Abstract

Currently a migraine attack is considered as originating in the brain. Triggers initiate depolarizing neu- roelectric and metabolic events resulting in spreading depression of Leao. This activates the headache and associated features of the attack by mechanisms involving either peripheral trigeminovascular or brains- tem pathways, or both. Interictal excitability of cell membranes that is in part genetically determined is the brain's susceptibility to attacks. Factors that increase or decrease neuronal excitability constitute the threshold for triggering attacks. Susceptibility to migraine attacks appears related to brain hyperexcitabi- lity. Recent functional neuroimaging techniques have shown the primary neural basis of migraine attack with secondary vascular changes(neuro-vascular mechanism). On this basis the prophylaxis for migraine should reduce the hyperexcitability and enhance the inhibitory activity of the sensitive migraine brain, thereby reducing the frequency, intensity, and duration of migraine attacks and enhancing the quality of life of migraine patients. Korean Journal of Headache 4(1):37-40, 2003