三叉神经痛患者血液降钙素基因相关肽的观察

目的：观察三叉神经痛发作时是否有降钙素基因相关肽参与，加深对三叉神经痛发病机理的认识。方法：用放射免疫法检测７例三叉神经痛患者疼痛发作时患侧颈外静脉血，肘静脉血及术后患颈外静脉血中降钙素基因相关肽的含量。结果：发现疼痛发作时患侧颈外静脉血中降钙素基因相关肽含量显著高于肘静脉血及术后患侧颈外静脉血中降钙素基因相关肽的含量。     

降钙素基因相关肽与三叉神经痛发病关系的临床研究

目的 :通过研究三叉神经痛患者疼痛发作时是否有降钙素基因相关肽 (calcitoningene -relatedpeptide ,CGRP)参与 ,痛支与非痛支神经组织中CGRP含量是否有所不同 ,加深对三叉神经痛发病机理的认识。方法 :用放射免疫法检测 16例三叉神经痛患者疼痛发作时患侧颈外静脉血、肘静脉血及术后患侧颈外静脉血中CGRP含量并以 10名同年龄组健康成人颈外静脉血中的CGRP含量作为正常对照 ;用免疫组织化学法标记 16例患者痛支与非痛支神经切片中CGRP免疫反应阳性颗粒 ,定量观察痛支与非痛支神经纤维中CGRP免疫反应阳性颗粒的数量、面积、平均光密度和平均面积 ,从免疫反应阳性颗粒的数量和面积两个方面来说明痛支与非痛支神经纤维中CGRP的含量有无差异 ;结果 :疼痛发作时患侧颈外静脉血中CGRP含量显著升高 ,与肘静脉血、术后患侧颈外静脉血及健康对照组颈外静脉血中的CGRP含量相比 ,差异非常显著 (P <0 .0 1) ,而后三者相比差异均不显著 (P >0 .0 5 ) ;痛支神经纤维中CGRP免疫反应阳性颗粒的数量、面积均明显高于非痛支中CGRP免疫反应阳性颗粒 ,差异非常显著 (P <0 .0 1) ;结论 :CGRP与三叉神经痛发病关系密切 ,三叉神经痛发作时局部确有CGRP的参与 ,三叉神经痛的痛支神经过度合成和释放降钙素基因相关肽可能促进了局     

三叉神经痛患者血浆血管活性肠肽的观察

目的:观察三叉神经痛发作时临近原发病灶的静脉血中是否有血管活性肠肽(VIP) 的参与。方法:用放射免疫法测定16 例三叉神经痛患者,疼痛发作时患侧颈外静脉血、肘静脉血及三叉神经颅底高位切断术后患侧颈外静脉血中VIP 含量,并与11 例正常自愿者颈外静脉血中VIP 的含量比较。结果:疼痛发作时患侧颈外静脉血中的VIP含量明显高于患者肘静脉血、术后患侧颈外静脉血及正常自愿者颈外静脉血中的VIP 含量。结论:三叉神经痛发作时临近原发病灶的静脉血中确有VIP 参与,其作用可能与增强P 物质在局部形成神经源性炎症有关。     

神经肽与三叉神经痛发病关系的临床研究

目的：观察三叉神经痛发病是否与P物质（SP）、降钙素基因相关肽（CGRP）、血管活性肠多肽（VIP）以及β内啡肽（β－EP）有关。方法：用放射免疫法检测患者疼痛发作时患侧颈外静脉血、肘静脉血及术后患侧颈外静脉血中SP、CGRP、VIP、β－EP含量，正常志愿者颈外静脉血中SP、CGRP、VIP、β－EP含量作正常对照；用免疫组织化学法观察患者痛支与非痛支神经组织中SP、CGRP免疫反应阳性颗粒的差异。结果：疼痛发作时患侧颈外静脉血中SP、CGRP、VIP含量明显升高，患者血浆β－EP含量显著降低；痛支神经组织中SP、CGRP免疫反应阳性颗粒的数量、总面积均显著多于、大于非痛支神经组织中的SP、CGRP免疫反应阳性颗粒。结论：患者体内神经肽的合成或释放异常可能与三叉神经痛的发病有关。     

P物质与三叉神经痛发病关系的临床研究

我们用放射免疫法检测三叉神经痛患者血浆Ｐ物质(ｓｕｂｓｔａｎｃｅＰ ,ＳＰ)的含量 ,用免疫组织化学法观察痛支与非痛支神经组织中ＳＰ免疫反应阳性颗粒的差异 ,报道如下。1 材料和方法 :原发性三叉神经痛住院患者 32例 ,自愿者 10名。用放射免疫法检测 16例患者疼痛发作时患侧颈外静脉血、肘静脉血及术后患侧颈外静脉血中ＳＰ含量 ,10名自愿者颈外静脉血中ＳＰ含量作为正常对照 ;用免疫组织化学法观察 16例患者痛支与非痛支神经组织中ＳＰ免疫反应阳性颗粒的差异。2 结果 :疼痛发作时患侧颈外静脉血中ＳＰ含量明显高于肘静脉血、术后患…     

三叉神经痛患者血浆β—内啡肽含量的观察

目的：确定血浆β－内啡肽与三叉神经痛发病的关系。方法：用放射免疫法检测12例患者疼痛发作时患侧颈外静脉血、健上静脉血、肘静脉血及术后患者颈外静脉血中β-内啡肽含量,12例正常自愿者颈外静脉血中β内啡肽含量作为正常对照。结果：患者血浆β-内啡肽含量显著低于正常人（P＜0．05）;疼痛发作时患者颈外静脉血中β-内啡肽含量与健侧颈外静脉血、肘静脉血中β－内啡肽含量无显著差异,与术后患者颈外静脉血中β－内啡肽含量也无显著差异（P＞0．05）。结论三叉神经痛患者血浆β－内啡肽含量降低,中枢内源性痛觉调制系统对疼能的抑可能减弱,外周神经源性炎症可能得不到有效的控制。     

三叉神经痛发作与降钙素基因相关肽的临床研究

降钙素基因相关肽（CGRP）与速激肽作为伤害性刺激的递质或调质而存在于感觉神经元中，可引起三叉神经“神经血管系”的神经元性炎症反应，参与三叉神经痛的发生。本研究对三叉神经痛治疗前后颈外静脉血中CGRP的含量进行观察并初步探讨CGRP浓度与疼痛强度的关系。     

三叉神经痛患者神经纤维降钙素基因相关肽的观察

目的 :观察三叉神经痛患者痛支与非痛支神经纤维中降钙素基因相关肽的含量变化 ,加深对三叉神经痛发病机理的认识。方法 :用免疫组织化学法观察 16例患者痛支与非痛支神经纤维组织中降钙素基因相关肽免疫反应阳性颗粒的差异。结果 :发现痛支神经组织中降钙素基因相关肽免疫反应阳性颗粒的数量、面积均显著多于、大于非痛支神经组织中的降钙素基因相关肽免疫反应阳性颗粒。结论 :我们认为 :三叉神经痛的痛支神经过度合成和释放降钙素基因相关肽可能促进了SP的释放 ,导致阵发性剧烈疼痛 ,并在局部形成神经源性炎症。     

三叉神经痛患者神经纤维降钙素基因相关肽的观察

目的：观察三叉神经痛患者痛支与非痛支神经纤维中降钙素基因相关肽的含量变化，加深对胡叉神经痛发病机理的认识。方法：用免疫组织化学法观察１６例患者痛支与非痛支神经纤维组织中降钙素基因相关肽免疫反应阳性颗粒的差异。结果：发现痛支神经组织中降钙素基因相关肽免疫反应阳性颗粒的数量、面积均显著多于、大于非痛支神经组织中的降钙素基因相关肽免疫反应性颗粒。结论：我们认为：三叉神经痛的痛支神经过度合成和释放降钙素基     

根治性颈淋巴清扫术改善术后肩功能的方法探讨

目的 探讨一种改进根治性颈清扫术式对术后肩功能的影响。方法 随机选择20例需行颈清扫术的患者分为2组，每组10例。试验组行根治性颈清扫术时保留颈丛深支，对照组行常规根治性颈清扫术。术后3周及6个月随访．对术后患侧斜方肌功能进行评价。结果 术后3周两组患者均有不同程度的肩功能受损；术后6个月试验组患者患侧肩部无明显下垂，患侧上肢外展稍超越水平线。对照组患侧肩部有不同程度下垂，肩部疼痛，麻木，上肢外展不能超过水平线。结论 保留颈丛深支的根治性颈淋巴清扫术能明显改善术后患侧的肩臂功能，减轻传统术式术后肩部的疼痛、麻木感。该术式不影响根治颈清扫术的疗效，易于临床开展。     

A novel technique of delivering viral vectors to trigeminal ganglia in rats

The objective of this study was to develop a viable and reliable technique of delivering viral vectors to rat trigeminal ganglia. Adult Sprague‐Dawley rats (200–300 g) were used, and lentiviral vectors containing enhanced green fluorescence protein and calcitonin gene‐related peptide short hairpin RNA (shRNA) were generated. Following general anesthesia, viral vectors were delivered to rat trigeminal ganglia using the technique described in this study. Both X‐ray and micro‐computed tomography (micro‐CT) were employed to verify the position of the needles when injecting the vectors. In vivo fluorescence imaging and immunostaining against enhanced green fluorescence protein were performed to determine the success of viral transduction.The levels of calcitonin gene‐related peptide in trigeminal ganglia were determined using real‐time PCR, and pain levels following injections were evaluated using the Rat Grimace Scale. Our results show that injection needles can be advanced precisely at the trigeminal fossa and that viral vectors can successfully transduce trigeminal ganglia. Moreover, the levels of calcitonin gene‐related peptide at trigeminal ganglia were down‐regulated on day 7 after viral transduction. Pain levels returned to baseline by day 7 following injection. Therefore, we suggest that our trigeminal ganglion‐targeting technique could be used for delivering genes or drugs to rat trigeminal ganglia.     

双侧颈内静脉结扎后颅内静脉回流通道的解剖学观察

目的:研究双侧根治性颈淋巴清扫术后颅内静脉血液回流通道的分布和开放情况。方法:选用猕猴,在双侧颈内静脉结扎情况下作经上矢状窦的染料灌注和动物尸检。结果:椎管静脉丛,颈外静脉,椎静脉,颈深静脉和咽食管静脉丛等明显充盈和染色。结论:颈内静脉阻断后,上述静脉均是颅内静脉血液的回流通道     

Neuropeptide Y Y1 receptor effects on pulpal nociceptors

Neuropeptide Y (NPY) is an important modulatory neuropeptide that regulates several physiological systems, including the activity of sensory neurons. We evaluated whether activation of the NPY Y1 receptor could modulate the activity of capsaicin-sensitive nociceptors in trigeminal ganglia and dental pulp. We tested this hypothesis by measuring capsaicin-stimulated calcitonin gene-related peptide release (CGRP) as a measure of nociceptor activity. Capsaicin-evoked CGRP release was inhibited by 50% (p < 0.05) in trigeminal ganglia and by 26% (p < 0.05) in dental pulp when tissues were pre-treated with [Leu(31),Pro(34)]NPY. The Y1 receptor was found to co-localize with the capsaicin receptor TRPV1 in trigeminal ganglia. These results demonstrate that activation of the Y1 receptor results in the inhibition of the activity of capsaicin-sensitive nociceptors in the trigeminal ganglia and dental pulp. These findings are relevant to the physiological modulation of dental nociceptors by endogenous NPY and demonstrate an important novel analgesic target for the treatment of dental pain.     

Spontaneous pain attacks: neuralgic pain

Paroxysmal orofacial pains can cause diagnostic problems, especially when different clinical pictures occur simultaneously. Pain due to pulpitis, for example, may show the same characteristics as pain due to trigeminal neuralgia would. Moreover, the trigger point of trigeminal neuralgia can either be located in a healthy tooth or in the temporomandibular joint. Neuralgic pain is distinguished into trigeminal neuralgia, glossopharyngeal neuralgia, Horton's neuralgia, cluster headache and paroxysmal hemicrania. In 2 cases trigeminal neuralgia is successfully managed with a neurosurgical microvascular decompression procedure according to Jannetta. Characteristic pain attacks resembling neuralgic pain result from well understood pathophysiological mechanisms. Consequently, adequate therapy, such as a Janetta procedure and specific pharmacological therapy, is available.     

Lipopolysaccharide from Porphyromonas gingivalis sensitizes capsaicin-sensitive nociceptors

Although odontogenic infections are often accompanied by pain, little is known about the potential mechanisms mediating this effect. In this study we tested the hypothesis that trigeminal nociceptive neurons are directly sensitized by lipopolysaccharide (LPS) isolated from an endodontic pathogen, Porphyromonas gingivalis. In vitro studies conducted with cultures of rat trigeminal neurons demonstrated that pretreatment with LPS produced a significant increase in the capsaicin-evoked release of calcitonin gene-related peptide (CGRP) when compared with vehicle pretreatment, thus showing sensitization of the capsaicin receptor, TRPV1, by LPS. Furthermore, confocal microscopic examination of human tooth pulp samples showed the colocalization of the LPS receptor (toll-like receptor 4, TLR4) with CGRP-containing nerve fibers. Collectively, these results suggest the direct sensitization of nociceptors by LPS at concentrations found in infected canal systems as one mechanism responsible for the pain associated with bacterial infections.     

LPS sensitizes TRPV1 via activation of TLR4 in trigeminal sensory neurons

Recent studies have demonstrated that the lipopolysaccharide (LPS) receptor (TLR4) is expressed in TRPV1 containing trigeminal sensory neurons. In this study, we evaluated whether LPS activates trigeminal neurons, and sensitizes TRPV1 responses via TLR4. To test this novel hypothesis, we first demonstrated that LPS binds to receptors in trigeminal neurons using competitive binding. Second, we demonstrated that LPS evoked a concentration-dependent increase in intracellular calcium accumulation (Ca(2+))(i) and inward currents. Third, LPS significantly sensitized TRPV1 to capsaicin measured by (Ca(2+))(i), release of calcitonin gene-related peptide, and inward currents. Importantly, a selective TLR4 antagonist blocked these effects. Analysis of these data, collectively, demonstrates that LPS is capable of directly activating trigeminal neurons, and sensitizing TRPV1 via a TLR4-mediated mechanism. These findings are consistent with the hypothesis that trigeminal neurons are capable of detecting pathogenic bacterial components leading to sensitization of TRPV1, possibly contributing to the inflammatory pain often observed in bacterial infections.