Migraine is caused simply by blood vessels constricting and then dilating.

For much of the twentieth century, migraine was explained mainly as a problem of blood vessels in and around the brain.

The classic sequence was simple: vessels first constricted, or narrowed, producing the visual and sensory symptoms called aura. They then dilated, or widened, and that expansion was supposed to cause the throbbing headache.

That model fit some observations, but not all of them.

Brain imaging and blood-flow studies showed that migraine attacks can begin without the predicted sequence of vessel narrowing and widening. Changes in blood-vessel size also do not track symptoms consistently enough to explain the whole disorder.

Research increasingly pointed to the nervous system itself. The trigeminal system becomes involved during attacks. Brain networks that regulate pain and sensory processing also change, and signaling molecules such as CGRP help transmit and amplify migraine-related signals.

Treatments that block CGRP or other neural pathways can prevent or relieve migraine without working as simple mechanical vasoconstrictors.

Blood vessels still matter, and migraine is often described as neurovascular because nerve and vessel processes interact. What disappeared was the idea that a migraine is simply a headache caused by an artery becoming wider.