Migraine is not a severe headache. It is a neurological disorder with a distinct biology, a predictable sequence of phases, and a set of treatments that only work if you understand which phase you are treating. Roughly one in twelve adults is affected, it is about three times more common in women than men, and it sits among the leading causes of years lived with disability worldwide.
That last point matters. Migraine is often treated as an inconvenience to be pushed through. When it occurs on fifteen or more days a month, it is a disabling condition, and effective treatment exists for most people who are not getting it.
Why migraine is not “just a headache”
During a migraine attack, the brain’s trigeminovascular system becomes activated, the peptide CGRP (calcitonin gene-related peptide) is released, blood vessels in the meninges dilate, and inflammatory signalling sensitises the pain pathways. Imaging studies show spreading waves of altered activity across the cortex.
None of that is ordinary headache physiology. It is why migraine can produce symptoms far beyond pain — nausea, light and sound sensitivity, visual disturbances, and cognitive fog — and why some attacks cause no head pain at all.
The four phases of an attack
1. Prodrome (hours to two days before)
Subtle warning signs: yawning, food cravings, irritability, neck stiffness, increased thirst, difficulty concentrating, or a distinctive mood shift. Not everyone gets it, but those who do often learn to recognise theirs — which is the window for preventive action rather than waiting for pain.
2. Aura (usually 5–60 minutes before pain)
Around a quarter of people experience aura. It is a fully reversible neurological symptom, most often visual: zigzagging lines, a shimmering blind spot that expands, flashes of light, or a pattern that spreads across the visual field. Other forms include pins and needles on one side, difficulty speaking, or weakness.
Aura reflects a phenomenon called cortical spreading depression — a slow wave of neuronal activation followed by suppression that moves across the cortex at a few millimetres per minute. That speed matches how an aura appears to travel.
3. Headache (4–72 hours untreated)
Typically one-sided and throbbing, worse with routine physical activity, and accompanied by nausea or vomiting plus sensitivity to light and sound. Both light and sound sensitivity are required for a formal diagnosis — one alone does not qualify.
Around a third of people experience attacks on both sides, or the side switches, so “always on the left” is not a reliable rule.
4. Postdrome (up to 24 hours after)
The “migraine hangover”: exhaustion, difficulty concentrating, mood changes, and sensitivity that lingers. Many people describe feeling emotionally flat or unusually clear-headed in the hours after pain resolves.
What actually triggers attacks
Triggers are individual, and the list published online is long enough that people blame food for what is actually sleep loss or stress. The most consistently reported:
| Trigger | Notes |
|---|---|
| Stress and its let-down | The most common — and the crash after stress ends is as provocative as stress itself |
| Disrupted sleep | Both too little and too much; weekend lie-ins are a classic trigger |
| Hormonal change | Menstruation, ovulation, and the drop after childbirth — the basis of menstrual migraine |
| Missed meals and dehydration | Skipping breakfast is highly reproducible |
| Alcohol | Especially red wine; both the alcohol and congeners contribute |
| Weather and barometric change | Reported frequently; harder to study because it is hard to isolate |
| Bright or flickering light | Including screens, though screen time alone rarely explains an attack |
| Strong smells | Perfume, paint, solvent |
| Aged cheese and processed meats | Tyramine; real but overstated relative to sleep and stress |
The practical approach is not to eliminate everything. It is to keep a short attack diary for six to eight weeks, identify your own top three triggers, and control those. Trying to avoid twenty triggers simultaneously produces anxiety and a worse diet without reducing attacks.
Sleep consistency deserves particular emphasis — our insomnia guide covers the wake-time discipline that serves both conditions.
Treatments that work
Treating an attack once it starts
Take medication early, while pain is still mild. Once a migraine is fully established and nausea has begun, oral medication is absorbed poorly and works less well.
- Simple analgesics — ibuprofen, aspirin or paracetamol, taken at first sign
- Triptans — the first-line specific treatment for moderate-to-severe attacks. They constrict cranial vessels and block CGRP release. They are contraindicated in people with cardiovascular disease, which is why a cardiovascular check comes first
- Gepants — CGRP receptor antagonists taken acutely; they do not constrict vessels, so they are an option where triptans are unsuitable
- Anti-nausea medication — metoclopramide or domperidone, particularly when vomiting threatens to return the analgesic
Preventive treatment
Recommended when attacks occur more than about four days a month, when acute medication is not working, or when attacks are predictably disabling. Options include beta-blockers such as propranolol, amitriptyline, topiramate, candesartan, and — for episodic migraine — CGRP monoclonal antibodies injected monthly.
Preventives generally need eight to twelve weeks at an adequate dose before you judge whether they work, and they should be reviewed rather than continued indefinitely without reassessment.
Supplements with reasonable evidence
Magnesium (commonly 400–600 mg daily of a well-absorbed form), riboflavin (400 mg daily), and coenzyme Q10 have the best evidence among adjunctive options. Magnesium is also worth checking if you experience muscle cramps or palpitations — see our blood pressure guide for where it sits in a broader dietary pattern.
Non-drug approaches
Regular aerobic exercise, on schedule rather than when convenient, reduces attack frequency in trials. Cognitive behavioural therapy, biofeedback and relaxation training have genuine evidence for prevention. So does consistent sleep — a real intervention, not generic advice.
The problem nobody warns you about
Medication overuse headache develops when acute painkillers are used too often: generally ten or more days a month for triptans and combination analgesics, or fifteen or more days a month for simple painkillers.
The mechanism is counterintuitive — the medication that treats pain gradually becomes the thing generating it. Withdrawal is necessary and unpleasant for two to four weeks, but the headache settles afterwards and preventives start working again. This is the single most common reason people with migraine end up in a headache clinic with daily pain.
Red flags: when to seek urgent care
Most migraine is benign. These patterns are not migraine until proven otherwise:
- Sudden, worst headache of your life reaching maximum intensity within seconds to minutes — possible subarachnoid haemorrhage
- Fever with neck stiffness or confusion
- New headache after age 50, or a progressive change in pattern
- Headache with weakness, visual loss, double vision or difficulty speaking
- Headache after a head injury, or worse with coughing, bending or exertion
- Headache with cancer or immunosuppression in the history
- Attacks lasting more than 72 hours (status migrainosus) — needs assessment
When to see a doctor
If you use acute medication more than twice a week, if attacks are increasing, if you are missing work or school regularly, if over-the-counter treatment stops helping, or if your pattern changes — book an appointment. Ask about preventive treatment and about whether medication overuse has already developed.
Diagnosis is clinical: there is no scan or blood test for migraine. A normal MRI is reassuring that nothing else is present, but it does not diagnose or exclude migraine. That distinction is worth understanding before imaging is ordered.
Frequently asked questions about migraine
Can migraine be cured?
There is no cure, but the aim of treatment is close to it: attacks reduced to the point where they no longer shape your choices. Some people achieve that with a trigger change alone; others need preventive medication. Hormonal migraine in particular can improve substantially after menopause.
Is a migraine always one-sided?
No. One-sided pain is typical and supports the diagnosis, but a substantial proportion of people have bilateral attacks, and the side can change between attacks. Doubles the diagnostic weight of the associated nausea, light sensitivity and activity intolerance.
Do I need to avoid all chocolate, cheese and wine?
Almost certainly not. The trigger lists circulated online are based partly on older studies with methodological problems. Restricting your diet broadly while ignoring sleep regularity and stress usually fails. Track your own attacks, find your actual triggers, and change those.
Are there options if triptans do not suit me?
Yes. Gepants do not carry the vasoconstrictive contraindication, ditans act on a different receptor entirely, and preventives reduce the number of attacks you need to treat. If a triptan has been ineffective, the dose or timing may simply be wrong before concluding the class does not work.
Do screens cause migraine?
Bright, flickering or glaring light can provoke attacks in people who are already susceptible, and screen light in the hours before bed can affect sleep. But screens alone rarely explain frequent attacks — sleep disruption, skipped meals and stress usually contribute more. Treat the pattern, not the device.
This article is for general information only and is not a substitute for professional medical advice. See our medical disclaimer.
