专家幻灯—偏头痛病理生理于生元.ppt

Key point: A secondary neuroinflammatory cascade could be generated in the dura involving the release of inflammatory mediators such as NO and the neuropeptides CGRP and substance P, which could contribute to the pain of migraine. 二次神经炎性在硬脑膜形成，涉及炎性递质的释放，包括NO，神经递质CGRP，P物质等，促使偏头痛疼痛。 It has been hypothesized that neurogenic inflammation develops in dura mater induced by the release of various vasoactive neuropeptides from trigeminal perivascular fibers, leading to a cascade of events characterized by vasodilation, plasma protein extravasation, and the release of proinflammatory mediators.假设激活的三叉神经血管外周的纤维释放各种血管活性神经肽引起硬脑膜下炎性反应，导致血管扩张，血浆蛋白外渗，炎性介质释放。 Among various substances that may be involved in the neurogenic inflammation process, CGRP is proposed to play the leading role in its genesis.1引起神经炎症的各种物质中，CGRP被认为是起主导作用。 Activated nociceptors of the trigeminal system release neuropeptides that include CGRP and substance P in the meninges.2激活的脑膜三叉神经系统伤害感受器，释放神经肽，包括CGRP，P物质等 A parasympathetic reflex triggered by the activation of the trigeminal system may also lead to the release of NO.3,4三叉神经系统的激活引起的副交感神经反射可能会导致NO的释放 Those neuromediators have a number of actions in the meninges:这些神经介质对脑膜有多种作用： CGRP,3 NO,4 and substance P4 induce blood vessel vasodilation.CGRP，NO，P物质引起血管扩张。 CGRP and substance P activate mast cell degranulation.5CGRP和P物质激活肥大细胞的脱颗粒作用 Substance P6 induces plasma extravasation.P物质引起血浆蛋白外渗 Mast cell degranulation induced by CGRP and substance P leads to the release of several substances, including histamine, serotonin, nerve growth factor, as well as proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6.7 CGRP和P物质诱发肥大细胞的脱颗粒作用，导致数种化学物质的释放，包括组胺，5羟色胺，神经生长因子，以及炎性细胞因子如肿瘤坏死因子(TNF)-α，白介素(IL)-1、IL-6。 According to the neurogenic theory, those factors released in the vicinity of sensory fibers innervating the meninges activate and sensitize peripheral nociceptors.1根据神经源性学说，这些释放在支配脑膜的感觉纤维周围的因子，激活和敏化外周痛觉感受器。1 A recent study provided