Understanding migraine: Potential role of neurogenic inflammation.
Understanding migraine: Potential role of neurogenic inflammation.
复制标题
DOI：
10.4103/0972-2327.182302
复制
发表时间：
2016-04
影响因子：
1.7
通讯作者：
Malhotra R
中科院分区：
文献类型：
--
作者：
Malhotra R
神经源性炎症是一种明确的病理生理过程，其特征是从激活的外周伤害性感觉神经末梢（通常是 C 和 A δ 纤维）释放强效血管活性神经肽，主要是降钙素基因相关肽 (CGRP)、P 物质 (SP) 和神经激肽 A。这些肽导致一系列炎症组织反应，包括小动脉血管舒张、血浆蛋白外渗和周围靶组织中肥大细胞脱颗粒。神经源性炎症过程长期以来被认为是涉及神经系统、呼吸系统、胃肠道、泌尿生殖道和皮肤等多种人类疾病的病理生理学的可能机制。最近开发的几种创新实验性偏头痛模型提供了证据，表明神经肽（SP、神经激肽 A 和 CGRP）与偏头痛有关。对三叉神经伤害性纤维的逆向刺激导致神经源性炎症反应，通过释放各种感觉神经肽，血浆蛋白从硬脑膜血管外渗显着增加。几种临床上有效的抗偏头痛药物，例如麦角和曲坦类药物，已被证明可以减弱神经肽的释放和神经源性血浆蛋白的外渗。这些发现为使用动物模型研究偏头痛神经源性炎症机制的有效性提供了支持。这些也进一步强化了偏头痛是一种神经炎症性疾病的概念。在临床背景下，医生对神经源性炎症在偏头痛中的作用缺乏了解和认识。对神经源性炎症的分子生物学、药理学和病理生理学的更好的理解可以为从业者提供特定背景的反馈，以确定新颖且最有效的治疗方法。为此，本综述总结了支持神经源性炎症和神经肽参与偏头痛病理生理学和药理学的证据，及其在更好地制定偏头痛或其他神经系统疾病治疗干预措施方面的潜在意义。此外，我们还简要强调了神经源性炎症在各种其他神经系统疾病中的病理生理学作用。
Neurogenic inflammation, a well-defined pathophysiologial process is characterized by the release of potent vasoactive neuropeptides, predominantly calcitonin gene-related peptide (CGRP), substance P (SP), and neurokinin A from activated peripheral nociceptive sensory nerve terminals (usually C and A delta-fibers). These peptides lead to a cascade of inflammatory tissue responses including arteriolar vasodilation, plasma protein extravasation, and degranulation of mast cells in their peripheral target tissue. Neurogenic inflammatory processes have long been implicated as a possible mechanism involved in the pathophysiology of various human diseases of the nervous system, respiratory system, gastrointestinal tract, urogenital tract, and skin. The recent development of several innovative experimental migraine models has provided evidence suggestive of the involvement of neuropeptides (SP, neurokinin A, and CGRP) in migraine headache. Antidromic stimulation of nociceptive fibers of the trigeminal nerve resulted in a neurogenic inflammatory response with marked increase in plasma protein extravasation from dural blood vessels by the release of various sensory neuropeptides. Several clinically effective abortive antimigraine medications, such as ergots and triptans, have been shown to attenuate the release of neuropeptide and neurogenic plasma protein extravasation. These findings provide support for the validity of using animal models to investigate mechanisms of neurogenic inflammation in migraine. These also further strengthen the notion of migraine being a neuroinflammatory disease. In the clinical context, there is a paucity of knowledge and awareness among physicians regarding the role of neurogenic inflammation in migraine. Improved understanding of the molecular biology, pharmacology, and pathophysiology of neurogenic inflammation may provide the practitioner the context-specific feedback to identify the novel and most effective therapeutic approach to treatment. With this objective, the present review summarizes the evidence supporting the involvement of neurogenic inflammation and neuropeptides in the pathophysiology and pharmacology of migraine headache as well as its potential significance in better tailoring therapeutic interventions in migraine or other neurological disorders. In addition, we have briefly highlighted the pathophysiological role of neurogenic inflammation in various other neurological disorders.