Migraine: Causes, Mechanism, and Treatment — a Full Overview

The International Classification of Headache Disorders (ICHD-3), the official diagnostic standard of the International Headache Society, distinguishes two main migraine subtypes. Migraine without aura is the more common form, involving attacks of one-sided, pulsating headache of moderate to severe intensity lasting 4 to 72 hours, worsened by physical activity, and accompanied by nausea, vomiting, and sensitivity to light and sound.

Migraine with aura, occurring in roughly a quarter to a third of people with migraine, is preceded by fully reversible neurological symptoms — most often visual (flashing lights, zigzag lines, blind spots), less often sensory (tingling spreading from the hand toward the face) or speech-related. Aura typically develops gradually over several minutes and resolves before or during the headache phase, usually lasting 20-60 minutes.

Migraine triggers are highly individual and rarely act in isolation — more often they add up, creating a threshold that, once crossed, results in an attack. The most commonly reported include: stress and — paradoxically — the period right after it eases (so-called weekend migraine), irregular sleep (both too little and too much), skipped meals and dehydration, hormonal changes across the menstrual cycle, certain foods and additives (though the evidence for specific foods is weaker than popular belief suggests), weather changes, and excessive caffeine intake or sudden withdrawal from it.

The practical implication of this individuality is that generic "foods to avoid with migraine" lists circulating online rarely hold up for any given person. Systematically noting potential triggers, sleep, meals, and cycle phase in a simple diary is far more effective, allowing an actual, individual pattern to emerge over time instead of following generic advice.

Modern understanding of migraine has moved away from the old purely vascular hypothesis (dilation of brain blood vessels as the main cause of pain) toward a neurovascular model. A key role is played by activation of the trigeminovascular system and the release of calcitonin gene-related peptide (CGRP) — a neurotransmitter with strong vasodilatory and pro-inflammatory effects that plays a central role in generating migraine pain. Aura, meanwhile, is linked to cortical spreading depression — a wave of altered electrical activity moving across the cerebral cortex.

Understanding CGRP's role was a breakthrough not just scientifically but therapeutically — it's the mechanism behind an entire new generation of preventive and acute drugs, described further below. Migraine also has a significant genetic component: risk is markedly higher in people whose first-degree relatives have migraine, though it isn't inherited in a simple, single-gene way (with the exception of rare familial hemiplegic migraine).

Acute treatment aims to abort an attack already underway and should be started as early as possible after symptoms appear. The International Headache Society (IHS) published unified global practice recommendations for acute migraine treatment in 2024, organizing a stepped approach based on attack severity.

Preventive treatment is usually considered when attacks are frequent (typically from about 4 migraine days per month), significantly impair functioning despite proper acute treatment, or when acute treatment is contraindicated or ineffective. Propranolol and other beta-blockers are among the longest-used and best-studied preventive medications in migraine, even though their exact anti-migraine mechanism isn't fully understood.

Besides beta-blockers, classic preventive options include certain anti-seizure medications (topiramate, valproate), tricyclic antidepressants (amitriptyline), and — for chronic migraine — botulinum toxin type A. The choice of drug depends on the side-effect profile, the patient's comorbidities, and individual tolerance, and preventive effect is usually assessed only after 8-12 weeks of regular use.

The discovery of CGRP's key role in migraine's pathomechanism led to a new drug class — monoclonal antibodies targeting CGRP or its receptor, given by injection once monthly or quarterly, specifically designed for migraine prevention, unlike older drugs "borrowed" from cardiology or psychiatry.

Alongside prescription drugs, questions often arise about specific supplements in the context of migraine — a topic extensive and evidence-based enough that we've dedicated separate, in-depth articles to it: on magnesium's role in migraine prevention, see our article on magnesium and migraine; on riboflavin (vitamin B2) for attack prevention, see riboflavin and migraine; and on ginger for easing an acute attack, see ginger and migraine. This article deliberately focuses on the overall disease picture and guideline-established drugs rather than repeating those more detailed analyses.

It's worth stressing that none of these supplements replace acute or preventive treatment in moderate-to-severe migraine — depending on the evidence quality described in each dedicated article, they may be considered as an add-on, especially for people preferring to start with interventions with a milder side-effect profile, but the decision to add them, especially alongside prescription drugs, should be discussed with your treating physician.

Migraine is a disease where patient education makes a real difference — understanding your own triggers, using acute medication judiciously and within limits (to avoid medication overuse headache), and knowing when to consider prevention can change quality of life as effectively as the choice of any single drug. The development of CGRP inhibitors also shows migraine is no longer treated as the "lesser" sibling of other neurological diseases — today it has its own targeted treatment built on a well-understood mechanism.