Migraines are not ordinary headaches. They are a neurological event driven by abnormal brain activity, nerve activation, and chemical imbalances that unfold in distinct phases. About one in seven people worldwide experience migraines, and women are roughly three times more likely to have them than men. Understanding why they happen starts with what’s going on inside the brain well before the pain begins.
It Starts in the Brain, Not the Blood Vessels
For decades, doctors assumed migraines were primarily a blood vessel problem, with arteries in the head expanding and pressing on nerves. That theory has been largely replaced. Migraines are now understood as a disorder of brain excitability, where neurons become overly reactive and trigger a cascade of events that eventually produce pain, nausea, and sensory disturbances.
The process often begins in deep brain structures hours before you feel any head pain. Imaging studies have shown early activation of the hypothalamus, a small region that regulates sleep, appetite, mood, and body temperature. This activation explains why many people experience warning signs, called the premonitory phase, that can start a full day before the headache arrives. Excessive yawning, food cravings, neck stiffness, unusual thirst, and fatigue are all linked to the hypothalamus ramping up activity and releasing signaling chemicals like neuropeptide Y and dopamine. Research published in Continuum found that altered connections between the hypothalamus and brainstem begin before pain onset, suggesting this region essentially “primes” the brain for a migraine attack.
What Happens During Aura
About one in four people with migraines experience aura: visual disturbances like zigzag lines, blind spots, or flashing lights that typically last 20 to 60 minutes before the headache phase. Aura is caused by a phenomenon called cortical spreading depression, a slow wave of intense electrical activity that moves across the surface of the brain, followed by a prolonged period of suppressed activity.
This was long theorized but only recently confirmed through direct brain recording. Researchers at the American Headache Society documented a case in which a patient experienced a migraine with aura while undergoing brain monitoring. The team observed brainwave activity flatten and remain suppressed for hours on one side of the brain, providing rare, direct evidence of cortical spreading depression in action. This wave of disrupted electrical activity is what produces the visual and sensory symptoms of aura, and it may also activate the pain pathways that follow.
How the Pain Signal Gets Generated
The headache phase of a migraine is driven by the trigeminovascular system, a network where sensory nerve fibers from the trigeminal nerve (the main pain nerve of the face and head) wrap closely around blood vessels in the meninges, the protective layers surrounding the brain. The outer layer, the dura, is packed with pain-sensing nerve fibers that originate in the trigeminal ganglion.
When these nerve fibers become activated, whether by cortical spreading depression, chemical triggers, or other signals, they release inflammatory proteins into the tissue surrounding the blood vessels. The most important of these is a molecule called CGRP (calcitonin gene-related peptide). During an attack, blood levels of CGRP rise and fall in direct proportion to headache intensity. CGRP causes blood vessels to dilate and surrounding tissue to become inflamed and swollen, which stimulates more pain-sensing nerves, creating a feedback loop that sustains the headache.
CGRP doesn’t just drive head pain. It also plays a role in nausea, changes in digestion, and sensitivity throughout the gut, which is why migraines so often come with stomach symptoms. This discovery was significant enough that an entire class of preventive migraine medications was developed specifically to block CGRP or its receptors.
The Role of Serotonin
Serotonin, a brain chemical involved in mood, sleep, and pain regulation, plays a central but complex role in migraines. People who get migraines appear to have chronically low baseline levels of serotonin in the brain. Research published in Neurology found that people with migraines may already have abnormally low serotonin, and that lowering levels further produced no additional effect, suggesting their brains are already operating near a threshold.
These low serotonin levels have wide-reaching consequences. Serotonin helps regulate the tone of blood vessels and modulates how pain signals are processed. When levels drop further, as they can before a migraine attack, blood vessels and nerves around the brain become more prone to inflammation. This serotonin connection also helps explain why migraines overlap with motion sickness, sleep disorders, and mood changes: all are influenced by the same chemical pathways.
Why Certain Things Trigger Attacks
Migraine triggers don’t cause migraines on their own. Instead, they push an already sensitive brain past its threshold. The most common triggers include stress, sleep disruption, skipped meals, alcohol, strong sensory stimuli (bright light, loud noise, strong smells), and hormonal shifts. Each of these works through the same underlying systems.
Hormonal Changes
Fluctuations in estrogen are one of the most reliable migraine triggers, which is a major reason migraines are far more common in women after puberty. The drop in estrogen that occurs just before menstruation is a well-documented trigger. Many women report migraines concentrated in the days immediately before or during their period. Pregnancy often brings relief because estrogen levels stay consistently high, but migraines frequently return after delivery when estrogen drops sharply. The pattern reinforces that it’s the change in hormone levels, not the absolute amount, that destabilizes the brain’s pain processing systems.
Weather and Environmental Shifts
Changes in barometric pressure, temperature swings, and high humidity are reported triggers for many people. The mechanism is not fully mapped, but weather changes may cause imbalances in brain chemicals, including serotonin, that lower the threshold for an attack. For people whose brains are already hovering near that threshold, a shift in atmospheric pressure can be enough to tip the balance.
Stress and Sleep
Stress activates the hypothalamus and alters levels of cortisol and other signaling chemicals, which can trigger the premonitory cascade. Interestingly, many people get migraines not during peak stress but during the “letdown” period afterward, like a weekend after a demanding work week. Sleep disruption works through similar pathways: the hypothalamus regulates both sleep cycles and migraine initiation, so poor sleep, oversleeping, or jet lag can all destabilize the system.
Why Some People Get Migraines and Others Don’t
Migraines run strongly in families. If one of your parents has migraines, you have roughly a 50% chance of developing them. If both do, the risk climbs to about 75%. This genetic component doesn’t point to a single “migraine gene” but rather to variations in dozens of genes that affect how excitable your neurons are, how efficiently your brain clears signaling chemicals, and how sensitive your trigeminovascular system is to activation.
The result is a brain that functions perfectly well most of the time but responds differently to certain stimuli. A migraine-prone brain has a lower threshold for the cascade of events described above. The same missed meal or poor night of sleep that causes no symptoms in one person can set off a full attack in someone whose neurological wiring is tuned differently. This is why migraines are considered a threshold disorder: the machinery for an attack exists in every brain, but the trigger point varies dramatically from person to person.
The Full Sequence of a Migraine Attack
Putting it all together, a typical migraine unfolds in up to four phases, though not everyone experiences all of them:
- Premonitory phase (hours to a day before pain): The hypothalamus activates, producing subtle symptoms like yawning, food cravings, irritability, neck stiffness, or difficulty concentrating. Most people learn to recognize these as warning signs over time.
- Aura (5 to 60 minutes): A wave of electrical disruption crosses the brain surface, causing visual disturbances, tingling, or speech difficulty. This phase occurs in roughly 25% of migraine sufferers.
- Headache phase (4 to 72 hours): Trigeminal nerve fibers release CGRP and other inflammatory compounds around meningeal blood vessels. Pain is typically throbbing, one-sided, and worsened by movement. Nausea, vomiting, and extreme sensitivity to light and sound are common.
- Postdrome (up to 48 hours after pain resolves): Often called a “migraine hangover,” this phase brings fatigue, difficulty concentrating, and mood changes as the brain recovers from the neurological disruption.
Each phase reflects a different stage of the same underlying process: a hyper-excitable brain generating and amplifying signals through pathways that connect deep brain structures, sensory nerves, and the blood vessels surrounding the brain. The pain is real and measurable, driven by inflammation and nerve activation, not tension or imagination.