A migraine is a recurrent neurological disorder most often recognised by a moderate-to-severe, throbbing or pounding pain that commonly affects one side of the head. Attacks typically last from a few hours up to several days and are often accompanied by nausea, vomiting, and heightened sensitivity to light, sound, and smell. Some people experience sensory disturbances called aura before or during an attack; others have migraine without head pain but with the same disabling features.

Symptoms, phases and common patterns

Migraine attacks may follow several phases, although not everyone experiences all of them. A prodrome (hours to days before pain) can include fatigue, mood change, neck stiffness, or food cravings. The headache phase is usually unilateral and pulsatile, often worsening with physical activity. Associated symptoms frequently include nausea, dizziness and sensory sensitivity. In some cases an aura precedes the headache: visual changes such as flashing lights, zigzag lines or blind spots are typical, but auras can also affect speech, movement or sensation. Attacks commonly last between four and 72 hours when untreated.

Types and diagnostic distinctions

Migraines are classified by their frequency and by the presence or absence of aura. When headaches occur fewer than 15 days per month they are usually termed episodic migraine; when they occur on 15 or more days per month for more than three months, with at least eight days meeting migraine criteria, the condition is often labelled chronic migraine. Other recognised types include vestibular migraine (prominent balance or dizziness symptoms), hemiplegic migraine (temporary motor weakness), and ocular or retinal migraine when visual loss is a prominent feature. Diagnosis relies on clinical history and symptom pattern rather than a single laboratory test.

Causes and mechanisms

Current understanding frames migraine as a disorder of brain excitability and brain–blood vessel interactions. A variety of neural pathways and chemical mediators are involved; one peptide that has received substantial attention is calcitonin gene-related peptide (CGRP), which can promote vasodilation and neurogenic inflammation in tissues surrounding the brain, including the meninges. CGRP is not the sole cause of migraine but is an important mediator for many sufferers. Genetic susceptibility, environmental factors and changes in brain networks all contribute to the risk of developing recurrent attacks.

Triggers and risk factors

Many people with migraine identify specific triggers that tend to precede attacks. Common triggers include sleep disturbance, stress, dehydration, skipped meals, certain foods or additives, alcohol, strong odors, bright lights and changes in weather. For women, fluctuations in estrogen levels around menstruation or menopause can be a prominent trigger. Family history is a strong risk factor: migraine often runs in families, indicating inherited components. Lifestyle modification and trigger management are central parts of prevention strategies for many patients; see the list below for typical examples.

  • Sleep regularity and hydration
  • Stress reduction and pacing of activity
  • Identification and avoidance of dietary triggers
  • Consistent meal and caffeine patterns

Impact, treatment approaches and public health

Migraine is a leading cause of disability in working-age adults because attacks can be both frequent and disabling. The World Health Organization and other public health bodies have highlighted the substantial societal costs of migraine care and lost productivity. In regional and policy discussions it has been described as among the most costly neurological problems for treatment and disability in areas such as the World Health Organization-referenced literature; examples cited in reports include the European Union and the United States.

Management broadly divides into acute treatments to relieve individual attacks and preventive strategies to reduce attack frequency and severity. Acute care may use simple analgesics, antiemetics, or migraine-specific medications; preventive options include oral medications, neuromodulation devices, behavioural therapies, and, for many patients, newer therapies that target CGRP signalling. Decisions on treatment are personalised, based on attack frequency, side effects, coexisting medical conditions and patient preference.

People should seek medical advice if headaches are new, change in pattern, are unusually severe, or are accompanied by neurological symptoms that persist beyond the typical aura. Prompt assessment helps to exclude secondary causes and to establish an effective management plan that reduces disability and improves quality of life. For general background on headache disorders and symptom descriptions see resources on headache and public health summaries of risk factors.