可持续很长时间,甚至可致患者残疾。目前神经病理性疼痛的治疗是医学界的难题,主要因其发病机制尚不明确。近年研究表明,神经元-小胶质细胞信号与神经病理性疼痛关系密切。本文在简述小胶质细胞与神经病理性疼痛关系的基础上,重点阐述神经元-小胶质细胞信号在神经病理性疼痛中的相互作用机制研究进展,为进一步研究脊神经慢性压迫性疼痛机制提供理论支持。     

肠神经胶质细胞在帕金森病中的作用研究进展

<正>帕金森病(PD)是一种黑质致密部多巴胺能神经元退行性变性、死亡,以残存神经元细胞质内α-突触核蛋白(α-syn)聚集形成路易小体为主要病理改变的运动障碍性疾病^[1]。目前PD尚无有效的治疗方法,随着其发病率的逐年上升,社会负担也逐渐加重,成为当今社会面临的重大挑战之一。造成这种局面的原因是PD病因及发病机制不明。虽然研究表明PD特征性α-syn病理沉积物首先出现在肠神经系统(ENS)^[2],与肠道微生物群引起的肠道局部炎症有关,但其中具体的细胞及分子机制尚不清楚。     

星形胶质细胞-小胶质细胞的交互对话在神经炎症中的双重作用

中枢神经系统(central nervous system,CNS)中的胶质细胞不仅是营养支持细胞,同时也是重要的神经炎症反应细胞.急性炎症反应一般有利于组织损伤的修复、细胞碎屑和病原体的清除.而慢性神经炎症是各种疾病的危险因素,如神经退行性疾病.星形胶质细胞和小胶质细胞是介导CNS神经炎症最重要的两类胶质细胞.它们不...     

胶质细胞在神经血管单元中的作用

神经血管单元是由微血管、神经胶质细胞、神经元及细胞外基质组成,各组分间的信号联系是保证神经元功能和正常脑血流的基础。其中星形胶质细胞介导了神经元和脑血流之间的功能偶联,是神经血管单元的重要组成部分,对维持血脑屏障的功能具有重要作用。此外,在脑缺血等病理情况下,胶质细胞对神经血管单元具有保护作用。     

胶质细胞参与疼痛中枢敏感化的机制

目的：近年来，审视胶质细胞-神经元网络成为日前神经科学研究领域的一个热门课题，本文综述了胶质细胞参与疼痛中枢敏感化机制的研究进展。 资料来源：应用计算机检索Medline1991-01／2005-06的关于胶质细胞和疼痛中枢敏感化的文章，检索词包括“glial cdis，astrocytes，neuropathic pain，central sensitization”等，并限定文章语言种类为English。同时检索万方数据库2000-01／2004-12关于胶质细胞和疼痛中枢敏感化的文章，检索词为：胶质细胞、疼痛、中枢敏感化、病理性疼痛。限定文章语言种类为中文。 资料选择：对资料进行初审，选择胶质细胞与疼痛中枢敏感化相关的文章，然后筛除胶质细胞与病理性疼痛无明显联系的文章。纳入标准：详细阐述胶质细胞与神经元之间信号交流特征的文献。排除标准：重复性研究。 资料提炼：共收集到122篇关于胶质细胞与疼痛中枢敏感化相关的文献，纳入26篇用于综述。 资料综合：胶质细胞与神经元间存在着广泛的信号交流，活化的胶质细胞产生和释放神经递质、细胞因子，通过突触、缝隙连接和细胞间信号交流，在受体、离子通道、信使传递、基因转录和翻译等多级水平全面影响和调节神经元的兴奋性，导致疼痛中枢敏感化的发生。 结论：胶质细胞在疼痛中枢敏感化机制发生过程中具有重要的作用，这不仅对于进一步揭示疼痛中枢敏感化机制具有重要的理论意义，而且对制定慢性顽固性疼痛的防治策略具有潜在的实用价值。     

小胶质细胞极化在神经病理性疼痛中的作用研究进展

神经病理性疼痛(neuropathic pain,NP)发病机制尚不完全清楚,一直以来是困扰人类的难题。越来越多的证据显示小胶质细胞活化以及随之发生的促炎反应在神经病理性疼痛中扮演着至关重要的作用。此外,在神经炎症过程中经常发生小胶质细胞极化为促炎的M1型或抗炎的M2型,并在神经系统中发挥有害或有益作用。本文从小胶质细胞极化与神经病理性疼痛的关系方面展开探讨,探寻如何利用M2型小胶质细胞的保护性、抗炎特性来开发控制神经病理性疼痛的新靶向药物,进而寻找治疗神经病理性疼痛的一种新途径。     

脊髓小胶质细胞活化状态与前列腺的炎性疼痛

目的：观察化学性刺激大鼠前列腺后相应脊髓节段小胶质细胞活化的状况。 方法：实验于2004-05／2005—11在第三军医大学神经生物学教研室实验室完成。①分组：健康雄性SD大鼠24只，随机分为4组：对照组6只；完全弗氏佐剂刺激3d组6只；完全弗氏佐剂刺激10d组6只；完全弗氏佐剂刺激28d组6只。②模型制备：对照组：取下腹部正中直切口，于前列腺腹侧叶注入生理盐水0．1mL，可吸收线缝合伤口；完全弗氏佐剂刺激组：取下腹部正中直切口，于前列腺腹侧叶注入完全弗氏佐剂0．1mL，可吸收线缝合伤口。③用免疫组织化学技术对不同时间段大鼠相应脊髓节段（L6和S1）的小胶质细胞活化进行检测。 结果：24只大鼠均进入结果分析。完全弗氏佐剂刺激大鼠前列腺后3，10，28d，L6～S1脊髓背角浅层和深层小胶质细胞的活化与对照组相比均显著增加，其中3d时已显著增强，10d时增强最显著，28d时较10d时活化有所减少，但仍显著高于对照组。 结论：完全弗氏佐剂刺激大鼠前列腺引起前列腺炎性疼痛，导致了相应节段L6-S1脊髓背角小胶质细胞的激活，提示小胶质细胞活化在前列腺炎性疼痛的神经病理过程可能发挥了重要作用。     

胶质细胞参与疼痛中枢敏感化的机制

目的:近年来,审视胶质细胞-神经元网络成为目前神经科学研究领域的一个热门课题,本文综述了胶质细胞参与疼痛中枢敏感化机制的研究进展。资料来源:应用计算机检索Medline1991-01/2005-06的关于胶质细胞和疼痛中枢敏感化的文章,检索词包括“glialcells,astrocytes,neuropathicpain,centralsensitization”等,并限定文章语言种类为English。同时检索万方数据库2000-01/2004-12关于胶质细胞和疼痛中枢敏感化的文章,检索词为:胶质细胞、疼痛、中枢敏感化、病理性疼痛。限定文章语言种类为中文。资料选择:对资料进行初审,选择胶质细胞与疼痛中枢敏感化相关的文章,然后筛除胶质细胞与病理性疼痛无明显联系的文章。纳入标准:详细阐述胶质细胞与神经元之间信号交流特征的文献。排除标准:重复性研究。资料提炼:共收集到122篇关于胶质细胞与疼痛中枢敏感化相关的文献,纳入26篇用于综述。资料综合:胶质细胞与神经元间存在着广泛的信号交流,活化的胶质细胞产生和释放神经递质、细胞因子,通过突触、缝隙连接和细胞间信号交流,在受体、离子通道、信使传递、基因转录和翻译等多级水平全面影响和调节神经元的兴奋性,导致疼痛中枢敏感化的发生。结论:胶质细胞在疼痛中枢敏感化机制发生过程中具有重要的作用,这不仅对于进一步揭示疼痛中枢敏感化机制具有重要的理论意义,而且对制定慢性顽固性疼痛的防治策略具有潜在的实用价值。     

髌股关节疼痛综合征患者的疼痛治疗

髌骨关节的异常排列和过度使用导致髌骨轨迹的滑轨是引起髌股关节疼痛的重要因素，髌股关节疼痛综合征患者的疼痛治疗正日益引起关注。本文讨论了此类患者评定疼痛的常用方法；总结疼痛的治疗方案，讨论了不同训练方案的有效性。     

剖胸术后镇痛

剖胸术后伤口疼痛剧烈，并伴有肺功能的显著下降，对患者术后康复不利。本文就目前临床常用的剖胸术后镇痛方法的镇痛效果及其对患者术后肺功能的影响进行综述。     

肌筋膜疼痛综合征的治疗进展

肌筋膜疼痛综合征的干预和康复手段在过去十余年中有着重大的发展和变化。本文综述最新的肌筋膜疼痛综合征的治疗方法及相关研究证据。     

Facilitated Pronociceptive Pain Mechanisms in Radiating Back Pain Compared With Localized Back Pain

Facilitated pain mechanisms and impaired pain inhibition are often found in chronic pain patients. This study compared clinical pain profiles, pain sensitivity, as well as pronociceptive and antinociceptive mechanisms in patients with localized low back pain (n = 18), localized neck pain (n = 17), low back and radiating leg pain (n = 18), or neck and radiating arm pain (n = 17). It was hypothesized that patients with radiating pain had facilitated pain mechanisms and impaired pain inhibition compared with localized pain patients. Cuff algometry was performed on the nonpainful lower leg to assess pressure pain threshold, tolerance, temporal summation of pain (increase in pain scores to 10 repeated stimulations at pressure pain tolerance intensity), and conditioning pain modulation (increase in pressure pain threshold during pain conditioning on the contralateral leg). Heat detection and heat pain threshold at the nonpainful hand were also assessed. Clinical pain intensity, psychological distress, and disability were assessed with questionnaires. Temporal summation of pain was increased in patients with radiating back pain compared with localized back pain (P < .03). Patients with radiating arm pain or localized low back pain demonstrated hyperalgesia to heat and pressure in nonpainful body areas (P < .05), as well as well as a facilitated clinical pain profile compared with patients with localized neck pain (P = .03). Patients with radiating pain patterns demonstrated facilitated temporal summation suggesting differences in the underlying pain mechanisms between patients with localized back pain and radiating pain.

涡流浴缓解疼痛的疗效与机制研究进展

涡流浴通过旋涡式流体力学与温热效应,调控疼痛闸门,促进血液循环,增加组织延展性,提高痛阈,可缓解骨关节炎疼痛,改善关节僵硬;减轻肌筋膜炎疼痛和焦虑症状;缓解运动后迟发性肌肉酸痛;降低产妇分娩后的痛觉敏感性;联合其他物理治疗,还能改善肩手综合征的肿胀、疼痛和痉挛症状。涡流浴通过外周温度、机械等刺激局部组织,提高血管渗透率,加快疼痛介质代谢,减少伤害性刺激对外周伤害感受器的影响;促进机体产生镇痛物质,调节自主神经系统,调控疼痛闸门,进而缓解疼痛。涡流浴的具体治疗参数在不同研究中区别较大,有待进一步规范。     

毫米波缓解疼痛临床研究进展

毫米波疗法可以改善血液循环、增强白细胞吞噬能力、促进炎症吸收、抑制细菌生长、提高组织功能和再生能力、促进内啡肽的释放、抑制肿瘤生长,从而对疼痛形成的各种诱因都发挥作用。在国内外的文献中,可见应用毫米波疗法缓解头痛、关节痛、术后痛、神经痛、癌痛等。     

Peripheral Acute Pain Mechanisms

Many studies in several species, including humans, have identified a subset of primary afferent nerve fibres that are activated by potential or actual tissue-damaging stimuli. Discharge patterns of these nociceptive afferents faithfully reproduce some aspects of the applied stimuli (e.g. shape of the stimulus-response function) but not others (e.g. time-course of a sustained stimulus). Since primary nociceptive afferents provide the input to the central nervous system, their encoding properties have to be considered when studying central processing. On the other hand, pain perception correlates with some aspects of nociceptor discharges (e.g. fatigue with repetition of brief heat pulses), but not with others (e.g. absolute thresholds). Therefore, the painfulness of a stimulus cannot be deduced from nociceptor discharges alone; central processing needs to be taken into account, particularly central summation. In addition to the immediate responses of nociceptive afferents to external stimulation, acute pain mechanisms also comprise the short-term plasticity of the nociceptive system as a consequence of prolonged noxious stimulation     

Central Acute Pain Mechanisms

This account will consider the events occurring in the spinal cord that give rise to acute pain. The transmission and control of acute pain is not immutable but subject to plasticity so that the dividing line between acute and chronic pain is difficult to draw. Very brief acute pain is transmitted in a simple way and rarely produces difficulties in treatment. The situation within the spinal cord changes if the stimulus continues. After only seconds of C-fibre stimulation, additional peptides are released from C fibres, and spinal N-methyl-D-aspartate (NMDA) receptor activation and nitric oxide production occur. Soon after, genes are induced in central neurones, and increases and decreases in diverse pharmacological systems involved in pain transmission and modulation occur over periods of only a few hours. This rapid plasticity has important implications for the pharmacological treatment of acute because both the level of pain transmission and pain modulation will be altering over time.     

Symptom Interactions as Mechanisms Underlying Symptom Pairs and Clusters

PURPOSE: To present a summary of the potential shared or interactive mechanisms underlying an exemplar symptom pair: sleep disturbances and pain. ORGANIZING CONSTRUCT: Understanding of the multidimensional shared and interactive mechanisms underlying symptoms pairs and clusters has the potential to enhance symptom management. METHODS: Reviews of the literature were conducted to search for information on shared or interactive mechanisms underlying sleep disturbances and pain; minimal data were available. Relevant information about individual symptoms was outlined and categorized in areas often used to describe the multidimensional nature of symptoms, including the physiological, psychological, behavioral, and sociocultural domains. This information was examined for relationships and commonalities. CONCLUSIONS: Many potential shared and interactive mechanisms underlying the symptom pair of sleep disturbances and pain were identified. These results indicate the need for further work and theory development in this area. The symptom interactional framework is a beginning conceptual perspective designed to facilitate this work. Implications for interdisciplinary translational research designed to optimize symptom management are discussed.     

Neuropathic Pain: Mechanisms and Treatment Options

Abstract : Neuropathic pain results from damage to the nervous system. The diseases responsible for neuropathic pain are diverse but they may have in common pathophysiological mechanisms. This review will focus on these mechanisms both in the peripheral as well as within the central nervous system. In addition, there will be discussion on the various treatment choices including both pharamcological and interventional options.