A migraine is a neurological disorder that causes recurring attacks of moderate to severe head pain, typically lasting 4 to 72 hours. Unlike a tension headache, migraine involves a cascade of changes in the brain and nervous system that produce not just pain but nausea, sensitivity to light and sound, and sometimes visual disturbances. It affects roughly three times more women than men, largely because of hormonal fluctuations tied to the menstrual cycle.
How Migraine Differs From a Regular Headache
A migraine attack is not simply a bad headache. The pain is usually pulsating, often concentrated on one side of the head, and gets worse with routine physical activity like walking up stairs or bending over. Most people also experience at least one of these: nausea, sensitivity to light, or sensitivity to sound. A tension headache, by contrast, tends to produce a steady, band-like pressure on both sides of the head without nausea or light sensitivity.
In children and teenagers, migraines look somewhat different. The pain is more often felt on both sides of the head and may last as little as two hours. The one-sided pattern that most adults recognize typically emerges in late adolescence or early adulthood.
The Four Phases of a Migraine Attack
Not every person experiences all four phases, but understanding them helps you recognize an attack early and respond faster.
Prodrome
Hours or even a day or two before the headache begins, you may notice subtle warning signs: neck stiffness, fatigue, food cravings, mood changes, or increased sensitivity to light and sound. These signals come from changes in brain activity that precede the pain itself.
Aura
About one in four people with migraine experience aura, a set of temporary neurological symptoms that build gradually over 5 to 60 minutes before the headache starts. The most common type is visual: shimmering zigzag lines, blind spots, or flashing lights that drift across your field of vision. Some people get tingling or numbness that creeps up one arm and into the face, or temporary difficulty finding words. Aura is caused by a slow wave of electrical activity that moves across the brain’s surface, temporarily disrupting normal function in each area it passes through.
Headache
This is the phase most people associate with migraine. The throbbing pain can last anywhere from 4 to 72 hours if untreated. During this time, nausea, vomiting, and extreme sensitivity to light, sound, and sometimes smell are common. Many people find that even normal conversation or overhead lighting becomes unbearable, and lying still in a dark, quiet room is the only tolerable position.
Postdrome
After the headache resolves, many people enter a “migraine hangover” that can last up to 48 hours. Common symptoms include difficulty concentrating, lingering fatigue, and neck stiffness. Some describe feeling washed out or mentally foggy, while others experience a brief period of mild euphoria.
What Happens in the Brain During a Migraine
Migraine is driven by the trigeminovascular system, a network of nerve fibers that runs along the blood vessels covering the brain. During an attack, these nerve fibers release a signaling molecule that is the most potent vessel-widening peptide known in the body. This molecule, called CGRP, triggers a chain reaction: blood vessels in the protective membranes around the brain dilate, immune cells called mast cells release inflammatory substances, and the surrounding nerve endings become increasingly sensitized to pain.
That sensitization creates a feedback loop. The inflamed tissue makes nearby nerves more excitable, which causes them to release even more CGRP, which amplifies the inflammation further. This is why migraine pain tends to build and worsen over time rather than arriving all at once. The signals travel from the nerve cluster near the temple up into deeper brain structures involved in processing pain and sensory input, which explains why light, sound, and touch all become painful during an attack.
Common Triggers
A trigger does not cause migraine on its own. It acts more like a match in someone whose nervous system is already primed to ignite. The most commonly reported triggers, drawn from studies of thousands of patients, include stress, skipping meals, poor or disrupted sleep, weather changes, strong smells, and alcohol. For women, menstruation is one of the most reliable triggers. The sharp drop in estrogen that occurs just before a period appears to destabilize the trigeminovascular system, making an attack more likely.
Triggers often stack. A single night of poor sleep might not set off an attack, but poor sleep combined with a skipped lunch and a stressful day at work can push you past the threshold. Research has found that people who report at least three simultaneous triggers (such as physical exertion, hunger, stress, and insomnia) have significantly more headache days per month than those with fewer triggers. Caffeine withdrawal, oversleeping, and physical activity are also notable triggers, particularly in people with more frequent attacks.
Episodic vs. Chronic Migraine
Migraine exists on a spectrum of frequency. Episodic migraine means fewer than 15 headache days per month. Chronic migraine means 15 or more headache days per month for at least three months, with migraine features on at least eight of those days. About 3% of people with episodic migraine transition to chronic migraine each year.
People who have 10 or more migraine days per month are at the highest risk of becoming chronic. Ironically, one of the biggest risk factors for that transition is overusing the very medications meant to treat individual attacks. Taking over-the-counter pain relievers on more than 15 days per month, or using prescription migraine medications on more than 10 days per month, can cause the brain to become dependent on these drugs and produce rebound headaches when they wear off.
How Migraine Attacks Are Treated
Treatment divides into two categories: stopping an attack that’s already started and preventing future attacks from happening.
For stopping an active attack, anti-inflammatory pain relievers are a first-line option for mild to moderate episodes. For more severe attacks, a class of medications called triptans has been the standard treatment for decades. These work by narrowing blood vessels and blocking pain signals in the trigeminal nerve. They are not suitable for people with heart disease or stroke history because of their effects on blood vessels.
A newer class of medications works by directly blocking the CGRP molecule that drives the inflammatory cascade. Unlike triptans, these do not constrict blood vessels, which makes them an option for people with cardiovascular risk factors. They can be used both to stop individual attacks and, in some formulations, to prevent them.
Timing matters enormously with any acute treatment. Taking medication early in the attack, ideally during the prodrome or at the first sign of pain, is far more effective than waiting until the pain is fully established. Once central sensitization kicks in (the point where even light touch on the scalp becomes painful), medications are much less likely to provide complete relief.
When Prevention Becomes the Goal
If you experience three or more migraine attacks per month, or at least eight headache days per month, preventive treatment is worth considering. Prevention is also appropriate when individual attacks are severe enough to be disabling despite proper acute treatment, or when you find yourself reaching for acute medication so often that overuse becomes a concern.
The goal of preventive therapy is not to eliminate every migraine. A 50% reduction in attack frequency or headache days is considered a successful outcome. Preventive regimens typically need several weeks to reach full effect. If migraines remain well controlled for 6 to 12 months, treatment is generally tapered down to see whether the improvement holds on its own.
Why Women Are Disproportionately Affected
Before puberty, boys and girls experience migraine at roughly equal rates. After puberty, the gap widens dramatically, with women affected about three times more often. The primary driver is estrogen. The sharp decline in estrogen levels that occurs in the days before menstruation is the most well-established hormonal trigger, first identified in the early 1970s. Estrogen influences pain processing directly within the trigeminovascular system, and some women appear to have a genetic sensitivity to these hormonal fluctuations that makes their nervous system more reactive to the drop. This is why migraines often improve during pregnancy (when estrogen levels stay high) and may change again around menopause.