Migraine

Migraine is a common primary headache disorder characterised by recurrent attacks of moderate-to-severe head pain, typically pulsating and one-sided, lasting hours to a few days and often accompanied by nausea and heightened sensitivity to light and sound. In some people attacks are preceded by an aura of transient neurological symptoms, most often visual. Migraine is not merely a bad headache but a disabling brain disorder, and it ranks among the leading causes of disability worldwide.

Definition

Migraine is a primary headache disorder defined by recurrent attacks of headache, characteristically unilateral, pulsating, of moderate or severe intensity, aggravated by routine physical activity, and associated with nausea and/or photophobia and phonophobia, with or without a preceding aura of reversible neurological symptoms.

Scope

This entry covers migraine as a clinical entity defined by the International Classification of Headache Disorders: its principal subtypes (migraine with and without aura), the phases of an attack, current understanding of its pathophysiology, and its epidemiology and burden. It is a reference description of the disorder and its mechanisms, not a guide to diagnosis or treatment of any individual.

Core questions

• What distinguishes migraine from other primary headaches such as tension-type headache?
• What is the aura, and what does it reveal about migraine mechanisms?
• Why does migraine cause such a large share of global disability?

Key concepts

• Migraine with aura and migraine without aura
• Prodrome, aura, headache, and postdrome phases
• Photophobia and phonophobia
• Calcitonin gene-related peptide (CGRP)
• Episodic versus chronic migraine
• Central sensitisation and cutaneous allodynia

Key theories

Trigeminovascular activation

Migraine pain is generated by activation and sensitisation of the trigeminovascular system, the network linking the trigeminal nerve to cranial blood vessels and central pain pathways, with neuropeptides including calcitonin gene-related peptide implicated in transmitting and amplifying the pain signal.

Cortical spreading depression and aura

The migraine aura is thought to reflect cortical spreading depression, a slowly propagating wave of neuronal and glial depolarisation followed by suppression of activity that moves across the cortex and corresponds to the marching neurological symptoms of aura.

Mechanisms

Migraine is increasingly understood as a disorder of the brain rather than primarily of the blood vessels. Attacks are thought to involve activation and sensitisation of the trigeminovascular system, with release of neuropeptides such as calcitonin gene-related peptide (CGRP) that promote pain signalling, alongside altered activity in brainstem and hypothalamic regions that may underlie the early premonitory phase. The aura is attributed to cortical spreading depression, a wave of neuronal depolarisation and subsequent suppression that spreads across the cortex and matches the evolving sensory or visual symptoms. Repeated activation can produce central sensitisation, clinically reflected in cutaneous allodynia during attacks.

Clinical relevance

Migraine is one of the most common reasons for neurological consultation and a major contributor to lost productivity and reduced quality of life. Recognising its characteristic pattern and distinguishing it from other primary and secondary headaches is central to evidence appraisal in neurology. This entry describes the disorder and its mechanisms for reference purposes and does not provide individualised diagnostic or treatment guidance.

Epidemiology

Migraine is highly prevalent, affecting a substantial fraction of the adult population, with a marked female predominance after puberty. Global Burden of Disease analyses consistently rank migraine among the leading causes of years lived with disability, particularly in people of working age, reflecting both its high prevalence and the disability imposed by attacks.

Evidence & guidelines

The International Classification of Headache Disorders, 3rd edition (ICHD-3) provides the diagnostic criteria that define migraine and its subtypes, while large-scale reviews and Global Burden of Disease analyses describe its epidemiology and burden.

History

Recurrent unilateral headache with visual disturbance has been described since antiquity, and the term migraine derives from the Greek hemicrania, meaning half the skull. Modern understanding shifted across the twentieth century from a purely vascular theory toward a neuronal and neurovascular model, consolidated by the recognition of cortical spreading depression as the substrate of aura and of CGRP signalling in attack generation.

Debates

Is migraine fundamentally vascular or neuronal in origin?

Earlier models attributed migraine to vasodilation of cranial vessels, but evidence on cortical spreading depression, trigeminovascular activation, and CGRP has shifted the consensus toward a primarily neuronal and neurovascular disorder in which vascular changes are secondary.

Seminal works

• ichd3-2018
• charles-2018
• ashina-2021

Frequently asked questions

What is a migraine aura?

An aura is a set of transient, fully reversible neurological symptoms, most often visual (such as flickering lights or a spreading blind spot), that precede or accompany the headache in some people with migraine. It is attributed to cortical spreading depression, a wave of altered brain activity.

Is migraine the same as a severe tension headache?

No. Although both are primary headaches, migraine is typically pulsating, often one-sided, aggravated by activity, and accompanied by nausea and light or sound sensitivity, whereas tension-type headache is usually a milder, pressing, bilateral pain without these associated features.