Pathogenesis of Migraine: A NEJM Review
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Migraine is a ubiquitous neurologic disorder that is estimated to affect approximately 1 billion people worldwide, predominantly females. According to the Global Burden of Disease Study 2016, migraine is the second leading cause of disability and accounts for more disability than all other neurologic disorders combined.

The diagnosis is based on clinical criteria provided by the International Classification of Headache Disorders, 3rd edition (ICHD-3). Broad clinical features suggestive of migraine are recurrent headache attacks of moderate-to-severe pain intensity, with a duration of 4 to 72 hours. A diagnosis of migraine should be considered if a typical attack of head pain is unilateral, pulsating, and aggravated by physical activity.

Common accompanying symptoms are nausea, vomiting, photophobia, and phonophobia. Some persons report that the migraine is preceded by an aura, which is characterized by reversible focal neurologic symptoms, typically comprising visual or hemisensory disturbances. Although the pathogenesis of migraine is incompletely understood, it is considered to involve the trigeminal nerve and its axonal projections to the intracranial vasculature (termed the trigeminovascular system).

Nociceptive signals from the trigeminovascular system are relayed to areas in the brain that yield the perception of migraine pain. Further progress in understanding the pathogenesis has been made with the identification of signaling molecules that are involved in the genesis of a migraine attack. This advance has facilitated the development of mechanismbased therapies for migraine.

This review describes the current understanding of the pathogenesis of migraine, which is based predominantly on clinical data published within the past 10 years, and outlines recommended practices for the treatment of acute migraine and for preventive treatment of migraine, emphasizing medications that have recently been approved.