Migraines happen because of a chain reaction in the brain involving overexcitable nerve cells, chemical signaling gone haywire, and a massive sensory nerve that amplifies pain signals across your head and face. Unlike a tension headache, a migraine is a neurological event with distinct phases, each driven by specific brain activity. Roughly 40% of the global population experiences headache disorders, with migraine being among the top three most common neurological conditions from childhood through old age.
The Chain Reaction Inside Your Brain
A migraine begins hours before you feel pain. The hypothalamus, a small structure deep in the brain that regulates hunger, sleep, and body temperature, becomes unusually active during what researchers call the premonitory phase. This early activation explains why many people experience food cravings, excessive yawning, or mood changes before a migraine hits. Brain imaging studies have confirmed heightened hypothalamic activity not just during migraine pain, but in the hours leading up to it.
In people who experience visual disturbances (aura) before the headache, the next step is a phenomenon called cortical spreading depression. A wave of intense electrical activity rolls across the surface of the brain, followed by a period where neurons go quiet. During this wave, brain cells lose control of their electrolyte balance: potassium floods out while sodium and calcium rush in. The brain burns through extra energy trying to restore normal conditions, and blood flow to affected areas fluctuates. This wave is what produces the shimmering lines, blind spots, or tingling sensations that characterize aura, typically lasting 20 to 60 minutes.
How the Pain Signal Travels
The trigeminal nerve is the key player in migraine pain. This large nerve network has sensors attached to blood vessels in the brain’s protective covering (the dura) and connects to the brainstem and cortex. When activated, trigeminal nerve fibers release a signaling molecule called CGRP, which dilates blood vessels and triggers inflammation around the brain.
CGRP levels are consistently elevated during migraine attacks. In women with chronic migraine, blood levels of CGRP measure roughly twice as high as those in women with occasional migraines and more than double the levels in people without migraines. This molecule is so central to the process that injecting it into people with migraine can trigger an attack, while it causes no headache in people without the condition. Newer migraine treatments work by blocking CGRP specifically.
Serotonin also plays a role. During a migraine, waves of excitable brain cell activity trigger serotonin release, which narrows blood vessels throughout the body. Shifts in serotonin levels change how sensitive your pain-processing system is, effectively lowering the threshold at which normal sensations become painful.
Why Light Makes It Worse
Most people with migraine become intensely sensitive to light during an attack, and the reason traces back to a specific pathway from the eye to the brain. Light-sensitive cells in the retina send signals to a relay station in the thalamus, where they converge with pain signals coming from the trigeminal nerve. Neurons in the thalamus that respond to pain from the dura are two to three times more likely to also respond to light compared to non-pain neurons. This convergence is why light physically intensifies headache pain rather than just being annoying.
Not all light is equal. Research measuring thalamic neuron firing rates found that blue and white light significantly increased neural activity in pain-related pathways, while green light did not. This matches what patients report: green light is the least likely color to worsen migraine symptoms, and some people find it mildly soothing.
Genetics Set the Stage
Migraine runs in families, and the genetic picture is complex. Large-scale genetic studies have identified more than 130 regions in human DNA linked to migraine susceptibility, with at least 53 specific genes whose activity levels correlate with migraine risk. These genes influence everything from how neurons fire to how blood vessels respond to chemical signals. You don’t inherit a single “migraine gene.” Instead, you inherit a collection of small genetic variations that together make your brain more reactive to triggers.
Hormones and the Gender Gap
Migraine affects significantly more women than men, and hormones are the primary reason. Migraine typically begins around puberty and peaks between ages 35 and 45, tracking closely with reproductive years. The pattern of attacks often follows the menstrual cycle, clustering in the days just before or during a period when estrogen levels drop sharply.
This estrogen withdrawal effect is well documented. After a sustained period of estrogen exposure lasting about a week or less, a sudden decline triggers attacks of migraine without aura. The relationship flips for migraine with aura: high estrogen states, such as those during certain phases of pregnancy or while taking hormonal contraceptives, are associated with aura-type attacks. Pregnancy often brings relief from migraine overall, likely because estrogen levels remain consistently high rather than fluctuating. Menopause, once hormone levels stabilize at a lower baseline, also tends to reduce migraine frequency for many women.
Common Triggers and Why They Work
Triggers don’t cause migraines on their own. They push an already susceptible brain past its threshold. The most reliably reported triggers include sleep disruption (too much or too little), skipped meals, dehydration, stress or the letdown after stress, alcohol, and strong sensory stimuli like bright lights, loud sounds, or intense smells.
What connects these seemingly unrelated triggers is that they all affect the brain’s energy balance or excitability. Skipping meals drops blood sugar, which stresses neurons that are already metabolically vulnerable. Poor sleep disrupts the hypothalamus, which is already implicated in migraine initiation. Stress hormones alter serotonin and other chemical messengers involved in pain processing. For most people, a single trigger on a good day won’t cause an attack. It’s the combination of triggers stacking up, sometimes called the “migraine threshold” model, that tips the balance.
Weather changes, particularly shifts in barometric pressure, are another frequently cited trigger, though the mechanism is less clear. One theory is that pressure changes affect the sinuses and blood vessels in ways that activate trigeminal nerve endings. Individual trigger profiles vary widely, which is why keeping a headache diary remains one of the most practical tools for identifying your personal patterns.
The Four Phases of an Attack
A full migraine episode can last anywhere from a few hours to three days and typically moves through up to four phases, though not everyone experiences all of them.
- Prodrome (hours to days before): Subtle warning signs driven by hypothalamic activation. These include food cravings, frequent yawning, neck stiffness, irritability, or difficulty concentrating. Many people learn to recognize these signals over time.
- Aura (5 to 60 minutes): Only about 25 to 30% of migraine sufferers experience aura. It’s caused by cortical spreading depression and most commonly involves visual disturbances like zigzag lines, flashing lights, or temporary blind spots. Some people get tingling in the face or hands, or have difficulty finding words.
- Headache (4 to 72 hours): Typically a throbbing or pulsating pain on one side of the head, worsened by physical activity, light, sound, or smell. This phase reflects full activation of the trigeminovascular system and the flood of inflammatory molecules like CGRP.
- Postdrome (up to 48 hours): Often called a “migraine hangover,” this phase involves fatigue, difficulty concentrating, and a washed-out feeling as the brain recovers from the metabolic disruption of the attack.
Understanding these phases matters practically. Treating a migraine during prodrome or early aura is significantly more effective than waiting until the headache phase is fully established. The earlier you intervene, the less momentum the neurological cascade has built.