Peripheral mechanisms for the initiation of pain following trigeminal nerve injury.
Peripheral mechanisms for the initiation of pain following trigeminal nerve injury.
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发表时间：
2004
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通讯作者：
P. Robinson;F. Boissonade;A. Loescher;Keith G. Smith;J. Yates;C. Elcock;E. V. Bird;S. Davies;Paula L. Smith;A. R. Vora
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作者：
P. Robinson;F. Boissonade;A. Loescher;Keith G. Smith;J. Yates;C. Elcock;E. V. Bird;S. Davies;Paula L. Smith;A. R. Vora
三叉神经分支的损伤可能导致受影响区域的慢性疼痛的发展。这种情况的病因尚不清楚，但有强有力的证据表明，从损伤部位自发和机械诱导的神经放电起着至关重要的作用。在实验室研究中，我们的特点是这种放电损伤后的下牙槽神经或舌神经，并已显示出时间与受损轴突中的神经肽的积累。P物质，降钙素基因相关肽，血管活性肠多肽都被发现能够增加放电时，全身应用，脑啡肽引起的减少。在损伤部位和三叉神经节中，特异性钠通道和一氧化氮合酶的表达也发生变化。对接受神经修复的患者的舌神经神经瘤的研究也显示了肽的积累，以及炎症和结构变化，但这些特征的存在与报告的症状没有直接关系。应用皮质类固醇激素的实验性损伤部位减少了机械诱导的放电，和抗惊厥药卡马西平减少了一些轴突的自发放电。三叉神经分支损伤引起的一些反应似乎与其他周围神经损伤后的反应不同。这些差异将需要考虑到在开发新的治疗方法来管理损伤引起的三叉神经痛。
Injury to a branch of the trigeminal nerve may lead to the development of chronic pain in the affected area. The etiology of this condition is not clear, but there is strong evidence to suggest that spontaneous and mechanically induced neural discharge from the injury site plays a crucial role. In laboratory studies, we have characterized this discharge following injury to the inferior alveolar or lingual nerves and have shown a temporal association with the accumulation of neuropeptides in the damaged axons. Substance P, calcitonin gene-related peptide, and vasoactive intestinal polypeptide were all found to be capable of increasing the discharge when applied systemically, and enkephalin caused a decrease. There were also changes in the expression of specific sodium channels and nitric oxide synthase, both at the injury site and in the trigeminal ganglion. Studies on lingual nerve neuromas taken from patients undergoing nerve repair also revealed accumulation of peptides, as well as inflammatory and structural changes, but the presence of these features did not correlate directly with the reported symptoms. The application of corticosteroids to an experimental injury site decreased the mechanically induced discharge, and the anticonvulsant carbamazepine reduced the spontaneous discharge in some axons. Some of the responses that result from damage to a branch of the trigeminal nerve appear to differ from those that follow damage to other peripheral nerves. These differences will need to be taken into account when developing new therapeutic approaches for the management of injury-induced trigeminal pain.