Up to one-third of people with migraine experience aura, a premonitory period of sensory disturbance widely accepted to be caused by cortical spreading depression at the onset of a migraine attack.[4] Although primarily considered to be a headache disorder, migraine is highly heterogenous in its clinical presentation and is better thought of as a spectrum disease rather than a distinct clinical entity.[6]Disease burden can range from episodic discrete attacks to chronic disease.[6][7]
Migraine is believed to be caused by a mixture of environmental and genetic factors that influence the excitation and inhibition of nerve cells in the brain.[8] An incomplete "vascular hypothesis" postulated that the aura of migraine is produced by vasoconstriction and the headache of migraine is produced by vasodilation. However, the vasoconstrictive mechanism has been disproven,[9] and the role of vasodilation in migraine pathophysiology is uncertain.[10][11] The accepted hypothesis suggests that multiple primary neuronal impairments lead to a series of intracranial and extracranial changes, triggering a physiological cascade that leads to migraine symptomatology.[12]
Initial recommended treatment for acute attacks is with over-the-counter analgesics (pain medication) such as ibuprofen and paracetamol (acetaminophen) for headache, antiemetics (anti-nausea medication) for nausea, and the avoidance of triggers.[13] Specific medications such as triptans, ergotamines, or CGRP inhibitors may be used in those experiencing headaches that are refractory to simple pain medications.[14] For individuals who experience four or more attacks per month, or could otherwise benefit from prevention, prophylactic medication is recommended.[15] Commonly prescribed prophylactic medications include beta blockers like propranolol, anticonvulsants like sodium valproate, antidepressants like amitriptyline, and other off-label classes of medications.[16] Preventive medications inhibit migraine pathophysiology through various mechanisms, such as blocking calcium and sodium channels, blocking gap junctions, and inhibiting matrix metalloproteinases, among other mechanisms.[17][18] Non-pharmacological preventive therapies include nutritional supplementation, dietary interventions, sleep improvement, and aerobic exercise.[19] In 2018, the first medication (Erenumab) of a new class of drugs specifically designed for migraine prevention called calcitonin gene-related peptide receptor antagonists (CGRPs) was approved by the FDA.[20] As of July 2023, the FDA has approved eight drugs that act on the CGRP system for use in the treatment of migraine.[21]
Globally, approximately 15% of people are affected by migraine.[22] In the Global Burden of Disease Study, conducted in 2010, migraine ranked as the third-most prevalent disorder in the world.[23] It most often starts at puberty and is worst during middle age.[24] As of 2016[update], it is one of the most common causes of disability.[25]
^ abPescador Ruschel MA, De Jesus O (2024), "Migraine Headache", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID32809622, retrieved 13 September 2024
^Shankar Kikkeri N, Nagalli S (December 2022). "Migraine With Aura". StatPearls Publishing. PMID32119498. Bookshelf ID: NBK554611. Archived from the original on 8 June 2023. Retrieved 23 August 2023.
^Kumar A, Kadian R (September 2022). "Migraine Prophylaxis". StatPearls Publishing. PMID29939650. Bookshelf ID: NBK507873. Archived from the original on 8 March 2023. Retrieved 22 August 2023.
^Gobel H. "1. Migraine". ICHD-3 The International Classification of Headache Disorders 3rd edition. Archived from the original on 24 October 2020. Retrieved 22 October 2020.