Migraines are caused by waves of abnormal electrical activity in the brain that trigger inflammation and pain signaling, not by blood vessel problems as scientists once believed. The process involves a cascade of events: shifts in brain chemistry, activation of pain-sensitive nerves around the skull, and the release of inflammatory molecules that produce the throbbing, often debilitating headache. Genetics account for roughly 40 to 50 percent of a person’s susceptibility, while the rest comes down to individual triggers and environmental factors.
The Electrical Wave That Starts It All
The clearest window into what physically happens during a migraine comes from a phenomenon called cortical spreading depression. It begins when a cluster of brain cells suddenly fires in an uncontrolled burst, flooding the space around them with potassium and excitatory chemicals like glutamate. Normally, tiny pumps on each cell rapidly rebalance these ions. During cortical spreading depression, the surge overwhelms those pumps, and the imbalance spreads outward like a ripple across the brain’s surface at roughly 3 to 5 millimeters per minute.
As this wave moves, it temporarily shuts down normal brain activity in its path. That shutdown is what produces the visual disturbances, tingling, or speech difficulties known as aura, which about a quarter of migraine sufferers experience. But even in migraines without aura, a version of this process may still occur in deeper brain regions that don’t produce obvious sensory symptoms.
The wave itself isn’t the painful part. Pain comes next, when the inflammatory molecules released during and after the wave reach the meninges, the sensitive membranes surrounding the brain. Once those membranes become inflamed, they activate branches of the trigeminal nerve, the main pain highway of the face and head. That’s when the headache begins.
How Brain Chemistry Shifts Before and During an Attack
Serotonin plays a central but somewhat paradoxical role. Between migraine attacks, serotonin levels in the blood tend to run low. Then, as an attack begins, serotonin spikes before dropping again. This pattern of chronically low baseline levels with a transient surge during attacks has been a foundational finding in migraine research for decades. The low baseline may explain why migraine sufferers are more sensitive to light, sound, and touch even on headache-free days, a phenomenon researchers call “deficient habituation,” meaning the brain fails to tune out repetitive stimuli the way it normally would.
Magnesium is another piece of the puzzle. Under normal conditions, magnesium sits inside a key receptor in the brain and acts like a gatekeeper, preventing calcium from flooding into nerve cells. When magnesium levels drop, that gate opens more easily, which ramps up excitatory signaling and can push the brain toward the kind of electrical instability that sparks a migraine. Research on magnesium levels in migraine patients has been mixed, with some studies finding clear deficiencies and others showing normal blood levels, partly because blood measurements don’t always reflect what’s happening inside the brain itself.
The Role of Genetics
If one of your parents gets migraines, your chances of getting them are significantly higher. Heritability estimates land at about 38 percent for men and 48 percent for women, meaning that genetic factors explain just under half of who develops migraines. The rest comes from environment, lifestyle, and individual biology. Familial factors contribute to less than 50 percent of all migraine cases overall.
The most direct genetic evidence comes from a rare subtype called familial hemiplegic migraine, where attacks cause temporary paralysis on one side of the body. Researchers identified the first gene linked to this condition in 1996: a gene that controls calcium channels in nerve cells. A second gene was later found that encodes part of the same sodium-potassium pump that gets overwhelmed during cortical spreading depression. At least a third gene exists, since some affected families don’t carry mutations in either of the first two. These discoveries confirm that migraines are, at their core, a disorder of how the brain manages electrical and chemical balance.
For common migraines (the kind most people get), no single gene is responsible. Instead, dozens of small genetic variations each nudge the brain slightly toward greater excitability or more reactive blood vessels, and the combined effect determines your threshold for an attack.
Common Triggers and Why They Work
A trigger doesn’t cause migraines in the way a virus causes the flu. Instead, triggers push an already susceptible brain past its threshold. The most consistently reported ones include hormonal fluctuations (especially the drop in estrogen before menstruation), sleep disruption, stress or the letdown after stress, skipped meals, alcohol, and certain foods. What’s important to understand is that triggers are highly individual. A food that reliably sets off one person’s migraine may be completely harmless to another.
Weather changes, particularly shifts in barometric pressure, are a well-recognized trigger. The mechanism likely involves pressure changes causing imbalances in brain chemicals, including serotonin. Many people find their migraines cluster around storm fronts or seasonal transitions, and while you can’t control the weather, tracking your attacks alongside weather patterns can help you identify whether atmospheric pressure is a meaningful trigger for you.
Sensory overload also plays a role. Bright or flickering lights, strong smells, and loud environments can all provoke attacks, especially given the “deficient habituation” that makes migraine brains less able to filter out intense stimulation. This sensitivity tends to worsen as an attack approaches, creating a feedback loop where the early stages of a migraine make you more reactive to the very stimuli that can intensify it.
Why Migraines Become Chronic
About 3 percent of people with occasional migraines progress to chronic migraine, defined as 15 or more headache days per month. This shift, called chronification, appears to involve physical changes in the brain. Recent imaging research found that people with chronic migraine show signs of impaired waste clearance in the brain. Specifically, the fluid exchange system that removes metabolic byproducts from brain tissue appears to function less effectively, with measurable changes in how water moves through the spaces around blood vessels in the brain. Overuse of pain medication accelerates this process, which is why frequent use of over-the-counter painkillers can paradoxically make migraines worse over time.
Repeated migraine attacks also appear to sensitize the trigeminal pain system, essentially lowering the threshold for future attacks. Each episode leaves the pain-processing circuits a little more reactive, which is one reason neurologists emphasize prevention over just treating attacks as they come. The goal is to interrupt this cycle before the brain’s pain system remodels itself into a more permanently reactive state.
Why Women Are Hit Harder
Women experience migraines roughly three times more often than men, and the higher heritability estimate in women (48 percent versus 38 percent) suggests that genetics and hormones interact in ways that amplify susceptibility. Estrogen influences serotonin activity, pain processing, and blood vessel tone, and the cyclical rise and fall of estrogen across the menstrual cycle creates a recurring window of vulnerability. Many women find their worst migraines occur in the two days before or the first three days of their period, when estrogen drops sharply. Migraines often improve during pregnancy (when estrogen stays high) and may change character again around menopause.