Schoenen J
Department of Neurology, University of Liège, Belgium.
Biomed Pharmacother. 1996;50(2):71-8. doi: 10.1016/0753-3322(96)84716-0.
According to recent evoked potential studies, a fundamental, probably protective, feature of cortical information processing, ie, response habituation during stimulus repetition, is abnormal in migraine between attacks. The deficient habituation is found for different sensory modalities and experimental paradigms: pattern-reversal visual evoked potentials (same stimulus at a constant intensity), cortical auditory evoked potentials (same stimulus at increasing intensities) and auditory event-related potentials obtained in a passive "oddball" paradigm (novel stimulus). The abnormal information processing is an interictal cortical dysfunction most likely due to inadequate control by the so-called "state-setting, chemically-addressed pathways" originating in the brain stem, in particular by the serotonergic pathway, leading to a low preactivation level of sensory cortices. We suggest that it may play a pivotal role in migraine pathogenesis in conjunction with the reported decrease of brain mitochondrial energy reserve, by favouring a rupture of metabolic homeostasis and biochemical shifts capable of activating the trigeminovascular system and thus capable of producing a migraine attack. We postulate that both the deficient habituation in information processing and the deranged oxygen metabolism may have behavioral correlates. Which of these abnormalities are inherited, acquired or both remains to be determined.
根据最近的诱发电位研究，皮质信息处理的一个基本特征，即刺激重复时的反应习惯化，这可能具有保护作用，在发作间期偏头痛患者中是异常的。在不同的感觉模式和实验范式中都发现了习惯化不足的情况：模式翻转视觉诱发电位（相同强度的恒定刺激）、皮质听觉诱发电位（强度增加时的相同刺激）以及在被动“oddball”范式（新异刺激）中获得的听觉事件相关电位。这种异常的信息处理是发作间期皮质功能障碍，很可能是由于源自脑干的所谓“状态设定、化学寻址通路”，特别是5-羟色胺能通路控制不足，导致感觉皮质的预激活水平较低。我们认为，它可能通过促进代谢稳态的破坏和生化变化，从而激活三叉神经血管系统并引发偏头痛发作，在偏头痛发病机制中与所报道的脑线粒体能量储备减少共同发挥关键作用。我们推测，信息处理中的习惯化不足和紊乱的氧代谢都可能与行为相关。这些异常是遗传性的、后天获得的还是两者皆有，仍有待确定。
