异丙酚对慢性神经痛大鼠脊髓诱导型一氧化氮合酶表达的影响

目的 研究不同剂量异丙酚对慢性神经痛大鼠触诱发痛痛阈及其脊髓组织诱导型一氧化氮合酶(iNOS)mRNA的影响。方法 Wistar大鼠40只,随机分为四组,Ⅰ组为空白对照;Ⅱ、Ⅲ、Ⅳ组结扎左侧坐骨神经。术后第7天,Ⅰ、Ⅱ组腹腔注射生理盐水50 ml·kg-1,Ⅲ、Ⅳ组腹腔注射异丙酚50 ml·kg-1或75ml·kg-1,每天一次共6 d。在术后第6、10和12天,使用Von Frey法分别测定各组大鼠触诱发痛痛阈,比较不同剂量的异丙酚对大鼠痛阈的影响。术后第12天取L4-5和L5-6节段脊神经节和脊髓组织,采用半定量RT-PCR法,对各组大鼠脊髓组织iNOS mRNA表达进行检测。结果 术后第10和12天,Ⅲ、Ⅳ组大鼠双侧的痛阈值高于Ⅱ组(P<0.05);术后第12天,Ⅲ、Ⅳ组大鼠脊髓组织iNOS mRNA表达低于Ⅱ组(P<0.05)。结论 异丙酚通过抑制脊髓组织iNOS mRNA转录,降低其表达,而起到一定的抗伤害作用。     

Combined open and laparoscopic approach to chronic pain following open inguinal hernia repair

Introduction: Chronic groin pain is the most common long-term complication after open inguinal hernia repair. Traditional surgical management of the associated neuralgia consists of injection therapy followed by groin exploration, mesh removal, and nerve transection. The resultant hernia defect may be difficult to repair from an anterior approach. We evaluate the outcomes of a combined laparoscopic and open approach for the treatment of chronic groin pain following open inguinal herniorrhaphy. Methods: All patients who underwent groin exploration for chronic neuralgia after a prior open inguinal hernia repair were prospectively analyzed. Patient demographics, type of prior hernia repair, and prior nonoperative therapies were recorded. The operation consisted of a standard three trocar laparoscopic transabdominal preperitoneal hernia repair, followed by groin exploration, mesh removal, and nerve transection. Outcome measures included recurrent groin pain, numbness, hernia recurrence, and complications. Results: Twelve patients (11 male and 1 female) with a mean age of 41 years (range 29–51) underwent combined laparoscopic and open treatment for chronic groin pain. Ten patients complained of unilateral neuralgia, one patient had bilateral complaints, and one patient complained of orchalgia. All patients failed at least two attempted percutaneous nerve blocks. Prior repairs included Lichtenstein (n=9), McVay (n=1), plug and patch (n=1), and Shouldice (n=1). There were no intraoperative complications or wound infections. With a minimum of 6 weeks follow up, all patients were significantly improved. One patient complained of intermittent minor discomfort that required no further therapy. Two patients had persistent numbness in the ilioinguinal nerve distribution but remained satisfied with the procedure. Conclusions: A combined laparoscopic and open approach for postherniorrhaphy groin pain results in good to excellent patient satisfaction with no perioperative morbidity. It may be the preferred technique for the definitive management of chronic neuralgia after prior open hernia repair.     

神经病理性疼痛老年大鼠海马CA1区突触长时程增强的变化

目的观察神经病理性疼痛老年大鼠海马CA1区突触长时程增强(LTP)的变化。方法老年雄性Wistar大鼠15只,随机均分为三组。模型组,结扎左侧L4/L5脊神经;D-2-氨基-5-磷酸戊酸(AP5)组,侧脑室输注AP5,余同模型组;假手术组,操作同模型组,但不结扎。观察大鼠行为变化,连续3周测定大鼠电痛阈值,1次/周;记录海马CA1区树突层兴奋性突触后膜电位(EPSP)、输入/输出曲线及LTP的变化。结果模型组与AP5组大鼠术后行为异常,术后各时点电痛阈值低于术前值及假手术组相应时点值(P<0.05);三组基础EPSP幅值稳定,最大基础EPSP幅值的50%组间比较差异无统计学意义;模型组LTP高于其他两组(P<0.05)。结论结扎老年大鼠L4/L5脊神经所致的神经病理性疼痛,不干扰海马CA1区突触及锥体细胞兴奋性,但可易化该区突触LTP。     

背根神经节Nav1.8磷酸化在大鼠糖尿病痛性周围神经病变中的作用

目的 本研究采用射频热凝毁损腰交感神经节,探讨背根神经节（DRG）Nav1．8磷酸化在大鼠糖尿病痛性周围神经病变中的作用。方法 采用腹腔注射链尿佐菌素诱导糖尿病痛性周围神经病变大鼠模型,取造模成功的大鼠20只,随机分为糖尿病对照组（D组）及交感神经节射频热凝组（R组）,每组10只,另取10只同月龄大鼠为正常对照组（C组）。R组大鼠在X光机介导下行右侧L3,4椎旁腰交感神经节射频热凝毁损。分别于射频热凝前、射频热凝后1、2周时,采用von Frey纤维丝测定大鼠右侧后爪对机械性刺激缩足反应的阈值（PWT）;射频热凝后2周,采用Western-blotting方法测定DRG细胞Nav1．8蛋白和苏氨酸磷酸化Nav1．8蛋白表达,并采用透射电镜观察大鼠腓肠神经超微病理结构。结果 与C组比较,射频热凝前D组和R组PWT降低（P＜0．01）。射频热凝后1～2周,R组较D组PWT升高,但仍较C组降低（P＜0．05）。C组髓鞘排列均匀,轴突内可见形态正常的线粒体;D组脱髓鞘明显,髓鞘板层排列紊乱、断裂、肿胀;R组脱髓鞘程度明显减轻,髓鞘板层局部排列紊乱、空泡形成。与C组比较,D组和R组Nav1．8蛋白表达降低（P＜0．05）,而苏氨酸磷酸化Nav1．8蛋白表达增高（P＜0．01）;R组苏氨酸磷酸化Nav1．8蛋白表达低于D组（P＜0．05）。结论 DRG细胞Nav1．8的磷酸化可能是糖尿病痛性周围神经病变大鼠痛觉过敏形成的机制之一。     

p38丝裂原活化蛋白激酶在糖尿病大鼠神经病理性痛中的作用

目的探讨p38丝裂原活化蛋白激酶（p38MAPK）在链脲菌素诱导的糖尿病大鼠神经病理性痛中的作用。方法雌性Wistar大鼠31只，3月龄，体重180～220g，随机分为3组：对照组（C组，n=10）、糖尿病神经病理性痛组（D组，n=11）和p38MAPK抑制剂组（Ⅰ组，n=10）。D组、Ⅰ组单次腹腔注射链脲菌素65mg／kg制备糖尿病模型。糖尿病模型制备成功后，Ⅰ组尾静脉注射p38MAPK抑制剂SB203580 0．5mg／kg，1次／周，连续4周；C组和D组尾静脉注射等体积的生理盐水。给药4周后，测定机械缩足反应阈值（MWT）、左侧坐骨神经传导速率（NCV）、背根神经节（DRG）和脊髓的磷酸化p38MAPK水平。结果与C组比较，D组、Ⅰ组MWT下降，NCV减慢，伴有脱髓鞘现象，DRG和脊髓的磷酸化p38MAPK水平升高；与D组比较，Ⅰ组MWT升高，NCV增快，脱髓鞘程度减轻，DRG和脊髓的磷酸化p38MAPK水平下降。结论p38MAPK信号转导通路参与了糖尿病大鼠神经病理性痛的形成。     

慢性神经病理性痛大鼠背根神经节P2Y2受体mRNA的表达

目的评价背根神经节（DRG）P2Y2受体mRNA的表达在大鼠慢性神经病理性痛中的作用。方法SPF级大鼠24只,体重150～200g,雌雄不拘,随机分为2组：假手术组（S组）和慢性神经痛组（N组）,每组12只。N组结扎左侧坐骨神经建立大鼠慢性压迫性损伤（CCI）模型,S组只暴露,不结扎左侧坐骨神经。2组分别于CCI前1d、CCI后1、4、7、10、14 d进行行为学观察,测定大鼠双后肢热痛阈和机械痛阈,并分别于CCI后7、14 d各取6只大鼠断颈处死,取双侧L（4-6）背根神经节,RT-PCR法测定P2Y2受体mRNA的表达。结果两组CCI后4 d热痛阈、机械痛阈明显降低（P〈0.05）,持续至CCI后14 d;N组左侧DRG P2Y2受体mRNA表达较右侧明显下调,CCI后14 d较CCI后7 d下调（P〈0.05）;与S组右侧比较,N组DRG P2Y2受体mRNA表达差异无统计学意义（P〉0.05）。结论背根神经节P2Y2受体mRNA的表达下调参与了大鼠慢性神经病理性痛的形成。     

针灸治疗三叉神经痛的文献述评

根据近10年所发表的针灸现代文献，对针灸治疗三叉神经痛的选穴特点、针灸治疗规律、疗效进行评价，并对目前临床研究中存在的问题及今后研究的重点提出了建设性的意见。     

深刺局部穴治疗三叉神经痛疗效观察

目的:寻找提高三叉神经痛疗效的有效方法.方法:将90例原发性三叉神经痛患者随机分为深刺组(45例)、常规针刺组(45例).常规针刺组以局部近取浅刺和循经远取手足阳明经穴位为主,深刺组在此基础上对局部穴位采用深刺达神经干的方法.治疗3个疗程后统计疗效.结果:两组均收到明显疗效,深刺组临床治愈12例,显效24例,好转7例,无效2例,有效率为95.6%;而常规针刺组分别为7例、15例、12例、11例、75.6%.深刺组疗效优于常规针刺组(P＜0.05).结论:针刺治疗三叉神经痛,局部穴位深刺加循经远取手足阳明经穴位,能明显提高疗效.     

Cómo y cuándo derivar un paciente con cefalea primaria y neuralgia craneofacial desde Urgencias y Atención Primaria: recomendaciones del Grupo de Estudio de Cefalea de la Sociedad Española de Neurología

IntroductionWhen a patient is diagnosed with primary headache or craniofacial neuralgia in the emergency department or in primary care, and is referred to a neurologist due to the complexity of the case, it is useful to know whether additional examination should be sought and the priority (urgent, preferential or normal) with which the patient should be seen. This will avoid unnecessary delays in patients with disabling headache and where organic causes are suspected.In order to issue recommendations on this matter, the Spanish Society of Neurology's Headache Study Group has decided to create a series of agreed recommendations constituting a referral protocol for patients with headache and/or craniofacial neuralgia.DevelopmentYoung neurologists with an interest and experience in headache were invited to draft a series of practical guidelines in collaboration with Spanish Society of Neurology's Headache Study Group Executive Committee. For practical reasons, the document was divided into 2 articles: this first article focuses on primary headaches and craniofacial neuralgias and the second on secondary headaches. In order for the recommendations to be helpful for daily practice they follow a practical approach, with tables summarising referral criteria, examinations to be performed, and referral to other specialists.ConclusionsWe hope to offer a guide and tools to improve decision-making regarding patients with headache, identifying complementary tests to prioritise and referral pathways to be followed, in order to avoid duplicated consultations and delayed diagnosis and treatment.     

Neuropathic Pain Model of Peripheral Neuropathies Mediated by Mutations of Glycyl-tRNA Synthetase

Charcot-Marie-Tooth disease (CMT) is the most common inherited motor and sensory neuropathy. Previous studies have found that, according to CMT patients, neuropathic pain is an occasional symptom of CMT. However, neuropathic pain is not considered to be a significant symptom associated with CMT and, as a result, no studies have investigated the pathophysiology underlying neuropathic pain in this disorder. Thus, the first animal model of neuropathic pain was developed by our laboratory using an adenovirus vector system to study neuropathic pain in CMT. To this end, glycyl-tRNA synthetase (GARS) fusion proteins with a FLAG-tag (wild type [WT], L129P and G240R mutants) were expressed in spinal cord and dorsal root ganglion (DRG) neurons using adenovirus vectors. It is known that GARS mutants induce GARS axonopathies, including CMT type 2D (CMT2D) and distal spinal muscular atrophy type V (dSMA-V). Additionally, the morphological phenotypes of neuropathic pain in this animal model of GARS-induced pain were assessed using several possible markers of pain (Iba1, pERK1/2) or a marker of injured neurons (ATF3). These results suggest that this animal model of CMT using an adenovirus may provide information regarding CMT as well as a useful strategy for the treatment of neuropathic pain.

Graphical Abstract

相似文献