Migraine is a complex neurological disorder characterised by recurring attacks of moderate-to-severe, typically unilateral, pulsating headache lasting 4-72 hours — accompanied by nausea and/or vomiting, and sensitivity to light (photophobia) and sound (phonophobia). The attacks are worsened by routine physical activity. An attack typically has four phases: prodrome (hours to days before — mood changes, food cravings, yawning); aura (focal neurological symptoms in approximately 30%); headache; and postdrome ("migraine hangover" — fatigue, cognitive impairment, lasting hours to a day).

What causes migraine?

Migraine is a neurological disorder caused by complex brain network dysfunction. The trigeminovascular system — sensory nerve fibres from the trigeminal nerve surrounding intracranial blood vessels — releases CGRP and other inflammatory peptides during attacks, causing pain. Cortical spreading depression — a wave of electrical silence spreading across the cortex at approximately 3mm/minute — is the mechanism of migraine aura. Genetic predisposition (70-80% heritability), hormonal factors (oestrogen), sleep disruption, stress, certain foods and weather changes are triggers in susceptible individuals.

What triggers migraine attacks?

Common triggers: hormonal changes (oestrogen fluctuations — menstrual migraine is the most predictable pattern); stress (during stress and — paradoxically — after stress relief); sleep disruption (too much or too little); skipping meals and dehydration; alcohol (especially red wine and beer); weather changes (barometric pressure, bright light); certain foods (processed meats, aged cheeses, MSG — in some individuals); strong odours; and sensory overload. Individual triggers vary greatly — a migraine diary helps identify personal patterns.

What is the difference between migraine with and without aura?

Migraine without aura (the most common — approximately 70%) proceeds directly to the headache phase. Migraine with aura (approximately 30%) has transient focal neurological symptoms before or during the headache — typically visual disturbances (scintillating scotoma — a crescent of flickering light growing across the visual field; fortification spectra — jagged "castle walls" pattern), sensory tingling, or speech/language difficulties. Aura symptoms last 20-60 minutes and are fully reversible. Migraine with aura doubles the risk of ischaemic stroke — particularly in women who smoke and use oestrogen-containing contraceptives.

What medications treat migraine attacks?

Mild attacks: simple analgesics (paracetamol, aspirin, NSAIDs — ibuprofen, naproxen); antiemetics (metoclopramide, prochlorperazine) for nausea. Moderate-severe attacks: triptans (sumatriptan 50-100mg oral or 6mg SC — the most effective class; faster onset with nasal spray or injection); gepants (ubrogepant, rimegepant — no vasoconstriction, safe in CVD); lasmiditan (a serotonin 5-HT1F agonist — no vasoconstriction). For severe attacks: IV treatments (valproate, metoclopramide, ketorolac, sumatriptan SC) in ED.

What are CGRP monoclonal antibodies?

CGRP-targeting monoclonal antibodies are the first migraine-specific preventive therapies. They target either the CGRP peptide (fremanezumab, galcanezumab — monthly or quarterly SC; eptinezumab — quarterly IV) or the CGRP receptor (erenumab — monthly SC). They reduce monthly migraine days by approximately 50% in 50-60% of patients, with approximately 25-30% achieving 75%+ reduction. Safe, well-tolerated, no organ toxicity. Disadvantages: injection requirement; high cost ($700/month in US); restricted access in many countries.

What is chronic migraine?

Chronic migraine (CM) — defined by the International Headache Society as ≥15 headache days per month for >3 months, ≥8 of which meet migraine criteria — affects approximately 2% of the population. It is among the most disabling conditions in medicine. CM typically develops from episodic migraine (transformation). Risk factors: medication overuse (the most important), stress, obesity, sleep disorders, caffeine overuse. Treatment: preventive medications (CGRP mAbs, topiramate, valproate, beta-blockers, amitriptyline, OnabotulinumtoxinA — Botox for CM); withdrawal of overused medications.

How does migraine affect women specifically?

Migraine is strongly influenced by oestrogen: it first appears in puberty, peaks during reproductive years, and declines after menopause in most women. Menstrual migraine — attacks occurring within 2 days of menstruation onset — affects approximately 50% of women with migraine and tends to be more severe and resistant to treatment. Combined oral contraceptives can worsen migraine with aura and should be avoided (increased stroke risk). Pregnancy often improves migraine; the postpartum period may trigger severe attacks.

How does GMJ News cover migraine?

GMJ News covers WHO migraine burden data, CGRP monoclonal antibody approvals, gepants evidence, migraine-stroke link in women, and the treatment gap. Migraine is a major neurological burden in Georgia — affecting a substantial proportion of working-age women — directly relevant to PHIG's neurological health priorities and the Georgian Medical Journal.

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Migraine

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Migraine is the second leading cause of disability globally — affecting approximately 1.13 billion people, predominantly women aged 20-50 — and responsible for the most disability years of any neurological condition and the highest disability burden in adults under 50 years of age (WHO). A neurological disorder — not just a headache — migraine involves complex brain network dysfunction causing recurring attacks of moderate-to-severe throbbing head pain, nausea, vomiting, photophobia and phonophobia lasting 4-72 hours. The CGRP (calcitonin gene-related peptide) pathway — targeted by gepants and monoclonal antibodies (erenumab, fremanezumab, galcanezumab) — has produced the first migraine-specific preventive therapies.

Key messages

1.13 billion people — 2nd leading disability cause

Migraine affects approximately 1.13 billion people globally and is the second leading cause of disability globally — and the leading cause in adults under 50 years of age. It causes more disability years than any other neurological condition (WHO/GBD).

A neurological disorder, not just a headache

Migraine is a complex neurological disorder involving brain network dysfunction — not simply a severe headache. Attacks involve multiple phases: prodrome, aura (in approximately 30%), headache and postdrome, with neurological, gastrointestinal and sensory features.

CGRP — the migraine molecule

Calcitonin gene-related peptide (CGRP) is released during migraine attacks and drives neurogenic inflammation. CGRP-targeted therapies — gepants (ubrogepant, rimegepant) for acute treatment and monoclonal antibodies (erenumab, fremanezumab, galcanezumab, eptinezumab) for prevention — are the first migraine-specific drug classes.

Women affected 3:1

Migraine affects women approximately 3 times more than men — predominantly during reproductive years. Hormonal fluctuations (oestrogen withdrawal before menstruation — menstrual migraine) are a major trigger.

Chronic migraine

Chronic migraine — defined as ≥15 headache days per month, ≥8 of which are migrainous — affects approximately 2% of the population and is among the most disabling conditions known. Medication overuse headache (MOH) frequently complicates chronic migraine.

Treatment gap

Less than 50% of migraine sufferers consult a doctor; only approximately 15-20% receive effective preventive treatment. WHO and WHO classify migraine as a public health priority but it receives minimal research investment relative to its burden.

Key statistics

1.13B

people with migraine globally

WHO/GBD

leading cause of disability globally

GBD

in under-50s

GBD 2016

3:1

female to male ratio

WHO

of population have chronic migraine

WHO/IHC

4-72hr

duration of an untreated migraine attack

IHS/WHO

Migraine prevalence by age and sex (%) — GBD 2016

Source: GBD 2016. Peak in reproductive-age women; declines after menopause in women.

Glossary of key terms

Migraine with aura
IHS/WHOMigraine associated with transient focal neurological symptoms (aura) — typically visual (scintillating scotoma, fortification spectra), sensory, speech/language or rarely motor — lasting 20-60 minutes before or during the headache. Present in approximately 30% of migraineurs. Aura reflects cortical spreading depression.

CGRP (calcitonin gene-related peptide)
ResearchA neuropeptide released by trigeminal nerve fibres during migraine attacks — a vasodilator and mediator of neurogenic inflammation. CGRP levels are elevated during attacks and normalise with successful treatment. The primary target of new migraine-specific treatments.

Triptans
WHO EMLSerotonin (5-HT1B/1D) receptor agonists — the most effective acute migraine treatments for the past 30 years. Sumatriptan (original), and multiple oral and injectable successors. Cause vasoconstriction and block CGRP release. Contraindicated in cardiovascular disease. On WHO Essential Medicines List.

CGRP monoclonal antibodies
FDA/EMAMonthly or quarterly SC or quarterly IV injections for migraine prevention: erenumab (anti-CGRP receptor), fremanezumab, galcanezumab, eptinezumab (anti-CGRP ligand). Reduce monthly migraine days by 50% in approximately 50-60% of patients. First migraine-specific preventives.

Gepants
FDA/EMASmall molecule CGRP receptor antagonists — ubrogepant and rimegepant for acute migraine treatment; rimegepant and atogepant for prevention. Oral, no vasoconstriction. Safe in cardiovascular disease — an advantage over triptans.

Medication overuse headache (MOH)
IHS/WHOHeadache occurring on ≥15 days/month in a person overusing acute migraine medications for ≥3 months — a very common complication of chronic migraine. Triptans, analgesics and ergotamines are responsible. Treatment requires withdrawal of the overused medication.