Abstract

The pathophysiology of migraine is not fully understood. Neuronal hyperexcitability can explain the interictal status of migraine. Cortical spreading depression appears to underlie the aura phase in patients with migraine aura. The pain of the headache phase is mediated by the trigeminal vascular system and central projection. Preventive medications may target brain excitability, consequently blocking triggers of aura or headache. Acute medications inhibit trigeminal activation from either a peripheral or central location. Triptans ameliorate migraine headache primarily by constricting the dilated cranial blood vessels and by inhibiting the neurogenic inflammation. Recently published clinical study has reported that a selective CGRP receptor antagonist is effective in treating acute migraine attacks without significant side effects. Several new targets will be reviewed in this article. Korean Journal of Headache 6(1):6-13, 2005