Migraine: What It Is, Why It Happens, and How It's Treated

Short Answer

Migraine is not just a bad headache. It is a neurological disorder that comes in recurrent attacks: moderate-to-severe head pain, often one-sided and throbbing or pulsing, usually with nausea and sensitivity to light and sound. Some people also get an aura — temporary nervous-system symptoms such as visual changes, tingling, numbness, weakness, or trouble speaking — before or during the attack. (mayoclinic.org)

It is also extremely common and genuinely disabling: one 2026 study describes migraine as "a debilitating neurological syndrome that affects approximately 15% of the global population, with a three-fold higher prevalence in females compared to males". (pubmed.ncbi.nlm.nih.gov) The female predominance isn't a coincidence — a 2026 review notes that "Estrogen fluctuations contribute to migraine expression and underlie the 3:1 female-to-male prevalence". (pubmed.ncbi.nlm.nih.gov)

Underneath the pain is a specific body system: the trigeminovascular system, where pain-processing trigeminal nerves interact with blood vessels and inflammatory signaling around the brain. One of the key messengers in that system is CGRP — calcitonin gene-related peptide — which is strongly tied to migraine biology and is now a major target for migraine-specific treatments. (pubmed.ncbi.nlm.nih.gov) Migraine is not “cured” in the simple sense of making the tendency disappear forever, but it is very treatable: acute medicines can help stop an attack, preventive treatments can reduce how often or how hard attacks hit, and lifestyle pattern work can help you spot what lowers your attack threshold. (mayoclinic.org)

A wearable cannot diagnose migraine. But tracking sleep, stress, HRV, resting heart rate, and your cycle can give you useful context: not a prediction, not a verdict, but a way to see when your nervous system may be more vulnerable. That matters because sleep changes, stress, hormonal shifts, caffeine, alcohol, sensory stimuli, skipped meals, and weather changes are all commonly reported migraine triggers — and a 2026 animal study found that sleep restriction can facilitate trigeminovascular sensitization, making migraine-like responses easier to trigger. (mayoclinic.org)

Migraine, the autonomic nervous system, and your patterns — what our data shows

Among 396 Welltory users who self-report migraine, compared with 3,749 users who do not, the pattern mirrors what we have seen in other chronic-condition cohorts: the felt burden is real, but a single wellness score does not capture it. Brain fog was the clearest separator. About 49% of the migraine group flagged self-reported brain fog, versus 25% of everyone else. That gap holds up even when we compare people carrying the same number of other conditions, so it tracks with migraine itself rather than simply with a heavier overall condition load.

The “hard” wearable numbers separated people much less. The morning HRV score was essentially identical in both groups: 3.11 vs 3.11. Resting heart rate ran only modestly higher in the migraine group — 65.5 vs 62.5 bpm — but that gap is real mainly in the sense that it reflects the cluster of co-occurring conditions this group tends to carry, not migraine on its own; it flattens once we compare people like-for-like. In plain English: a single wearable reading like HRV or resting heart rate does not cleanly separate people who self-report migraine from those who do not. Your tracker can look normal in the morning while your brain still feels foggy, overloaded, and migraine-prone. That does not make the symptoms less real. It means one daily recovery number is too blunt to carry the whole migraine signal — the more useful signal is your own baseline and trigger pattern over time.

This is a first-party pattern from a self-identified group of Welltory users, not a clinical diagnosis, and it is not a way to diagnose or predict migraine. The figures are self-reported, anonymized, and aggregated; no individual user is identifiable. The reportable finding is the brain-fog gap (49% vs 25%), which held up on like-for-like comparison; the wearable numbers are shown for honesty, not as a migraine test.

Migraine at a glance

Migraine is a recurrent neurological disorder, not “just a headache.” An attack can move through your whole nervous system: moderate-to-severe head pain, nausea or vomiting, sensitivity to light and sound, trouble concentrating, fatigue, and sometimes aura. "Migraine is a debilitating neurological syndrome that affects approximately 15% of the global population, with a three-fold higher prevalence in females compared to males" Migraine is also commonly summarized as affecting about 1 in 7 people worldwide, and women are affected more often than men. (pubmed.ncbi.nlm.nih.gov)

Most migraine is without aura. About one-quarter of people with migraine experience aura — most often visual changes such as flashing lights, blind spots, or zig-zag lines, though aura can also involve numbness, speech difficulty, dizziness, or other reversible neurologic symptoms. Aura can come before the headache or overlap with it. "Migraine with aura is a risk factor for ischemic stroke" That does not mean a stroke is likely for any one person, but it does mean aura has a different vascular-risk profile and is worth discussing with a clinician, especially if symptoms are new, one-sided, sudden, or unlike your usual pattern. (medlineplus.gov)

The pain pathway starts deep in the trigeminovascular system — the network where trigeminal nerve fibers, brain coverings, blood-vessel signaling, and inflammatory peptides talk to each other. When this system is activated, trigeminal neurons release signaling molecules, especially CGRP, which helps amplify pain transmission and sensitivity. "the release of vasoactive peptides by trigeminal ganglion (TG) neurons, such as CGRP and PACAP, plays a crucial role" (pubmed.ncbi.nlm.nih.gov)

Migraine is usually described as episodic or chronic based on frequency. Chronic migraine means headache on 15 or more days per month for more than 3 months, with migraine features on at least 8 days per month; fewer headache days is generally considered episodic migraine. That distinction matters because frequent attacks can train the nervous system to stay more sensitive, and treatment often shifts from “stop this attack” to “reduce the whole attack load.” (pmc.ncbi.nlm.nih.gov)

Migraine is not currently “cured” in the way an infection can be cured. But it is highly manageable. Acute treatment can help stop an attack once it starts; preventive treatment can reduce how often attacks happen, how severe they feel, and how long they last; and trigger management — sleep rhythm, meals, stress load, hormones, alcohol, light, weather, overuse of pain medicine — can lower the chance that your nervous system crosses its migraine threshold. (ninds.nih.gov)

What migraine is — a neurological disorder, not "just a headache"

Migraine is a neurological disorder of the brain’s pain-signaling and sensory-processing systems, not a simple headache you should be expected to “push through.” During an attack, the pain is often moderate to severe, one-sided, throbbing or pulsing, and worse with ordinary movement like walking upstairs. It commonly travels with nausea, vomiting, and sensitivity to light and sound — which is why a bright room, a loud conversation, or even normal activity can suddenly feel unbearable. Clinically, migraine is recognized by this pattern: recurrent attacks, characteristic pain features, associated symptoms, and the fact that another diagnosis does not better explain what is happening. (ncbi.nlm.nih.gov)

It is common and disabling in equal measure: "Migraine is a debilitating neurological syndrome that affects approximately 15% of the global population, with a three-fold higher prevalence in females compared to males". (pubmed.ncbi.nlm.nih.gov)

That framing matters. If your scan looks normal, it does not mean the pain is imaginary or “just stress.” Migraine is usually diagnosed from your history, exam, attack pattern, and diagnostic criteria because the problem is often functional — how pain pathways, the trigeminal system, brainstem networks, chemicals such as CGRP, and sensory circuits behave during an attack — rather than a visible structural injury on routine imaging. Primary headaches, including migraine, can occur without a detectable underlying cause, and imaging is usually reserved for red flags or unusual changes in the headache pattern. (ncbi.nlm.nih.gov)

So the useful question is not “Is it only a headache?” It is: “Does this attack behave like migraine?” The ICHD-3 diagnostic feature set looks for attacks lasting 4–72 hours when untreated or unsuccessfully treated, at least two core pain features — such as one-sided location, pulsating quality, moderate-to-severe intensity, or worsening/avoidance of routine activity — plus nausea and/or vomiting, or both light and sound sensitivity, with no better explanation from another headache diagnosis. (ncbi.nlm.nih.gov)

Migraine with aura, migraine without aura, and the phases of an attack

Migraine without aura is the most common form of migraine. In plain language, that means the attack is built around head pain and the usual migraine companions — nausea, light sensitivity, sound sensitivity, throbbing or one-sided pain, and worsening with movement — but there is no separate neurological “warning” beforehand. Migraine with aura adds that warning layer: temporary, fully reversible nervous-system symptoms that usually come on gradually. Most often they are visual — zig-zag lines, blind spots, flashing lights, shimmering shapes — but aura can also be sensory, like tingling, or language-related, like trouble finding words. In ICHD-3-based criteria summarized by NCBI Bookshelf, individual aura symptoms typically last 5–60 minutes, and the symptoms may spread gradually over at least 5 minutes or occur one after another. (ncbi.nlm.nih.gov)

Aura is not just a symptom quirk — it changes the medical context. A 2025 stroke-risk study states plainly that "Migraine with aura is a risk factor for ischemic stroke". That does not mean most people with aura will have a stroke. It means your aura history matters when a clinician is thinking through your whole vascular-risk picture, especially around choices that can affect clotting risk, such as estrogen-containing contraception or hormone therapy. Reviews and consensus papers on contraception and migraine make the same practical point: aura is one of the details clinicians weigh before recommending estrogen-containing options. (pubmed.ncbi.nlm.nih.gov)

The phases of a migraine attack are another reason migraine can feel bigger than “just a headache.” Many attacks move through recognizable stages, although not everyone gets every stage every time. The prodrome can start hours to one or two days before pain, with body-level clues such as yawning, food cravings, mood shifts, neck stiffness, increased urination, or fatigue. Then comes aura for people who have it. The headache/attack phase is the painful part itself. Afterward, the postdrome can feel like a migraine hangover: drained, foggy, worn out, or briefly more sensitive to movement. Mayo Clinic describes the same four-stage pattern — prodrome, aura, attack, postdrome — and notes that some people skip stages. (mayoclinic.org)

That phased pattern is why prediction research is so interested in the prodrome. Before the pain peaks, the nervous system may already be changing. One 2026 wearable study set out "to evaluate the use of wearable sensor technology in predicting migraine attacks by monitoring changes in the ANS during the prodrome phase". The study analyzed sleep-time heart-rate-variability signals from wearable sensors and framed HRV as a noninvasive window into autonomic nervous system activity — promising, but still early and variable person to person. (pubmed.ncbi.nlm.nih.gov)

What causes migraine? Trigeminovascular activation, CGRP, and the autonomic link

There isn’t one single cause of migraine. It’s better understood as a neurologic disorder of sensitivity and threshold: your brain and pain-processing networks are more likely to overreact to internal or external change, especially when genetics, sleep, hormones, stress, meals, caffeine, and the environment stack up at the same time. NINDS describes the start of primary headaches as uncertain, but involving a cascade of blood-vessel, nerve, inflammatory, and nerve-cell activity changes; NCBI’s clinical overview similarly frames migraine as a mix of genetic, environmental, and neurologic factors rather than one simple trigger. (ninds.nih.gov)

The trigeminovascular system and CGRP. During an attack, one key circuit is the trigeminovascular system — trigeminal nerve pathways connected to pain-sensitive blood vessels and the meninges around the brain. When this circuit is activated, trigeminal ganglion neurons release vasoactive signaling molecules, especially CGRP (calcitonin gene-related peptide), which helps amplify pain signaling and inflammation-like sensitivity. As a 2026 study describes it, "the release of vasoactive peptides by trigeminal ganglion (TG) neurons, such as CGRP and PACAP, plays a crucial role" in migraine. This is not just theory: CGRP is now the target of major migraine treatment classes, including monoclonal antibodies and gepants, and the American Headache Society position statement says CGRP-targeting therapies are a first-line option for migraine prevention. (pubmed.ncbi.nlm.nih.gov)

The autonomic nervous system. Migraine is also tightly linked to the autonomic nervous system — the “automatic” system that regulates heart rate, blood-vessel tone, digestion, sweating, sleep-wake physiology, and stress response. That matters for Welltory because wearables do not measure migraine directly, but they can measure signals related to autonomic state, especially heart-rate variability. A 2026 wearable-sensor study notes that "Current evidence suggests that autonomic nervous system (ANS) alterations play a significant role in migraine pathophysiology", and that "Heart rate variability (HRV), a well-established, noninvasive marker of ANS function, is associated with migraine severity and treatment efficacy". So HRV, sleep, and stress are not “migraine detectors.” They are context signals from the same body system that helps set migraine threshold, recovery, and vulnerability (see §6). (pubmed.ncbi.nlm.nih.gov)

Triggers lower the threshold. Common triggers — irregular or short sleep, skipped meals, caffeine changes, stress, dehydration, hormonal shifts, weather changes, bright or flashing light, strong smells, alcohol, and too much or too little sleep — usually do not “cause” migraine from nowhere. They lower the attack threshold in a brain that is already susceptible. NINDS lists many of these as migraine triggers and emphasizes that triggers vary from person to person. A 2026 experimental study gives this everyday advice a biological mechanism: "SR facilitates trigeminovascular sensitization, promoting migraine-like responses in a sex-specific manner and highlighting caffeine as an enhancer of this interaction". In plain English: sleep restriction made the migraine pain circuit easier to activate in rats, and caffeine strengthened that effect. (ninds.nih.gov)

Other contributors. Genetics also matter: migraine often runs in families, and its genetic basis appears complex rather than controlled by one migraine gene. Researchers are also studying why migraine becomes chronic in some people, including changes in pain networks, CGRP biology, neuroinflammation, and brain waste-clearance pathways. One 2026 imaging study of chronic migraine reported region-specific enlarged perivascular spaces — MRI-visible markers linked to glymphatic system dysfunction — and concluded that "Chronic migraine is associated with an increased prevalence of high-grade EPVS in specific brain regions, suggesting an underlying GS dysfunction". That does not mean every person with migraine needs brain imaging; it means migraine is increasingly studied as a whole-brain, whole-body network disorder, not just a bad headache. (ncbi.nlm.nih.gov)

Who gets migraine — the female predominance and the hormonal story

Migraine disproportionately affects women, and the reason is largely hormonal. A 2026 review states that "Migraine is a neurologic disorder that disproportionately affects women and undergoes important changes across the menopausal transition", and that "Estrogen fluctuations contribute to migraine expression and underlie the 3:1 female-to-male prevalence". In plain terms: when estrogen rises, falls, or becomes erratic, the migraine brain can become more reactive — to pain signals, sleep loss, stress, light, smell, and normal body rhythms that might not bother someone else. (pubmed.ncbi.nlm.nih.gov)

Menstrual migraine. For many women, attacks cluster around the drop in estrogen just before or during a period — “menstrual migraine,” "a hormone‐related migraine type" that is frequently underdiagnosed. The ICHD appendix criteria describe pure menstrual migraine and menstrually related migraine as migraine without aura attacks that occur around menstruation — day 1 ± 2, meaning from 2 days before bleeding starts through day 3 — in at least 2 out of 3 menstrual cycles; pure menstrual migraine happens only in that window, while menstrually related migraine also happens at other times of the cycle. (pmc.ncbi.nlm.nih.gov)

Menstrual attacks tend to be more severe, longer-lasting, and harder to treat, partly because the estrogen drop is not just a “trigger” outside the body — it changes the body’s pain chemistry and can interact with CGRP, prostaglandins, sleep disruption, cramps, mood symptoms, and inflammation. Premenstrual symptom burden compounds the picture: a 2026 report describes that "Females with MM had significantly higher PSST and HIT-6 scores" (more premenstrual symptoms and greater headache impact) than women with non-menstrual migraine, and that "the presence of PMDD was associated with an increase of 3.113 points in HIT-6 scores". HIT-6 is a headache-impact score from 36 to 78 where higher scores mean headaches interfere more with work, home life, and social functioning; even small point changes can matter at a group level. (pmc.ncbi.nlm.nih.gov) (For prevention timing and options, see our migraine treatment page and PMS/period and perimenopause guides.)

Across the menopausal transition. The pattern shifts with life stage. Perimenopause is often the messy part: estrogen and progesterone do not simply “decline” in a straight line — they fluctuate, sometimes sharply — so migraine can become less predictable. The 2026 review summarizes the longer arc this way: "Migraine without aura often improves after menopause, whereas migraine with aura tends to persist and independently increases the risk of ischemic stroke and other vascular events". This is why aura status and vascular risk matter so much when choosing treatment in midlife: the question is not only “what stops the headache?” but also “what is safest for this person’s blood vessels, hormones, sleep, bones, mood, and metabolic health?” (pubmed.ncbi.nlm.nih.gov)

How migraine is treated (acute, preventive, and where medicine belongs)

There is no cure for migraine, but that does not mean you are stuck “just living with it.” Migraine treatment usually has two jobs: acute treatment, which tries to stop or shorten an attack that has already started, and preventive treatment, which tries to make attacks happen less often, feel less disabling, or both. Trigger management sits alongside both — because your brain is more likely to tip into migraine when sleep, meals, hydration, caffeine, hormones, stress, or recovery are unstable. For a full treatment and medication guide, see our migraine treatment page. (mayoclinic.org)

Medication choice, dose, and suitability are clinical decisions — this page does not give drug or dose instructions. In broad strokes, acute treatment can range from over-the-counter pain relievers for milder attacks to migraine-specific prescription medicines when attacks are more severe, longer, or harder to stop. Triptans are a long-standing mainstay: a 2026 review notes "Triptans have established efficacy and are widely prescribed for the acute treatment of migraine", but also that "triptans may not be recommended for some individuals due to cardiovascular contraindications and precautions" — which is exactly why self-prescribing is unsafe. Newer non-vasoconstrictive migraine-specific options include gepants and ditans for acute treatment; CGRP-targeting therapies also include preventive gepants and CGRP monoclonal antibodies. The American Headache Society’s 2024 position statement says CGRP-targeting therapies can be considered a first-line option for migraine prevention, and chronic migraine prevention may also involve injection-based treatments for the right patient. Which drug, which dose, and whether any of this is right for you depends on your migraine type, aura status, cardiovascular and pregnancy status, other diagnoses, other medicines, and your attack pattern — and must be decided with a clinician. See our migraine treatment page. (pubmed.ncbi.nlm.nih.gov)

A note on medication in pregnancy. Some common migraine drugs carry pregnancy cautions, and “natural to you” does not automatically mean safe for a pregnancy. A 2026 CPRD cohort study found that "Having migraine was associated with an 8% higher relative risk of miscarriage", and that triptan, amitriptyline, and NSAID exposure were also associated with higher odds of miscarriage. This kind of study shows association, not proof that a medicine caused the outcome — but it is still a strong reason not to DIY migraine medication during pregnancy or when trying to conceive. Your clinician has to weigh the risks of the medicine against the risks of untreated migraine, vomiting, dehydration, poor sleep, and uncontrolled pain. (pubmed.ncbi.nlm.nih.gov)

Non-drug and lifestyle levers. Consistent sleep, regular meals, hydration, steady caffeine habits, stress management, and identifying personal triggers are first-line migraine support — not because migraine is “just lifestyle,” but because your nervous system is less reactive when the body’s basic rhythms are predictable. A headache diary or tracker can help you see patterns you would otherwise miss: the attack after two short nights, the skipped-lunch migraine, the caffeine swing, the stress letdown after a hard week. These levers can complement medication, reduce avoidable load on the nervous system, and give your clinician cleaner information to work with — especially if attacks are changing over time. See §6 for how tracking fits in. (mayoclinic.org)

Migraine, sleep, stress, and HRV — the Welltory angle

Migraine is not “just a headache.” It is a nervous-system event that involves pain pathways, sensory processing, blood vessels, hormones, and the autonomic nervous system — the same body-control network that shifts your heart rate, recovery, stress response, and sleep depth. That matters because some of migraine’s most common day-to-day triggers are also measurable from the outside: short sleep, irregular sleep, stress load, caffeine changes, and cycle-related hormone shifts. Mayo Clinic lists stress, sleep changes, caffeine, alcohol, and hormonal changes among migraine triggers, and it also recommends keeping a headache diary to learn your own pattern over time. (mayoclinic.org)

This is where HRV becomes useful context. Not as a diagnosis. Not as a magic warning system. But as a way to see whether your body was already under strain before the attack showed up. The research says the autonomic link directly: "Heart rate variability (HRV), a well-established, noninvasive marker of ANS function, is associated with migraine severity and treatment efficacy". A 2026 wearable-sensor study also tested nocturnal HRV features before migraine episodes and found that physiological responses varied a lot from person to person — exactly why your own timeline matters more than a generic “migraine trigger list.” (pubmed.ncbi.nlm.nih.gov)

A wearable still can’t diagnose migraine, replace a neurological exam, or reliably predict an individual attack for everyone. Migraine diagnosis is clinical: it depends on your history, symptoms, and a physical and neurological exam; imaging is used when the pattern is complex, sudden, or concerning. (mayoclinic.org) What a wearable can do is help you ask better questions: Did attacks cluster after two short nights? After a week of high stress? On low-HRV mornings? After caffeine swings? For many women, do they tend to appear in the days before or around bleeding, when estrogen withdrawal can make the trigeminovascular system more vulnerable? (pmc.ncbi.nlm.nih.gov)

That distinction is important for the Welltory angle. In our own migraine cohort, the signal that separated people wasn’t the morning HRV score — that read essentially identical between groups — it was how they felt, especially brain fog. That fits migraine as a whole-body neurological condition: sometimes the wearable metric is not “the answer,” but the context around the answer. Your sleep, stress, HRV, resting heart rate, and cycle notes can turn “I think bad sleep and stress set me off” into a concrete timeline you can bring to a clinician. Related reading: HRV, anxiety, PMS/period, and perimenopause.

How we made it

This page was drafted with AI tools, then edited, fact-checked, and medically reviewed by the Welltory team. Medical claims were checked against authoritative migraine references, including NINDS, Mayo Clinic, MedlinePlus Genetics, ICHD-3 diagnostic criteria coverage on NCBI Bookshelf, and recent peer-reviewed studies on migraine biology, hormonal factors, and the autonomic nervous system.

The cohort figures in this page come from a self-identified group of Welltory users, not from clinically diagnosed patients. All figures are reported as anonymized, aggregated data; no individual user is identifiable. They describe patterns in our app data — not a way to diagnose, predict, or measure migraine for any individual person. The reportable finding is the self-reported brain-fog gap (49% vs 25%), which held up when comparing people carrying the same number of other conditions; the wearable numbers are included for honesty, not as a migraine test.

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