Malick A, Burstein R
Department of Neurobiology, Program in Neuroscience, Harvard Medical School, Boston, MA, USA.
Funct Neurol. 2000;15 Suppl 3:28-35.
Current theories propose that the pain of migraine is caused by chemical activation of meningeal perivascular fibers. In an animal model of migraine, we have recently shown that chemical activation of meningeal primary afferent nociceptors that innervate the dura could lead to the following: a) peripheral sensitization of these nociceptors to intracranial mechanical stimulation; b) central sensitization of second-order trigeminovascular neurons that receive convergent input from the dura and skin to extracranial mechanical and thermal stimulation; and c) facilitated cardiovascular pressor responses that are usually indicative of pain. These findings provide the first set of evidence for the induction of peripheral and central sensitization along trigeminovascular pain pathways by visceral input from the intracranial dura. We propose that the throbbing pain of migraine is mediated mainly through peripheral and to a lesser extent through central sensitization, and that the development of scalp tenderness is mediated mainly through central sensitization.
当前理论认为，偏头痛的疼痛是由脑膜血管周围纤维的化学激活引起的。在偏头痛的动物模型中，我们最近发现，支配硬脑膜的脑膜初级传入伤害感受器的化学激活可导致以下情况：a）这些伤害感受器对颅内机械刺激的外周敏化；b）接受来自硬脑膜和皮肤的汇聚输入的二级三叉神经血管神经元对颅外机械和热刺激的中枢敏化；c）通常指示疼痛的心血管升压反应增强。这些发现为颅内硬脑膜的内脏输入沿三叉神经血管疼痛通路诱导外周和中枢敏化提供了第一组证据。我们提出，偏头痛的搏动性疼痛主要通过外周介导，在较小程度上通过中枢敏化介导，而头皮压痛的发展主要通过中枢敏化介导。
