Migraines start deep in the brain, not in the blood vessels as doctors once believed. The current scientific consensus points to a central nervous system origin, where a cascade of electrical and chemical events unfolds over hours or even a full day before head pain begins. Understanding this sequence helps explain why migraines feel so different from ordinary headaches, and why early warning signs matter.
The Prodrome: Early Warnings Up to 24 Hours Before
The first phase of a migraine can begin up to 24 hours before any head pain arrives. During this window, areas deep in the brain become unusually active. Brain imaging studies have identified heightened activity in the hypothalamus, the brainstem’s periaqueductal gray region, and several cortical areas during this early stage. These are regions responsible for regulating sleep, mood, appetite, and pain processing, which explains the oddly specific symptoms people notice.
Prodrome symptoms include fatigue, difficulty concentrating, mood changes, trouble sleeping, nausea, increased hunger and thirst, and frequent urination. Many people don’t connect these early signs to the migraine that follows, but they represent the brain’s shifting chemistry. The hypothalamus in particular acts as the body’s internal thermostat for things like energy, hydration, and hormonal balance, so when it becomes overactive, you feel it in ways that seem unrelated to headache.
What Happens in the Brain During Aura
About one in four migraine sufferers experience aura, a phase lasting anywhere from 5 to 60 minutes that produces visual disturbances, tingling, or difficulty speaking. The mechanism behind it is called cortical spreading depression: a slow wave of intense electrical activity that sweeps across the brain’s surface, followed by a prolonged period of suppressed nerve firing.
Functional MRI studies have tracked this wave in real time. It begins near the back of the brain, where central vision is processed, and moves forward at roughly 3.5 millimeters per minute. As the wave passes through each area, it first causes a burst of neural activity (producing the shimmering, scintillating visuals many people describe), then leaves suppressed, quiet tissue in its wake (creating the blind spots or scotomas that follow the shimmer). Recovery takes about 15 minutes for each affected area to return to roughly 80% of its normal function.
Not everyone with migraine experiences aura, and the headache phase can begin independently of it. But when aura does occur, it provides a visible marker of the electrical disruption already underway inside the skull.
How Pain Signals Get Activated
The actual pain of a migraine originates from a network of nerve fibers called the trigeminovascular system. These are sensory fibers from the trigeminal nerve that wrap around blood vessels in the membranes covering the brain. When these fibers become activated, either by the electrical wave of cortical spreading depression or by chemical signals from overexcited brain regions, they release powerful inflammatory molecules into the vessel walls.
The key molecule in this process is a neuropeptide called CGRP. When trigeminal nerve fibers fire, they release CGRP along with other inflammatory signals like substance P. CGRP is a potent vasodilator that also sensitizes pain receptors and promotes inflammation in surrounding tissues. People who experience migraine attacks without aura tend to have even higher CGRP concentrations during an attack than those with aura, and women, people over 30, and those who had a recent headache before the current attack all show elevated levels.
This inflammatory cascade does two things simultaneously. It sends pain signals up through the trigeminal nerve to the brainstem, and it spreads the inflammatory response to adjacent tissues through a process where nerve fibers conduct signals in both directions. This bidirectional firing helps explain why migraine pain can intensify and expand over time rather than staying static.
Why Light, Sound, and Smell Become Painful
One of the hallmarks of migraine is extreme sensitivity to sensory input. Light sensitivity in particular has a specific neural explanation. In the thalamus, the brain’s central relay station, researchers have identified a group of neurons that respond to both pain signals from the skull’s membranes and to light. These dual-purpose neurons project to the brain’s visual, sensory, and association areas simultaneously, which means that during a migraine, ordinary light gets routed through the same pathways already carrying pain information.
This is why dimming the lights helps during an attack. Visual stimulation activates pain-processing areas in the brainstem, and this connection is even stronger in people with chronic migraine. The thalamus essentially loses its ability to filter sensory input properly, so stimuli that would normally be harmless get amplified into something overwhelming.
The Role of Blood Vessels
For decades, migraines were considered a vascular disorder, caused by blood vessels constricting and then dilating. That theory has been largely replaced. Changes in blood flow do occur during a migraine, but they are now understood as a consequence of the underlying neural events rather than the cause. When serotonin levels shift during the cascade, blood vessels narrow. Hormonal fluctuations, particularly drops in estrogen, can also trigger vessel contractions that contribute to throbbing pain.
The vascular component still matters for how the pain feels. The pulsating quality of migraine pain correlates with blood vessel changes in the inflamed meningeal tissues. But treating only the blood vessel changes, without addressing the neural inflammation, is why older migraine treatments often fell short. Modern treatments that block CGRP or target the trigeminal pathway work because they interrupt the process closer to its source.
Common Triggers That Set the Process in Motion
While the internal cascade is well mapped, the initial spark varies from person to person. Environmental triggers interact with a brain that is already predisposed to migraine. Changes in barometric pressure, for instance, may create a small imbalance between the pressure inside the skull and the outside environment, directly stimulating pain-sensitive nerves and triggering inflammation. Low oxygen levels also appear to play a role: in controlled studies, prolonged exposure to reduced oxygen caused a significant rise in CGRP levels in migraine-prone individuals.
Other well-established triggers include sleep disruption, skipped meals, dehydration, hormonal shifts, stress (or the letdown period after stress), strong smells, and bright or flickering light. These triggers likely work by pushing an already excitable brain past its threshold, activating the hypothalamic and brainstem circuits that initiate the prodrome. This is why the same trigger doesn’t always produce a migraine. Your brain’s baseline excitability on any given day determines whether a trigger tips you into an attack.
The Full Timeline of an Attack
A complete migraine episode moves through up to four distinct phases, though not everyone experiences all of them:
- Prodrome (up to 24 hours): Fatigue, food cravings, mood shifts, neck stiffness, frequent yawning, difficulty concentrating.
- Aura (5 to 60 minutes): Visual disturbances like zigzag lines or blind spots, tingling in the face or hands, difficulty speaking. Only affects about 25% of migraine sufferers.
- Headache (4 to 72 hours): Gradually intensifying pain, often on one side of the head, with nausea, vomiting, and sensitivity to light, sound, and smell.
- Postdrome (a few hours to 48 hours): Sometimes called a “migraine hangover,” with lingering fatigue, stiff neck, dizziness, difficulty concentrating, and continued light sensitivity.
The total duration from first prodrome symptom to the end of the postdrome can stretch well beyond three days. Treating a migraine early in the process, ideally during the prodrome or at the very start of pain, is more effective because it interrupts the inflammatory cascade before central sensitization takes hold. Once the trigeminal system is fully activated and pain signals have been amplified in the brainstem, the attack becomes much harder to stop.