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神经痛

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The exact mechanism might be that adriamycin destroyed SP and CGRP gangliocytes in trigeminal ganglions to decrease SP and CGRP synthesis and release therefore to inhibit the transmittion of nociceptin stimulation.

我们认为,将阿霉素直接注入神经干后,通过轴浆的逆行运输作用,阿霉素可到达三叉神经节,并选择性地破坏相应的节细胞,起到&化学切断&的作用,阻断中枢神经系统与三叉神经周围支之间的信息传递,从而达到治疗三叉神经痛的目的。

Massage also can decline the excitement of nerve ending, so it is often used as pain killing of neuritis and nerve ache, etc.

同时推拿可降低神经末梢的兴奋性,故常用于止痛,如神经炎,神经痛等。

The bee venom for in jection project has taken a technology to seperate the painful materials from Sesibilizatim materials It is used to cure The pain of rhenmarthritis,nearitis,neuralgia and it also do benefit for patients with cancer and reduce the pain of tlem to live longer this projects is original creation in our country production per your is 5millim pcs,output valuce per year is 90 million yuan ,profits and taces can reach 54 million yuan.

注射用蜂毒项目采用超临界萃取技术将蜂毒致敏物质和颈痛物质分离除去采用冷冻干燥技术制成供注射用的冻干粉针剂,主要用于治疗风湿性关节炎,类风湿性关节炎、周围神经炎及神经痛以及对中晚期癌症病人镇痛都有很好的疗效,用该品种不但可以让病人停用杜冷丁,大大减轻病人痛苦,而且明显延长病人存活期。

Exccesive synthetise and release of calcitonin gene-related peptide in trigeminal nerve may promote release of substance P, cause the intense paroxysmal pain and form a local neurogenic inflammation.

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P物质的释放,导致阵发性剧烈疼痛,并在局部形成神经源性炎症。

Exccesive synthetise and release of calcitonin gene-related peptide in trigeminal nerve may promote release of substance P, cause the intense paroxysmal pain and form a local neurogenic inflammation.

我们认为: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P物质的释放,导致阵发性剧烈疼痛,并在局部形成神经源性炎症。

Exccesive synthetise and release of calcitonin gene-related peptide in trigeminal nerve may promote release of SP, cause the intense paroxysmal pain and form a local neurogenic inflammation.

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。

Conclusion摘要: Exccesive synthetise and release of calcitonin gene-related peptide in trigeminal nerve may promote release of substance P, cause the intense paroxysmal pain and form a local neurogenic inflammation.

结论摘要:我们认为摘要: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P物质的释放,导致阵发性剧烈疼痛,并在局部形成神经源性炎症。

Exccesive synthetise and release of calcitonin gene-related peptide in trigeminal nerve may promote release of su tance P, cause the inte e paroxysmal pain and form a local neurogenic inflammation.

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P物质的释放,导致阵发性剧烈疼痛,并在局部形成神经源性炎症。

Objective To evaluate the therapeutic effect and mechanisms of microvascular decompression in treating typical and atypical trigeminal neuralgia.

目的探讨微血管减压术治疗典型及非典型三叉神经痛的不同疗效及其可能机制。

ABSTRACT: Objective To probe into a better therapy for primary trigeminal neuralgia.

摘 要]目的:探索治疗原发性三叉神经痛的较佳疗法。

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