Migraine

• Migraine without aura — the most common form: recurrent attacks of moderate-to-severe, often one-sided, pulsating head pain lasting 4–72 hours, worsened by routine activity and accompanied by nausea and/or light and sound sensitivity.
• Migraine with aura — around a third of people, in whom attacks are preceded by reversible neurological symptoms developing over 5–20 minutes and lasting under an hour: most often visual (zigzag lines, scotoma), sometimes sensory, speech or motor. Aura is cortical, not vascular.
• Chronic migraine — headache on 15 or more days a month for over three months, with migraine features on at least eight. It usually evolves out of episodic migraine, and medication overuse is the single most common driver of that transformation.
• Menstrual migraine — attacks reliably clustered around the perimenstrual oestrogen withdrawal; typically longer, more severe and less responsive to acute treatment.
• Vestibular migraine — recurrent vertigo as the dominant symptom, with or without head pain; a leading cause of episodic dizziness and frequently misattributed to the inner ear.
• Migraine with brainstem aura and hemiplegic migraine — rarer forms with brainstem symptoms or motor weakness, both of which change the safety calculus, since vasoconstrictor acute treatments are contraindicated.

The old “vascular theory” is wrong, and it still shapes a lot of herbal writing about migraine. For most of the twentieth century migraine was explained as vasoconstriction causing aura followed by rebound vasodilation causing pain — which is why so much traditional advice reaches for vasodilators and “circulatory” herbs. Modern evidence describes something else: migraine is a disorder of a hyperexcitable brain and of the trigeminovascular system, and the vascular changes are a downstream consequence rather than the cause.

Aura corresponds to cortical spreading depression — a slow wave of neuronal and glial depolarization moving across the cortex at 2–5 mm per minute, followed by suppression, which matches the march of visual aura almost exactly. Pain arises when trigeminal sensory fibres innervating the meninges are activated and sensitized, releasing calcitonin gene-related peptide (CGRP) and other neuropeptides. CGRP is the pivotal molecule: infusing it triggers migraine in susceptible people, and blocking it aborts and prevents attacks — which is the basis of the gepants and the CGRP monoclonal antibodies that have reshaped treatment since 2018.

Central sensitization explains why an established attack becomes harder to treat and why the scalp becomes tender (allodynia), and it is the pharmacological reason acute treatment works far better taken early. Between attacks the migraine brain shows altered habituation to sensory input — it does not damp down repeated stimuli the way most brains do, which is the plausible substrate for trigger sensitivity.

Migraine carries a strong genetic component and clusters with depression, anxiety, epilepsy, irritable bowel syndrome, fibromyalgia and insomnia. Migraine with aura is associated with a modestly increased risk of ischaemic stroke, an association that becomes clinically important alongside smoking and combined hormonal contraception.

Migraine is diagnosed clinically, on pattern, using the ICHD-3 criteria: at least five attacks lasting 4–72 hours, with at least two of (one-sided, pulsating, moderate-to-severe, aggravated by routine activity), and at least one of (nausea/vomiting, or light and sound sensitivity). No scan or blood test confirms it, and imaging in someone with a typical history and normal examination is generally unhelpful.

Imaging and prompt assessment are warranted for red-flag features — a sudden “worst ever” thunderclap headache, headache with fever or neck stiffness, new headache after age 50, progressive daily worsening, headache with abnormal neurological signs, or a headache pattern that changes distinctly in an established migraine sufferer.

Two diagnostic traps send people toward self-treatment. “Sinus headache” is very often migraine — facial pain, congestion and tearing are trigeminal-autonomic features of migraine itself, not evidence of sinus infection. And medication-overuse headache develops when acute treatment is taken too often (roughly 10+ days a month for triptans, opioids and combination analgesics, 15+ for simple analgesics), producing a daily headache that only worsens as more treatment is taken. It is common, frequently missed, and it resolves on withdrawal.

Acute treatment. NSAIDs and aspirin work well for many attacks. Triptans are the migraine-specific standard and are most effective taken early, though they are contraindicated in uncontrolled hypertension, ischaemic heart disease and hemiplegic or brainstem-aura migraine. Gepants (CGRP receptor antagonists) and ditans are newer options without vasoconstrictor effects, useful precisely where triptans cannot be used. Anti-emetics are therapeutic in migraine, not just symptomatic, since gastric stasis during an attack impairs absorption of everything taken by mouth.

Preventive treatment is considered when attacks are frequent, disabling or poorly responsive. Established options include beta-blockers (propranolol, metoprolol), topiramate, sodium valproate, amitriptyline and candesartan. Since 2018 the CGRP monoclonal antibodies — erenumab, fremanezumab, galcanezumab, eptinezumab — have offered the first preventives designed for migraine rather than borrowed from other conditions, and onabotulinumtoxinA is established for chronic migraine.

Any preventive needs an adequate trial — typically 8–12 weeks at target dose — before being judged, and the realistic goal is fewer and less severe attacks, not their abolition.

Migraine is unusual in that several nutritional agents carry formal guideline recognition, which is a much higher bar than “some trials exist.”

Riboflavin (vitamin B2) at 400 mg/day has the cleanest result. In a randomized controlled trial, riboflavin was superior to placebo in reducing attack frequency, with 59% of riboflavin patients responding against 15% on placebo and a number-needed-to-treat of 2.3 ^{12Reference 12Schoenen et al. · 1998RCTEffectiveness of high-dose riboflavin in migraine prophylaxis — randomised controlled trial (400 mg/day; 59% vs 15% responders, NNT 2.3)View study →}. A 2025 review concludes it can be recommended for migraine prevention in adults, with minimal side effects, while noting effectiveness in children remains unproven ^{13Reference 13Tepper et al. · 2025ReviewNutraceuticals and headache 2024: riboflavin, coenzyme Q10, feverfew, magnesium, melatonin, and butterbur — reviewView study →}. The dose matters: 400 mg is far above nutritional intake, and ordinary B-complex products do not deliver it.

Magnesium is recommended for migraine prevention by the same review, and intravenously for acute attacks ^{13Reference 13Tepper et al. · 2025ReviewNutraceuticals and headache 2024: riboflavin, coenzyme Q10, feverfew, magnesium, melatonin, and butterbur — reviewView study →}. The AAN/AHS guideline rates it probably effective, though individual trials conflict ^{11Reference 11Holland et al. · 2012Evidence-based guideline update: NSAIDs and other complementary treatments for episodic migraine prevention in adults — AAN/AHS Quality Standards Subcommittee reportView study →}. Doses used are typically 400–600 mg/day of elemental magnesium; loose stools are the usual limiting factor, and the citrate and glycinate forms are better tolerated than oxide.

Coenzyme Q10 carries Level C evidence with few adverse effects ^{13Reference 13Tepper et al. · 2025ReviewNutraceuticals and headache 2024: riboflavin, coenzyme Q10, feverfew, magnesium, melatonin, and butterbur — reviewView study →}.

Butterbur (Petasites hybridus) has the strongest efficacy evidence of any botanical in migraine prevention, and a real concern for hepatotoxicity ^{13Reference 13Tepper et al. · 2025ReviewNutraceuticals and headache 2024: riboflavin, coenzyme Q10, feverfew, magnesium, melatonin, and butterbur — reviewView study →}. Unlicensed products were withdrawn in several countries after cases of liver injury, and raw butterbur additionally contains hepatotoxic and carcinogenic pyrrolizidine alkaloids that must be removed by processing. Anyone considering it should check current national safety guidance first, not a supplement label.

Melatonin shows weak evidence and is weakly recommended only where sleep disturbance is part of the picture — with the added caveat that the purity of melatonin sold in the US is poor ^{13Reference 13Tepper et al. · 2025ReviewNutraceuticals and headache 2024: riboflavin, coenzyme Q10, feverfew, magnesium, melatonin, and butterbur — reviewView study →}.

Feverfew is the traditional migraine herb. The Cochrane review found six trials in 561 patients, low-quality evidence, with one larger rigorous trial showing a reduction of 0.6 attacks per month and two other rigorous trials finding no significant difference ^{4Reference 4Wider et al. · 2015Systematic reviewFeverfew for preventing migraine — systematic reviewView study →}. It appears safe, and it may help; the evidence does not yet support a confident claim, and extract stability varies widely between products.

Ginger is best understood as acting on the nausea rather than the headache — which, given how much of migraine’s disability is gastrointestinal, is not a small thing. 5-HTP’s migraine literature is dated and heterogeneous, and no recent placebo-controlled trial supports it as a first-line preventive.

Everyday measures matter most: regular sleep, regular meals, hydration, exercise, and identifying genuine personal triggers rather than eliminating foods wholesale. Keeping a headache diary is the single most useful self-directed intervention, because it distinguishes real triggers from coincidence and reveals medication-overuse patterns that neither the patient nor the prescriber may have noticed.

Supplements, nutrients and compounds used for migraine.