离子通道与神经病理性疼痛

神经病理性疼痛是由神经系统损伤所致的一种慢性疼痛,发病机制复杂.已经证实异位放电是痛觉异常的电生理学基础,并且离子通道改变是形成异常放电的主要原因.就现有文献报道的感觉神经元中一些重要离子通道在神经病理性疼痛中的变化作一简单综述.     

神经病理性疼痛机制研究进展

神经病理性疼痛程度重、治疗效果差,严重影响患者生活质量.神经病理性疼痛的病因有创伤、压迫、神经毒性药物、感染、自身免疫性疾病、肿瘤、维生素缺乏等,模拟这些病因的神经病理疼痛动物模型已大部分建立起来,极大地促进了对神经病理性疼痛的研究.神经病理性疼痛的发病机制复杂,目前认为既有外周神经敏化又有中枢神经系统敏化,除受损神经敏化,未受损神经以及胶质细胞也参与发病过程.现对近10年来的神经病理性疼痛机制研究的进展作一综述.     

神经病理性疼痛的治疗进展

神经病理性疼痛(Neuropathic pain)是与多种周围神经障碍相关的一组共同表现的症状,包括与糖尿病(DN)、甲状腺功能低下、尿毒症、营养缺乏和化疗(长春新碱、顺铂、扎西他宾和紫杉醇)相关的神经障碍。也包括其他疾病:格-巴二氏综合征(GBS)、带状疱疹后神经痛(PHN)、进行性神经病性(腓骨)肌萎缩(CMT)病、复合性局部疼痛综合征I型(CRPs-I)和缺血性神经病变。最近几年神经病理性疼痛治疗方面     

白介素和神经病理性疼痛

近来实验发现免疫细胞活化对于人类和实验动物神经病理性疼痛的病因和症状有密切联系,而免疫细胞活化的一类产物--白介素在疼痛形成和维持过程中发挥重要作用.此文讨论白介素-1(白介素-1α、白介素-1β、白介素-1ra)、白介素-6和白介素-10在神经病理性疼痛的产生和维持过程的作用,探讨白介素在神经病理性疼痛治疗的前景.     

神经病理性疼痛的背根神经节机制

背根神经节是痛觉传人的第一级神经元，它的异位放电是神经病理性疼痛的重要机制，这种异位放电与背根神经节中的离子通道变化密切相关，它可能源于受损神经和／或邻近未受损神经中的A类和(或)C类传入神经纤维。     

巨噬细胞在神经病理性疼痛中的作用

神经病理性疼痛（neuropathic pain, NP）是指由躯体感觉系统的损害或疾病导致的疼痛。NP的发病机制复杂,与免疫调节有关。巨噬细胞是体内重要的免疫细胞,在体内通过自身极化和神经免疫相互作用参与神经损伤后的外周及中枢敏化形成过程,促进NP的发展。文章对巨噬细胞在NP中的作用进行综述,研究巨噬细胞在NP形成与...     

神经病理性疼痛的药物治疗

“神经病理性疼痛”在本质上与“伤害感受性疼痛”有所不同。伤害感受性疼痛由伤害感受器被激活(介导)并沿固定的通路传递电化学冲动到达较高级的背角中枢而引起，其传入有害冲动的调节发生在脊髓水平。神经病理性疼痛则与之相反，其出现可提示体内已有神经组织损害，虽没有固定的通路，但原先     

神经病理性疼痛86例临床分析

目的分析神经病理性疼痛的常见临床类型及治疗方法。方法将86例神经病理性疼痛分为周围性神经病理疼痛和中枢性神经病理疼痛,并根据其临床类型给予相应的药物治疗。结果 86例神经病理性疼痛治愈68例,占79.1%,有效13例,占15.1%。结论神经病理性疼痛的治疗应首先查明病因,应用药物,结合理疗、针灸、心理治疗以及康复治疗等综合措施。     

鞘内注射Roscovitine缓解大鼠慢性神经病理性疼痛

目的 在SD大鼠脊髓后根神经节慢性压迫(CCD)模型上观察鞘内注射Roscovitine的镇痛效果.方法 用不锈钢棒(长4 mm,直径0.7 mm)持续件压迫脊髓背根神经节(DRG)建立慢性神经病理性疼痛模型.术后第7天鞘内注射溶解于DMSO 10 μl中的Roscovitine 50 μg(R组);同时设CCD术后第7天只给予鞘内注射二甲基亚砜(DMS0)10 μl的CCD组(C组)和非CCD处理、并给予鞘内注射DMSO 10 μl的假手术组(S组).三组均于CCD术前、术后第7天(给药前)及给药后2、24、72 h榆测机械痛缩足阈值(PWMT)和热痛缩足潜伏期(PWTL).CCD术前及给药后72 h用免疫组化技术检测脊髓背角N-甲基-D天冬门氨酸(NMDA)受体2A亚基(NR2A)的表达水平.结果 R组和C组给药前PWMT均较术前显著降低[(3.64±0.40)g vs.(14.38±1.53)g,(3.50±0.77)g vs(13.25±2.21)g],也明显低于S组的(11.31±1.13)g(P<0.05).R组和C组给药前PWTL均较术前显著缩短[(9.28±1.18)s vs(18.34±1.23)s,(8.91±1.08)s vs.(18.59±1.92)s],也短于S组的(18.45±1.44)s(P<0.05).R组PWMT在给药后24 h较给药前和C组显著增加[(7.32±0.69)g vs.(3.64±0.40)g,(3.86±1.14)g](P<0.05),而给药后2 h PWTL,较给药前和C组显著延长[(15.464±1.51)s vs.(9.28±1.18)s,(9.91±1.07)s(P<0.05).给药后72 h,R组脊髓背角NR2A受体表达水平明显低于C组[(0.21±0.02)vs.(0.26±0.01)](P<0.05).结论 鞘内注射Roseovitine能有效改善CCD大鼠痛行为学反应;其作用可能与抑制脊髓背角NR2A受体表达有关.     

神经病理性疼痛中阿片类药物的应用

阿片类药物作为一种较为有效的药物用来治疗重度疼痛以及包括神经病理性疼痛在内的慢性疼痛.然而在神经病理性疼痛中,阿片类药物的疗效存在争议.长期持续的运用阿片类药物容易产生耐受的现象,表现为需要增加药物剂量来维持疼痛的缓解程度.但最近的几个研究都表明阿片类药物在神经病理痛中的应用是有效的.现就神经病理性疼痛中阿片类药物的耐受及应用发展作一阐述.     

Lidocaine 5% patch for localized chronic neuropathic pain in adolescents: report of five cases

We describe a case series of five adolescents who were managed with lidocaine 5% patches for chronic localized neuropathic pain from a variety of causes with minimal adverse effects. Treatment was effective in four of five patients with only one patient complaining of minimal pain relief. 5% Lidocaine patches have been used for treatment of chronic neuropathic pain in adults and we have found this to be effective in management of localized neuropathic pain in children and adolescents.     

Mechanisms of neuropathic pain

Br J Anaesth 2001; 87: 12–26     

不同功率的低强度激光对神经病理性疼痛大鼠痛阈及脊髓背角5-HT、GABA表达的影响

目的探讨低强度激光对神经病理性疼痛大鼠的镇痛作用、机制及最佳照射参数。方法56只雄性SD大鼠随机分为假手术组,模型组,10 nw和30 nw激光照射组四个组,模型组以及激光照射组制成坐骨神经缩窄性损伤模型。每组14只,分别于术前1 d、术后1 d、激光照射后3 d、12 d测定大鼠热水甩尾潜伏期(tail flick latency,TFL)。于激光照射后3 d、12 d各取7只采用免疫组化方法检测大鼠脊髓背角GABA、5-HT的表达。结果与假手术组比较,模型组以及激光照射组术后1 d大鼠痛阈降低(P0.05);与模型组比较,术后12 d,激光照射组TFL明显延长(P0.05),脊髓背角5-HT、GABA的表达显著增加(P0.05),30 nw优于10 nw(P0.05)。结论低强度激光能提高神经病理性疼痛大鼠的痛阈,激光治疗强度30nw优于10nw,其治疗机制可能与促进神经递质5-HT、GABA的表达有关。     

Post-surgical neuropathic pain

Surgeons and anaesthetists are involved in Pain Medicine, as they have a responsibility to contribute to postoperative pain management and are often consulted about longer-term pain problems as well. A large component of persistent pain after surgery can be defined as neuropathic pain (NP). Nerves are injured during surgery and pain can persist after the surgical wound has healed. NP is because of a primary lesion or dysfunction of the peripheral or central nervous system. Prevalence estimates indicate that 2-3% of the population in the developed world experience NP. Persistent post-surgical NP is a mostly unrecognized clinical problem. The chronicity and persistence of post-surgical NP is often severely debilitating and impinges on the psychosocial, physical, economic and emotional well-being of patients. Options for treatment of any neuropathic factors are based on understanding the pain mechanisms involved. The current understandings of the mechanisms involved are presented. There is reasonable evidence for the efficacy of pharmacological management for NP. The aim of this article was to appraise the prevention, diagnostic work-up, the physical and particularly the pharmacological management of post-surgical NP and to provide a glimpse of advances in the field. It is a practical approach to post-surgical NP for all surgeons and anaesthetists. The take-home message is that prevention is better than waiting for post-surgical NP to become persistent.     

The effectiveness of intravenous ketamine and lidocaine on peripheral neuropathic pain

BACKGROUND: Neuropathic pain is often severe and resistant to pharmacological treatment. The aims of the present study were to assess the analgesic effect of ketamine and lidocaine and to investigate if measurement of different variables of sensibility could be used to identify responders. We also wanted to study if treatment resulted in changes of sensibility. METHODS: Twelve patients with long-lasting peripheral neuropathic pain of traumatic origin were included. The effects of ketamine hydrochloride (Ketalar, Parke Davis) 0.4 mg/kg and lidocaine hydrochloride (Xylocain, Astra) 2.5 mg/kg were investigated. Saline was used as placebo. The intensity of continuous pain was measured by a visual analogue scale (VAS). Warm and cold perception as well as heat and cold pain thresholds were assessed. Sensibility to touch was also tested. Systemic plasma concentrations of lidocaine and ketamine were assessed. RESULTS: The mean reduction in VAS-scores was 55%, 34% and 22% for ketamine, lidocaine and placebo, respectively. A significant difference was registered between ketamine and placebo (P = 0.009). Response to treatment (50% reduction in VAS-score during infusion) was recorded in 7/12 in the ketamine, 4/12 in the lidocaine and 2/12 in the placebo group. Quantitative sensory testing (QST) of thermal sensitivity and sensory tests for mechanical stimuli could not separate responders from non-responders and neither were the results from these assessments changed by the infusion of the drugs. Lidocaine and particularly ketamine were associated with frequent side-effects, the most common being somnolence and dizziness. CONCLUSION: Ketamine showed a significant analgesic effect. The clinical usefulness is, however, limited by disturbing side-effects.     

Efficacy of intravenous magnesium in neuropathic pain

Background. Postherpetic neuralgia is a complication of acuteherpes zoster characterized by severe pain and paraesthesiain the skin area affected by the initial infection. There isevidence that the N-methyl-D-aspartate receptor is involvedin the development of hypersensitivity states and it is knownthat magnesium blocks the N-methyl-D-aspartate receptor. Method. A double-blind, placebo-controlled, cross-over studywas conducted in which magnesium sulphate was administered asan i.v. infusion. Spontaneous pain was recorded and qualitativesensory testing with cotton wool was performed in seven patientswith postherpetic neuralgia before and after the i.v. administrationof either magnesium sulphate 30 mg kg^–1 or saline. Results. During the administration, pain scores were significantlylower for magnesium compared with placebo at 20 and 30 min (P=0.016)but not at 10 min. I.V. magnesium sulphate was safe, well-toleratedand effective in patients with postherpetic neuralgia. Conclusion. The present study supports the concept that theN-methyl-D-aspartate receptor is involved in the control ofpostherpetic neuralgia. Br J Anaesth 2002; 89: 711–14     

丝裂原活化蛋白激酶家族与病理性疼痛

病理性疼痛包括炎性痛和神经病理性痛。炎性痛是由创伤、细菌或病毒感染及外科手术等引起的外周组织损伤导致的炎症而引起的疼痛;神经病理性疼痛是由于外周或中枢神经系统的直接损伤或功能紊乱引起的疼痛,其共同的临床表现有自发性疼痛、痛觉过敏、触诱发痛等。许多脊髓或高级中枢神经病理生理的改变都可引起或参与病理性神经痛的形成。目前的研究认为,脊髓背角神经元及脊髓胶质细胞丝裂原活化蛋白激酶家族活化与病理性疼痛有关[1,2]。现就MAPKs在病理性疼痛的发生、发展过程中所起的作用作一综述。1 MAPKsMAPKs在所有真核细胞中均有表…     

Complex neuropathic pain states

In this article we discuss complex neuropathic pain states: diabetic peripheral neuropathic pain (DPNP), phantom limb pain (PLP), central post-stroke pain (CPSP), and complex regional pain syndrome (CRPS). Pain in these conditions can often be severe, significantly affect quality of life and be resistant to current treatment options. Multidisciplinary assessment and treatment is essential.     

Complex neuropathic pain states

In this article we discuss complex neuropathic pain states: diabetic peripheral neuropathic pain (DPNP), phantom limb pain (PLP), central post-stroke pain, and complex regional pain syndrome (CRPS). Pain in these conditions can often be severe, significantly affect quality of life and be resistant to current treatment options. Multidisciplinary assessment and treatment are essential.