2021 Volume 38 Issue 3 Pages 180-184
Migraine is characterized by recurrent headache attacks of moderate to severe intensity accompanied by nausea, vomiting, and photophobia/phonophobia. This disabling headache disease causes an enormous financial burden on society. Although the pathophysiology of migraine remains largely unknown, it is now much appreciated that migraine is primarily a neural disease. Migraine headache is caused by abnormal activation of the trigeminal system with calcitonin gene–related peptide (CGRP) playing a pivotal role in the development of sensitization. Triptans, 5–HT1B/1D/1F agonists, are the mainstay of migraine acute therapy. For prophylaxis, calcium channel blockers, anti–epileptic drugs, and tricyclic antidepressants are used with a view to rectifying abnormal neural activity. In addition, CGRP–targeted therapy, which consists of CGRP–related monoclonal antibodies and small–molecule CGRP receptor antagonists, has been launched into migraine management. In particular, CGRP–related antibodies are shown to exert efficacy even in difficult–to–treat cases.