Migraine

Migraine
Woman during a migraine attack
SpecialtyNeurology
SymptomsHeadaches coupled with sensory disturbances such as nausea, sensitivity to light, sound, and smell
Usual onsetAround puberty
DurationRecurrent, long term
CausesEnvironmental and genetic
Risk factorsFamily history, female sex
Differential diagnosisSubarachnoid hemorrhage, venous thrombosis, idiopathic intracranial hypertension, brain tumor, tension headache, sinusitis, cluster headache
PreventionPropranolol, amitriptyline, topiramate,Calcitonin gene-related peptide receptor antagonists (CGRPs)
MedicationIbuprofen, paracetamol (acetaminophen), triptans, ergotamines
Prevalence~15%

Migraine (UK: /ˈmɡrn/, US: /ˈm-/)[1][2] 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.[3][4] Other characterizing symptoms may include nausea, vomiting, cognitive dysfunction, allodynia, and dizziness.[3] Exacerbation of headache symptoms during physical activity is another distinguishing feature.[5]

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 calcitonin gene-related peptide receptor antagonist (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, it is one of the most common causes of disability.[25]

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