Abstract
Migraine is clinically characterized by recurrent throbbing headache attacks of moderate to severe intensity accompanied by nausea, vomiting, and photophobia/phonophobia. This debilitating and common headache disorder predominantly affects young people and causes an enormous financial burden on society. Although the pathophysiology of migraine remains elusive, it is now appreciated that migraine is primarily a neural disease. Hypothalamic dysfunction seems to be implicated in the emergence of migraine prodrome. Migraine aura is caused by cortical spreading depression/depolarization. Abnormal activation of the trigeminal system is responsible for the generation of migraine headache, wherein calcitonin gene-related peptide （CGRP） plays a pivotal role in provoking peripheral sensitization. Triptans, 5-HT1B/1D/1F agonists, are the mainstay of migraine acute therapy. It is envisioned that the anti-migraine action of triptans is mediated mainly by inhibition of CGRP release from the trigeminal nerves. For prophylaxis, calcium channel blockers, anti-epileptic drugs, and tricyclic antidepressants are empirically used with a view to rectifying abnormal neural activity. There are unmet needs in the current pharmacological management of migraine. CGRP-targeted therapy, which consists of CGRP-related monoclonal antibodies and small-molecule CGRP receptor antagonists, has recently been launched into migraine management. In particular, CGRP-related antibodies are shown to exert efficacy even in difficult-to-treat cases. We are now entering a new era of migraine treatment.
