Migraine
Disorder resulting in recurrent moderate-severe headaches / From Wikipedia, the free encyclopedia
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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 | |
---|---|
Woman with migraine headache | |
Specialty | Neurology |
Symptoms | Headaches, nausea, sensitivity to light, sound, and smell[1][2] |
Usual onset | Around puberty[1] |
Duration | Recurrent, long term[1] |
Causes | Environmental and genetic[3] |
Risk factors | Family history, female[4][5] |
Differential diagnosis | Subarachnoid hemorrhage, venous thrombosis, idiopathic intracranial hypertension, brain tumor, tension headache, sinusitis,[6] cluster headache[7][unreliable medical source?] |
Prevention | Propranolol, amitriptyline, topiramate[8] |
Medication | Ibuprofen, paracetamol (acetaminophen), triptans, ergotamines[5][9] |
Prevalence | ~15%[10] |
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[update], it is one of the most common causes of disability.[26]