Migraine — Causes, Aura, Triggers & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Migraine is a primary headache disorder characterised by recurrent episodes of moderate to severe, often throbbing, unilateral headache lasting 4-72 hours, associated with nausea, vomiting, photophobia (light sensitivity), and phonophobia (noise sensitivity). It is classified as the third most prevalent disease and second leading cause of disability worldwide by the Global Burden of Disease Study. Approximately 1 billion people are affected globally, with a 3:1 female predominance — peaking in prevalence during the reproductive years (30-40 years). One-third of migraine sufferers also experience aura — transient neurological symptoms preceding the headache (visual disturbances, sensory changes, speech difficulties). Migraine without aura is the most common type. Chronic migraine is defined as 15 or more headache days per month, with features of migraine on at least 8 days — affecting 1-2% of the population and associated with significant disability and medication overuse headache.

Migraine is a complex neurological disorder with a strong genetic component (heritability estimated at 40-65%). Familial hemiplegic migraine (FHM) involves identified mutations in calcium channel, sodium channel, and ATP pump genes — providing insight into migraine neurobiology. The current understanding of migraine pathophysiology centres on: cortical spreading depression (CSD) — a wave of neuronal depolarisation followed by suppression propagating across the cortex, correlating with aura symptoms; calcitonin gene-related peptide (CGRP) — a neuropeptide released from trigeminal nerve fibres that plays a key role in neurogenic inflammation and central sensitisation of the trigeminovascular system; brainstem and hypothalamic involvement in generating the prodrome and initiating attacks. Triggers (precipitating individual attacks in susceptible individuals): hormonal changes (perimenstrual migraine — oestrogen withdrawal is the most common trigger in women), sleep disturbance (too much or too little), stress and stress let-down, alcohol (especially red wine and beer), specific foods (processed meats — nitrites; aged cheese — tyramine; MSG), bright or flickering lights, strong smells, dehydration, fasting, and weather changes.

Migraine attacks classically occur in four phases. Prodrome (hours to days before): fatigue, mood changes, food cravings (particularly for sweet foods), neck stiffness, yawning, and concentration difficulties — these are generated by hypothalamic and brainstem activation. Aura (30% of migraineurs; each symptom typically develops over 5-20 minutes and lasts under 60 minutes): visual aura (most common) — scintillating scotoma (zigzag fortification spectrum expanding across visual field), photopsia, hemianopia; sensory aura — unilateral tingling or numbness, typically spreading from hand to face (cheiro-oral distribution); motor aura (hemiplegic migraine); speech aura (dysphasia, dysarthria); retinal aura (monocular visual disturbance — carotid occlusion must be excluded). Headache phase: moderate to severe throbbing or pulsating pain, typically unilateral (60%) but may be bilateral; aggravated by routine physical activity; associated nausea (up to 90%), vomiting (50%), photophobia, phonophobia, and osmophobia. Postdrome: fatigue, cognitive slowing, and mood change persisting for up to 24 hours after headache resolution — the 'migraine hangover'.

Migraine is a clinical diagnosis based on the International Classification of Headache Disorders (ICHD-3) criteria. Migraine without aura: at least 5 attacks lasting 4-72 hours with at least 2 of: unilateral location, pulsating quality, moderate-to-severe intensity, aggravation by activity; plus at least 1 of: nausea/vomiting or photophobia and phonophobia. Migraine with aura: at least 2 attacks with at least 1 fully reversible aura symptom, each lasting 5-60 minutes, followed by headache. Investigations are not required for typical presentations in a young adult with normal neurological examination. MRI brain with contrast: indicated for atypical features, new headache pattern in adults over 50, progressive headache, neurological deficits, or clinical suspicion of secondary headache. Red flag features requiring urgent investigation (SNOOP4 mnemonic): Systemic symptoms (fever, weight loss), Neurological signs, Onset sudden ('thunderclap' — rule out subarachnoid haemorrhage), Onset after age 50, Previous headache history change, Precipitated by Valsalva, Postural variation, Papilloedema. Brain imaging should be performed promptly for all red flag headaches.

Acute treatment (stratified care — treat based on attack severity from the outset): mild attacks — paracetamol 1000 mg or ibuprofen 400-600 mg, ideally combined with a prokinetic antiemetic (metoclopramide or prochlorperazine — hasten gastric emptying and improve drug absorption; also relieve nausea). Moderate to severe attacks: triptans (selective 5-HT1B/1D agonists — sumatriptan 50-100 mg oral/6 mg SC/20 mg intranasal, rizatriptan 10 mg, eletriptan 40-80 mg, zolmitriptan 2.5-5 mg) — effective in 60-80% of patients; contraindicated in hemiplegic migraine, basilar migraine, cardiovascular disease, and uncontrolled hypertension. Gepants (small-molecule CGRP receptor antagonists — ubrogepant, rimegepant): effective for triptan non-responders and those with cardiovascular contraindications; rimegepant also has a preventive role taken every other day. Ditans (lasmiditan — 5-HT1F agonist): effective without vasoconstriction — for patients with cardiovascular disease. Preventive treatment: indicated for 4+ migraine days/month causing significant disability, or 2+ attacks responding poorly to acute treatment. First-line prevention: propranolol 40-120 mg/day, topiramate 25-100 mg/day (teratogenic — avoid in pregnancy), amitriptyline 10-75 mg nocte. CGRP monoclonal antibodies (erenumab — anti-CGRP receptor; fremanezumab, galcanezumab — anti-CGRP ligand): approved for chronic and episodic migraine; 50% reduction in monthly migraine days in ~50% of patients; monthly or quarterly SC injection.

Migraine carries several serious and long-term complications that extend beyond the immediate attack. Chronic migraine: episodic migraine transforms to chronic migraine (15+ headache days per month) in 2.5% of sufferers annually, most commonly from medication overuse headache (MOH) — occurring when triptans are used on 10+ days/month or simple analgesics on 15+ days/month. MOH causes rebound cycles requiring supervised medication withdrawal. Migrainous infarction: a rare complication where a persistent aura is associated with ischaemic stroke confirmed on neuroimaging — occurring in fewer than 1% of migraine with aura sufferers but representing a recognised risk. Persistent aura without infarction (PAWOI): aura symptoms persisting beyond 1 week without corresponding neuroimaging changes — cause unknown. Depression and anxiety: present in 40-50% of chronic migraine patients — pain and mood disorders share serotonergic and noradrenergic pathways. Significant occupational and social disability: migraineurs lose an average of 4-6 work days per month during high-frequency periods; the condition costs the UK economy an estimated 4 billion GBP annually. Serotonin syndrome risk: rarely occurs when triptans are combined with SSRIs or SNRIs. Medication-related complications from opioid use in poorly managed migraine include dependence and cognitive impairment.

Maintain a migraine diary (paper or app — Migraine Buddy, Healow) to identify personal triggers, menstrual pattern, medication use, and attack frequency — essential for demonstrating preventive treatment need and avoiding medication overuse headache. Medication overuse headache (MOH — 'rebound headache'): regular use of triptans on 10+ days/month or simple analgesics on 15+ days/month can transform episodic to chronic migraine. Managing MOH requires withdrawal of the overused medication with guidance from a headache specialist. Lifestyle: maintain regular sleep schedule (consistent wake time even weekends), regular hydration (2-3 L/day), avoid skipping meals, and regular aerobic exercise 3x weekly (evidence for reduction in attack frequency). Hormonal migraine management: perimenstrual triptan prophylaxis (frovatriptan 2.5 mg daily for 6 days around menstruation) or continuous combined OCP (avoiding hormone-free interval) can reduce menstrual migraine. Note: combined OCP with aura increases stroke risk — progestogen-only or non-hormonal contraception preferred for migraine with aura. CBT and biofeedback: evidence-based non-pharmacological prevention — particularly for stress-triggered migraine. CGRP monoclonal antibodies provide the most consistent and targeted prevention available.

Seek emergency care immediately for a sudden, severe 'thunderclap' headache (worst headache of life) — subarachnoid haemorrhage must be excluded with urgent CT brain and lumbar puncture. Also seek emergency care for: headache with fever, neck stiffness, and photophobia (meningitis); headache with focal neurological deficit not matching typical migraine aura; headache after head trauma; new severe headache in a person over 50; and any headache with papilloedema or reduced consciousness. See your GP or neurologist for: frequent migraines (4+ days/month) to discuss preventive treatment, poor response to over-the-counter analgesics, rapidly escalating headache frequency, or headache requiring frequent acute medication (risk of medication overuse headache). Specialist referral is appropriate for chronic migraine, migraine with atypical aura, or for CGRP therapy assessment.