Migraines happen because the brain overreacts to signals that wouldn’t bother most people. The underlying cause is a combination of genetic wiring, an overly excitable nervous system, and a cascade of chemical events that amplify pain signals far beyond what the situation calls for. About 40% of the global population experiences headache disorders, and migraine is among the top three most common neurological conditions across nearly every age group, from age 5 through 80.
The Brain’s Alarm System Misfires
At the core of every migraine is a network called the trigeminovascular system, a connection between the trigeminal nerve (the main sensory nerve of the face and head) and the blood vessels lining the brain. When this system activates inappropriately, nerve fibers release powerful signaling molecules that cause blood vessels in the brain’s outer lining to swell and become inflamed. One of the most important of these molecules, calcitonin gene-related peptide (CGRP), is so central to migraine pain that an entire class of newer migraine drugs works by blocking it.
Think of it this way: your brain has a pain alarm system designed to warn you of real threats. In people with migraines, that alarm goes off in response to triggers that pose no actual danger, like bright light, a glass of wine, or a shift in barometric pressure. Once the alarm fires, it sets off a chain reaction of inflammation and nerve sensitization that feeds on itself, which is why migraines can last hours or even days.
What Happens During an Aura
About a quarter of people with migraines experience aura, the visual disturbances, tingling, or temporary speech difficulties that can precede the headache. This is caused by cortical spreading depression (CSD), a slow wave of intense electrical activity that rolls across the surface of the brain, followed by a prolonged period of suppressed activity. Researchers at the American Headache Society recently documented this directly in a patient whose brainwave activity went flat and stayed suppressed for hours on one side of the brain during a migraine with visual aura. That recording provided rare, direct human evidence of a mechanism scientists had theorized about for decades but struggled to observe in real time.
CSD doesn’t just cause the aura itself. As the wave moves across the brain, it’s thought to activate the trigeminal nerve endings in the brain’s outer lining, which kicks off the pain phase. This is why aura typically comes first, followed by the headache 20 to 60 minutes later.
Genetics Set the Stage
Migraines run in families, and researchers have identified dozens of genes that raise susceptibility. Most of these genes affect how nerve cells handle electrical signals, particularly how ions like potassium and calcium flow in and out of brain cells. In one well-studied example, a mutation in a gene called KCNK18 disrupts a potassium channel in the nervous system and was traced through four generations of a family where migraine with aura followed a clear inheritance pattern. That particular mutation turned out to be rare (only one case among 621 migraine patients screened), but it illustrates the principle: small changes in how your neurons manage electrical activity can lower the threshold for a migraine attack.
Most people don’t inherit migraine through a single gene. Instead, they carry a collection of common gene variants that each nudge the brain toward greater excitability. Layer enough of these together, add the right environmental trigger, and a migraine becomes likely.
Why Women Get Migraines More Often
Migraine is significantly more common in women, and the primary reason is hormonal. Estrogen and progesterone directly influence pain-related chemicals in the brain, and it’s the fluctuation in estrogen levels, not the absolute amount, that matters most. The sharp drop in estrogen that occurs just before menstruation is one of the most reliable migraine triggers known. Many women notice their worst attacks cluster in the two days before and the first three days of their period.
Steady estrogen levels tend to improve migraines, which is why some women find relief during the second and third trimesters of pregnancy, when estrogen is consistently high. Conversely, the hormonal roller coaster of perimenopause often makes migraines worse before they improve after menopause. Migraine most commonly begins at puberty and peaks between ages 35 and 45, a window that aligns closely with a woman’s reproductive years.
The Hypothalamus and Everyday Triggers
People with migraines often report that specific things set off an attack: bright lights, strong smells, weather changes, skipped meals, poor sleep. These aren’t random sensitivities. High-resolution brain imaging has shown that the hypothalamus, a small structure deep in the brain that regulates sleep, hunger, and body temperature, acts as a central hub between attack-triggering factors and the brain’s pain-control system.
In people with chronic migraines (15 or more headache days per month), the hypothalamus shows increased activation compared to those with occasional attacks. This heightened activity appears to lower the threshold for generating an attack, which helps explain why chronic migraineurs can be set off by triggers that wouldn’t faze someone who gets migraines only occasionally. It also explains the premonitory symptoms many people recognize hours before a headache: food cravings, yawning, mood changes, and neck stiffness all originate in or near the hypothalamus.
The Role of Magnesium and Brain Excitability
One of the clearest nutritional links to migraines involves magnesium. This mineral acts as a natural brake on nerve cell excitability. It sits in a receptor called the NMDA receptor and blocks calcium from flooding into nerve cells. When magnesium levels drop, that brake weakens, making neurons more likely to fire excessively and release glutamate, the brain’s main excitatory chemical. Both of these processes are directly involved in triggering migraines.
Magnesium also helps stabilize the electrical charge of nerve cell membranes, making them less reactive to stimulation. People with migraines tend to have lower magnesium levels than those without, and supplementation has shown enough benefit that many headache specialists consider it a reasonable first-line option, particularly for people who prefer to start with something other than medication.
How Migraines Change the Brain Over Time
Migraines aren’t just painful episodes that leave no trace. Brain imaging studies have found that people with migraines show measurable reductions in gray matter, the tissue that processes sensory information and makes decisions. Over just one year, researchers observed gray matter loss in areas involved in processing pain and sensory input, including the somatosensory cortex (where touch and pain signals are interpreted) and the hippocampus (involved in memory and stress responses).
The white matter, which connects different brain regions, appears to change more slowly and may take years of chronic migraines to show measurable differences. These structural changes don’t mean migraines cause permanent cognitive damage in most people, but they do suggest that the brain physically adapts to repeated migraine attacks. It’s one more reason neurologists emphasize reducing attack frequency rather than simply treating each headache as it comes.
Why Some People and Not Others
The fundamental answer to “why do people have migraines” is that their brains are wired to be more reactive. Genetics load the gun by making neurons more excitable, hormones and metabolic factors influence how close to the firing threshold someone sits at any given time, and environmental triggers pull the final trigger. Once the cascade starts, the trigeminovascular system amplifies the signal into a full-blown attack complete with throbbing pain, nausea, and sensitivity to light and sound.
This is why the same trigger, say a glass of red wine, can cause a migraine on one day but not another. It depends on where you are on that threshold at that moment: how well you slept, where you are in your hormonal cycle, whether you’ve eaten, and how stressed you are. All of these factors converge in the hypothalamus and brainstem, and when enough of them stack up, the brain tips over into a migraine. Understanding this threshold model is the single most useful thing for managing the condition, because it shifts the focus from avoiding one specific trigger to keeping your overall level of brain excitability as low and stable as possible.