加巴喷丁治疗神经病理性疼痛的小样本随机对照临床研究

目的 观察抗癫药物加巴喷丁治疗神经病理性疼痛的临床疗效及安全性.方法 采用前瞻性随机对照研究方法观察神经病理性疼痛患者对加巴喷丁的临床治疗效果,根据视觉模拟评分(VAS)评价患者治疗前后疼痛改善程度,记录药物不良反应发生率.结果 83 例患者完成试验,1 例脱落.与治疗前相比,加巴喷丁组患者治疗后第1、2、4 和8 周末VAS 评分显著减少(均P = 0.001),且自治疗第2 周末开始各测量时间点VAS 评分均低于卡马西平组(P = 0.011,0.001,0.001).治疗第8 周末加巴喷丁组患者治疗有效率为87.50%(35/40),高于卡马西平组的67.44%(29/43;χ2 = 4.723,P = 0.030).两组患者治疗过程中药物不良反应发生率差异无统计学意义(Z = 0.324,P = 0.373),实验室检查未出现具有临床意义的异常变化.结论 加巴喷丁治疗神经病理性疼痛安全、可靠,值得临床推广应用.     

己酮可可碱预处理对癫痫发作大鼠海马损伤的影响

目的观察己酮可可碱(Ptx)预处理对癫痫发作大鼠海马损伤的影响。方法健康、成年雄性Wistar大鼠分为3组:对照组、癫痫组和Ptx预处理组。对照组腹腔注射生理盐水(127mg·kg~(-1));癫痫组和Ptx组大鼠用氯化锂-匹罗卡品(Li-Pc)诱发癫痫发作,先腹腔注射氯化锂(127mg·kg~(-1)),20h后背部皮下注射匹罗卡品(15mg·kg~(-1));Ptx组大鼠在匹罗卡品注射前30min通过腹腔给予Ptx(60mg·kg~(-1))。观察大鼠癫痫发作情况,利用Timm和Thionin染色分别观察海马苔藓纤维发芽(MSF)和神经元损伤情况。结果癫痫组大鼠在海马苔藓纤维发芽明显增多,并伴有海马神经元的损伤和脱失,Ptx预处理降低了Li-Pc诱发大鼠的癫痫发作率和癫痫发作程度,延长了其癫痫发作潜伏期,减轻了Li-Pc诱发大鼠海马的苔藓纤维出芽及神经元的损伤。结论 Ptx预处理缓解了Li-Pc诱发大鼠的癫痫发作和海马损伤,可能成为治疗癫痫的一种方法。     

纳络酮对全脑缺血大鼠的神经保护作用研究

全脑缺血后如何保护脑功能、减轻缺血/再灌注损伤是目前研究热点,但有效的神经保护剂并不多,仅tempol、MK-801等在实验中证明有效。纳络酮,作为传统意义的阿片受体拮抗剂,在许多实验和临床研究中亦被证明有神经保护作用,但仍存在较多争议。最近研究揭示纳络酮具有抑制钙超载的作用,本文通过研究其对钙结合蛋白表达的影响来探讨纳络酮的神经保护作用。1材料与方法实验选用健康SD大鼠29只,雌雄不拘,体重185.5～294.0g,建立窒息 艾司洛尔的大鼠心肺骤停模型[1],实验参数设计和记录均参照实验研究的Utstein模型。实验动物随机分为4组:假手术组…     

强弱阿片类药物对神经病理性疼痛的干预作用

目的研究强弱阿片类药物对神经病理性疼痛的干预效果。方法抽选2013-05—2014-06我院收治的神经病理性疼痛患者86例,随机法分为强药组(n=43)和弱药组(n=43),强药组给予盐酸羟考酮缓释片治疗;弱药组给予盐酸曲马多片治疗,比较2组用药前后疼痛程度及睡眠质量改善率,比较不良反应发生情况。结果强药组用药1周后及用药2月后疼痛程度(3.2±1.5)分、(3.4±1.2)分较对照组(4.1±2.0)分、(4.3±1.8)分显著较低(P0.05);2组睡眠质量总改善率比较无统计学差异(P0.05);强药组便秘发生率76.7%与弱药组55.8%比较显著增高(P0.05);其他不良反应发生率比较无统计学差异(P0.05)。结论强阿片类药物比弱阿片类药物对神经病理性疼痛患者疼痛改善效果略好,但不良反应相对较高,临床用药可根据患者病情及既往用药史酌情选择。     

氨酚氢可酮联合神经阻滞治疗带状疱疹急性期疼痛的疗效观察

目的观察氨酚氢可酮联合神经阻滞治疗带状疱疹急性期疼痛的疗效。方法选择郑州大学第一附属医院就诊的带状疱疹急性期患者61例,按照随机数字表法分为常规治疗+神经阻滞组(对照组)、常规治疗+神经阻滞+氨酚氢可酮组(实验组)。分别记录所有患者治疗前后视觉模拟评分(VAS),睡眠质量评分(AIS),红外热像扫描皮肤温差(△dT),带状疱疹后遗神经痛(PHN)及其他不良反应发生率。结果与治疗前相比,2组患者治疗后各时间点VAS、AIS评分和红外热像扫描皮肤温差均明显降低(P0.05);与对照组相比,实验组患者治疗后3 d、7 d、14 d VAS评分及AIS评分更低(P0.05),且治疗前后△dT明显更大(P0.05)。2组患者PHN及不良反应的发生率相比未见显著性差异(P0.05)。结论常规治疗联合神经阻滞能够有效缓解带状疱疹急性期疼痛,改善睡眠质量,在此基础上联合氨酚氢可酮使疱疹急性期病程缩短,治疗效果更显著。     

己酮可可碱对癫痫大鼠黑质多巴胺能神经元的影响

目的观察己酮可可碱(Ptx)预处理对癫痫发作大鼠多巴胺(DA)能神经元的影响。方法健康、成年雄性Wistar大鼠分为3组:对照组、癫痫组和Ptx预处理组(PTX组)。对照组腹腔注射生理盐水(127mg·kg~(-1));癫痫组和PTX组大鼠用氯化锂-匹罗卡品(Li-Pc)诱发癫痫发作,先腹腔注射氯化锂(Li,127mg·kg~(-1)),20h后背部皮下注射匹罗卡品(Pc,20mg·kg~(-1));PTX组大鼠在Pc注射前30min通过腹腔给予Ptx(60mg·kg~(-1))。观察大鼠癫痫发作情况;利用免疫细胞化学、蛋白印迹和液质联用检测黑质(SN)DA能神经元功能活动;通过分光光度法检测SN和尾壳核(CPu)处丙二醛(MDA)、谷胱甘肽(GSH)含量及超氧化物岐化酶(SOD)活性,探讨Ptx预处理对Li-Pc诱发癫痫大鼠DA能神经元的影响及氧化应激的参与。结果 (1)Ptx预处理降低了Li-Pc诱发大鼠的癫痫发作率,显著延长了大鼠的癫痫发作潜伏期(P0.01);(2)免疫细胞化学和蛋白印迹显示癫痫组大鼠SN和CPu处TH免疫反应强度和蛋白含量比对照组明显降低;与癫痫组相比,PTX组大鼠SN和CPu的TH免疫反应强度和蛋白含量显著增加(均P0.05);(3)癫痫组大鼠CPu的DA、二羟苯乙酸(DOPAC)和高香草酸(HVA)含量较对照组明显降低;与癫痫组相比,PTX组大鼠DA、DOPAC和HVA含量显著增加(均P0.05);(4)与对照组相比,癫痫组大鼠SN和CPu的MDA含量明显增多,GSH含量明显减少,SOD活性显著降低;与癫痫组相比,PTX组大鼠SN和CPu的MDA含量明显降低,GSH含量和SOD活性明显升高(均P0.05)。结论 Ptx预处理缓解了Li-Pc诱发癫痫大鼠脑内的氧化应激状态和DA能神经元功能活动的降低。     

吡格列酮对脑缺血再灌注损伤大鼠的神经保护作用及其机制的研究

目的 探讨吡格列酮对脑缺血再灌注(CIR)损伤大鼠的神经保护作用及其机制.方法 将80只SD大鼠随机分为假手术组(A组)、CIR模型组(B组)、吡格列酮干预组(C组)、GW9662+吡格列酮组(D组)及二甲基亚砜组(E组),每组16只.用线栓法制作CIR损伤大鼠模型,于术前3d起分别给予各组大鼠相应药物(A组和B组大鼠为生理盐水)静脉注射;均为每天1次,连续3d.在缺血再灌注24 h后给各组大鼠进行神经功能缺损评分(NDS),用ELISA法测定大鼠脑组织核因子-κB (NF-κB)及干扰素-γ(IFN-γ)水平,HE染色观察缺血区病理学改变,尼氏染色和原位末端标记染色检测神经元数及凋亡细胞数.对大鼠脑组织NF-κB与IFN-γ水平(B组,C组)的相关性作直线相关分析.结果 与A组相比,其他4组的NDS、脑组织NF-κB和IFN-γ水平、细胞凋亡数均明显升高,健存神经细胞数明显减少(P ＜0.05 ～0.01).与C组相比,B组、D组、E组的NDS、NF-κB和IFN-γ水平、细胞凋亡数均显著升高,健存神经细胞数明显减少(均P＜0.05).B组、C组大鼠脑组织NF-κB与IFN-γ水平呈正相关(r=0.952,r =0.978,均P＜0.001).结论 吡格列酮对CIR损伤有显著的神经保护作用.其可能通过下调脑组织NF-κB的表达,减少IFN-γ,的释放,使健存神经细胞增加、神经细胞凋亡减少,从而发挥神经保护作用的.     

鞘内注射LXM-10对神经病理性疼痛大鼠Fos蛋白和P2X3受体表达的影响

目的 研究鞘内注射新型镇痛药LXM-10（2,4-dimethyl-9-β-phenylethyl-3-oxo-6,9-diazaspiro[5,5]undecane chloride,2,4-乙烷基-9-β-苯乙酸-3-oxo-6,9-二氮杂螺环-[5,5]十二烷基盐酸盐,LXM-10）对神经病理性疼痛（neuropathic pain,NPP）大鼠脊髓背角和背根神经节Fos蛋白和P2X3受体表达的影响。方法 选取SD大鼠108只,随机分为假手术组（S组）、对照组（C组）和药物组（L组）,对照组和药物组制备坐骨神经慢性压迫模型（chronic constriction injury of the sciatic nerve,CCI-SN）。假手术组、药物组和对照组根据给药时间不同分为3个亚组（n=12只）,药物组和对照组分别在CCI-SN造模成功后1、5、12d开始向蛛网膜下腔注射生理盐水10μl,连续3d,分别设为C3组、C7组、C14组,或向蛛网膜下腔注射LXM-10 6μg/kg,连续3d,分别设为L3组、L7组、L14组;假手术组仅在相应时间点向鞘内注射生理盐水,设为S3组、S7组、S14组。连续注射3d后于末次给药后2h处死动物,取腰膨大脊髓节段和腰4～6背根神经节分别进行免疫组化实验检测Fos蛋白和P2X3受体的表达情况。结果 对照组各时间点Fos蛋白随着时间延长表达增强,Fos蛋白主要表达于脊髓背角。药物组在各时间点脊髓背角Fos蛋白免疫反应阳性（Fos-like immunoreactivity,F-LI）细胞均较相应时间点对照组明显减少（（L3组 vs C3组,P =0.003;L7组 vs C7组,P =0.023;L14组 vs C14组,P =0.005）。背根神经节中Fos蛋白变化趋势同脊髓背角（L3组 vs C3组,P =0.002;L7组 vs C7组,P =0.003;L14组 vsC14组,P =0.002）。P2X3在CCI-SN造模成功后3～14d,表达逐渐升高,主要在背根神经节表达。在脊髓背角药物组各时间点P2X3阳性细胞表达均较对照组对应时间点降低（L3组 vs C3组,P =0.043;L7组 vs C7组,P =0.008;L14组 vs C14组,P=0.005）。在背根神经节鞘内给药后,各时间点P2X3阳性细胞表达明显减少（L3组 vs C3组,P =0.034;L7组 vs C7组,P =0.001;L14组 vs C14组,P =0.003）。结论 对于NPP大鼠,CCI-SN后脊髓背角和背根神经节中Fos蛋白和P2X3受体表达均明显增强。LXM-10鞘内给药可明显降低二者表达。     

加巴喷丁联合盐酸羟考酮缓释片对癌性神经痛患者疼痛介质的影响

目的研究加巴喷丁联合盐酸羟考酮缓释片对癌性神经痛患者疼痛介质的影响。方法选取我院2014-07—2015-07收治的癌性神经痛患者70例,抽签随机分为观察组与对照组各35例,对照组给予盐酸羟考酮缓释片治疗,观察组给予加巴喷丁联合盐酸羟考酮缓释片治疗。比较2组临床疗效、治疗前后视觉模拟评分法(VAS)评分,比较2组去甲肾上腺素(NE)、多巴胺(DA)、5-羟色胺(5-HT)含量变化情况及不良反应发生率。结果观察组临床总有效率为82.86%,较对照组的60%显著较高(P0.05);观察组VAS评分(1.72±1.02)分,显著低于对照组的(2.83±1.04)分(P0.05);观察组5-HT水平(706.51±147.48)ng/g,显著低于对照组的(812.18±178.62)ng/g(P0.05)。结论加巴喷丁联合盐酸羟考酮缓释片治疗癌性神经痛疗效显著,能显著降低患者体内疼痛介质水平,是一种安全可靠的治疗方法,值得临床应用推广。     

臭氧对大鼠神经病理性疼痛镇痛作用的实验研究

目的 探讨臭氧对大鼠神经病理性疼痛起镇痛作用的部位和所需的臭氧浓度.方法 应用成年雄性SD大鼠建立部分坐骨神经损伤(SNI)模型,采用随机数字表法分四组.即手术局部组、坐骨神经组、L5脊神经组、联合组(手术局部和L5脊神经),每组6只,于对应部位注射50μg/mL臭氧.另外,取SNI模型建立后12 d大鼠,采用随机数字表法分四组,每组6只.四个组分别以40μg/mL、50μg,mL、60μg/mL和70μg/mL臭氧浓度对联合注射部位处理.采用大鼠50%的机械刺激撤足阈值(PWT)为观察项目.结果 联合组和L5脊神经组在臭氧干预后机械痛阈明显升高,与其他处理组相比差异有统计学意义(P<0.05).在联合部位注射不同浓度臭氧的处理后,不同浓度间痛阈改变差异无统计学意义(P>0.05).结论 臭氧对神经病理性疼痛镇痛的作用部位在手术局部和L5脊神经处.40～70μg/mL的臭氧对神经病理性疼痛均有镇痛效果.     

Meteorin reverses hypersensitivity in rat models of neuropathic pain

Neuropathic pain is caused by a lesion or disease to the somatosensory nervous system and current treatment merely reduces symptoms. Here, we investigate the potential therapeutic effect of the neurotrophic factor Meteorin on multiple signs of neuropathic pain in two distinct rat models. In a first study, two weeks of intermittent systemic administration of recombinant Meteorin led to a dose-dependent reversal of established mechanical and cold hypersensitivity in rats after photochemically-induced sciatic nerve injury. Moreover, analgesic efficacy lasted for at least one week after treatment cessation. In rats with a chronic constriction injury (CCI) of the sciatic nerve, five systemic injections of Meteorin over 9days dose-dependently reversed established mechanical and thermal hypersensitivity as well as weight bearing deficits taken as a surrogate marker of spontaneous pain. The beneficial effects of systemic Meteorin were sustained for at least three weeks after treatment ended and no adverse side effects were observed. Pharmacokinetic analysis indicated that plasma Meteorin exposure correlated well with dosing and was no longer detectable after 24hours. This pharmacokinetic profile combined with a delayed time of onset and prolonged duration of analgesic efficacy on multiple parameters suggests a disease-modifying mechanism rather than symptomatic pain relief. In sciatic nerve lesioned rats, delivery of recombinant Meteorin by intrathecal injection was also efficacious in reversing mechanical and cold hypersensitivity. Together, these data demonstrate that Meteorin represents a novel treatment strategy for the effective and long lasting relief from the debilitating consequences of neuropathic pain.     

N-methyI-D-aspartate receptor effects on p38 mitogen activated protein kinase and its role in a rat model of diabetic neuropathic pain

BACKGROUND： Activated N-methyl-D-aspartate （NMDA） receptor is involved in the formation of chronic neuropathic pain, and its antagonist, ketamine, exhibits effective amelioration of diabetic neuropathic pain （DNP）. However, the mechanisms of NMDA receptor participation in the formation and maintenance of DNP remain poorly understood. OBJECTIVE： To evaluate the role NMDA receptor plays in DNP and effects on p38 mitogen activated protein kinase （p38 MAPK） in a rat model of DNP. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Human Embryonic Stem Cell Research Institute of Yunyang Medical College Affiliated Taihe Hospital between July 2005 and September 2007. MATERIALS： Streptozotocin was provided by Sigma, USA; p38 MAPK inhibitor （SB203580） was provided by Shanghai KangChen Biotech, China; NMDA receptor antagonist （MK-801） was purchased from Shanghai Yope Biotech, China. METHODS： A total of 128 healthy, Wistar rats of clean grade, aged 3 months and weighing 180- 220 g, were randomly assigned to 4 groups： control, DNP model, p38 MAPK, and NMDA receptor. Each group contained 32 rats. DNP was established in all groups except for the control group by intraperitoneal injection of streptozocin （65 mg/kg）. Subsequently, 1 mg/kg SB203580 and 1 mg/kg MK-801 were injected once each week via intraperitoneal injection in the p38 MAPK and NMDA receptor groups, respectively. MAIN OUTCOME MEASURES： At the end of 2, 4, 6, and 8 weeks following streptozotocin injection, mechanical withdrawal threshold was measured in 8 animals from each group following von Frey filament stimulation. The rats were anesthetized and nerve conduction velocity of the left sciatic nerve was measured. Subsequently, the right sciatic nerve, the lumbar segment of the spinal cord, and dorsal root ganglia were removed from the L3-6 segment for microscopic examination, p38 MAPK expression was determined using immunohistochemistry and Western blot analysis. Expression of NMDA receptor 1 mRNA in dorsal root ganglion and spinal cord neurons was detected using RT-PCR. RESULTS： Mechanical withdrawal threshold and nerve conduction velocity were significantly reduced, and p38 MAPK and NMDA receptor 1 mRNA expression in the spinal cord and dorsal root ganglia were significantly increased, in the model, p38 MAPK, and NMDA receptor groups compared with the control group at all time points （P 〈 0.05）. At 4-8 weeks following successful DNP model establishment, SB203580 and MK-801 increased mechanical withdrawal threshold, accelerated nerve conduction velocity, and attenuated p38 MAPK expression, compared with the model group. The NMDA receptor group exhibited downregulated mRNA expression of NMDA receptor 1 compared with the model and p38 MAPK groups （P 〈 0.05）. CONCLUSION： NMDA receptor was highly expressed in the brains of DNP rats and was involved in DNP development via activation of the p38 MAPK signal pathway.     

A brief,high-dose remifentanil infusion partially reverses neuropathic pain in a subgroup of post herpetic neuralgia patients

Mechanism-based therapy for chronic pain is desperately needed. Recent basic science research demonstrated that remifentanil can reverse long-term potentiation at C-fiber synapses in the dorsal horn of rats. In this exploratory, single group study, patients with chronic post-herpetic pain were treated with a single, one-hour, high-dose remifentanil infusion. The mean overall change of pain intensity seven days after treatment was −18 (−7.5; −28.5, 95%CI, p < 0.001) points on the numeric rating scale (0–100) (−33 (±11) points amongst responders only). Eleven of 20 patients responded to treatment (≥30% reduction in pain), the mean relative reduction in pain from baseline amongst responders was 61.0%. These promising preliminary results suggest that a mechanism-based reversal of chronic pain may be impending.     

脊髓电刺激治疗神经病理性疼痛的测试效果及其影响因素分析

目的探讨采用脊髓电刺激(SCS)治疗神经病理性疼痛(NP)的测试效果及其影响因素。方法回顾性分析2012年1月至2019年12月首都医科大学宣武医院功能神经外科采用SCS治疗的81例NP患者的临床资料。对所有患者选择双极刺激模式,频率为30~60 Hz,脉宽为180~260μs,电压为0.5~2.0 V。以疼痛改善率作为SCS测试是否有效的主要评估指标,计算公式为:疼痛改善率=[术前视觉模拟评分(VAS)-术后VAS]/术前VAS×100%;其中疼痛改善率>50%为测试有效,≤50%为测试无效。采用单因素和多因素logistic回归分析法分析影响NP患者SCS测试效果的危险因素。结果81例患者均成功植入电极。81例患者术后疼痛改善率为(45.9±2.9)%;术后VAS为(4.5±2.5)分,较术前[(8.3±1.2)分]显著下降(t=13.67,P<0.01)。根据SCS测试有效的评估标准,45例患者为测试有效,36例为测试无效;测试有效率为55.6%(45/81)。单因素分析结果显示,年龄、性别、病程、术前VAS、病因、疼痛侧别及疼痛区感觉均不是SCS测试效果的影响因素(均P>0.05),而疼痛部位是SCS测试效果的影响因素(P<0.05)。进一步多因素logistic回归分析结果显示,疼痛位于下肢是影响SCS测试效果的保护因素(OR=3.14,95%CI:1.26~7.83,P=0.013)。结论采用SCS治疗NP的测试有效率较高;疼痛位于四肢,特别是下肢的NP患者测试效果较好。     

EFNS guidelines on pharmacological treatment of neuropathic pain

Neuropathic pain treatment remains unsatisfactory despite a substantial increase in the number of trials. This EFNS Task Force aimed at evaluating the existing evidence about the pharmacological treatment of neuropathic pain. Studies were identified using first the Cochrane Database then Medline. Trials were classified according to the aetiological condition. All class I and II controlled trials (according to EFNS classification of evidence) were assessed, but lower-class studies were considered in conditions that had no top level studies. Only treatments feasible in an outpatient setting were evaluated. Effects on pain symptoms/signs, quality of life and comorbidities were particularly searched for. Most of the randomized controlled trials included patients with postherpetic neuralgia (PHN) and painful polyneuropathies (PPN) mainly caused by diabetes. These trials provide level A evidence for the efficacy of tricyclic antidepressants, gabapentin, pregabalin and opioids, with a large number of class I trials, followed by topical lidocaine (in PHN) and the newer antidepressants venlafaxine and duloxetine (in PPN). A small number of controlled trials were performed in central pain, trigeminal neuralgia, other peripheral neuropathic pain states and multiple-aetiology neuropathic pains. The main peripheral pain conditions respond similarly well to tricyclic antidepressants, gabapentin, and pregabalin, but some conditions, such as HIV-associated polyneuropathy, are more refractory. There are too few studies on central pain, combination therapy, and head-to-head comparison. For future trials, we recommend to assess quality of life and pain symptoms or signs with standardized tools.     

Wireless peripheral nerve stimulation increases pain threshold in two neuropathic rat models

Neurostimulation approaches including spinal cord and peripheral nerve stimulation are typically used to treat intractable chronic pain in individuals who are refractory to pain medications. Our earlier studies have shown that a voltage controlled capacitive discharge (VCCD) method of stimulation of nerve activation is able to selectively recruit activity in large myelinated nerve fibers. In this study, we were able to wirelessly activate the sciatic nerve using the VCCD waveform. The purpose of this study was to determine whether this waveform can effectively improve two of the most troublesome pain symptoms experienced by patients with chronic neuropathic pain mechanical and cold hyperalgesia. Neuropathic mechanical hyperalgesia was reproduced using the Spinal Nerve Ligation (SNL) rat model whereas cold allodynia was reproduced using the Chronic Constriction Injury (CCI) model in male rats. Von Frey and cold plate tests were used to evaluate paw withdrawal threshold and latency to withdrawal before and after stimulation in experimental and control rats. Paw withdrawal threshold increased significantly compared to post-lesion baseline after VCCD stimulation in SNL rats. We also observed a significant improvement in cold allodynia in the active implant CCI rats after stimulation. These results suggest that the VCCD stimulation using a wireless microstimulator may be effective in the treatment of neuropathic pain.     

Interest of registries in neuropathic pain research

Neuropathic pain is frequent in the general population, with 7 to 10% of adults presenting with chronic neuropathic pain. To date, the gold standard to evaluate treatments is based on randomized controlled trials. Nonetheless, such design is run on a limited sample and for a limited period. Moreover, many treatments will never be compared directly in sufficiently large and representative populations. A way to overcome several of these limitations is to use real-world data. Indeed, the International Association for the Study of Pain (IASP) includes a special interest group focusing on pain registries and promoting the use of such approaches. In this short narrative review, several of the main chronic pain registries are presented. The strengths and weaknesses of this approach are presented. Indication bias is frequent in observational studies because the choice of treatment is generally influenced by the patients’ characteristics. However, a propensity score can be computed to adjust for these differences. The use of propensity score is briefly explained. Some data specific to neuropathic pain are discussed.