A migraine starts long before the headache hits. The process begins deep in the brain, often hours or even days ahead of the pain, with a cascade of electrical and chemical changes that ripple outward through your nervous system. Understanding this sequence can help you recognize early warning signs and make sense of why certain situations push you over the edge into an attack.
The Threshold That Determines When an Attack Begins
Every person with migraine has a biological threshold, a tipping point that determines when an attack gets triggered. On any given day, you sit somewhere below that line. How close you are depends on a combination of factors: sleep quality, hydration, stress levels, hormonal fluctuations, and sensory input like bright light or strong smells. A single trigger on a good day might not push you over. But stack a few together, and you cross the threshold.
Think of it like a cup slowly filling with water. One person’s trigger might be red wine. A few sips on a well-rested day might not be enough to start anything. But a full glass of red wine after a skipped meal and a poor night’s sleep fills the cup to overflowing. This cumulative model explains why the same trigger can cause an attack one week and not the next. Your proximity to the threshold shifts constantly.
The Prodrome: Your Brain’s Early Warning System
The first detectable phase of a migraine is the prodrome, sometimes called the premonitory phase. It can begin several hours before the headache, and in some cases, it stretches across one or two days. Not everyone experiences it, and the symptoms vary from person to person, but they tend to be subtle enough that many people don’t connect them to migraine until they learn what to look for.
Common prodrome symptoms include unusual fatigue, difficulty concentrating, food cravings, yawning repeatedly, irritability, neck stiffness, increased urination, sensitivity to light or sound, and mood changes like feeling unusually down or restless. Some people notice nausea or difficulty with reading and speaking. These symptoms reflect early shifts in brain activity, particularly in regions that regulate sleep, appetite, mood, and sensory processing. Your brain is already changing before pain signals have fired.
Cortical Spreading Depression: The Electrical Wave
In the roughly 25 to 30 percent of migraine sufferers who experience aura (visual disturbances, tingling, or speech difficulty), a specific electrical event called cortical spreading depression is the direct cause. It’s a slow wave of intense nerve cell firing that rolls across the surface of the brain, followed immediately by a period of electrical silence.
Here’s what happens at the cellular level. Neurons suddenly open their gates to sodium and calcium ions, flooding inward in concentrations so large that the cell’s normal pumping system can’t keep up. As a result, potassium spills out into the surrounding space. That buildup of potassium shifts neighboring neurons closer to their own firing threshold, causing them to depolarize too. The wave spreads outward at a few millimeters per minute, which is why aura symptoms tend to build gradually over at least five minutes and can last up to 60 minutes. In about 20 percent of people who get aura, symptoms persist longer than an hour.
The wave also releases glutamate, an excitatory brain chemical, which further fuels the chain reaction. This is not a blood flow problem. Brain imaging shows that blood flow drops modestly during aura, but the reduction follows the electrical wave rather than blood vessel territories. The flow decrease is a consequence of reduced brain metabolism, not the cause of symptoms.
How Pain Signals Get Activated
The headache itself comes from a network called the trigeminovascular system, a set of nerve fibers from the trigeminal nerve that wrap around blood vessels in the membranes covering the brain. Once cortical spreading depression reaches the brain’s surface, hydrogen and potassium ions leak into these membranes and activate pain-sensing nerve endings there.
Those activated nerve endings release a cocktail of inflammatory signaling molecules. The most important one is calcitonin gene-related peptide, or CGRP, now a proven therapeutic target. CGRP is a potent vasodilator, meaning it widens blood vessels, but more critically, it drives a sterile inflammatory response in the tissue surrounding the brain. This inflammation sensitizes the nerve endings further, creating a feedback loop: inflammation triggers more nerve firing, which releases more CGRP, which increases inflammation.
CGRP levels in the blood rise during migraine attacks, though baseline levels vary enormously between individuals. The trigeminal nerve acts as a final common pathway, meaning regardless of what initially set the migraine in motion (stress, hormones, sensory overload), the pain ultimately funnels through this same system.
Why Migraine Is a Brain Event, Not a Blood Vessel Problem
For decades, scientists believed migraine was fundamentally a vascular disorder, caused by blood vessels in the brain constricting and then painfully dilating. That theory has largely been replaced. The current understanding frames migraine as primarily a neurological process, with blood vessel changes happening as a secondary effect rather than the root cause.
The strongest evidence for this comes from brain imaging. In people who have migraine without aura, which is the majority, no consistent blood flow changes have been found at all. Even during aura, the blood flow reduction is too mild to explain the symptoms on its own. Meanwhile, brainstem imaging during attacks shows activation in specific areas involved in pain regulation and sensory processing that persists even after medication resolves the blood flow changes. The brain’s pain-regulation circuitry appears to malfunction, allowing sensory signals that would normally be filtered out to instead register as intense, throbbing pain.
The Role of Genetics in Migraine Susceptibility
Migraine runs in families, and specific gene mutations help explain why some brains are more excitable than others. The clearest examples come from a rare inherited form called familial hemiplegic migraine, where single gene mutations have been identified. The CACNA1A gene, which controls calcium channels in neurons, was the first discovered and is the most commonly affected. ATP1A2, which encodes part of the sodium-potassium pump responsible for resetting neurons after they fire, accounts for about 20 percent of another subtype. A third gene, SCN1A, affects sodium channels.
These mutations all converge on the same problem: they make it easier for the electrical wave of cortical spreading depression to get started. When ion channels don’t open or close properly, or when the pump that restores normal ion balance after firing is sluggish, neurons sit closer to their activation threshold at baseline. It takes less provocation to set off the cascade. While most people with migraine don’t have these specific rare mutations, the same ion channel pathways are thought to operate at subtler levels of dysfunction across the broader migraine population.
What the Full Attack Looks Like in Phases
A complete migraine attack unfolds in up to four phases, though not everyone experiences all of them.
- Prodrome lasts hours to days, with mood changes, cravings, fatigue, and neck stiffness signaling the brain’s early shift.
- Aura affects roughly one in four migraine sufferers and typically lasts 5 to 60 minutes, producing visual disturbances (zigzag lines, blind spots), tingling, or speech difficulty as the electrical wave crosses the cortex.
- Headache is the main attack phase, lasting anywhere from 4 to 72 hours. It typically involves pulsating pain, often on one side of the head, worsened by routine physical activity like walking or climbing stairs. Nausea, vomiting, and extreme sensitivity to light and sound are common companions. In children and adolescents, the headache phase can be as short as two hours.
- Postdrome is the recovery period after the headache resolves, often described as feeling drained or foggy.
A clinical migraine diagnosis typically requires at least five attacks matching this pattern. Fewer than five attacks with otherwise classic features are classified as probable migraine. The key distinguishing features are the combination of moderate to severe pulsating pain, worsening with movement, and the presence of nausea or sensitivity to light and sound. A headache that lacks these characteristics is more likely a tension-type headache or another condition entirely.