Amery W K
Cephalalgia. 1985 May;5 Suppl 2:131-3. doi: 10.1177/03331024850050S224.
It is postulated that a migraine attack is a specific reaction pattern to an episode of focal cerebral hypoxia. This hypothesis holds that any type of focal brain hypoxia (and thus not only a vasospasm) may provoke a migraine attack. Indeed, as hypoxia is a result of an imbalance between energy supply and energy use, the former can be decreased and/or the latter be increased. Spreading cortical depression, leading to the aura, is believed to be another consequence of brain hypoxia occurring in classical migraine. There are no other genuine differences between classical and common migraine, according to the cerebral hypoxia theory. The latter theory may improve our understanding of the mode of action of antimigraine drugs. Certain calcium entry blockers have a direct protective effect on brain hypoxia, but some other pharmacotherapeutic approaches may also prevent cerebral hypoxia via an effect on brain metabolism, vasomotion or platelet behavior.
据推测，偏头痛发作是对局灶性脑缺氧发作的一种特定反应模式。该假说认为，任何类型的局灶性脑缺氧（因此不仅是血管痉挛）都可能引发偏头痛发作。事实上，由于缺氧是能量供应与能量消耗失衡的结果，前者可能减少和/或后者可能增加。导致先兆的皮质扩散性抑制被认为是典型偏头痛中脑缺氧的另一个后果。根据脑缺氧理论，典型偏头痛和普通偏头痛之间没有其他真正的区别。后一种理论可能会增进我们对抗偏头痛药物作用方式的理解。某些钙通道阻滞剂对脑缺氧有直接保护作用，但其他一些药物治疗方法也可能通过对脑代谢、血管运动或血小板行为的影响来预防脑缺氧。
