Robinson Peter P, Boissonade Fiona M, Loescher Alison R, Smith Keith G, Yates Julian M, Elcock Claire, Bird Emma V, Davies Shelley L, Smith Paula L, Vora Amit R
Department of Oral and Maxillofacial Surgery, School of Clinical Dentistry, University of Sheffield, Claremont Crescent, Sheffield S10 2TA United Kingdom.
J Orofac Pain. 2004 Fall;18(4):287-92.
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.
三叉神经分支损伤可能导致患区出现慢性疼痛。这种情况的病因尚不清楚，但有强有力的证据表明，损伤部位自发的和机械诱导的神经放电起着关键作用。在实验室研究中，我们已经对下牙槽神经或舌神经损伤后的这种放电进行了特征描述，并表明其与受损轴突中神经肽的积累存在时间关联。发现P物质、降钙素基因相关肽和血管活性肠肽在全身应用时均能增加放电，而脑啡肽则导致放电减少。在损伤部位和三叉神经节，特定钠通道和一氧化氮合酶的表达也发生了变化。对接受神经修复患者的舌神经神经瘤的研究还发现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联。在实验性损伤部位应用皮质类固醇可减少机械诱导的放电，抗惊厥药物卡马西平可减少一些轴突的自发放电。三叉神经分支损伤产生的一些反应似乎与其他周围神经损伤后的反应不同。在开发治疗损伤性三叉神经痛的新治疗方法时，需要考虑这些差异。
