However, up to 5% of patients may develop chronic migraine 5 (Box 1). Most patients have the episodic form of migraine, with clearly defined attacks and attack-free periods. The duration of an entire attack is in fact longer if premonitory and postdromal symptoms are included (Fig. ![]() The median duration of untreated migraine headache is one day, but can range from 4 h (2 h in children) to 3 days 3, 21. Accordingly, the total number of attacks experienced by an individual over a lifetime can vary considerably between individuals, from only a few to several thousand. Attack frequency and durationĪmong those with active migraine, the median monthly attack frequency is 1.5, a quarter have weekly attacks, and up to 5% have chronic migraine (see below) 3, 8, 21, 22. Precise incidence and lifetime prevalence figures are sometimes difficult to obtain because some people do not recognize early attacks and, particularly older people, forget they have had migraine attacks. Between 30 and 50 years of age the prevalence of migraine in women (30%) is three to four times higher than in men after 50 years of age, the prevalence declines to ~5% in both men and women 18, 19, 20. In puberty, the prevalence of migraine rises, but more so in girls than in boys. Until puberty, the prevalence of migraine is similar in boys and girls (~5%). In one large study, the median age at onset was 23–25 years, with a peak between 15 and 19 years 17. Migraine attacks may begin at any age, typically in puberty and adolescence but only rarely after 50 years of age 3, 4. In addition, the bright future of migraine therapy, featuring several new emerging acute and preventive migraine-specific medications, is highlighted. This Primer focuses on the clinical presentation, epidemiology, pathophysiology and management of migraine. Of note, although chronic migraine may persist for a long time, the term may be confusing as it actually denotes ‘very high frequency migraine’ rather than ‘a disorder that persists for a long time’, which is the usual connotation for the term chronic. Most patients have episodic migraine, although some patients develop chronic migraine (the presence of ≥15 headache days per month, at least eight of which meet the criteria for migraine, or respond to a triptan or ergotamine derivative). Migraine attacks and patients are diagnosed using the International Classification of Headache Disorders (ICHD) diagnostic criteria and defines patients with migraine as ‘people ever having had at least two attacks of migraine with aura or at least five attacks of migraine without aura’. In women, migraine attack frequency is influenced by fluctuations in sex hormone levels attacks typically begin in puberty, frequently occur perimenstrually, temporarily disappear during pregnancy and while breastfeeding, and usually worsen and increase in frequency during menopause, often substantially decreasing in frequency or disappearing afterwards (for review see refs 15, 16). The presence, characteristics, severity, duration, frequency and associated features of migraine attacks show wide, partly sex-dependent, interindividual variability, and can also substantially vary within patients across a lifetime. The emergence of new treatment targets and therapies illustrates the bright future for migraine management. Several neuromodulation modalities have been approved for acute and/or preventive migraine treatment. ![]() ![]() Intramuscular onabotulinumtoxinA may be helpful in chronic migraine (migraine on ≥15 days per month) and monoclonal antibodies targeting CGRP or its receptor, as well as two gepants, have proven effective and well tolerated for the preventive treatment of migraine. CGRP receptor antagonists (gepants) and lasmiditan, a selective 5HT1 F receptor agonist, have emerged as effective acute treatments. Because of cardiovascular safety concerns, unreliable efficacy and tolerability issues, use of ergots to abort attacks has nearly vanished in most countries. Management includes analgesics or NSAIDs for mild attacks, and, for moderate or severe attacks, triptans or 5HT 1B/1D receptor agonists. Despite earlier beliefs, vasodilation is only a secondary phenomenon and vasoconstriction is not essential for antimigraine efficacy. Spreading depolarization probably causes aura and possibly also triggers trigeminal sensory activation, the underlying mechanism for the headache. ![]() Depression, epilepsy, stroke and myocardial infarction are comorbid diseases. The aetiology is multifactorial with rare monogenic variants. Migraine is a common, chronic, disorder that is typically characterized by recurrent disabling attacks of headache and accompanying symptoms, including aura.
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