芍药甘草汤加味联合苏肽生治疗周围神经损伤后疼痛临床观察

目的:观察芍药甘草汤加味联合苏肽生治疗周围神经损伤后神经病理性疼痛临床疗效。方法:将136例周围神经损伤后疼痛患者随机分为2组,每组68例。对照组西医常规治疗,治疗组在西药常规治疗的基础上加用芍药甘草汤加味联合苏肽,疗程10d。观察患者治疗前后有效率、疼痛消失时间、睡眠时间变化情况和满意度的情况变化。结果:治疗组疼痛消失时间和患者满意度与对照组比较,具有明显差异;治疗组有效率88.24%,明显高于对照组45.59%;治疗组睡眠时间在治疗的第1天、第4天、第7天和第10天与对照组比较,均具有明显差异。结论:芍药甘草汤加味联合苏肽生治疗能够明显减轻周围神经损伤后神经病理性疼痛。     

背根神经节射频热凝对老年带状疱疹后遗神经痛疗效的影响

<正>Ma Ke等[1]胸神经脉冲射频治疗带状疱疹后神经痛(postherpetic neuralgia,PHN)取得了良好的疗效,Kim等[2]背根神经节脉冲射频明显缓解了PHN患者的疼痛,凌地洋等[3]选择性背根神经节脉冲射频联合普瑞巴林、袁燕等[4]经皮背根神经节脉冲射频联合加巴喷丁治疗PHN,迅速缓解了患者的疼痛症状,改善了睡眠质量。PHN是一种顽固性神经病理性疼痛性疾病,背根神经节脉冲射频同传统射频     

维生素B_(12)与鼠神经生长因子联合使用对神经性耳鸣患者睡眠SPIEGEL评分的影响

目的:研究分析采用维生素B12联合鼠神经生长因子治疗神经性耳鸣患者的疗效及对睡眠SPIEGEL评分的影响。方法:选取2018年3月至2019年3月山东省德州市陵城区人民医院耳鼻喉科收治的神经性耳鸣患者100例,随机分为观察组和对照组,每组50例。观察组采用维生素B12联合鼠神经生长因子治疗,对照组采用维生素B12治疗,比较2组患者治疗临床效果、睡眠SPIEGEL评分和生命质量评分。结果:观察组在治疗总有效率、睡眠SPIEGEL评分、生命质量评分方面明显较高,2组比较差异有统计学意义(P 0. 05)。结论:在神经性耳鸣患者中采用维生素B12联合鼠神经生长因子治疗,能提高患者治疗的临床总有效率,还能提高睡眠SPIEGEL评分。     

普瑞巴林或加巴喷丁药物联合神经阻滞治疗带状疱疹后神经痛的疗效比较

【目的】对比分析普瑞巴林联合神经阻滞和加巴喷丁联合神经阻滞治疗带状疱疹（HZ）后神经痛（PHN）的疗效和安全性。【方法】收集PHN患者100例,按照治疗方法分为两组,每组50例,A组采用口服普瑞巴林联合神经阻滞治疗,B组采用加巴喷丁联合神经阻滞治疗,共治疗3周。用视觉模拟评分（visual an-alogue scale,VAS）和24 h睡眠时间来评价治疗效果,同时观察两组并发症及药物不良反应。【结果】在3周住院期间,两组患者治疗后各时点与治疗前相比疼痛评分随时间下降,睡眠时间均增加（P ＜0．05）;A组的VAS评分下降大于B组,24 h睡眠时间增加大于B组（P＜0．05）;两组未出现并发症及严重的药物副作用。【结论】普瑞巴林联合神经阻滞及加巴喷丁联合神经阻滞治疗 PHN,均可迅速缓解疼痛,改善睡眠质量,但前者疗效优于后者。     

重复经颅磁刺激治疗脊髓损伤后慢性神经病理性疼痛8例报道

目的探讨重复经颅磁刺激(rTMS)对脊髓损伤后慢性神经病理性疼痛的疗效。方法 2014年6月至2015年12月,8例脊髓损伤后慢性神经病理性疼痛患者应用rTMS治疗5周,治疗前后采用疼痛数字分级量表和睡眠状况自评表进行评定。结果治疗后,患者疼痛数字分级评分下降4~6分,疼痛程度由重度降至轻中度;睡眠状况自评分下降9~20分。结论 rTMS对部分脊髓损伤后慢性神经病理性疼痛有效,可与药物联合治疗。     

时间护理在慢性神经病理性疼痛中的应用研究

目的探讨时间护理在慢性神经病理性疼痛中的应用效果。方法选取62例慢性神经病理性疼痛患者为研究对象,分为试验组和对照组各31例,对照组给予常规护理,试验组在此基础上遵循时间护理原则,结合认知情况、用药护理、音乐疗法及心理治疗等进行护理干预。对比两组患者住院第1天、第3天、第7天,进行疼痛视觉模拟评分、睡眠质量评分和满意度评分。结果住院第3天、第7天,试验组疼痛视觉模拟评分明显低于对照组(P0.01),试验组睡眠质量评分明显优于对照组(P0.01);住院第1天、第3天、第7天,试验组护理满意度评分均高于对照组(P0.01)。结论时间护理能显著缓解患者慢性神经病理性疼痛,提高睡眠质量和护理满意度。     

普瑞巴林联合神经妥乐平治疗脊髓损伤患者神经病理性疼痛的疗效观察

目的:探讨神经妥乐平对于脊髓损伤后神经病理性疼痛的临床疗效,同时比较单独使用神经妥乐平与联合使用普瑞巴林和神经妥乐平对神经病理性疼痛的缓解程度、对患者情绪以及睡眠状况的改善情况。方法:选取符合入组标准的脊髓损伤伴神经病理性疼痛患者62例,电脑随机分2组,分别为神经妥乐平组、普瑞巴林联合神经妥乐平组,神经妥乐平组起始剂量为4U bid,普瑞巴林联合神经妥乐平组起始剂量为普瑞巴林75mg bid+神经妥乐平4U bid,间隔3d调整药物剂量,疗程为4周。采用视觉模拟评分量表(visual analogue scale,VAS)、医院焦虑抑郁量表(hospital anxiety and depression scale,HAD)、匹茨堡睡眠质量指数量表(Pittsburgh sleep quality index,PSQI)对患者进行疼痛、情绪和睡眠质量的评估。由专业的康复治疗师对患者服药前和疗程结束后的疗效分别进行评估。结果:单独使用神经妥乐平可以缓解脊髓损伤患者神经病理性疼痛,同时改善患者睡眠质量,治疗前后比较差异有显著性意义(P0.05);而联合使用普瑞巴林和神经妥乐平治疗后,患者的VAS和HAD评分均较神经妥乐平组明显降低,差异有显著性意义(P0.05)。结论:神经妥乐平可以缓解脊髓损伤患者的疼痛症状,联合使用普瑞巴林和神经妥乐平不仅明显缓解脊髓损伤神经病理性疼痛患者的疼痛症状,同时显著改善了患者的焦虑抑郁情绪,提高患者睡眠质量,进而提升患者生存质量,是一种有效的临床治疗方法。     

皮内注射联合口服药物治疗胸背部带状疱疹后神经痛的临床观察

目的:观察皮内注射联合口服药物治疗胸背部带状疱疹后神经痛的临床疗效和安全性。方法:60例确诊为胸背部带状疱疹后神经痛的患者,采用数字表法随机均分为两组,对照组(n=30):口服加巴喷丁、神经妥乐平和盐酸曲马多;观察组(n=30):在口服药物的基础上联合疼痛区域的皮内注射治疗。观察治疗前及治疗后不同时期(治疗后7 d、14 d和28 d)疼痛程度和睡眠质量的变化。采用视觉模拟评分(visual analogue scale,VAS)及睡眠质量(quality of sleep,QS)综合评定治疗效果,并记录并发症和不良反应的发生率。结果:两组治疗后各时期VAS评分均较治疗前明显降低,睡眠质量评分均较治疗前明显增加(P<0.01);观察组在治疗后各时期VAS评分较对照组同期明显降低,睡眠质量评分较对照组同期明显升高(P<0.01)。观察组在治疗后24 h内未出现局部血肿。两组患者在口服药物后出现程度不等的不良反应,患者均可耐受。结论:皮内注射联合口服药物治疗胸背部带状疱疹后神经痛效果好,可以迅速缓解疼痛症状、改善患者睡眠质量,且安全性良好。     

加巴喷丁与普瑞巴林治疗带状疱疹后神经痛的效果比较

目的观察加巴喷丁和普瑞巴林治疗带状疱疹后神经痛(post-herpetic neuralgia,PHN)的效果以及对患者睡眠的影响。方法 60例PHN患者按随机数字表法分为加巴喷丁组和普瑞巴林组各30例,分别给予加巴喷丁900 mg/d口服和普瑞巴林150 mg/d口服,疗程均为28天。观察治疗前后疼痛和睡眠的改善情况及药物不良反应。结果两组患者治疗后各时点与治疗前相比疼痛评分随时间下降,睡眠时间增加(P<0.05);普瑞巴林组治疗后各时点的疼痛视觉模拟评分(Visualanalogue scale,VAS)低于加巴喷丁组(P<0.05),24小时睡眠时间大于加巴喷丁组(P<0.05);两组未出现严重的药物不良反应,普瑞巴林组嗜睡发生率明显低于加巴喷丁组(P<0.05),其余不良反应发生率两组间比较差异均无统计学意义(P>0.05)。结论普瑞巴林治疗PHN更安全有效,优于加巴喷丁。     

注射用鼠神经生长因子联合吡拉西坦对脑梗死后血管性痴呆MMSE评分及日常生活能力的影响

目的:探讨注射用鼠神经生长因子联合吡拉西坦对脑梗死后血管性痴呆患者MMSE评分及日常生活能力的影响。方法:选取我院2015年3月~2017年8月脑梗死后血管性痴呆患者82例,按照治疗方法不同分为观察组和对照组各41例。两组均给予常规治疗,对照组加用注射用鼠神经生长因子治疗,观察组用注射用鼠神经生长因子及吡拉西坦治疗。比较两组临床疗效及治疗前后MMSE、ADL评分。结果:观察组治疗总有效率明显高于对照组(P<0.05);治疗前,两组MMSE、ADL评分比较无显著性差异(P>0.05);治疗后,观察组MMSE、ADL评分均高于对照组(P<0.05)。结论:注射用鼠神经生长因子联合吡拉西坦治疗脑梗死后血管性痴呆效果确切,可显著提高患者认知功能及日常生活能力。     

Analysis and treatment of different types of neuropathic cancer pain

Neuropathic pain is a major problem in the treatment of cancer pain. We performed a retrospective analysis of 213 cancer patients with neuropathic pain treated by a pain service following the World Health Organization guidelines for relief of cancer pain. Of these, 79% presented with nerve compression pain, 16% with nerve injury pain, and 5% with sympathetically-maintained pain. Whereas nerve compression and nerve injury pain were caused most frequently by cancer growth, sympathetically-maintained pain was caused most frequently by cancer treatment. There were no significant differences in the use of analgesics, the mean pain intensity, or the efficacy of analgesic treatment among the three groups. Nerve injury pain and sympathetically-maintained pain were treated more frequently with adjuvant analgesics, especially antidepressants and anticonvulsants. The variety of different neuropathic pain syndromes should be separated in future studies of the efficacy of different treatment approaches.     

阿片类药物在慢性非癌性疼痛中的应用

目的:回顾性分析卡马西平和加巴喷丁治疗原发性三叉神经痛、带状疱疹以及带状疱疹后遗神经痛的疗效、安全性和不良反应。方法:102位患者进入本研究,比较卡马西平或加巴喷丁治疗前后患者疼痛强度的改变和对睡眠影响的改善;依据药物分类,比较两种药物的副作用和不良反应。结果:卡马西平治疗原发性三叉神经痛起效较加巴喷丁快,二者长期疗效相当;加巴喷丁治疗带状疱疹和带状疱疹后神经痛的疗效优于卡马西平;疗效随治疗时间的延长而增加。卡马西平的副作用和不良反应事件发生率较加巴喷丁高。结论:抗癫痫药物卡马西平和加巴喷丁是治疗神经病理性疼痛的有效药物,可以改善患者的睡眠,但副作用和不良反应发生率高。     

A role for inflammation in chronic pain

Recent studies indicate that inflammatory events induced by nerve injury play a central role in the pathogenesis of neuropathic pain. These involve inflammatory cells (eg, macrophages), the production of molecules that mediate inflammation (cytokines/interleukins), and the production of nerve growth factor (NGF). However, in many instances, neuropathic pain is associated with nerve inflammation, neuritis, in the absence of nerve injury. Studies on the role of cytokines in neuropathic pain have only recently begun, mostly in model systems that involve nerve injury. Little is known about the role of inflammation in neuropathic pain in the absence of nerve injury. We developed an animal model to study neuropathic pain and underlying inflammatory mechanisms in a system in which neuropathic pain is induced by nerve inflammation in the absence of injury, neuritis. Neuritis is provoked by local application of complete Freund’s adjuvant (CFA) on the sciatic nerve. The following events in the course of experimental neuritis are described: 1) the time course of neuropathic pain, 2) the structural changes in axons and myelin, and 3) the spontaneous electrical activity (peripheral sensitization). It is conceivable that biochemical and physiologic changes (inflammatory mediators) that occur along the “pain pathway” (nociceptors, peripheral nerve, dorsal root ganglion [DRG]), dorsal root, neurons in the spinal cord) may sensitize one or all these sites along the pain pathway and hence lead to chronic pain).     

损伤大鼠L5脊神经及其前后根对痛行为的影响

目的:观察大鼠腰5脊神经和脊神经根不同部位损伤对诱导神经病理性疼痛的不同作用。方法:采用腰5脊神经结扎加切断(lumbar5 spinal nerve ligation,L5 SNL)、腰5前根切除(lumbar5 ventral rhizotomy,L5 VR)和腰5背根切除(lumbar5 dorsal rhizotomy,L5 DR)诱导大鼠痛觉过敏,结合痛行为学测试观察病理性疼痛的发展过程。结果:(1)L5SNL可引起大鼠病理性疼痛。双侧后肢50%撤足阈值(paw withdrawal threshold,PWT)和撤足潜伏期(paw withdrawal latency,PWL)于术后1d明显下降,痛觉过敏的症状,在同侧后肢持续了5周,在对侧后肢也保持3周。(2)L5 VR也可诱导大鼠产生病理性疼痛。双侧后肢50%PWT和PWL于术后1d明显降低,并维持到了术后第5周。(3)L5DR没有引起大鼠产生痛觉过敏症状。与术前基础值和假手术组比较,L5DR后50%PWT和PWL均无明显变化。结论:选择性损伤运动纤维和损伤脊神经均能诱导大鼠产生病理性疼痛,但脊神经背根损伤不引起痛觉过敏。     

An Improved Rodent Model of Trigeminal Neuropathic Pain by Unilateral Chronic Constriction Injury of Distal Infraorbital Nerve

The number of studies on trigeminal nerve injury using animal models remains limited. A rodent model of trigeminal neuropathic pain was first developed in 1994, in which chronic constriction injury (CCI) is induced by ligation of the infraorbital nerve (IoN). This animal model has served as a major tool to study trigeminal neuropathic pain. Unfortunately, the surgical procedure in this model is complicated and far more difficult than ligation of peripheral nerves (eg, sciatic nerve). The aim of this study was to improve on the current surgical procedure of IoN ligation to induce trigeminal neuropathic pain in rats. We show that the IoN can be readily accessed through a small facial incision. CCI can be induced by ligation of a segment at the distal IoN (dIoN). This dIoN-CCI procedure is simple, minimally invasive, and time-saving. Our data show that the dIoN-CCI procedure consistently induced acute as well as chronic nociceptive behaviors in rats. Daily gabapentin treatment attenuated mechanical allodynia and reduced face-grooming episodes in dIoN-CCI rats.

Modality of hyperalgesia tested,not type of nerve damage,predicts pharmacological sensitivity in rat models of neuropathic pain

Although many types of nerve damage can cause neuropathic pain, there are substantial commonalities in neuropathic pain symptoms, and patients can be divided into sub‐groups based on their symptom profile rather than etiology. Mechanism‐based treatment suggests that pharmacotherapy should be chosen be based shared commonalities of symptoms rather than etiology. The aim of the present study was to determine whether type of injury (etiology) or behavioral endpoint (symptom) is a better predictor of pharmacological responsivity in the most commonly used rodent models of neuropathic pain. We used the chronic constriction injury (CCI) model to directly compare the temporal and pharmacological characteristics of four different types of evoked stimuli; heat, pressure, acetone cooling and punctate mechanical. We then compared heat hyperalgesia and mechanical allodynia endpoints across etiologies using the spinal nerve ligation (SNL) model. Evoked pain responses in both models had strikingly different temporal characteristics. We then tested three standard therapies for neuropathic pain from different drug classes, oxycodone, gabapentin, and amitriptyline. Notably, regardless of the model tested, or the time of onset, common endpoints showed near‐identical pharmacological responses, and not all endpoints were equally sensitive to drug intervention within one model. Hypersensitivity to heat and pressure were highly responsive to oxycodone, gabapentin, and amitriptyline; whereas cold and mechanical allodynia were more difficult to reverse. Moreover, CCI‐ and SNL‐induced mechanical allodynia was completely insensitive to amitriptyline treatment. We conclude that regardless of model and time course of presentation, different symptoms of peripheral neuropathy have unique pharmacological responses.     

Tramadol and several anticonvulsants synergize in attenuating nerve injury-induced allodynia

Neuropathic pain results from injury or dysfunction of the central or peripheral nervous system. The treatment of neuropathic pain is challenging, in part because of its multiple etiologies. The present study explores combinations of the analgesic tramadol and each of four anticonvulsants in the treatment of surgically induced (ligation of the L5 spinal nerve) allodynia in rats. Each of the five drugs studied exhibited a dose-dependent antiallodynic effect. When studied in combination, tramadol and each of two of the anticonvulsants (topiramate and RWJ-333369) interacted synergistically at all three ratios studied, whereas tramadol and each of the other two anticonvulsants (gabapentin and lamotrigine) exhibited a synergistic antiallodynic effect at only one of three ratios investigated. In addition, tramadol and topiramate were found to interact synergistically in a nociceptive pain model, the mouse hot-plate test. These studies suggest the benefit of using combinations of analgesics and anticonvulsants in the relief of neuropathic pain.     

Gabapentin in traumatic nerve injury pain: a randomized, double-blind, placebo-controlled, cross-over, multi-center study

A double-blind, randomized, placebo-controlled cross-over multi-center study was conducted to evaluate the efficacy and safety of gabapentin in the treatment of neuropathic pain caused by traumatic or postsurgical peripheral nerve injury, using doses up to 2400 mg/day. The study comprised a run-in period of two weeks, two treatment periods of five weeks separated by a three weeks’ washout period. The primary efficacy variable was the change in the mean pain intensity score from baseline to the last week of treatment. Other variables included pain relief, health related quality of life (SF-36), interference of sleep by pain, Clinician and Patient Global Impression of Change, and adverse effects. Nine centers randomized a total of 120 patients, 22 of whom withdrew. There was no statistically significant difference between the treatments for the primary outcome efficacy variable. However, gabapentin provided significantly better pain relief (p = 0.015) compared with placebo. More patients had at least a 30% pain reduction with gabapentin compared with placebo (p = 0.040) and pain interfered significantly less with sleep during gabapentin treatment compared with placebo (p = 0.0016). Both the Patient (p = 0.023) and Clinician (p = 0.037) Global Impression of Change indicated a better response with gabapentin compared with placebo. Gabapentin was well tolerated. The most common adverse effects were dizziness and tiredness.     

Gabapentin suppresses ectopic nerve discharges and reverses allodynia in neuropathic rats

Repetitive ectopic discharges from injured afferent nerves play an important role in initiation and maintenance of neuropathic pain. Gabapentin is effective for treatment of neuropathic pain but the sites and mechanisms of its antinociceptive actions remain uncertain. In the present study, we tested a hypothesis that therapeutic doses of gabapentin suppress ectopic afferent discharge activity generated from injured peripheral nerves. Mechanical allodynia, induced by partial ligation of the sciatic nerve in rats, was determined by application of von Frey filaments to the hindpaw. Single-unit afferent nerve activity was recorded proximal to the ligated sciatic nerve site. Intravenous gabapentin, in a range of 30 to 90 mg/kg, significantly attenuated allodynia in nerve-injured rats. Furthermore, gabapentin, in the same therapeutic dose range, dose-dependently inhibited the ectopic discharge activity of 15 injured sciatic afferent nerve fibers through an action on impulse generation. However, the conduction velocity and responses of 12 normal afferent fibers to mechanical stimulation were not affected by gabapentin. Therefore, this study provides electrophysiological evidence that gabapentin is capable of suppressing the ectopic discharge activity from injured peripheral nerves. This action may contribute, at least in part, to the antiallodynic effect of gabapentin on neuropathic pain.