临床药师参与1例癌性神经病理性疼痛的药物治疗

目的 探索临床药师在癌痛药物治疗中的作用。方法 临床药师以会诊的形式参与1例重度癌痛患者的药物治疗。通过开展癌痛评估,结合患者用药史及临床表现,临床药师判断患者合并癌性神经病理性疼痛,出现阿片类药物耐受,针对性调整药物止痛治疗方案并指导患者用药。结果 临床药师的参与有效减轻了患者的疼痛程度,提高了患者的生活质量。结论 临床药师在癌痛的药物治疗中发挥了有效作用。     

羟考酮治疗晚期结肠癌癌性神经病理性疼痛的临床疗效分析

目的分析羟考酮治疗晚期结肠癌癌性神经病理性疼痛的临床疗效。方法选取我院2015年7月至2016年5月收治的88例晚期结肠癌癌性神经病理性疼痛患者予以分组,按照硬币法分为对照组和研究组,每组44例,对照组予以常规治疗,研究组在此基础上予以羟考酮治疗,观察并比较2组治疗前后疼痛情况和生活质量。结果研究组治疗后疼痛评分、生活质量评分均低于对照组,组间表现出的差异具有统计学意义(P <0.05)。结论羟考酮可显著减轻晚期结肠癌癌性神经病理性疼痛程度,改善生活质量,值得在临床中推广和普及应用。     

普瑞巴林联合羟考酮治疗癌性神经病理性疼痛的临床效果

目的 观察普瑞巴林联合羟考酮治疗癌性神经病理性疼痛的临床效果.方法 回顾性选取2018年11月—2020年4月广东省深圳市人民医院收治的癌性神经病理性疼痛患者107例,根据治疗方法不同分为观察组(n=53)和对照组(n=54).观察组给予普瑞巴林联合羟考酮治疗,对照组给予羟考酮治疗,2组患者均治疗14 d.比较2组患者...     

芬太尼透皮贴剂联合加巴喷丁治疗癌性神经病理性疼痛21例疗效观察

目的观察芬太尼透皮贴剂联合加巴喷丁治疗癌性神经病理性疼痛的镇痛疗效及毒性反应。方法 21例神经病理性疼痛的癌症患者接受治疗。芬太尼初治剂量25μg/h,前曾用过强阿片类药物者根据用药情况进行剂量转换给药;用药后观察24h,疼痛缓解欠佳时进行剂量滴定,按25μg/h增加剂量,直至疼痛缓解。加巴喷丁初始剂量为100mg/次,3次/d,每间隔1~2d,增加剂量300mg/d,直至疼痛缓解或见难以耐受的副作用。1周后采用NPS评分标准评价镇痛疗效及毒性反应。结果有效率90.5%（19/21）,其中,完全缓解率28.6%（6/21）,明显缓解率为47.6%（10/21）,轻度缓解率14.3%（3/21）。主要不良反应是头晕、恶心、便秘、嗜睡、皮肤痛痒等,但发生率较低。无呼吸抑制、成瘾现象发生。结论芬太尼透皮贴剂联合加巴喷丁治疗癌性神经病理性疼痛疗效确切,毒性反应轻,值得临床应用。     

盐酸羟考酮缓释片联合复方苦参注射液治疗癌性神经病理性疼痛

目的:观察盐酸羟考酮缓释片联合复方苦参注射液治疗癌性神经病理性疼痛患者的近期疗效和不良反应.方法:将 72 例癌性神经病理性疼痛患者随机分为两组各 36 例,治疗组口服盐酸羟考酮缓释片 40 mg,q 12 h,联合复方苦参注射液 30 ml 稀释后静脉滴注,qd.对照组口服盐酸羟考酮缓释片 40 mg,q 12 h.两组治疗后第 3、7 和 14 d 进行疗效比较.结果:治疗后第 7 d 治疗组、对照组疼痛治疗有效率分别为 88. 9% 和61. 1%(P = 0. 014);治疗后第 14 d 治疗组、对照组疼痛治疗有效率分别为 91. 7% 和 75. 0% ;差异均有统计学意义(P < 0. 05).14 d 内人均羟考酮剂量调整次数,治疗组(1. 44 ± 1. 40)次,对照组为(2. 47 ± 1. 97)次,差异有显著性(P < 0. 05).治疗组恶心呕吐发生率为 33. 3% ,显著低于对照组恶心呕吐发生率 61. 1%(P < 0. 05).结论:盐酸羟考酮缓释片联合复方苦参注射液治疗癌性神经病理性疼痛效果良好,并可降低恶心呕吐发生率.     

癌性疼痛联合用药

癌症病人有疼痛症状的占50～70％，癌症导致病人情绪上的忧郁、绝望又使疼痛加剧，如此恶性循环。统计数字表明：癌性疼痛77％由癌症本身引起，19％由治疗引起．4％为与癌症无关的其他因素。同时，研究证实，4%以上的癌痛病人的疼痛原因有2个以上。药物治疗，作为癌症止痛的首选疗法，可使80％病人的疼痛得以缓解。     

2011-2012年厦门市第二医院癌性疼痛镇痛药应用分析

目的：了解癌性疼痛评估方法及癌性疼痛镇痛药在临床的用药趋势,并评价癌性疼痛镇痛药临床使用的合理性,为临床合理用药提供参考。方法：随机抽查我院2011年及2012年每年癌性疼痛治疗病历各60份,收集癌性疼痛镇痛药使用数据,并对其使用趋势进行分析。结果：2012年我院癌性疼痛镇痛药的总用量比2011年有所增长;吗啡制剂用量最大,居首位。结论：所抽查病历中癌性疼痛镇痛药用药结构趋于规范化,使用情况总体趋于合理化。     

富氢液联合羟考酮控释片对癌性神经病理性疼痛的临床疗效观察

目的：探讨富氢液（HRW）联合盐酸羟考酮控释片（OHCT）对癌性神经病理性疼痛（MNP）的临床疗效。方法：选择80例 MNP 患者随机分成 OHCT 治疗组（A 组）和 HRW 联合 OHCT 治疗组（B 组）,观察两组患者的 VAS 评分、爆发痛情况、疼痛缓解率、OHCT 用量及药物不良反应。结果：用药治疗后两组患者的 VAS 评分和爆发痛发作次数均较治疗前显著降低（P ＜0.05）;在治疗第14 d 和28 d 后 VAS 评分、疼痛缓解率、爆发痛发作次数及 OHCT 用量等方面 B 组比 A组患者改善更明显（P ＜0.05）,且便秘、恶心和呕吐等不良反应明显减少（P ＜0.05）。结论：HRW 联合 OHCT 治疗能更有效改善 MNP 临床症状,并减少 OHCT 用量及药物不良反应。     

2010—2012年濮阳市油田总医院癌性疼痛患者镇痛药应用分析

目的：了解我院肿瘤科门诊及住院癌性疼痛患者镇痛药的使用情况,为临床规范化治疗癌性疼痛提供依据。方法：通过HIS系统统计2010—2012年我院肿瘤科门诊及住院癌性疼痛患者所使用的镇痛药种类、数量及销售金额,采用世界卫生组织（WHO）推荐的限定日剂量（DDD）、用药频度（DDDs）和限定日费用（DDC）等进行统计、分析。结果：2010—2012年我院盐酸羟考酮缓释片（10 mg）的DDDs在住院患者中逐年上升;硫酸吗啡缓释片（30 mg）的DDDs在门诊患者中稳居第1位;DDC最高的为芬太尼透皮贴剂。结论：我院癌性疼痛患者镇痛药的使用基本合理。     

NMDA受体及其拮抗剂的研究进展

N-甲基-D-天冬氨酸(NMDA)受体是一种离子型谷氨酸受体,在中枢神经系统兴奋性的突触传递、可塑性和兴奋毒性中起着关键作用,与机体的记忆、学习和情绪密切相关.本文从结构分布和生理活性这两方面详细总结了N-甲基-D-天冬氨酸受体各亚型的特点,介绍并汇总了目前研究较多的N-甲基-D-天冬氨酸受体拮抗剂,为N-甲基-D-天...     

Topical analgesics in neuropathic pain

Neuropathic pain can be difficult to treat clinically, as current therapies involve partial effectiveness and significant adverse effects. Following the development of preclinical models for neuropathic pain, significant advances have been made in understanding the neurobiology of neuropathic pain. This includes an appreciation of the molecular entities involved in initiation of pain, the role of particular afferents (small and large diameter, injured and uninjured), and the contribution of inflammation. Currently, topical formulations of capsaicin (cream) and lidocaine (patch) are available for treating neuropathic pain in humans. Preclinical studies provide evidence that peripheral applications of opioids, alpha-adrenergic agents, and antidepressants also may be beneficial in neuropathic pain, and some clinical reports provide support for topical applications of such agents. An appreciation of the ability of drug application, to sites remote from the site of injury, to alleviate aspects of neuropathic pain will provide a significant impetus for the further development of novel topical analgesics for this condition.     

Current treatment options in neuropathic pain

Neuropathic pain results from damage to the nervous system due to many diverse processes. It causes persistent, distressing pain that is reputedly unresponsive to conventional analgesics. Treatment is best managed in a multi-therapy pain clinic setting and pharmacotherapy is one facet of this treatment. There is no single effective drug treatment and patients have been empirically treated with antidepressants and antiepileptics in the past. This review focuses on evidence from randomized controlled trials to assess the efficacy of the currently available drug treatments.     

氨酚曲马多联合普瑞巴林治疗癌性神经病理性疼痛的疗效观察

目的探究氨酚曲马多片联合普瑞巴林胶囊治疗癌性神经病理性疼痛的临床疗效。方法选取2015年4月—2017年4月郑州大学附属郑州中心医院收治的癌性神经病理性疼痛患者150例为研究对象,所有患者随机分为普瑞巴林组、氨酚曲马多组和联合治疗组,每组各50例。普瑞巴林组口服普瑞巴林胶囊,75 mg/次,2次/d;氨酚曲马多组口服氨酚曲马多片,100 mg/次,1次/d;联合治疗组口服普瑞巴林胶囊和氨酚曲马多片,用法同上。所有患者均连续治疗4周。观察两组的临床疗效,比较两组的疼痛数字(NRS)评分、生活质量(QOL)评分和睡眠质量(MOS)评分。结果治疗后,普瑞巴林组、氨酚曲马多组、联合治疗组疼痛总缓解率分别为62.00%、64.00%、82.00%,联合治疗组与普瑞巴林组、氨酚曲马多组比较差异具有统计学意义(P0.05)。治疗后,3组NRS评分均显著降低,同组治疗前后比较差异具有统计学意义(P0.05);且联合治疗组NRS评分明显低于普瑞巴林组、氨酚曲马多组,两组比较差异具有统计学意义(P0.05)。治疗后,3组QOL评分均显著降低,同组治疗前后比较差异具有统计学意义(P0.05);且联合治疗组QOL评分明显低于普瑞巴林组、氨酚曲马多组,两组比较差异具有统计学意义(P0.05)。治疗后,普瑞巴林组、联合治疗组睡眠干扰(SLPD)、睡眠量(SLPQ)评分显著降低,睡眠充足度(SLPA)评分显著升高,同组治疗前后比较差异具有统计学意义(P0.05);且联合治疗组这些观察指标的改善程度明显优于普瑞巴林组、氨酚曲马多组,3组比较差异具有统计学意义(P0.05)。结论氨酚曲马多片联合普瑞巴林胶囊治疗癌性神经病理性疼痛具有较好的临床疗效,可缓解患者癌性疼痛,改善患者生活质量和睡眠质量,安全性较好,具有一定的临床推广应用价值。     

神经病理性疼痛的治疗和药物发现现状

神经病理性疼痛(neuropathic pain,NP)是一直困扰人类的医学难题,严重影响人民生活质量.尽管近年来关于NP的研究取得了很大进展,但是依旧有很多患者对现有的治疗无效.目前药物治疗依旧是缓解疼痛的主要方法,然而药物不良反应阻碍了疗效的发挥,寻找新型药物靶点及减少现有药物的不良反应迫在眉睫.本综述将主要阐述神...     

局部皮下注射神经妥乐平治疗神经源性疼痛的临床观察

目的通过临床观察评价神经妥乐平局部皮下注射治疗神经源性疼痛的疗效与安全性。方法21例神经源性疼痛患者皮下注射神经妥乐平3.6 U/次,1周2次,连续3周为1个疗程,采用疼痛视觉模拟评分法(VAS法)评定疗效并进行统计学分析。结果治疗后患者疼痛强度显著性降低(P<0.05),未出现明显不良反应。结论神经妥乐平皮下注射治疗神经源性疼痛,有效、安全、简便。     

Mechanisms of neuropathic pain

Neuropathic pain is a disease of global burden. Its symptoms include spontaneous and stimulus-evoked painful sensations. Several maladaptive mechanisms underlying these symptoms have been elucidated in recent years: peripheral sensitization of nociception, abnormal excitability of afferent neurons, central sensitization comprising pronociceptive facilitation, disinhibition of nociception and central reorganization processes, and sympathetically maintained pain. This review aims to illustrate these pathophysiological principles, focussing on molecular and neurophysiological findings. Finally therapeutic options based on these findings are discussed.     

Antinociception induced by rosuvastatin in murine neuropathic pain

Background

Neuropathic pain, and subsequent hypernociception, can be induced in mice by paclitaxel (PTX) administration and partial sciatic nerve ligation (PSNL). Its pharmacotherapy has been a clinical challenge, due to a lack of effective treatment. In two models of mouse neuropathic pain (PTX and PSNL) the antinociception induced by rosuvastatin and the participation of proinflammatory biomarkers, interleukin (IL)- 1β, TBARS and glutathione were evaluated.

Pathobiology of neuropathic pain.

This review deals with physiological and biological mechanisms of neuropathic pain, that is, pain induced by injury or disease of the nervous system. Animal models of neuropathic pain mostly use injury to a peripheral nerve, therefore, our focus is on results from nerve injury models. To make sure that the nerve injury models are related to pain, the behavior was assessed of animals following nerve injury, i.e. partial/total nerve transection/ligation or chronic nerve constriction. The following behaviors observed in such animals are considered to indicate pain: (a) autotomy, i.e. self-attack, assessed by counting the number of wounds implied, (b) hyperalgesia, i.e. strong withdrawal responses to a moderate heat stimulus, (c) allodynia, i.e. withdrawal in response to non-noxious tactile or cold stimuli. These behavioral parameters have been exploited to study the pharmacology and modulation of neuropathic pain. Nerve fibers develop abnormal ectopic excitability at or near the site of nerve injury. The mechanisms include unusual distributions of Na(+) channels, as well as abnormal responses to endogenous pain producing substances and cytokines such as tumor necrosis factor alpha (TNF-alpha). Persistent abnormal excitability of sensory nerve endings in a neuroma is considered a mechanism of stump pain after amputation. Any local nerve injury tends to spread to distant parts of the peripheral and central nervous system. This includes erratic mechano-sensitivity along the injured nerve including the cell bodies in the dorsal root ganglion (DRG) as well as ongoing activity in the dorsal horn. The spread of pathophysiology includes upregulation of nitric oxide synthase (NOS) in axotomized neurons, deafferentation hypersensitivity of spinal neurons following afferent cell death, long-term potentiation (LTP) of spinal synaptic transmission and attenuation of central pain inhibitory mechanisms. In particular, the efficacy of opioids at the spinal level is much decreased following nerve injury. Repeated or prolonged noxious stimulation and the persistent abnormal input following nerve injury activate a number of intracellular second messenger systems, implying phosphorylation by protein kinases, particularly protein kinase C (PKC). Intracellular signal cascades result in immediate early gene (IEG) induction which is considered as the overture of a widespread change in protein synthesis, a general basis for nervous system plasticity. Although these processes of increasing nervous system excitability may be considered as a strategy to compensate functional deficits following nerve injury, its by-product is widespread nervous system sensitization resulting in pain and hyperalgesia. An important sequela of nerve injury and other nervous system diseases such as virus attack is apoptosis of neurons in the peripheral and central nervous system. Apoptosis seems to induce neuronal sensitization and loss of inhibitory systems, and these irreversible processes might be in common to nervous system damage by brain trauma or ischemia as well as neuropathic pain. The cellular pathobiology including apoptosis suggests future strategies against neuropathic pain that emphasize preventive aspects.