A migraine is a neurological event that unfolds in up to four distinct phases, each driven by specific changes in brain activity, nerve signaling, and chemical release. The full process can last anywhere from a few hours to several days. Far from being “just a headache,” a migraine involves a cascade of electrical and inflammatory events that affect how your brain processes pain, light, sound, and even touch.
It Starts in the Brain, Not the Blood Vessels
For decades, scientists debated whether migraines were caused by blood vessels expanding in the head or by abnormal nerve activity. The current consensus is that both systems are involved, but the process begins with the neurons. Deep brain structures fire abnormally, triggering a chain reaction that eventually recruits blood vessels and pain-sensing nerves into a full-blown attack.
One of the earliest players is the hypothalamus, a small region near the base of the brain that regulates sleep, hunger, mood, and body temperature. Brain imaging studies using PET scans have shown that the hypothalamus activates during the earliest stage of a migraine, sometimes 48 hours before pain begins. This helps explain why the first signs of an approaching migraine often look like disruptions to basic body functions: changes in appetite, mood swings, excessive yawning, or trouble sleeping.
The Prodrome: Your Brain’s Early Warning
The prodrome is the first phase, and it can begin hours or even days before headache pain arrives. Symptoms include fatigue, irritability, difficulty focusing, neck stiffness, sensitivity to light and sound, nausea, and changes in bowel habits. Some symptoms are particularly distinctive to this phase: repeated yawning, unusual food cravings, and frequent urination. Not everyone notices their prodrome, but people who learn to recognize these signals can use them as a cue to take medication early, which tends to be more effective than waiting for pain to set in.
The Electrical Wave Behind Aura
About one in four people with migraines experience aura, a phase of reversible neurological symptoms that typically lasts 5 to 60 minutes, though it can stretch beyond an hour in roughly 20% of cases. The most common aura symptoms are visual: shimmering lights, geometric patterns, or blind spots that slowly expand across your field of vision. Some people experience tingling in their hands or face, or temporary difficulty finding words.
Aura is caused by a phenomenon called cortical spreading depression. A wave of intense electrical activity sweeps slowly across the surface of the brain, followed immediately by a period of silence where neurons stop firing altogether. During this wave, sodium and calcium flood into brain cells faster than they can be pumped back out, while potassium builds up in the space between cells. The wave also triggers the release of excitatory brain chemicals like glutamate, which push the depolarization further across the cortex. As the wave passes through the visual processing area, you see the characteristic light disturbances. As it moves into sensory areas, you feel tingling.
This electrical wave does more than produce strange visual effects. It releases inflammatory molecules that drift toward the meninges, the protective membranes surrounding the brain. Once those inflammatory signals reach the meninges, they set the stage for pain.
How the Pain Phase Develops
The headache phase typically lasts several hours to three days. The pain is generated through a system called the trigeminovascular pathway, which connects the trigeminal nerve (the main sensory nerve of the face and head) to the blood vessels lining the brain’s surface.
When the trigeminal nerve is activated, its fibers release a signaling molecule called CGRP. This molecule is a powerful vasodilator, meaning it causes blood vessels to widen. More importantly, CGRP triggers a process called neurogenic inflammation: the nerve endings themselves drive an inflammatory response in the tissues surrounding the brain. Blood vessel walls become leaky, surrounding tissue swells, and pain-sensing nerve fibers become increasingly sensitized. Each heartbeat sends a pulse of blood through these inflamed, swollen vessels, which is why migraine pain often throbs in rhythm with your pulse.
The pain is usually felt on one side of the head, though it can affect both sides. Alongside the pain, most people experience nausea, sensitivity to light, sound, and smell, anxiety, and difficulty sleeping. These symptoms reflect the widespread nature of the neurological disruption. This isn’t just a pain problem; it’s a brain-wide shift in how sensory information is processed.
Why Normal Touch Becomes Painful
Many people with migraines develop a symptom called cutaneous allodynia, where normally painless sensations become painful. Brushing your hair, wearing a hat, resting your head on a pillow, or even feeling the shower hit your skin can hurt. This happens because of a process called central sensitization.
As the trigeminal nerve continues to send pain signals during an attack, the relay neurons in the brainstem that receive those signals become hypersensitive. They start responding to inputs that wouldn’t normally register as painful. This sensitization first affects the head and face, which is why touching your scalp hurts. If it progresses further and reaches relay neurons in the thalamus (the brain’s central sensory switchboard), the sensitivity can spread to your arms, chest, or legs. At that point, even wearing a watch or having fabric brush your forearm can feel uncomfortable.
Once central sensitization is established, it can maintain itself even without ongoing input from the original pain source. This is one reason why treating a migraine early matters: once the central nervous system ramps up to this state, the attack becomes harder to interrupt.
The Postdrome: The Migraine Hangover
After the headache fades, most people enter the postdrome, often called the “migraine hangover.” An electronic diary study published in Neurology found that tiredness or weariness was the most common symptom, reported in 88% of postdromes. Difficulty concentrating affected 56% of participants, and 42% had a stiff neck. Many people also experienced lingering nausea, light sensitivity, sound sensitivity, and a mild residual head discomfort that falls short of the full headache but still feels present.
The duration of the postdrome varies from person to person and attack to attack. Some people feel off for a few hours, while others take a full day or more to feel normal again. The cognitive fog and fatigue can be significant enough to affect work and daily tasks, even though the pain phase has ended.
Genetics and the Migraine-Prone Brain
Why some brains are vulnerable to this cascade and others aren’t comes down partly to genetics. Migraines run in families, and researchers have identified specific gene mutations that make the brain more excitable and therefore more prone to the electrical and chemical events described above.
The clearest example comes from familial hemiplegic migraine, a rare inherited form of the condition. Mutations in the CACNA1A gene on chromosome 19 alter a calcium channel found specifically in the brain. These channels control how much calcium flows into neurons, and when they’re mutated, neurons become more easily excitable. At least 13 different mutations in this single gene have been identified across affected families. While most people with common migraines don’t carry these specific mutations, studying them has confirmed that migraines are fundamentally a disorder of neuronal excitability. The migraine-prone brain sits closer to a tipping point, requiring less provocation to launch the full cascade of spreading depression, trigeminal activation, and inflammatory pain signaling.