雌激素对慢性神经病理性疼痛大鼠热痛觉过敏的影响

目的探讨雌激素对慢性神经病理性疼痛大鼠热痛觉过敏的影响。方法 SD雌鼠18只,体重180～200 g,出生8～10周,随机分为三组:A组(n=6):低雌激素组,接受卵巢切除;B组(n=6):高雌激素组,外源性注射雌激素;C组(n=6):正常雌激素水平组。3周后,监测雌激素水平已达稳态,所有动物均进行坐骨神经不完全结扎手术。在术前、术后3、7、14以及21 d分别进行热板实验,记录后肢回缩时间(PWL),同时监测血雌激素水平。结果 三组动物行坐骨神经结扎后的PWL,与术前比较差异有显著性(P<0.01),对热痛觉刺激的敏感性加强,B组更为明显。结论 雌激素能够提高慢性神经病理性疼痛大鼠的热痛觉过敏性,使动物对热刺激更加敏感。     

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。     

利多卡因与神经病理性疼痛

神经病理性疼痛是一种严重影响人类健康的疼痛性疾病,至今仍缺乏有效的治疗手段,其机制也未能完全阐明.大量临床和实验研究证实,局部麻醉药利多卡因对多种神经病理性疼痛有明显的疗效.正如慢性神经病理性疼痛机制破的复杂性一样,利多卡因对慢性神经病理性疼痛的镇痛机制也不是单一的,此文就利多卡因对神经病理性疼痛镇痛机制研究的进展作一综述.     

神经病理性疼痛病因及其机制研究进展

神经病理性疼痛是神经系统损伤引起的一种慢性状态，国际疼痛研究协会称之“来源于或者由神经系统的功能紊乱引起”，包括确切存在的神经损伤，比如神经缺血或其他病变，也包括缺少确切损伤状态下的疼痛，比如复合区域性疼痛综合征Ⅰ型和某些三叉神经痛。急性疼痛对机体具有警示和“保护”作用，而神经病理性疼痛与之不同，它可以持续存在，对机体无益，甚至会严重影响生活质量。其自发的疼痛，可以描述为针刺、电灼、撕裂、刀割样疼痛，也可表现为诱发的疼痛，被称作感觉异常和痛觉过敏。     

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.     

脊髓背角补体异常活化与神经病理性疼痛关系的实验研究

目的 观察神经病理性疼痛(neuropathic pain,NPP)模型大鼠脊髓背角补体C3变化,并探索脊髓补体异常活化在NPP形成中的作用.方法 实验分两部分:①84只SD大鼠随机分为正常对照组、假手术后1、3、7 d组及坐骨神经结扎后1、3、7 d组,每组12只.分别在建模后1、3、7 d测定大鼠机械痛阈值.并按照分组在规定时间处死大鼠,采用RT-PCR、免疫组化和免疫比浊等测定脊髓中补体C3的表达情况.②48只SD大鼠随机分假手术+生理盐水组、CCI+生理盐水组、CCI+CVF组(持续尾静脉注射CVF组)和CCI+生理盐水+CVF组(单次尾静脉注射CVF组),每组12只.分别在术前和术后1、3、7、14 d测定大鼠机械痛阈值,两周后处死大鼠,用免疫组化和免疫比浊技术测定大鼠L4～L6脊髓中补体C,含量;并用分光光度法测定L4～L6脊髓匀浆中超氧化物歧化酶(superoxide dismutase,SOD)和丙二醛(malondialdehyde,MDA),同时透射电镜观察L4～L6脊髓背角神经元内部结构变化.结果 CCI大鼠坐骨神经结扎侧后1、3、7 d脊髓L4～L6背角补体C,蛋白及mRNA都显著表达,并呈进行性升高趋势.而假手术组无明显变化;Pearson相关分析显示,CCI大鼠脊髓背角补体异常活化状况与大鼠痛觉过敏程度相关.单次尾静脉注射CVF可一过性提高模型大鼠痛觉阈值,并随着药物的代谢作用逐渐减弱;持续给予CVF可抑制大鼠痛觉过敏的发生.给予CVF可逆转模型大鼠脊髓中SOD活力并降低MDA产物含量.给予CVF可减轻模型大鼠脊髓背角神经元线粒体肿胀及核膜损伤程度(P<0.05).结论 外周神经损伤诱发的NPP大鼠脊髓背角发生了补体异常活化现象,并且该处的补体活化参与NPP的痛觉过敏形成.     

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.     

脊髓背角补体异常活化与神经病理性疼痛关系的实验研究

目的 观察神经病理性疼痛(neuropathic pain,NPP)模型大鼠脊髓背角补体C3变化,并探索脊髓补体异常活化在NPP形成中的作用.方法 实验分两部分:①84只SD大鼠随机分为正常对照组、假手术后1、3、7 d组及坐骨神经结扎后1、3、7 d组,每组12只.分别在建模后1、3、7 d测定大鼠机械痛阈值.并按照分组在规定时间处死大鼠,采用RT-PCR、免疫组化和免疫比浊等测定脊髓中补体C3的表达情况.②48只SD大鼠随机分假手术+生理盐水组、CCI+生理盐水组、CCI+CVF组(持续尾静脉注射CVF组)和CCI+生理盐水+CVF组(单次尾静脉注射CVF组),每组12只.分别在术前和术后1、3、7、14 d测定大鼠机械痛阈值,两周后处死大鼠,用免疫组化和免疫比浊技术测定大鼠L4～L6脊髓中补体C,含量;并用分光光度法测定L4～L6脊髓匀浆中超氧化物歧化酶(superoxide dismutase,SOD)和丙二醛(malondialdehyde,MDA),同时透射电镜观察L4～L6脊髓背角神经元内部结构变化.结果 CCI大鼠坐骨神经结扎侧后1、3、7 d脊髓L4～L6背角补体C,蛋白及mRNA都显著表达,并呈进行性升高趋势.而假手术组无明显变化;Pearson相关分析显示,CCI大鼠脊髓背角补体异常活化状况与大鼠痛觉过敏程度相关.单次尾静脉注射CVF可一过性提高模型大鼠痛觉阈值,并随着药物的代谢作用逐渐减弱;持续给予CVF可抑制大鼠痛觉过敏的发生.给予CVF可逆转模型大鼠脊髓中SOD活力并降低MDA产物含量.给予CVF可减轻模型大鼠脊髓背角神经元线粒体肿胀及核膜损伤程度(P<0.05).结论 外周神经损伤诱发的NPP大鼠脊髓背角发生了补体异常活化现象,并且该处的补体活化参与NPP的痛觉过敏形成.     

脊髓背角补体异常活化与神经病理性疼痛关系的实验研究

目的 观察神经病理性疼痛(neuropathic pain,NPP)模型大鼠脊髓背角补体C3变化,并探索脊髓补体异常活化在NPP形成中的作用.方法 实验分两部分:①84只SD大鼠随机分为正常对照组、假手术后1、3、7 d组及坐骨神经结扎后1、3、7 d组,每组12只.分别在建模后1、3、7 d测定大鼠机械痛阈值.并按照分组在规定时间处死大鼠,采用RT-PCR、免疫组化和免疫比浊等测定脊髓中补体C3的表达情况.②48只SD大鼠随机分假手术+生理盐水组、CCI+生理盐水组、CCI+CVF组(持续尾静脉注射CVF组)和CCI+生理盐水+CVF组(单次尾静脉注射CVF组),每组12只.分别在术前和术后1、3、7、14 d测定大鼠机械痛阈值,两周后处死大鼠,用免疫组化和免疫比浊技术测定大鼠L4～L6脊髓中补体C,含量;并用分光光度法测定L4～L6脊髓匀浆中超氧化物歧化酶(superoxide dismutase,SOD)和丙二醛(malondialdehyde,MDA),同时透射电镜观察L4～L6脊髓背角神经元内部结构变化.结果 CCI大鼠坐骨神经结扎侧后1、3、7 d脊髓L4～L6背角补体C,蛋白及mRNA都显著表达,并呈进行性升高趋势.而假手术组无明显变化;Pearson相关分析显示,CCI大鼠脊髓背角补体异常活化状况与大鼠痛觉过敏程度相关.单次尾静脉注射CVF可一过性提高模型大鼠痛觉阈值,并随着药物的代谢作用逐渐减弱;持续给予CVF可抑制大鼠痛觉过敏的发生.给予CVF可逆转模型大鼠脊髓中SOD活力并降低MDA产物含量.给予CVF可减轻模型大鼠脊髓背角神经元线粒体肿胀及核膜损伤程度(P<0.05).结论 外周神经损伤诱发的NPP大鼠脊髓背角发生了补体异常活化现象,并且该处的补体活化参与NPP的痛觉过敏形成.     

Neuropathic pain following multilevel surgery in children with cerebral palsy: a case series and review

Six children with cerebral palsy are presented who developed neuropathic pain following multilevel orthopedic surgery. This significant complication is previously unreported. The diagnosis and treatment options are reviewed. Treatment should be kept as simple and noninvasive as possible, and aim to enable physiotherapy to continue. Early recognition and interdisciplinary treatment is important to prevent a downward spiral of increasing pain and decreased function. A good outcome in respect of improved pain and functioning was achieved in five of these six children. It is our opinion that this complication should form part of informed consent for multilevel surgery and that anesthetists should be aware of this complication when managing postoperative pain control.     

Mechanisms of neuropathic pain

Br J Anaesth 2001; 87: 12–26     

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.     

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     

黑皮质素受体在神经病理性疼痛中的介导作用

国际疼痛研究会将神经病理性疼痛定义为:“原发或原发病灶引发的或神经系统的功能障碍所引起的疼痛”[1]。神经系统内的损伤或功能障碍,被认为是外周神经病理性疼痛或中枢性疼痛的主要病因。Dvorkin[2]认为神经病理性疼痛即是通常所指的慢性疼痛,即持续超过3个月或在疾病治愈后持续时间超出正常范围的疼痛。感染、创伤、机体代谢性疾病、恶性肿瘤的化疗、外科手术、射线、神经毒性药物、神经受压、炎症和肿瘤的侵袭都可以引起外周神经病理性疼痛和中枢神经病理性疼痛。神经病理性疼痛的发病率近年来有逐渐增加的趋势。原因主要在于以下几方…     

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.     

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.