What Happens in a Migraine
A migraine is not just a bad headache — it is a whole-brain event, and the science has moved far past “blood vessels.” It begins deep, in the brainstem and hypothalamus (why yawns and cravings can warn you hours ahead); the shimmering aura is a slow wave of cortical spreading depression creeping across the surface at about 3 mm per minute; and the pain comes when the trigeminal nerve wrapped around the brain’s vessels fires and floods the meninges with CGRP. Press play and watch one attack unfold — then give it a triptan or a CGRP blocker and watch it calm down.
Try this: let it run into the Pain phase and turn on ☀ Bright light to feel photophobia spike the pain — then hit Treatment and watch CGRP and pain both fall.
Live migraine readout
What's happening
Real values here: cortical spreading depression really does creep at about 3 mm/min, and pain is shown on the standard 0–10 clinical scale. The CGRP index is a simplified 0–100% model of peptide release, not a lab number — measured plasma CGRP varies widely between people and labs.
The Science in Plain Language
1. A migraine is a brain event — not a “blood-vessel headache”
For most of the 20th century, migraine was taught as a vascular disease: blood vessels in the head were said to constrict (causing the aura) and then swell (causing the throb). We now know that story is backwards. The primary driver is neural — excitable brain tissue misbehaving. Blood-vessel dilation happens, but it is a downstream consequence of nerve activity, not the cause. Migraine is a genuine, heritable neurological disorder that affects roughly 1 in 7 people worldwide and is consistently ranked among the leading causes of years lived with disability. It is not “just stress” and it is not a weakness.
2. It starts deep: the premonitory phase
An attack often begins hours to a day before any pain, in the hypothalamus and brainstem — primitive control centres for sleep, appetite, thirst and arousal. Brain-imaging studies show the hypothalamus lighting up in this premonitory (prodrome) phase. That is why the warning signs are so bodily and so specific: yawning, food cravings (often for sweets), fatigue, neck stiffness, mood swings, and sensitivity to light building before the headache. People who learn to read their own prodrome can sometimes treat early and blunt the whole attack. Watch the deep glow pulse in the Premonitory phase.
3. The aura: a wave you can actually clock
About a third of people get an aura — shimmering zigzag lines (a “fortification” pattern), a growing blind spot, sparkles, or sometimes tingling that marches up an arm. The cause is cortical spreading depression (CSD): a slow wave of intense neuronal firing immediately followed by a wave of electrical silence, rolling across the surface of the cortex. Its speed is the giveaway — it travels at roughly 3 mm per minute (measured range about 2–6 mm/min), which exactly matches how fast the visual disturbance expands across a person’s field of view. Because vision is mapped onto the occipital cortex at the back of the brain, a wave that starts there and creeps forward produces a shimmer that starts near the centre of sight and drifts outward over 20–60 minutes, then clears. That is the bright-then-dark band you see sweeping the cortical ribbon.
4. Where the pain comes from: the trigeminovascular system and CGRP
The brain itself feels no pain, but the meninges (the membranes around it) and their blood vessels are richly wrapped by branches of the trigeminal nerve — the great sensory nerve of the face and head. When this trigeminovascular system is activated, the nerve endings release a burst of inflammatory messengers, and the star of the show is CGRP (calcitonin gene-related peptide). CGRP is one of the most potent vasodilators in the body: it widens the meningeal vessels and, crucially, sensitises the pain pathway so that ordinary signals become painful. That is the throbbing, one-sided, pounding head pain of a migraine — and it is why injecting CGRP can trigger a migraine in susceptible people, and why blocking it stops one.
5. Central sensitisation: why light, sound and even your pulse hurt
As the attack matures, the pain system turns up its own gain — a process called central sensitisation. Neurons in the brainstem and thalamus that relay head pain become hyper-responsive, so inputs that are normally harmless start to hurt. This is why the scalp and even brushing your hair become tender (allodynia), why the rhythmic stretch of an artery with each heartbeat is felt as a throb, and why light (photophobia) and sound (phonophobia) become unbearable and drive people to a dark, quiet room. Turn on Bright light during the pain phase to watch the readout jump — that is photophobia feeding straight back into the pain.
6. Triptans: calming the trigeminal release
The first migraine-specific drugs, the triptans (sumatriptan, rizatriptan, eletriptan and others), arrived in the 1990s and are still front-line for treating an attack in progress. They are serotonin (5-HT1B/1D) receptor agonists: they act on the trigeminal nerve endings to shut down the release of CGRP and other peptides, and they modestly constrict the dilated vessels. Taken early, they abort many attacks. Their main limitation is that mild vessel-constriction, so they are generally avoided in people with established heart or stroke disease — which is exactly the gap the newer drugs fill.
7. CGRP blockers: gepants and antibodies, aimed at one molecule
Understanding CGRP produced a whole class of designer drugs that target that exact peptide — a rare and satisfying case of mechanism leading straight to medicine. The gepants (rimegepant, ubrogepant, atogepant) are small pills that block the CGRP receptor; they can both stop an attack and, taken regularly, prevent them, and they do not constrict vessels, so they are safer for people with cardiovascular risk. The monoclonal antibodies — erenumab (which blocks the receptor) and galcanezumab, fremanezumab and eptinezumab (which mop up CGRP itself) — are given by injection or infusion every one to three months purely to prevent migraines. Choosing Treatment in the animation drops the CGRP index and the pain together, the way these drugs do in real life.
8. Triggers: a susceptible brain nudged over threshold
Triggers do not cause migraine; they nudge an already-susceptible brain over its firing threshold. The best-documented ones are a “let-down” after stress (attacks often strike on the first day off, not during the crunch), changes in sleep (too little or too much), hormonal shifts (the drop in oestrogen around menstruation is a classic), skipped meals and dehydration, alcohol (especially red wine), and, in some people, specific foods. Importantly, the threshold moves day to day, so the same trigger may cause an attack one week and nothing the next — which is why chasing single “forbidden foods” usually disappoints. Tap Add trigger during the premonitory phase to push the model over the edge into an attack.
9. What this means for you
Because the biology is real and staged, so is the practical advice. Keep a simple diary to learn your own prodrome and pattern; steady your sleep, meals and hydration to raise your threshold; and treat early — a triptan or gepant works far better taken at the first twinge than once central sensitisation has set in. If you have four or more headache days a month, ask about prevention, which now includes CGRP antibodies alongside older options. And know the red flags that are not ordinary migraine and need urgent care: a sudden “worst headache of your life,” a headache with fever and a stiff neck, new weakness or trouble speaking, or a distinctly new headache after age 50. This page explains a mechanism; it is not a diagnosis.