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Migraine

This article is about the disorder. For other uses, see Migraine (disambiguation).

Migraine
Woman with migraine headache
SpecialtyNeurology
SymptomsHeadaches, nausea, sensitivity to light, sound, and smell[1][2]
Usual onsetAround puberty[1]
DurationRecurrent, long term[1]
CausesEnvironmental and genetic[3]
Risk factorsFamily history, female[4][5]
Differential diagnosisSubarachnoid hemorrhage, venous thrombosis, idiopathic intracranial hypertension, brain tumor, tension headache, sinusitis,[6] cluster headache[7][unreliable medical source?]
PreventionPropranolol, amitriptyline, topiramate[8]
MedicationIbuprofen, paracetamol (acetaminophen), triptans, ergotamines[5][9]
Prevalence~15%[10]

Migraine (UK: /ˈmiːɡreɪn/, US: /ˈmaɪ-/)[11][12] is a genetically influenced complex neurological disorder characterized by episodes of moderate-to-severe headache, most often unilateral and generally associated with nausea and light and sound sensitivity.[1] Other characterizing symptoms may include vomiting, cognitive dysfunction, allodynia, and dizziness. Exacerbation of headache symptoms during physical activity is another distinguishing feature.[13] Up to one-third of migraine sufferers experience aura, a premonitory period of sensory disturbance widely accepted to be caused by cortical spreading depression at the onset of a migraine attack.[13] 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.[14] Disease burden can range from episodic discrete attacks, consisting of as little as several lifetime attacks, to chronic disease.[14][15]

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.[3] An older "vascular hypothesis" postulated that the aura of migraine is produced by vasoconstriction and the headache of migraine is produced by vasodilation, but the vasoconstrictive mechanism has been disproven,[16] and the role of vasodilation in migraine pathophysiology is uncertain.[17][18] 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.[19]

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.[9] Specific medications such as triptans, ergotamines, or CGRP inhibitors may be used in those experiencing headaches that are refractory to simple pain medications.[20] For individuals who experience four or more attacks per month, or could otherwise benefit from prevention, prophylactic medication is recommended.[21] Commonly prescribed prophylactic medications include beta blockers like propranolol, anticonvulsants like sodium valproate, antidepressants like amitriptyline, and other off-label classes of medications.[8] 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.[22][23] Nonpharmacological preventative therapies include nutritional supplementation, dietary interventions, sleep improvement, and aerobic exercise.[24]

Globally, approximately 15% of people are affected by migraine.[10] In the Global Burden of Disease Study, conducted in 2010, migraines ranked as the third-most prevalent disorder in the world.[25] It most often starts at puberty and is worst during middle age.[1] As of 2016, it is one of the most common causes of disability.[26]

  1. ^ a b c d e "Headache disorders Fact sheet N°277". October 2012. Archived from the original on 16 February 2016. Retrieved 15 February 2016.
  2. ^ Cite error: The named reference Amin2009 was invoked but never defined (see the help page).
  3. ^ a b Piane M, Lulli P, Farinelli I, Simeoni S, De Filippis S, Patacchioli FR, et al. (December 2007). "Genetics of migraine and pharmacogenomics: some considerations". The Journal of Headache and Pain. 8 (6): 334–9. doi:10.1007/s10194-007-0427-2. PMC 2779399. PMID 18058067.
  4. ^ Lay CL, Broner SW (May 2009). "Migraine in women". Neurologic Clinics. 27 (2): 503–11. doi:10.1016/j.ncl.2009.01.002. PMID 19289228.
  5. ^ a b Cite error: The named reference Bart10 was invoked but never defined (see the help page).
  6. ^ Swanson JW, Sakai F (2006). "Diagnosis and Differential Diagnosis of Migraines". In Olesen J (ed.). The Headaches. Lippincott Williams & Wilkins. p. 424. ISBN 978-0-7817-5400-2. Archived from the original on 8 September 2017.
  7. ^ "Cluster Headache". American Migraine Foundation. 15 February 2017. Archived from the original on 9 May 2018. Retrieved 23 October 2017.
  8. ^ a b Kumar A, Kadian R (September 2022). "Migraine Prophylaxis". StatPearls Publishing. PMID 29939650. Bookshelf ID: NBK507873. Archived from the original on 8 March 2023. Retrieved 22 August 2023.
  9. ^ a b Gilmore B, Michael M (February 2011). "Treatment of acute migraine headache". American Family Physician. 83 (3): 271–280. PMID 21302868.
  10. ^ a b Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, et al. (December 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMC 6350784. PMID 23245607.
  11. ^ Wells JC (2008). Longman Pronunciation Dictionary (3rd ed.). Longman. ISBN 978-1-4058-8118-0.
  12. ^ Jones D (2011). Roach P, Setter J, Esling J (eds.). Cambridge English Pronouncing Dictionary (18th ed.). Cambridge University Press. ISBN 978-0-521-15255-6.
  13. ^ a b Headache Classification Subcommittee of the International Headache Society (2004). "The International Classification of Headache Disorders: 2nd edition". Cephalalgia. 24 (Suppl 1): 9–160. doi:10.1111/j.1468-2982.2004.00653.x. PMID 14979299.
  14. ^ a b Katsarava Z, Buse DC, Manack AN, Lipton RB (February 2012). "Defining the differences between episodic migraine and chronic migraine". Current Pain and Headache Reports. 16 (1): 86–92. doi:10.1007/s11916-011-0233-z. PMC 3258393. PMID 22083262.
  15. ^ Shankar Kikkeri N, Nagalli S (December 2022). "Migraine With Aura". StatPearls Publishing. PMID 32119498. Bookshelf ID: NBK554611. Archived from the original on 8 June 2023. Retrieved 23 August 2023.
  16. ^ Amin FM, Asghar MS, Hougaard A, Hansen AE, Larsen VA, de Koning PJ, et al. (May 2013). "Magnetic resonance angiography of intracranial and extracranial arteries in patients with spontaneous migraine without aura: a cross-sectional study". The Lancet. Neurology. 12 (5): 454–461. doi:10.1016/S1474-4422(13)70067-X. PMID 23578775. S2CID 25553357. Archived from the original on 28 July 2023. Retrieved 28 July 2023.
  17. ^ Mason BN, Russo AF (2018). "Vascular Contributions to Migraine: Time to Revisit?". Frontiers in Cellular Neuroscience. 12: 233. doi:10.3389/fncel.2018.00233. ISSN 1662-5102. PMC 6088188. PMID 30127722.
  18. ^ Jacobs B, Dussor G (3 December 2016). "Neurovascular contributions to migraine: moving beyond vasodilation". Neuroscience. 338: 130–144. doi:10.1016/j.neuroscience.2016.06.012. ISSN 0306-4522. PMC 5083225. PMID 27312704.
  19. ^ Burstein R, Noseda R, Borsook D (April 2015). "Migraine: multiple processes, complex pathophysiology". The Journal of Neuroscience. 35 (17): 6619–6629. doi:10.1523/JNEUROSCI.0373-15.2015. PMC 4412887. PMID 25926442.
  20. ^ Tzankova V, Becker WJ, Chan TL (January 2023). "Diagnosis and acute management of migraine". CMAJ. 195 (4): E153–E158. doi:10.1503/cmaj.211969. PMC 9888545. PMID 36717129. Archived from the original on 4 July 2023. Retrieved 22 August 2023.
  21. ^ Silberstein SD (August 2015). "Preventive Migraine Treatment". Continuum. 21 (4 Headache): 973–989. doi:10.1212/CON.0000000000000199. PMC 4640499. PMID 26252585. Archived from the original on 25 August 2023. Retrieved 22 August 2023.
  22. ^ Noseda R, Burstein R (December 2013). "Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, CSD, sensitization and modulation of pain". Pain. 154 (Suppl 1): S44–S53. doi:10.1016/j.pain.2013.07.021. PMC 3858400. PMID 24347803.
  23. ^ Spierings EL (July 2001). "Mechanism of migraine and action of antimigraine medications". The Medical Clinics of North America. 85 (4): 943–958, vi–vii. doi:10.1016/s0025-7125(05)70352-7. PMID 11480266. Archived from the original on 1 March 2023. Retrieved 22 August 2023.
  24. ^ Haghdoost F, Togha M (1 January 2022). "Migraine management: Non-pharmacological points for patients and health care professionals". Open Medicine. 17 (1): 1869–1882. doi:10.1515/med-2022-0598. PMC 9691984. PMID 36475060.
  25. ^ 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.
  26. ^ Vos T, Abajobir AA, Abate KH, Abbafati C, Abbas KM, Abd-Allah F, et al. (GBD 2016 Disease and Injury Incidence and Prevalence Collaborators) (September 2017). "Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016". Lancet. 390 (10100): 1211–1259. doi:10.1016/S0140-6736(17)32154-2. PMC 5605509. PMID 28919117.

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