Migraines start deep in the brain, not in the blood vessels as doctors once believed. About 14% of the global population gets them, and the process involves a chain reaction of nerve activation, chemical release, and inflammation that unfolds over hours or even days before the headache peaks. Understanding how this chain reaction works helps explain why certain people get migraines, why specific things trigger them, and why the experience goes far beyond a bad headache.
What Happens Inside the Brain
A migraine begins well before you feel pain. Hours or even a day or two earlier, the hypothalamus, a small structure at the base of the brain that regulates sleep, hunger, and mood, starts behaving differently. Its connections to the brain’s emotional and arousal circuits ramp up steadily in the lead-up to an attack, then collapse once the headache phase begins. This is why many people experience warning signs like food cravings, yawning, irritability, or neck stiffness before a migraine hits. The hypothalamus is essentially losing its grip on the circuits it normally keeps in check.
Once the process tips over, the trigeminal nerve, the brain’s main pain highway for the head and face, becomes activated. This nerve has branches that reach into the protective membranes surrounding the brain and their blood vessels. When those nerve endings fire, they release a signaling molecule called CGRP, which does two things: it dilates blood vessels inside and outside the skull, and it amplifies pain signals traveling back to the brain. The result is throbbing, pulsing pain that worsens with movement, often concentrated on one side of the head.
CGRP also triggers a cascade of inflammation around those blood vessels, which further sensitizes the nerve endings. This is why migraines tend to build in intensity rather than arriving all at once, and why touching your scalp, bending over, or even feeling your own pulse can become painful during an attack. The entire pain-sensing system in your head becomes dialed up to maximum sensitivity.
Why Some People Get Aura
About a quarter of people with migraines experience aura, a set of neurological symptoms that usually appear 20 to 60 minutes before the headache. The most common is visual: shimmering zigzag lines, flickering lights, or blind spots that slowly expand across your field of vision. Some people get tingling in their hands or face, difficulty finding words, or a sense that the world looks distorted.
Aura is caused by a slow electrical wave that rolls across the surface of the brain. Neurons first fire intensely, then go quiet for several minutes. Brain imaging has captured this wave moving across the visual cortex at roughly 3.5 millimeters per minute. As it passes through, the initial burst of activity produces the shimmering or flickering (scintillations), and the quiet phase that follows creates the blind spots. The wave moves from the back of the brain toward the front, which is why visual aura typically starts in the center of your vision and drifts outward over several minutes. It doesn’t jump between brain regions. It creeps forward in a continuous line, crossing different visual processing areas without pause.
Genetics and Family History
Migraines run in families, though the inheritance pattern isn’t straightforward. More than half of people with migraines have at least one close family member with the condition. There’s no single “migraine gene.” Instead, researchers have identified variations across dozens of genes that each contribute a small amount of risk. Many of these genes are active in the smooth muscle surrounding blood vessels in the brain, which fits with what we know about vascular changes during attacks. Others regulate glutamate, the brain’s main excitatory chemical, or control how easily nerve cells fire.
What you inherit isn’t migraines themselves but a brain that’s more reactive to certain changes. People with migraine-prone brains have a lower threshold for the chain reaction described above. Stimuli that a non-migraine brain would absorb without issue, like a skipped meal, a bright light, or a night of poor sleep, can be enough to push a sensitized brain past its tipping point.
Hormones and the Menstrual Cycle
More than 50% of women with migraines report a link between their attacks and menstruation, with the highest frequency of attacks occurring in the first few days of a period. The trigger isn’t low estrogen itself but the drop in estrogen. After estrogen levels hold steady for about a week (as they do in the late luteal phase), the sudden withdrawal that starts menstruation can set off an attack. Clinical trials have confirmed this pattern: sustained estrogen exposure followed by a rapid decline reliably triggers migraines without aura.
Interestingly, migraine with aura follows a different hormonal pattern. High estrogen levels appear to be the trigger, not the drop. Women who experience aura have been found to have estrogen levels roughly double those of women without migraines during certain phases of their cycle. This distinction matters practically: hormonal contraceptives, pregnancy, and menopause all shift estrogen levels in ways that can either improve or worsen migraines depending on the type.
Common Triggers and Why They Work
Triggers don’t cause migraines on their own. They push an already-susceptible brain past its threshold. This is why the same trigger might cause a migraine one week but not the next: your threshold shifts depending on sleep, stress, hydration, and hormonal status. Multiple smaller triggers can stack up to cross the line when none of them alone would have been enough.
Sleep disruption is one of the most reliable triggers. Research from the University of Arizona found that sleep deprivation significantly increases the likelihood of a migraine attack, while migraine pain itself doesn’t disrupt normal sleep. In other words, poor sleep feeds migraines, but migraines don’t cause poor sleep. This makes sleep quality one of the most actionable levers for prevention.
Certain foods trigger migraines through specific compounds. Tyramine, found in aged cheeses, cured meats, fermented foods, and some wines, causes nerve cells in the brain to release norepinephrine. The resulting spike in brain chemicals can trigger vascular changes and headache. People who break down tyramine slowly, whether due to genetics or certain medications, are especially vulnerable. Other dietary triggers include nitrates (in processed meats), alcohol (especially red wine), and caffeine withdrawal.
Stress operates differently. It doesn’t usually trigger migraines during the stressful period itself but during the “let-down” phase afterward, when cortisol and adrenaline levels drop. This explains the common pattern of getting a migraine on the first day of a vacation or after a major deadline passes.
The Four Phases of an Attack
A full migraine unfolds in up to four phases, though not everyone experiences all of them. The prodrome comes first, lasting hours to a day or two before the headache. Symptoms include mood changes, food cravings (especially for sweets), frequent yawning, neck stiffness, and increased urination. These are driven by that early hypothalamic activity shift.
Aura, if it occurs, follows the prodrome and typically lasts 20 to 60 minutes. Then comes the headache phase, which can last anywhere from 4 to 72 hours. The pain is usually moderate to severe, pulsating, and worse on one side. Nausea, vomiting, and extreme sensitivity to light, sound, and sometimes smell are hallmarks. These aren’t side effects of the pain. They’re part of the same neurological event, driven by the widespread sensitization of sensory processing in the brain.
The postdrome, sometimes called a “migraine hangover,” follows the headache. It can last another day or two and leaves people feeling drained, foggy, or mildly confused. Sudden head movements during this phase can briefly bring the pain back.
What Makes Migraines Different From Headaches
Tension headaches produce a dull, pressing sensation on both sides of the head. Migraines are a neurological event that happens to include head pain as one symptom among many. The involvement of the trigeminal nerve and CGRP release explains why migraines cause nausea (the trigeminal nerve connects to brainstem areas that control vomiting), light sensitivity (sensory processing centers become hyperexcitable), and why physical activity makes the pain worse (increased blood flow through dilated vessels amplifies the throbbing).
A formal migraine diagnosis requires attacks lasting 4 to 72 hours with at least two of these features: one-sided pain, pulsating quality, moderate to severe intensity, or worsening with routine physical activity. At least one additional symptom, nausea or sensitivity to light and sound, must also be present. People who get both migraine with aura and migraine without aura have two separate conditions that can occur independently.