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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。
Objective: To observe the changes of calcitonin gene-related peptide in painful and non-painful nerve fibers of trigeminal neuralgia and to deepen the understanding of the pathogenesis of trigeminal neuralgia. Methods: Immunohistochemical method was used to observe the difference of calcitonin gene-related peptide immunopositive granules in the painful and non-painful nerve fibers of 16 patients. Results: The number and area of calcitonin gene-related peptide immunoreactive granules in the painful nerve tissue were significantly higher than that of the calcitonin gene-related peptide immunopositive granules in the non-painful nerve tissue. CONCLUSIONS: We believe that excessive synthesis and release of calcitonin gene-related peptide in the pain-supporting nerves of trigeminal neuralgia may promote the release of SP leading to paroxysmal severe pain and local neurogenic inflammation.