巴氯芬联合腺苷钴胺治疗三叉神经痛的临床研究

目的探讨巴氯芬联合腺苷钴胺治疗三叉神经痛的临床疗效。方法选取2015年6月—2016年6月在天津市宝坻区人民医院进行治疗的三叉神经痛患者82例,根据治疗方案的差别分为对照组(41例)和治疗组(41例)。对照组患者肌肉注射注射用腺苷钴胺,1次/d。治疗组在对照组的基础上口服巴氯芬片,初始剂量为5 mg/次,3次/d,每4天增加5 mg,直至所需剂量,最大剂量不超过100 mg/次。两组均连续治疗4周。观察两组患者临床疗效,同时比较两组患者治疗前后生活质量评分、血清C反应蛋白(CRP)、白细胞介素-1β(IL-1β)、IL-6、肿瘤坏死因子-α(TNF-α)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)水平以及疼痛评分变化。结果治疗后,对照组和治疗组总有效率分别为80.49%和95.12%,两组总有效率比较差异具有统计学意义(P0.05)。治疗后,两组患者行动能力和自我照顾能力等各项生活质量评分均明显降低(P0.05);且治疗组的生活质量评分降低程度优于对照组(P0.05)。治疗后,两组患者血清CRP、IL-1β、IL-6及TNF-α水平明显低于治疗前(P0.05);且治疗组上述指标水平优于对照组(P0.05)。治疗后,两组患者血清SOD、GSH-Px水平明显高于治疗前(P0.05);与对照组相比,治疗组增高的更明显(P0.05)。治疗后,两组患者VAS评分明显降低(P0.05);且治疗组比对照组降低的更明显(P0.05)。结论巴氯芬联合腺苷钴胺治疗三叉神经痛效果显著,可明显提高患者睡眠质量,减轻机体炎性反应和应激反应,具有一定的临床推广应用价值。     

改良微骨孔完全显微血管减压术治疗三叉神经痛的临床疗效及并发症分析

目的 分析改良微骨孔完全显微血管减压术治疗三叉神经痛的临床疗效及并发症.方法 本研究所选观察对象为本院2010年2月至2016年1月收治的三叉神经痛患者80例,按照数字随机方式将全部患者分成两组,每组40例,两组患者分别给予传统显微血管减压术治疗、改良微骨孔完全显微血管减压术治疗;对两组患者的临床疗效和并发症发生情况进行观察比较.结果 实验组有效率为97.5％,对照组有效率为95.0％,两组比较差异无统计学意义(P＞0.05);实验组发生并发症3例(7.5％),实验组发生并发症7例(17.5％),实验组显著低于对照组(P＜0.05).结论 在对三叉神经痛患者进行治疗时,改良微骨孔完全显微血管减压术治疗具有比较显著的临床疗效,而且并发症发生率低,具有临床应用价值.     

原发性三叉神经痛的治疗新进展

原发性三叉神经痛( idiopathic trigeminal neuralgia,ITN) 是一种在三叉神经分布区内剧烈的短暂发作
的面部疼痛性疾病。病人常常难以忍受,严重影响其生活质量。三叉神经痛的治疗方法多种多样,药物治疗对
于初治病人作为首选,目前效果较好的手术治疗主要有射频热凝术( Ｒadiofrequency thermocoagulation,ＲFT) 、微
血管减压术( microvascular decompression,MVD) 和立体定向放射外科治疗( stereotactic radiosurgery,SＲS) 等。现
就原发性三叉神经痛目前最常用的治疗手段及其最新进展进行综述。     

Organization within the cranial IX-X complex in ranid frogs: a horseradish peroxidase transport study

Cranial nerves IX and X in frogs have been described as originating from a nuclear group referred to as the IX-X complex. We studied the central nervous system components of this complex in Rana pipiens and R. catesbiana by labeling peripheral branches of cranial nerves IX and X and identifying the central nervous system contributions of these branches. Various peripheral nerves (IX and the cardiac, gastric, pulmonary, and laryngeal branches of X) were identified and soaked in horseradish peroxidase (HRP). One to 2 weeks later, the frogs were killed and processed for HRP by the tetramethylbenzidine method. Glossopharyngeal efferents originated from a small ventrolateral cell group found at the level of IX root exit. Vagal efferents formed a single column of cells in a ventrolateral position from the level of the brainstem exist of the vagus nerve (approximately 2,000 micrometers above the obex) to 200 micrometers below the obex (values given are for an 80-g frog). This cell group was separate from and just caudal to efferent cells of the glossopharyngeal nerve. Within the vagal portion of the column, cells projecting through the gastric branch were found throughout the rostral-caudal extent of the nucleus. "Cardiac" cells tended to be more rostral than "pulmonary" cells, and both groups of cells were located in the middle of the nucleus. "Laryngeal" cells were located more caudally in the nucleus. This peripheral representation within the vagal nucleus corresponds more closely to the organization found in the mammalian nucleus ambiguus, rather than to the apparent lack of organization found in the mammalian dorsal motor nucleus. Afferents of IX and X entered slightly rostral to the ventral roots of their respective nerves and descended in two tracts. The majority entered the tractus solitarius and descended in a medial position to cervical spinal cord. A portion of the afferents from the vagus nerve crossed the midline in the lower myelencephalon just dorsal to the central canal and ascended a short distance on the contralateral side. Within the solitary tract, vagal afferents were located in a ventrolateral position as they descended to below the obex. Glossopharyngeal afferents filled the remainder of the tract. A smaller portion of afferents from both IX and X did not enter the solitary tract but descended in the spinal tract of V and the dorsolateral funiculus of the spinal cord (Lissauer's tract) to thoracic levels. Afferents of IX also formed a rostral bundle which extended in the solitary tract to the caudal metencephalon.     

Familial trigeminal neuralgia in charcot-marie-tooth disease

Summary A family is reported in which two members were found to have a peculiar association of Charcot-Marie-Tooth disease with familial trigeminal neuralgia. Electrophysiological studies showed abnormalities of blink reflex and facial nerve conduction. These data, together with otoneurological examination and hypertrophic demyelinating features of peripheral nerve involvement, suggest a common underlying disorder causing a cranial nerve as well as a peripheral neuropathy. It is not possible to exclude a central component at brain stem level.

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Zusammenfassung Anhand zweier Fälle wird der Zusammenhang zwischen einer familiären Charcot-Marie-Tooth-Erkrankung und einer familiären Trigeminusneuralgie diskutiert. Es fanden sich elektrophysiologisch Anomalien des Blinkreflexes und der Erregungsleitung im Nervus facialis. Dies sowie das Ergebnis der oto-neurologischen Untersuchung sowie der Nachweis von hypertrophischen und demyelinisierenden Veränderungen im peripheren Nerven legen den Verdacht einer gemeinsamen Ursache der Störung des Hirnnerven und der peripheren Nerven in den Extremitäten nahe. Eine zentrale Störung im Bereiche des Hirnstammes allerdings kann nicht mit Sicherheit ausgeschlossen werden.

     

上矢状窦神经分布及其临床意义

用5例新鲜成人硬脑膜标本,固定后将上矢状窦按前、中、后三段进行冰冻纵、横切片,银染后在光镜下观察。结果表明,上矢状窦各壁均有神经分布。其中后段神经最多,中段次之,前段最少。此结果一方面说明上矢状窦可能与头痛有关;另方面它的神经可参与调节上矢状窦的血流,从而影响脑表面的静脉回流。     

枕大神经痛诊治的解剖学基础

目的 介绍枕大神经痛的诊断与局部注射的治疗方法。方法 选择门诊确诊为枕大神经痛的患者30余例，采用强的松龙混悬液加局部麻药的局部注射神经通过第二颈椎横突上方一段的治疗方法。结果 所有病例皆在注射后短时完全止痛，多数病例一周后痊愈，少数经2－3次注射后痊愈，少数病人失访。结论 对诊断明确的病例，采用强的松龙注射法，可以获得满意的效果。     

枕大神经痛的解剖学基础

目的：探讨枕大神经痛发病的解剖学基础。方法：防腐固定10例(20侧)和新鲜标本5例(10侧)，以经骨性外耳门中点的水平线和后正中线为轴建立坐标系，定位枕大神经浅出点，观察枕大神经走行分布及其与枕动脉的毗邻关系。结果：(1)枕大神经皮下浅出点位于坐标原点旁开17～20mm；以浅出点为界，枕大神经可分为皮下段和肌内段。(2)皮下段与浅筋膜紧密附着，活动度小，为固定区；肌内段走行于半棘肌和斜方肌腱膜间，神经活动度大，为活动区。结论：颈部运动使活动区和固定区交界部位的神经处于“扭折”状态；浅出点腱膜组织对神经的固定作用造成了神经的“卡压”，此双重作用是构成枕大神经卡压的解剖学基础。     

电针对大鼠三叉神经尾侧脊束核内P物质影响的免疫及超微免疫细胞化学研究

用免疫细胞化学及免疫电镜方法研究了电针对大鼠三叉神经尾侧脊束核内ＳＰ的影响以及含ＳＰ的轴突终末的突触联系。结果表明,电针大鼠“人中”、“承浆”穴后痛阈明显提高（Ｐ＜０．０１）,三叉神经尾侧脊束核内ＳＰ免疫反应活性也较对照组明显增加（Ｐ＜０．０１）。三叉神经尾侧脊束核内含ＳＰ轴突终末内含有密集的清亮透明小泡、少量大颗粒小泡及线粒体,轴突终末内的ＳＰ免疫反应产物分布于大颗粒小泡内和清亮小泡壁上。含ＳＰ的轴突终末主要与三叉神经尾侧脊束核内神经元的树突形成轴－树突触;极少数ＳＰ阴性轴突终末与ＳＰ阳性轴突形成轴－轴突触或接触。电针可能通过轴－轴突触的突触前抑制方式,抑制了三叉神经初级传入细纤维ＳＰ的释放,从而参与针刺镇痛过程。     

Somatic sensory responses in the rostral sector of the posterior group (POm) and in the ventral posterior medial nucleus (VPM) of the rat thalamus.

The rodent barrel field cortex integrates somatosensory information from two separate thalamic nuclei, the ventral posterior medial nucleus (VPM) and the rostral sector of the posterior complex (POm). This paper compares the sensory responses of POm and VPM cells in urethane-anesthetized rats as a first step in determining how cortex integrates multiple sensory pathways. A complete representation of the contralateral body surface was identified in POm. Trigeminal receptive fields (RFs) of POm and VPM cells were mapped by computer-controlled displacement of individual whiskers; responses were quantified by using peristimulus time histograms. Average RF size was similar in POm (5.1 whiskers) and VPM (4.4 whiskers), but evoked responses in the two nuclei differed significantly according to all other measures. VPM cells were maximally responsive to one single whisker--the "center RF." Stimulating this whisker evoked, on average, a response of 1.4 spikes/stimulus at a latency of 7 ms; surrounding whiskers evoked responses of less than 1 spike/stimulus at latencies of greater than 8 ms. In contrast, POm cells were nearly equally responsive to several whiskers. Quantitative criteria allowed us to designate a single whisker as the "center RF" and stimulating this whisker evoked, on average, a response of 0.5 spikes/stimulus at a latency of 19 ms. VPM cells, but not POm cells, were able to "follow" repeated whisker deflection at greater than 5 Hz. We conclude that, when a single whisker is deflected, VPM activates the related cortical barrel-column at short latency--before the onset of activity in POm. The timing of activation could allow POm cells to modulate the spread of activity between cortical columns.