Migraines happen because of a chain reaction in your nervous system: nerves in and around your brain become abnormally activated, release inflammatory chemicals, and send amplified pain signals through a major nerve pathway in your head. About 1.16 billion people worldwide live with migraines, making it one of the most common neurological conditions on the planet. The full picture involves genetics, hormones, environmental triggers, and a brain that processes sensory information differently than average.
What Happens Inside Your Brain During a Migraine
A migraine is not just a bad headache. It’s a complex neurological event that unfolds in stages, driven by specific changes in brain chemistry and nerve signaling.
The process centers on a network called the trigeminovascular system. Nerve fibers that wrap around blood vessels in the protective membranes covering your brain (the meninges) become activated and sensitized. Once fired up, these fibers send pain signals through the trigeminal nerve, the largest nerve in your head, into a relay station in your brainstem called the spinal trigeminal nucleus. From there, the signals travel up through the thalamus and into higher brain regions where you consciously experience pain.
When these nerve fibers activate, they release a signaling molecule called CGRP. During an attack, CGRP levels in your blood rise and fall in lockstep with headache intensity. CGRP causes nearby arteries to dilate and triggers inflammation around those blood vessels, which further stimulates pain-sensing nerves. It also plays a role in the nausea and vomiting many people experience, because the same brainstem areas that process migraine pain signals connect directly to the brain’s vomiting center.
Why Light and Sound Become Unbearable
One of the hallmarks of a migraine is extreme sensitivity to light, sound, and sometimes smell. This isn’t just a side effect of pain. Specific neurons in the thalamus, the brain’s sensory relay hub, actually integrate light signals from your eyes with pain signals from the meninges. These neurons become dramatically more active under normal room lighting and calm down only in darkness. That’s why a dark, quiet room feels like the only bearable place during an attack: you’re removing the sensory input that these cross-wired neurons are amplifying.
This same thalamic activity can produce whole-body skin sensitivity, where even light touch on your arms or scalp feels painful. It’s a sign that the pain signaling has spread beyond the original trigeminal pathway and started affecting how your brain interprets touch everywhere.
The Role of Cortical Spreading Depression
About one in four people with migraines experience aura, the visual disturbances (flashing lights, geometric patterns, blind spots) that can precede the headache. Aura is caused by a phenomenon called cortical spreading depression: a slow wave of electrical activity that sweeps across the surface of the brain, exciting neurons briefly and then suppressing them. During this wave, cells lose their ability to maintain normal levels of potassium, sodium, and calcium. Excitatory chemicals like glutamate flood the spaces between neurons, propagating the wave further.
This wave typically builds over at least five minutes and lasts up to 60 minutes, though in roughly 20% of people it can persist longer. The visual symptoms you see correspond to the wave moving across your visual cortex. Even in people who don’t experience aura, similar but less intense cortical changes may still occur, which is why researchers believe the underlying brain excitability is a shared feature across migraine types.
Genetics Set the Stage
Migraine runs in families, and twin studies estimate that about 42% of your risk is genetic. You don’t inherit migraines from a single gene. Instead, dozens of small genetic variations each nudge your brain toward being more excitable and more reactive to triggers. These variations tend to affect ion channels (the gates that control electrical signaling in neurons), neurotransmitter systems, and vascular function.
There are rare exceptions. A severe subtype called hemiplegic migraine, which causes temporary paralysis on one side of the body, can be traced to mutations in specific genes that control calcium channels, sodium-potassium pumps, and sodium channels. But for the vast majority of people, migraine susceptibility comes from the combined effect of many common gene variants, none of which would cause migraines on their own.
Hormones as a Trigger
Roughly a third of women with migraines identify menstruation as a trigger, and the mechanism is well understood. When estrogen levels drop in the days before and during a period, this directly stimulates the release of CGRP, the same molecule that drives pain and inflammation during any migraine attack. The falling estrogen essentially lowers the threshold for a migraine to start.
This estrogen connection explains several patterns: why migraines often begin around puberty, why they’re roughly two to three times more common in women than men during reproductive years, why attacks sometimes worsen in the days surrounding a period, and why many women see improvement after menopause when hormonal fluctuations settle down. Pregnancy, oral contraceptives, and hormone replacement therapy can all shift migraine patterns in either direction, depending on how they affect estrogen stability.
Common Environmental Triggers
Your genes and hormones determine how sensitive your brain is. Triggers are the things that push it over the edge on any given day. In large surveys of migraine patients, the most frequently reported triggers are sleep disturbance (reported by about 71% of people), stress (67%), and fatigue (64%). These three dominate, but they rarely act alone. Most people have multiple triggers, and attacks are more likely when several converge.
Other well-established triggers include:
- Weather changes, particularly shifts in barometric pressure
- Skipped meals or dehydration
- Alcohol, especially red wine
- Strong sensory input like bright lights, loud noise, or heavy perfume
- Hormonal shifts, as described above
Triggers are personal and inconsistent. The same glass of wine might cause a migraine one week and not the next, because your threshold fluctuates based on sleep, stress, hydration, and where you are in your hormonal cycle. Thinking of it as a “threshold model” is helpful: your brain has a tipping point, and triggers stack up to push you past it.
The Four Phases of an Attack
Migraines don’t just switch on and off. They unfold across up to four distinct phases, though not everyone experiences all of them.
The prodrome can begin hours or even days before the headache. Symptoms include mood changes, food cravings, frequent yawning, neck stiffness, fatigue, and difficulty concentrating. Many people learn to recognize these as early warning signs. The aura phase, when it occurs, typically lasts 5 to 60 minutes and most commonly involves visual disturbances in both eyes.
The headache phase lasts anywhere from 4 to 72 hours if untreated. The pain is usually pulsating, moderate to severe, and often worse on one side of the head, though it can shift sides or spread to both. Physical activity like walking or climbing stairs typically makes it worse. Nausea, vomiting, and extreme sensitivity to light, sound, and smell are common throughout.
After the pain resolves, the postdrome (sometimes called a “migraine hangover”) can leave you feeling fatigued, foggy, dizzy, and achy for hours or longer. Understanding that this phase is a real part of the attack, not just lingering tiredness, helps explain why you might feel off even after the headache itself is gone.
Why Some People Get Migraines and Others Don’t
The short answer is that migraine brains are wired differently. They’re more electrically excitable, more reactive to changes in the environment, and less efficient at returning to baseline after stimulation. This isn’t a defect in the usual sense. It’s a variation in how the brain processes information, rooted in genetics and shaped by hormones, life circumstances, and overall health.
This is why migraine management focuses not just on treating attacks when they happen, but on stabilizing the brain’s environment: keeping sleep regular, managing stress, staying hydrated, eating consistently, and for people with frequent attacks, using preventive medications that reduce overall neural excitability or block CGRP signaling. The goal is to raise your threshold so that everyday triggers are less likely to set off the cascade.