A migraine is not simply a bad headache. It’s a complex neurological event that unfolds in stages, driven by waves of abnormal electrical activity in the brain, inflammatory chemicals released around blood vessels, and a pain-signaling network that becomes increasingly sensitized as the attack progresses. The World Health Organization ranks migraine as the third highest cause of disability worldwide, behind only stroke and a condition affecting newborns.
Understanding how migraines actually work has changed dramatically over the past few decades. The old explanation, that blood vessels in the skull simply expand and cause pain, turned out to be incomplete. The modern picture is far more interesting and starts well before any pain begins.
It Starts in the Brain, Not the Blood Vessels
For most of the 20th century, doctors believed migraine pain came from dilated blood vessels mechanically pressing on surrounding nerve fibers. This “vascular theory” made intuitive sense: blood vessels widen, nerves get squeezed, pain follows. But research eventually showed that vessel dilation doesn’t always line up with when pain starts, and vessel constriction doesn’t always coincide with pain relief.
The current understanding places the brain itself at the center. A migraine begins with changes in brain activity that cascade outward, triggering inflammation and pain signaling along the way. Blood vessel changes still play a role, but they’re a downstream consequence rather than the root cause. This shift matters because it reframes migraine as a neurological disorder, not a vascular one, and it explains why migraines produce such a wide range of symptoms beyond head pain.
The Four Phases of a Migraine Attack
A full migraine attack can stretch across days and moves through up to four distinct phases. Not everyone experiences all four, but recognizing them helps explain why migraines feel so different from ordinary headaches.
Prodrome
Hours or even days before pain begins, the brain starts sending early warning signals. You might notice unusual food cravings, frequent yawning, neck stiffness, mood changes, fatigue, or trouble concentrating. These symptoms trace back to the hypothalamus, a small region deep in the brain that regulates sleep, appetite, and mood. Brain imaging studies published in Neurology have found that the hypothalamus becomes unusually active during this pre-pain window, and it’s thought to play a direct role in initiating the attack. In people with chronic migraine, this region appears to stay in a heightened state of activation, lowering the threshold for the next attack to begin.
Aura
About one in four migraine sufferers experiences aura, a phase of temporary neurological symptoms that typically builds over five minutes and lasts up to an hour (though in roughly 20% of cases, it can persist longer). The most common form is visual: shimmering lights, geometric patterns, or blind spots that slowly expand across your field of vision.
Aura is caused by a phenomenon called cortical spreading depression, a slow wave of intense electrical excitation that rolls across the surface of the brain at a rate of about 3 to 5 millimeters per minute. As this wave passes through a given area, neurons fire intensely and then go temporarily silent. When it crosses the visual processing area at the back of the brain, you see the characteristic visual disturbances. When it crosses areas responsible for sensation or language, you might feel tingling in your hand or have difficulty finding words. The wave’s slow, steady march explains why aura symptoms build and shift gradually rather than appearing all at once.
The Pain Phase
The headache itself typically lasts several hours to three days. Pain is usually throbbing, often concentrated on one side of the head, and frequently accompanied by nausea, sensitivity to light, sound, and smell, anxiety, and difficulty sleeping. This phase is driven by the trigeminovascular system, a network connecting the trigeminal nerve (the largest nerve in your head) to the blood vessels lining your brain and its protective membranes.
Postdrome
After the pain subsides, many people enter a “migraine hangover” that can last a variable amount of time. Fatigue, body aches, difficulty concentrating, dizziness, and lingering light sensitivity are common. This phase is often overlooked but can be just as disruptive as the headache itself.
How Pain Signals Build and Intensify
The pain phase of a migraine centers on the trigeminovascular system. Nerve fibers from the trigeminal nerve wrap around the large blood vessels of the brain, the venous sinuses, and the dura mater (the tough membrane surrounding the brain). When these fibers become activated, whether by cortical spreading depression, hormonal fluctuations, or other triggers, they release inflammatory molecules at the nerve endings.
The most important of these molecules is a peptide called CGRP. It does two things that matter: it powerfully dilates blood vessels, and it helps transmit and amplify pain signals. CGRP release sets off a chain of events sometimes called neurogenic inflammation. The blood vessels swell, surrounding tissue becomes inflamed, and the nerve fibers themselves become sensitized, meaning they start responding to stimuli that wouldn’t normally cause pain. This is why, during a migraine, the normal pulsing of blood through your arteries can feel like a hammer, and why bending over or coughing makes the pain worse.
This sensitization can also spread to central pain-processing areas in the brainstem and spinal cord. Once that happens, even light touch on the scalp or face can become painful, a phenomenon called allodynia that many migraine sufferers recognize. The longer the attack continues, the more entrenched this sensitization becomes, which is one reason why treating a migraine early tends to be more effective than waiting.
Serotonin’s Role in the Cycle
Serotonin, a chemical messenger involved in mood, sleep, and pain regulation, fluctuates in a specific pattern around migraine attacks. Between attacks, people with migraine tend to have lower circulating serotonin levels but higher rates of serotonin turnover in the brain, meaning the brain is producing and breaking down serotonin faster than normal. During an attack, this pattern reverses: circulating serotonin rises while the rate of breakdown drops.
These fluctuations help explain why many migraine triggers, such as disrupted sleep, stress letdown, and hormonal shifts, share a common thread: they all affect serotonin signaling. It also explains why the most widely used class of acute migraine medications works by mimicking serotonin’s effects on specific receptors, calming the overactive trigeminovascular system.
Why Some People Get Migraines and Others Don’t
Genetics accounts for a substantial portion of migraine risk. Heritability is estimated at roughly 48% for women and 38% for men, meaning about half the variation in who gets migraines can be traced to inherited factors. If one of your parents has migraines, your chances are significantly higher than average.
The clearest genetic links come from a rare subtype called familial hemiplegic migraine, where researchers identified specific genes affecting ion channels in nerve cells. The first, discovered in 1996, encodes part of a calcium channel that controls how neurons fire. A second gene affects sodium-potassium pumps that maintain the electrical balance across nerve cell membranes. These discoveries reframed at least some forms of migraine as a “channelopathy,” a disorder of the tiny gated pores that control the flow of charged particles in and out of brain cells. When these channels don’t function properly, the brain becomes more susceptible to the waves of electrical disruption that kick off an attack.
For common migraine without these rare mutations, the genetics are more complicated. Dozens of genes each contribute a small amount of risk, affecting everything from how easily neurons become excited to how efficiently the brain clears inflammatory molecules. This is why migraine tends to run in families without following a simple inheritance pattern, and why two siblings with the same genetic predisposition may have very different experiences with the condition depending on their hormones, stress levels, sleep habits, and other environmental factors.
Why Migraines Throb
The throbbing quality of migraine pain was long assumed to match the heartbeat, with each pulse of blood stretching a dilated artery. The reality is more nuanced. While blood vessel changes contribute, the throbbing sensation is largely driven by the sensitized state of the trigeminovascular nerve fibers. Once these nerves become hyperreactive through neurogenic inflammation, they fire in response to the normal, rhythmic pressure changes that occur with each heartbeat. You’re not feeling your blood vessels expanding abnormally. You’re feeling normal vascular pulsation through a nervous system that has temporarily lost its ability to filter out that signal.
This is also why migraine pain can shift from one side of the head to the other, or become bilateral as the attack progresses. The sensitization gradually recruits additional nerve fibers and pain-processing areas, spreading the zone of hypersensitivity beyond where the attack originally began.