What does Migraine do in the body?

Story

Migraine

Last updated September 2026

In one pass Migraine is an attack that starts in the brain: endings of the trigeminal nerve, which supplies the meninges (the membranes wrapped around the brain), release several peptide signaling molecules, and the key one is CGRP (calcitonin gene-related peptide).

Educational content, not medical advice — consult a clinician.

Chapter 1

Migraine · not just a headache

Migraine is an attack that starts in the brain: endings of the trigeminal nerve, which supplies the meninges (the membranes wrapped around the brain), release several peptide signaling molecules, and the key one is CGRP (calcitonin gene-related peptide). It is not an ordinary tension-type headache, and it should not be blamed on the sinuses or the neck by default.

An attack is often a throbbing pain on one side of the head, with sensitivity to light and sound and nausea, and a wish to crawl into a dark, quiet room. It is treatable, and it is not a matter of willpower.

Red flags (get medical care immediately): the worst headache of your life; an explosive headache that peaks within seconds to minutes; fever plus a stiff neck; steadily worsening over days to weeks; new after age 50; persistent weakness, double vision, trouble speaking or reduced awareness; a new severe headache during pregnancy.

Clinical · How migraine is recognized

Migraine is recognized by the shape of the attacks, not by sinus thickening or neck-bone spurs on a scan.

For migraine without aura, the criteria of the International Classification of Headache Disorders, 3rd edition (ICHD-3), run roughly like this: at least 5 attacks; each lasting 4–72 hours if untreated; at least two of these four features — one-sided, throbbing, moderate to severe, made worse by routine activity; at least one of these two — nausea or vomiting, or sensitivity to both light and sound; and no other condition that explains it better.

Migraine with aura means that, before or during the attack, there is a visual, sensory or speech disturbance: zigzag flashing lights, hemianopia (losing half of the visual field), numbness, or a moment of not finding words, usually lasting 5–60 minutes. That light corresponds to a slowly spreading electrical wave across the visual cortex, not to a problem in the eye or the nose.

Children can have migraine too, about 7–8% of them, and it sometimes shows up first as tummy pain or bouts of cyclical vomiting rather than a throbbing temple. Men get it as well; it is not a women-only condition.

Red flag · Which headaches need care right now

Several kinds of headache look like migraine but work differently, so they are treated differently.

Tension-type: a pressing pain on both sides, mild to moderate, without nausea. Cluster: more common in men, an excruciating pain around one eye, with tearing, a runny nose and a change in the pupil on the same side. For secondary headaches, doctors need to rule out a brain tumor, changes in pressure inside the skull, temporal arteritis (an inflammation of blood vessels seen mostly in older people) and subarachnoid hemorrhage — a thunderclap headache is an emergency.

Red flags (immediate care):

This is the worst headache of my life (subarachnoid)Thunderclap, peaking in seconds to minutesFever plus neck stiffness (meningitis)Progressive worsening over days or weeksNew-onset headache after 50 (rule out temporal arteritis)Persistent neurological signs: weakness, diplopia, speech, consciousnessPregnancy plus a new severe headache
Treating early works better than toughing it out. Taking more and more painkillers can lead into medication-overuse headache (MOH, where taking acute painkillers too often makes headaches more frequent); that is covered in detail in Triggers and how to use medicines.

Numbers · How common and disabling migraine is

In 2020, Steiner and colleagues went back through the headache data of the Global Burden of Disease study (GBD 2019). Counted in years lived with disability (years of healthy life lost to living with a condition), migraine remains the world's second-leading cause of disability, behind only low-back pain. About 14–15% of people worldwide have migraine (about 17% of women and 8% of men); surveys in China estimate about 9%, or about 130 million people. It runs strongly in families; a commonly quoted estimate from family studies is that if one parent has it, a child's chance is about 50%, and if both do, about 75%.

One estimate puts China's yearly cost of migraine, in lost workdays plus medical care, on the order of 100 billion yuan. Hard-to-get appointments and slow dose adjustment are real frictions in long-term care, not a lack of persistence on the patient's part.

Some beliefs keep people stuck: men do not get it; children do not get it; it is just tiredness or poor sleep; the worse the pain, the more painkillers you should take. The first three do not fit the numbers or the mechanism above; the last one feeds medication-overuse headache (MOH). Migraine deserves a complete path of diagnosis and management, not endurance.

Chapter 2

How a migraine attack unfolds

When a migraine hurts, the key molecule is CGRP (calcitonin gene-related peptide) in the meninges, the membranes around the brain. Trigeminal nerve endings release it, blood vessels widen, local inflammation follows, and the pain signal travels on to the thalamus and the cortex. Changes in blood flow look more like a result than the cause; the old theory that explained migraine by vessels first narrowing and then widening is no longer the mainstream view.

The aura (warning signs before an attack, such as flashing lights or tingling) comes from a slow electrical wave spreading across the cortex, called cortical spreading depression (CSD). Infusing CGRP into people with migraine can set off an attack much like their usual ones, so CGRP is not a bystander.

The antibodies and small-molecule drugs aimed at CGRP are prescription medicines to discuss with a headache specialist, not something to buy and try on your own.

Mechanism · CSD ignites, CGRP amplifies at the meninges

A 2018 review by Edvinsson and colleagues framed CGRP as the target of the new migraine drugs. Laid out as a path you can follow step by step, it is more useful than memorizing "vessels narrow, then widen."

Step one: cortical spreading depression (CSD) appears on the cortex. Neurons and their support cells (glia) depolarize together — a brief burst of activity followed by silence — forming a wave that advances about 3–5 mm per minute. It is thought to be the neural basis of the aura; the zigzag flashing lights correspond to this wave crossing the visual cortex. Stress, hormonal swings, sleep loss, some foods and bright light are all thought to be able to set it off. Where attacks without aura begin is not yet settled.

Step two: in animal experiments, the wave activates the trigeminal sensory fibers that supply the meninges, and their endings release CGRP along with substance P and neurokinin A. CGRP is one of the most potent blood-vessel wideners known, and it drives neurogenic inflammation (inflammation triggered by substances released from nerve endings themselves).

Step three: widened meningeal vessels, mast cells releasing their contents, and inflammation send pain signals through the trigeminal nucleus to the thalamus and cortex. With repeated attacks, this pathway becomes centrally sensitized: the threshold keeps dropping, until a small trigger is enough.

Why CGRP is a lead actor rather than a bystander: infusing it into people with migraine can trigger attacks, and blood levels of CGRP rise clearly during attacks. From 2018, antibodies against the CGRP receptor or against CGRP itself entered clinical use — the first class of preventive drugs aimed squarely at this mechanism. Oral small-molecule gepants followed, for both acute attacks and prevention. These are specialist prescriptions, not the next item on a supplement shelf.

Why riboflavin, magnesium and coenzyme might touch this chain is a separate line of thinking: by the mechanism, better-fueled mitochondria should make CSD harder to set off. That step has not been measured directly in people; the trials and doses are in Three nutrients with evidence.

Mechanism · How hormones, food and sleep feed in

This CGRP chain is also wired to other parts of the body, which is why triggers look so varied; in the current understanding, most of them press on the same threshold.

The drop in estrogen before a period is thought to make receptors for serotonin (, a nerve-signaling chemical) more sensitive and to raise CGRP production — the most common explanation for menstrual migraine. Some foods contain substances that act on blood vessels, such as tyramine and phenylethylamine. Sleep loss and stress are thought to lower the trigger threshold through the stress axis. The older preventive drugs (beta-blockers, tricyclics, some antiseizure drugs) work in different ways, and how they help in migraine is not fully understood, but none of them blocks CGRP directly; among them, the tricyclic amitriptyline affects the reuptake of serotonin and norepinephrine.

Riboflavin, magnesium and coenzyme may help further up this chain: by the mechanism, better mitochondrial function gives brain neurons more , so CSD is harder to set off and attacks become less frequent. That is an explanation, not a measurement — the trials counted attacks and did not measure CSD directly. Doses and trials are in Three nutrients with evidence; hormones, periods and pregnancy are handled in Triggers and how to use medicines. For the whole menstrual cycle, see Menstrual Cycle; for perimenopause, see Perimenopause.

Clinical · How the four CGRP antibodies compare

From 2018, four monoclonal antibodies against CGRP came to market one after another — the latest stretch of a roughly thirty-year path from discovering this mechanism to drugs that target it. They are prescription preventives decided on by a neurologist or headache specialist, not a wellness step to inject on your own.

Drug	Brand	Target	Form + frequency	US annual price	China launch
Erenumab	Aimovig	CGRP receptor	70-140 mg SC / month	$7,000	2023 (Amgen)
Fremanezumab	Ajovy	CGRP ligand	225 mg monthly or 675 mg quarterly	$7,000	2024
Galcanezumab	Emgality	CGRP ligand	120 mg / month + 240 mg loading	$7,000	pending
Eptinezumab	Vyepti	CGRP ligand	100-300 mg IV / quarter	$14,000	pending

In the table, "ligand" means the CGRP molecule itself, "loading" is a doubled first dose, SC means under the skin and IV means into a vein. Erenumab targets the receptor; the other three target the ligand. In theory, ligand antibodies still let CGRP act through a related calcitonin receptor, while a receptor antibody blocks more completely; in practice, all four work about equally well in the clinic, and there is no clear head-to-head winner. The first three can be injected under the skin at home (like an insulin pen); eptinezumab needs an IV infusion in hospital.

Across the , results fall roughly in this range: 1.5 to 2.5 more monthly migraine days cut than with placebo; about 50–60% of people halve their migraine days, against about 30–40% on placebo; about 70% cut them by at least a third; and in hard-to-treat migraine where three drugs have already failed, about 30–40% still respond. The main side effects are injection-site reactions, constipation (erenumab) and, rarely, allergic reactions.

Compared with traditional preventives such as topiramate or amitriptyline, they work about as well, but act faster (1–3 months against 3–6), cause fewer side effects, and once-a-month dosing is easier to stick with. The drawbacks are cost and long-term data beyond ten years that are still being gathered.

The American Headache Society (AHS) 2019 position statement set the conditions for starting them roughly as: two or three traditional preventives have failed (at an adequate dose, for at least 3 months each); disabling migraine (grade III–IV on the Migraine Disability Assessment, MIDAS, meaning moderate to severe disability); or chronic migraine (headache on at least 15 days a month, at least 8 of them migraine, for 3 months or more). The AHS 2024 update listed CGRP-targeting therapies as a first-line option for prevention, no longer requiring two older oral preventives to fail first — especially suitable for people who cannot take, or cannot tolerate, the traditional drugs. In China, cost and insurance limits mean they are still mostly used second- or third-line in practice.

ahs-2024-cgrp-first-line-migraine

Clinical · Oral gepants, and access in China

Oral gepants (small-molecule drugs that block the CGRP receptor) have been used for prevention since about 2021. Rimegepant (Nurtec ODT), 75 mg every other day, covers both acute attacks and prevention; atogepant (Qulipta), 10–60 mg a day, is for prevention only. They are a little less effective than the antibodies, but they are taken by mouth and cost less. Rimegepant's advantage is that the occasional acute attack and long-term prevention can be handled with the same pill.

In China, access as of 2024–2025 looks roughly like this: erenumab (sold in China as Anshining) launched in 2023 at about 3,000–5,000 yuan a month, with some provinces covering some doses under public insurance since 2024; the other three antibodies are under review; and gepants are partly available through the Boao Lecheng pilot medical zone. The barriers are cost, insurance coverage, doctors' familiarity with the drugs, and approval for specific uses.

In practice, people with hard-to-treat or chronic migraine who can afford it can discuss these drugs with a neurologist or headache specialist. Usually the three nutrients (riboflavin, magnesium and coenzyme ) and two or three traditional preventives will have been tried, medication-overuse headache ruled out and lifestyle adjusted before an antibody is considered. For people whose migraine truly resists treatment, it can change their lives; it is still not a first step to start on your own. Data in pregnancy and breastfeeding are lacking, so avoid them for now.

Further down the research pipeline (2025 onward): an antibody against another nerve peptide, PACAP (Lu AG09222); a combined CGRP-plus-PACAP approach that might work together in theory and is still waiting for Phase III trials; and choosing drugs by genotype, which is not yet in clinical use. None of these is the next thing you can buy over the counter.

Watch the mechanism

Chapter 3

Three nutrients with evidence

Riboflavin (vitamin B2), magnesium and coenzyme meet migraine at the mitochondria: by the mechanism, brain neurons get more , so the CSD wave becomes harder to set off. Each has small placebo-controlled trials behind it, and the 2012 guideline of the American Academy of Neurology (AAN) and the American Headache Society (AHS) (Holland 2012) rated riboflavin and magnesium as probably effective and coenzyme Q10 as possibly effective.

The doses used in the trials were riboflavin 400 mg a day, elemental magnesium 400–600 mg and coenzyme Q10 100–300 mg. That magnesium dose is above the tolerable upper intake level () for supplemental magnesium, which makes it a treatment dose to take under a doctor's guidance. All three are generally safe, inexpensive and do not clash with prescription preventives, but they take two to three months to work, so two weeks without a change is no reason to stop. They do not replace the preventive drugs a specialist prescribes.

Evidence · What each of the three trials found

Riboflavin, 400 mg a day. In Schoenen's 1998 in Neurology (N = 55), three months of riboflavin cut attack frequency (p = 0.005) and headache days more than placebo. In the body it becomes FAD (a cofactor that helps enzymes pass electrons along), which keeps complex II of the mitochondria running. It is very safe; at most it turns urine bright yellow, which is harmless. The 2012 AAN and AHS guideline (Holland 2012) rated it probably effective. How riboflavin itself works in energy metabolism is covered separately — see Riboflavin.

Magnesium, 400–600 mg of elemental magnesium a day, which is above the tolerable upper intake level () for supplemental magnesium, so take it under a doctor's guidance. People with migraine often have lower magnesium in plasma, red blood cells and even brain tissue; that is an observed association. In Peikert's 1996 multicenter, randomized, double-blind trial, 600 mg of magnesium a day for three months reduced attack frequency more than placebo, and the same guideline also rated magnesium probably effective. By the mechanism, it blocks NMDA receptors (glutamate receptors that excite nerve cells), damps down CSD, relaxes the smooth muscle of blood vessels and helps regulate serotonin (). Magnesium glycinate or citrate is absorbed well; magnesium oxide is cheap but tends to cause diarrhea; magnesium threonate reached the brain in larger amounts in animal studies, but it is expensive. High doses cause diarrhea, and people with poor kidney function should be cautious. For magnesium's role in relaxation and sleep, see Magnesium.

Coenzyme , 100–300 mg a day. Sándor's 2005 randomized, double-blind trial in Neurology (N = 42) used 100 mg three times a day; by the third month it beat placebo on attack frequency, headache days and days with nausea. In Slater's 2011 pediatric trial, attacks fell in both groups with no difference between them. The 2012 AAN and AHS guideline rated it possibly effective, one step below riboflavin and magnesium. It is a cofactor in the mitochondrial electron-transport chain. Some studies suggest the reduced form (ubiquinol) is absorbed better; it costs more than the standard oxidized form (ubiquinone).

In practice · Combining them, and what not to add

Some headache specialists prescribe all three together. People vary a lot, but many respond to at least one of them. They are generally safe, moderately priced and do not clash with prescription preventives, which makes them especially suitable for people who are not ready for prescription drugs, are planning a pregnancy (riboflavin and magnesium are already common supplements in pregnancy), or are sensitive to drug side effects. They are still not a substitute for a CGRP antibody.

They work slowly: it takes two to three full months before you can tell, so do not stop after two weeks with no change. Keep a headache diary alongside (number of attacks, severity, which medicines you took) so you can judge whether they are really working.

Do not bundle other nutritional or herbal remedies into a must-take set with these three. One specific extract of feverfew was rated probably effective by the 2012 AAN and AHS guideline. Butterbur was rated higher in the same guideline, as effective, but some products contain liver-damaging pyrrolizidine alkaloids, so only preparations labeled as free of them (PA-free) should be used — it stays off the must-take list because of safety concerns, not because of effect. The guideline judged the evidence for omega-3 conflicting or inadequate; vitamin D shows some signal only in people who are deficient; and interacts with and prescription migraine drugs, so use it with caution. For the wider picture of mitochondrial cofactors, see Niacin and α-Lipoic acid (ALA).

Chapter 4

Triggers and how to use medicines

Triggers do not create a new disease. They lower the threshold of a CGRP chain that is already there: hormonal swings, sleep loss, a sudden let-up in stress, some foods, and bright light or strong smells. People differ a lot, so use a headache diary to find your own rather than copying someone else's blacklist.

Take acute medicines early. But if you take them too often, watch for medication-overuse headache (MOH): the more you take, the less they work. Depending on the drug, the threshold lies between 10 and 15 days a month — 10 days or more for triptans or combination painkillers, 15 days or more for simple painkillers — for three months in a row.

For people with aura, estrogen-containing contraceptives raise the risk of stroke; the usual switch is to a progestin-only method, made together with a doctor.

In practice · A diary tests your own triggers

Hormones: before a period, ovulation, perimenopause. Sleep: too little, too much, irregular hours, jet lag, shift work. A sudden let-up in stress: tense all week, then an attack as soon as the weekend relaxes you — hence the name weekend headache. Environment: bright or flickering light, noise, and strong smells such as perfume, smoke or paint. Weather: changes in air pressure, heat, wind, the turn of the seasons. For people with aura, estrogen-containing contraceptives raise the risk of stroke, and the usual switch is to a progestin-only method. For the sleep side, see Obstructive Sleep Apnea and Shift Work; for perimenopause, see Perimenopause.

Foods that are often named: tyramine in aged cheese, red wine and cured meat; phenylethylamine in chocolate (one common explanation is that the prodrome — the warning phase a few hours to a day or two before the headache — already brings a craving for sweets, which is then mistaken for chocolate causing the attack); , which is fine for most people; nitrites in ham and sausage; alcohol, especially red wine and brandy (tyramine and histamine, plus a direct effect on blood vessels); drinking a lot of caffeine on weekdays and suddenly stopping at the weekend; and fasting, skipped meals and low blood sugar. Aspartame is the sweetener named most often, but Schiffman's 1987 double-blind crossover trial specifically recruited people who said aspartame gave them headaches — and headaches after aspartame were not significantly more common than after placebo (numerically they were even slightly less common). So it belongs in your own diary as something to test, not on a list of accepted triggers. For dietary triggers, see Alcohol Metabolism and Artificial & Non-nutritive Sweeteners.

In practice · Treating an attack, and why early

Mild to moderate attacks: nonsteroidal anti-inflammatory drugs (), such as ibuprofen 600–800 mg, naproxen 500–1000 mg or diclofenac; or a combination of aspirin, acetaminophen and caffeine (in the US, the Excedrin Migraine type).

The classic drugs for moderate to severe attacks are the triptans — sumatriptan, zolmitriptan, rizatriptan, naratriptan and eletriptan — which selectively activate the serotonin receptors 5-HT1B/1D. Take them when the headache has just started and is still mild, rather than waiting for the full pain; people with aura usually wait until the headache itself begins, because the benefit of taking a triptan during the aura is uncertain. Taking them late works worse than taking them early. Side effects include chest tightness and a tight neck; people with cardiovascular disease should not take them; and there is a monthly limit on the total dose, to avoid rebound.

Newer acute drugs from the 2020s: gepants (rimegepant 75 mg, ubrogepant 50–100 mg) block the CGRP receptor and have a better cardiovascular safety profile; ditans (lasmiditan 50–200 mg) activate the 5-HT1F receptor instead, do not narrow blood vessels, and can be an option for people with a history of coronary heart disease. These are prescription drugs too, not an upgrade pack sold over the counter.

Clinical · Preventives, MOH and children

Preventive drugs come into the discussion at 4 or more attacks a month, or when attacks are severely disabling; the choice is made with a specialist, not by adding an injection yourself.

The evidence for the classic preventives comes mostly from , with certainty ranging from moderate to high: beta-blockers (propranolol 80–240 mg, metoprolol); the tricyclic amitriptyline 25–100 mg (a lower dose than for depression); the antiseizure drugs topiramate 25–100 mg and valproate; flunarizine, a calcium-channel drug commonly used in China; and, more recently, the blood-pressure drug candesartan 16 mg.

Newer prevention since 2018: anti-CGRP antibodies injected monthly or quarterly (erenumab, fremanezumab, galcanezumab, eptinezumab). In trials, about 50–70% of people respond (attacks cut by half or by a third, depending on the yardstick), with lower rates in people whose migraine has already resisted several drugs, and safety is good. They launched in China in 2023 and are still expensive (3,000–5,000 yuan a month), with partial insurance coverage. Oral gepants for prevention: rimegepant 75 mg every other day, atogepant 10–60 mg a day. The details are in How a migraine attack unfolds; this is not a page to start them from.

The most important warning is medication-overuse headache (MOH, where taking acute medicines too often makes headaches more frequent). Using acute medicine on 10–15 or more days a month, depending on the drug (10 days for triptans or combination painkillers, 15 for simple painkillers), for 3 months makes the headache worse and sets up a rebound cycle. The fix is to stop the overused drug under professional guidance and start a preventive. If you find yourself taking more, getting less relief, and wanting more still, treat that as an alarm and see a doctor soon to adjust your treatment.

In children, migraine may show up as tummy pain (cyclical vomiting, abdominal migraine). Treatment follows the same logic as in adults, with more conservative drug choices: avoid long-acting triptans, and use even low-dose amitriptyline with caution. The evidence for the nutrients is thinner in children than in adults: in Slater's 2011 pediatric trial of coenzyme , both groups improved and there was no difference between them. Cognitive behavioral therapy is also often used alongside medicines in children.

Clinical · Short-term prevention of menstrual migraine

Menstrual migraine is the most common type in women of reproductive age, and its drug logic differs from ordinary attacks. The main explanation is estrogen withdrawal: late in the cycle, (E2, the main estrogen) falls, which is thought to make serotonin () receptors more sensitive and raise CGRP production, with magnesium-related changes as well, so the migraine threshold drops. The estrogen peak around ovulation can also trigger attacks — possibly the swing itself, not just a low absolute level. Somerville's classic 1972 experiments first proposed that the key is the fall in estrogen.

The International Classification of Headache Disorders (ICHD-3) describes two types: pure menstrual migraine, with attacks only between 2 days before a period and its third day and never at other times, which is uncommon at about 7%; and menstrually related migraine, with attacks in that window and at other times too, which accounts for about half of migraine in women. These attacks are often more severe and longer (about 72 hours against 24–48), harder to stop with , and more likely to come back; aura is actually less common.

Short-term prevention starts 2 days before the period and lasts 5–7 days: naproxen 550 mg twice a day; the long-acting triptan naratriptan 1–2.5 mg twice a day; zolmitriptan 2.5 mg two or three times a day; frovatriptan 2.5 mg twice a day; or magnesium 600 mg a day from 2 weeks before the period until it ends, with some studies positive — a dose above the tolerable upper intake level () for supplemental magnesium, so take it under a doctor's guidance. Hormonal strategies include a continuous low-dose estradiol patch of 0.1 mg starting 7 days before the period, keeping levels steady and avoiding the withdrawal; extended-cycle contraception (for example 84 days of active pills plus 7 inactive days) can reduce attacks. People with aura should avoid estrogen-containing combined oral contraceptives: case-control studies estimate a roughly 8-fold rise in stroke risk. WHO and ACOG both advise against combined oral contraceptives for people with aura; observational studies estimate that migraine with aura, smoking and a combined pill together raise stroke risk more than 30-fold. The usual switch is to a progestin-only method, a copper IUD, or an IUD releasing levonorgestrel (LNG). For the whole menstrual cycle, see Menstrual Cycle.

Safety · Medicines in pregnancy and after birth

Most women with migraine improve during pregnancy (about 60–70%), because estrogen stays steadily high; a minority get worse or develop migraine for the first time. In the first weeks after birth, estrogen drops steeply and attacks often return.

For an acute attack, acetaminophen 500–1000 mg comes first, along with ice, a dark room and rest, enough water and no skipped meals. Long-term, high-dose acetaminophen in mid-to-late pregnancy has a disputed link with ADHD and autism in children, so it is still something to discuss with your obstetrician. The traditional practice for was occasional short use in the second trimester (14–30 weeks) and no use in late pregnancy (after 30 weeks), because a vessel in the fetal heart, the ductus arteriosus, may close too early; whether you can use them, and for how long, is for your obstetrician to decide. Among the triptans, a single 6 mg injection of sumatriptan under the skin has the most data (about 4000 exposures, with no clear signal of birth defects or preterm birth). Short-term metoclopramide can stop nausea and also ease the headache.

Strictly avoid: ergotamine (it causes uterine contractions and reduces blood flow to the placenta); valproate (neural-tube defects, effects on intellectual development), which women who could become pregnant should avoid altogether; and topiramate, which carries a risk of cleft lip and palate and should be avoided in pregnancy.

Prevention during pregnancy: riboflavin 400 mg a day and magnesium 400 mg a day are relatively safe and often recommended — though that magnesium dose is above the tolerable upper intake level () for supplemental magnesium, so use it under your obstetrician's guidance. Coenzyme has little data, so discuss it with your obstetrician. Propranolol can be continued, but in late pregnancy it slightly raises the risk of restricted fetal growth. Anti-CGRP antibodies and gepants lack data and are not recommended — this is not a gap to fill on your own.

The first 1–2 weeks after birth often bring worse attacks (the estrogen plunge plus lack of sleep). During breastfeeding, sumatriptan is relatively safe, since very little reaches breast milk; CGRP antibodies are not recommended while breastfeeding. Postpartum depression and migraine often come together and need to be managed together. Related reading: see Perimenopause, Menstrual Cycle.

Chapter 5

Keep a diary, then treat by frequency

If you often get headaches, first keep a diary for four weeks, then decide whether it is migraine, and then treat in tiers by how often attacks come. One-sided, throbbing, moderate-to-severe pain with nausea or sensitivity to light and sound strongly suggests migraine; get it confirmed by a neurologist or headache specialist.

With fewer than 4 attacks a month, acute medicines are often enough; with 4 or more a month, or severe disability, add prevention. If you use acute medicine on 10 days in any month for three months running, rule out medication-overuse headache (MOH, where taking painkillers too often makes headaches more frequent) first.

If any red flag appears, get medical care immediately — do not take this slow path.

In practice · Steps 4–6: prevention, menses, long term

The diary records the date and time, how long it lasted, severity on a 0–10 scale, where it hurt and what it felt like, your period, sleep, stress, food, weather, and which medicine you took. An app or a simple table both work. Compare it with the attack pattern described in Migraine · not just a headache, rather than giving yourself a label and stopping there.

Step four, prevention. Lifestyle first: 7–9 hours of sleep at consistent times, weekends included; no skipped meals; enough water; 150 minutes a week of moderate aerobic exercise (a sudden hard session can trigger an attack); less alcohol, especially red wine; mindfulness, cognitive behavioral therapy or yoga to manage stress; and avoiding your own bright-light and strong-smell triggers. Try the three nutrients — riboflavin, magnesium and coenzyme — at the published doses for three months: riboflavin 400 mg a day, elemental magnesium 400–600 mg (above the tolerable upper intake level, or , for supplemental magnesium, so take it under a doctor's guidance) and coenzyme Q10 100–300 mg. They work slowly, so do not stop early. Prescription prevention is chosen with a neurologist: first-line is often propranolol, topiramate or amitriptyline (depending on your other conditions); second-line is valproate, flunarizine or an angiotensin receptor blocker (); for hard-to-treat cases, anti-CGRP antibodies or gepant prevention come up next — still a specialist's decision, not an injection you start yourself. Whether aspartame triggers you is something to test in your diary; do not read Schiffman's negative 1987 crossover trial as confirmation.

Step five, menstrual migraine: a short course of naproxen 500 mg twice a day, or naratriptan, starting 2 days before the period. People with aura must not use estrogen-containing contraceptives (stroke risk rises); switch to a progestin-only method or an IUD.

Step six, the long term: treat migraine as a manageable chronic condition, not a matter of willpower. Find your own trigger pattern, avoid it, and use acute medicine early.

Red flags (get medical care immediately): the worst headache of your life; a sudden explosive headache; fever plus a stiff neck; progressive worsening; new onset after 50; persistent neurological symptoms.

Beliefs that do not hold up: tough it out without medicine; it is just tiredness; men and women are the same; children do not get it; every headache is migraine; the more painkillers, the better.

Further reading: for mitochondrial cofactors, see Riboflavin, niacin and α-Lipoic acid (ALA); for more on magnesium, see Magnesium; for hormonal swings, see Perimenopause; for sleep, see Insomnia, plus Obstructive Sleep Apnea and Shift Work; for dietary triggers, see Alcohol Metabolism and Artificial & Non-nutritive Sweeteners. Many people who combine the three nutrients, prescription prevention, lifestyle changes and (in a specialist's hands) the newer antibodies improve clearly within 6–12 months. If you have gone years without a systematic look, it is worth walking the path again.

References · 8

Steiner, T. J., Stovner, L. J., Jensen, R., Uluduz, D., Katsarava, Z., & Lifting The Burden. (2020). Migraine remains second among the world's causes of disability. Journal of Headache and Pain, 21(1), 137. 10.1186/s10194-020-01208-0
Edvinsson, L., Haanes, K. A., Warfvinge, K., & Krause, D. N. (2018). CGRP as the target of new migraine therapies. Nature Reviews Neurology, 14(6), 338-350. 10.1038/s41582-018-0003-1
Schoenen, J., Jacquy, J., & Lenaerts, M. (1998). Effectiveness of high-dose riboflavin in migraine prophylaxis: a randomized controlled trial. Neurology, 50(2), 466–470. 10.1212/WNL.50.2.466
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