Welch K M, D'Andrea G, Tepley N, Barkley G, Ramadan N M
Department of Neurology, Henry Ford Hospital, Detroit, Michigan.
Neurol Clin. 1990 Nov;8(4):817-28.
This article explores the hypothesis that migraine with aura is associated with a state of central neuronal hyperexcitability. The authors propose that this central neuronal hyperexcitability involves overactivity of the excitatory amino acids, glutamate, and possibly aspartate. Stimuli that activate the migraine attack evoke neuronal depolarization, slow depolarization shifts, and spreading suppression of spontaneous neuronal activity possible by glutamate and K+ dependent mechanisms. A low brain Mg2+ and consequent reduced gating of glutamatergic receptors may provide the link between the physiologic threshold for a migraine attack and the mechanisms of the attack itself by promoting glutamate hyperactivity, neuronal hyperexcitability, and susceptibility to glutamate-dependent spreading depression.
本文探讨了伴先兆偏头痛与中枢神经元兴奋性过高状态相关的假说。作者提出，这种中枢神经元兴奋性过高涉及兴奋性氨基酸（谷氨酸，可能还有天冬氨酸）的过度活动。激活偏头痛发作的刺激通过谷氨酸和钾离子依赖机制诱发神经元去极化、缓慢去极化偏移以及对自发神经元活动的扩散性抑制。低脑镁离子以及随之而来的谷氨酸能受体门控减少，可能通过促进谷氨酸过度活动、神经元兴奋性过高以及对谷氨酸依赖性扩散性抑制的易感性，在偏头痛发作的生理阈值与发作机制之间建立联系。
