The Migraine Weather Station — 72-Hour Forecast, CGRP, and Acute Care

Section 01 · The mechanism

What drives a migraine — the trigeminovascular storm.

Migraine is a disorder of the brain's pain-processing system, not a disorder of blood vessels or sinuses or the neck. It begins when trigeminal nerve endings around cranial blood vessels release neuropeptides — particularly calcitonin gene-related peptide (CGRP), substance P, and neurokinin A. These peptides dilate vessels, sensitize nerve endings, and trigger a self-amplifying inflammatory response that produces the throbbing, pulsating pain characteristic of a migraine attack.

The signal then travels centrally through the trigeminal ganglion to the trigeminal nucleus caudalis in the brainstem, and from there to the thalamus and cortex. This central sensitization explains why migraine pain worsens with movement, light, and sound — the brain becomes hyperexcitable, and normal sensory input becomes painful. That process is what makes the headache phase so disabling, and why most patients need to lie down in a dark, quiet room.

Cortical spreading depression (CSD) is the mechanism underlying aura. A wave of neuronal depolarization spreads slowly across the cortex at about 3 to 5 millimeters per minute, followed by a period of suppressed activity. The rate and direction of this wave match the classic visual aura symptoms — the scintillating scotoma that expands across the visual field over 20 to 60 minutes. CSD can trigger trigeminal activation on its own, which is why some patients get headaches after aura without an obvious external trigger.

What makes a brain susceptible is partly genetic. Over 40 genetic loci have been associated with migraine, and rare familial forms (familial hemiplegic migraine) involve mutations in ion channel genes. In the common forms, the inheritance is polygenic, and the trait is best understood as a lower threshold for the trigeminovascular system to activate. That threshold shifts with hormonal state, sleep, stress, and other triggers — which is why the same person may have attacks on some days and not others.

Section 02 · The four phases

Prodrome, aura, headache, postdrome — each with its own treatment window.

Not everyone experiences all four phases, and aura is absent in about 75 percent of cases. But when present, the phase structure is remarkably consistent — and understanding it opens treatment options at multiple points.

Phase 01

Prodrome — hours to a day before

Subtle warning signs that many patients only recognize in retrospect: food cravings, yawning, neck stiffness, mood shifts, irritability, fluid retention, and difficulty concentrating. These are driven by hypothalamic activation and can last from a few hours to 24 hours. Some patients can learn to recognize prodrome and treat preventively at this stage.

Phase 02

Aura — 20 to 60 minutes

Fully reversible neurological symptoms, most often visual: scintillating scotoma, fortification spectra, flashing lights, or blind spots. Less commonly sensory (tingling that spreads from the fingers to the face) or language (transient difficulty finding words). Symptoms develop over 5 minutes and last 5 to 60 minutes. Aura without headache is a recognized variant.

Phase 03

Headache — 4 to 72 hours

Moderate to severe, often unilateral, throbbing pain that worsens with activity. Nausea, vomiting, photophobia, and phonophobia are hallmark associated features. Untreated or under-treated attacks usually last 4 to 72 hours. This is the phase where acute medications — triptans, gepants, NSAIDs, antiemetics — work best, and where early treatment improves outcomes.

Phase 04

Postdrome — 24 to 48 hours

Often called the "migraine hangover." Fatigue, cognitive fogginess, mood changes, and residual head sensitivity that persist after the pain resolves. Patients often feel drained and slow for a full day. Recognizing postdrome matters because it is frequently misattributed to other causes, and because patients may need to plan their schedule around it.

Section 03 · Triggers

What "sets off" an attack — and what the evidence actually supports.

Triggers are individual. What reliably triggers one patient may do nothing for another. The most useful approach is a headache diary for 4 to 8 weeks to identify personal patterns, rather than avoiding long lists of theoretical triggers.

Commonly reported triggers

Ranked by frequency in patient diaries

Stress and post-stress letdown

The most commonly reported trigger. Notably, attacks often occur after the stress resolves — the "weekend headache" pattern — rather than during peak stress.

Hormonal fluctuation

Estrogen withdrawal around menstruation is a well-documented trigger. Menstrual migraine is a distinct subtype that often requires a tailored treatment approach.

Sleep disruption

Both too little and too much sleep — as well as irregular sleep schedules — are triggers. Consistent sleep timing matters more than total hours.

Weather and barometric change

Rapidly falling barometric pressure, high humidity, and temperature swings are commonly reported. Not modifiable, but useful for anticipation and pre-treatment.

Fasting and dehydration

Skipping meals and inadequate fluid intake are reliable triggers. Regular meals and consistent hydration reduce attack frequency for many patients.

Dietary triggers

Alcohol (especially red wine), aged cheese, processed meats, and monosodium glutamate are frequently reported. Evidence for most specific dietary triggers is weak — caffeine withdrawal is one of the few well-established dietary triggers.

Sensory stimuli

Bright or flickering lights, strong odors (perfume, smoke, cleaning products), and loud noise can trigger or worsen attacks. Many patients are hypersensitive to these even between attacks.

Medication overuse

Frequent use of acute medications paradoxically increases attack frequency. This is a trigger that patients often cause unknowingly, and one of the most important to recognize.

Section 04 · Acute treatment

Stopping an attack — and why timing is everything.

Acute treatment works best when taken early in the headache phase — ideally within 20 to 30 minutes of onset. Once central sensitization is established, response rates to all acute medications drop substantially. This is why patients are taught to treat early, not to "wait and see."

NSAIDs · First-line for mild-moderate

Ibuprofen, naproxen, aspirin

Effective for mild to moderate attacks, and often sufficient for patients with infrequent migraines. Best taken at the earliest sign, sometimes with caffeine to enhance absorption. Available over the counter.

Avoid chronic daily use — medication overuse headache is a real risk. NSAIDs are also not appropriate for patients with kidney disease, GI bleeding risk, or on anticoagulation.

ibuprofen · naproxen sodium · aspirin · combination products with caffeine

TRIPTANS · 5-HT1B/1D agonists

Triptans

The most effective class for moderate to severe migraine. Block CGRP release, constrict dilated cranial vessels, and inhibit trigeminal signaling. Available as tablets, orally disintegrating tablets, nasal sprays, and subcutaneous injections — the injectable form is fastest.

Contraindicated in coronary artery disease, uncontrolled hypertension, prior stroke, and certain migraine subtypes with aura (in some countries). Do not combine with MAO inhibitors or ergots. Recurrence within 24 hours affects up to 40% of patients and may require a second dose.

sumatriptan · rizatriptan · eletriptan · almotriptan · zolmitriptan · naratriptan

GEPANTS · CGRP receptor antagonists

Ubrogepant, rimegepant

A newer class of oral CGRP receptor antagonists. Do not constrict blood vessels, so they are appropriate for patients with cardiovascular contraindications to triptans. Effective for acute treatment, and generally well tolerated.

Rimegepant can also be used every other day as a preventive — a dual-use option. Lasmiditan, a ditan, is a related option with a different mechanism that also avoids vasoconstriction.

ubrogepant (Ubrelvy) · rimegepant (Nurtec) · lasmiditan (Reyvow) · zavegepant (Zavzpret, nasal)

ANTIEMETICS & ADJUNCTS

Antiemetics and dopamine blockers

Nausea is a core migraine symptom, and antiemetics are not just supportive — they improve migraine outcomes by promoting gastric emptying (which improves absorption of oral medications) and by modulating dopaminergic pathways.

Metoclopramide and prochlorperazine are used in emergency departments for severe attacks. Avoid in patients with movement disorders or QTc prolongation.

metoclopramide · prochlorperazine · promethazine · ondansetron

Section 05 · Preventive treatment

Reducing attacks before they start — and the CGRP revolution.

Preventive therapy is considered when migraines occur 4 or more days per month, cause significant disability, or are inadequately controlled by acute treatment. The goal is a 50 percent reduction in attack frequency, which is considered a clinically meaningful response.

ORAL PREVENTIVES · traditional

Beta-blockers, TCAs, AEDs

These older classes are generic, inexpensive, and supported by decades of evidence. Propranolol and metoprolol are first-line; amitriptyline is often chosen in patients with comorbid insomnia or tension-type headache; topiramate and valproate are effective antiseizure medications used as preventives.

Require weeks to months to work and are often limited by side effects — cognitive slowing with topiramate, weight gain with amitriptyline, exercise intolerance with beta-blockers. Valproate is teratogenic and avoided in women of childbearing potential.

propranolol · metoprolol · amitriptyline · topiramate · valproate · candesartan · lisinopril

CGRP · monoclonal antibodies

CGRP monoclonal antibodies

The biggest advance in migraine prevention in decades. Fully humanized monoclonal antibodies that bind either CGRP ligand or its receptor, producing sustained reduction in attack frequency. Given monthly or quarterly by subcutaneous injection, or quarterly by IV infusion.

Well tolerated. Main side effects are injection-site reactions and constipation (more with erenumab). No dose titration required — patients often respond within 4 to 8 weeks. Coverage varies by insurance; manufacturer programs help substantially.

erenumab (Aimovig) · fremanezumab (Ajovy) · galcanezumab (Emgality) · eptinezumab (Vyepti, IV)

GEPANTS · oral CGRP

Atogepant, rimegepant

Oral CGRP receptor antagonists for prevention. Atogepant is taken daily; rimegepant every other day. Convenient alternative to injectables for patients who prefer oral therapy, and generally well tolerated.

Less effective on average than the monoclonal antibodies, but with a lower burden of administration and no injection. Useful for patients who have failed or cannot access the injectable CGRP class.

atogepant (Qulipta) · rimegepant (Nurtec, dual-use)

BOTOX · chronic migraine

OnabotulinumtoxinA

FDA-approved for chronic migraine — defined as headache on 15 or more days per month, with at least 8 migraine days. Administered by a trained clinician in a fixed pattern of 31 injection sites across the scalp, temples, neck, and shoulders, every 12 weeks.

Response is not immediate — typically assessed after 2 to 3 treatment cycles. Well tolerated; main side effects are temporary brow droop and neck stiffness. Often used in patients who have failed multiple oral preventives.

onabotulinumtoxinA (Botox) · 155–195 units every 12 weeks

Section 06 · Safety

What to watch — and why timing matters for every medication.

SAFETY · MIGRAINE MEDICATIONS

Migraine medications are generally safe — but they require attention to interactions, frequency, and monitoring. These checks matter.

Medication overuse headache

Taking acute medications 10 or more days per month (triptans, ergots, combination analgesics) or 15 or more days (simple analgesics) can cause a chronic daily headache that worsens with more medication. This is one of the most important things to monitor.

Triptan cardiovascular contraindications

Triptans constrict blood vessels. They are contraindicated in coronary artery disease, uncontrolled hypertension, prior stroke or TIA, and peripheral arterial disease. Gepants and lasmiditan avoid this — a real advantage for patients with cardiovascular risk.

Serotonin syndrome

Triptans combined with SSRIs, SNRIs, MAO inhibitors, or other serotonergic drugs can rarely cause serotonin syndrome — agitation, tremor, hyperthermia, and clonus. Symptoms require prompt medical attention.

Topiramate and pregnancy

Topiramate and valproate are associated with birth defects and cognitive effects in offspring. Discuss contraception and alternatives before starting either medication in patients who could become pregnant.

Drug interactions

Preventive medications interact with many other drugs — beta-blockers with calcium channel blockers, topiramate with carbonic anhydrase inhibitors, triptans with MAO inhibitors. Every prescriber and pharmacist should have a complete medication list. A useful example of how routine interaction screening works appears in this reference on Metformin dosage, and the same principle applies to migraine medications.

Monitoring on preventives

Beta-blockers: heart rate and blood pressure. Topiramate: metabolic panel, kidney stones, cognition. Valproate: liver function, blood counts. A headache diary is also essential — it is how both patient and clinician judge whether a preventive is working.

Section 07 · What to watch for

Signs that require urgent medical evaluation.

Most headaches are migraine and are not dangerous. But certain patterns — summarized by the mnemonic SNOOP — raise concern for a secondary headache, meaning a headache caused by something else. These warrant prompt evaluation.

Urgent evaluation

If any of these appear, seek immediate medical attention — do not treat as a routine migraine.

Thunderclap headache — sudden, severe pain that reaches maximum intensity within 60 seconds. May indicate subarachnoid hemorrhage and requires emergency evaluation.

Headache with fever, neck stiffness, or rash. Possible meningitis or encephalitis — medical emergency.

Headache after head injury, especially if worsening over hours to days. Could indicate intracranial bleeding.

New neurological symptoms — weakness, numbness, confusion, difficulty speaking, vision loss, or seizure — with or without headache.

New headache pattern after age 50, or a significant change in an established headache pattern. Especially concerning with weight loss, jaw claudication, or scalp tenderness — possible giant cell arteritis.

Headache with papilledema, vision changes, or persistent vomiting, or a headache that is worse when lying down or on waking. Possible raised intracranial pressure.

Section 08 · Access & affordability

Migraine care is effective — but coverage varies and pharmacy pricing matters.

Traditional oral preventives and acute medications are largely generic and inexpensive — propranolol, amitriptyline, topiramate, sumatriptan, and naproxen are all available on $4 prescription lists at major pharmacies. The newer CGRP class — monoclonal antibodies and gepants — is expensive, typically $600 to $1,000 per month at list price. Manufacturer copay programs cover most of the out-of-pocket cost for commercially insured patients; foundation grants help Medicare and uninsured patients. Botox for chronic migraine is covered by most commercial plans and by Medicare Part B with prior authorization.

For any patient on multiple chronic medications — which is common in migraine, given the frequent coexistence of anxiety, depression, sleep disorders, and other conditions — pharmacy-level pricing differences can add up meaningfully. The same generic drug can cost several times more at one licensed pharmacy than another. A quick comparison before each refill is worth the two minutes. A reference like this one on is it safe to buy Metformin online walks through the compliant ordering process, and it is worth asking contact Metformin4You about the standards used to select sellers.

Before filling from any seller — online or local — verify them. A working VIPPS seal that resolves to a live NABP record, a real U.S. street address, and a prescription requirement that cannot be waived. Migraine medications are chronic and often taken over years — using a pharmacy you cannot hold accountable is not worth the risk.

Section 09 · Questions

Five asked most often in the headache clinic.

Q·01 What is migraine? +

Migraine is a neurological disorder characterized by recurrent attacks of moderate to severe headache, often on one side, with associated symptoms such as nausea, light sensitivity, and sound sensitivity. It is not simply a bad headache — it is a complex brain disorder involving the trigeminovascular system and the neuropeptide CGRP. About 40 million Americans live with migraine.

Q·02 What is the difference between acute and preventive migraine treatment? +

Acute treatments are taken at the start of an attack to stop it — NSAIDs, triptans, gepants, and antiemetics. Preventive treatments are taken regularly to reduce the frequency and severity of attacks over time — beta-blockers, tricyclic antidepressants, antiseizure medications, CGRP monoclonal antibodies, and Botox. Patients with frequent attacks typically need both.

Q·03 Are CGRP monoclonal antibodies safe? +

CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab, eptinezumab) are generally well tolerated, with injection-site reactions and constipation as the most common side effects. They are given monthly or quarterly, do not require dose titration, and have no known major organ toxicity. Long-term safety data continues to accumulate, but the class has been widely used since 2018. For a useful example of how a broader class of chronic medications is understood at the patient level, see this reference on the Metformin FAQ.

Q·04 What is medication overuse headache? +

Medication overuse headache (MOH) occurs when acute migraine medications are used too frequently — typically 10 or more days per month for triptans, ergots, or combination analgesics, or 15 or more days for simple analgesics. It produces a chronic daily headache that worsens with more medication. Treatment involves stopping the overused medication under medical supervision and starting an appropriate preventive.

Q·05 When should I worry about a headache? +

Seek urgent medical attention for a thunderclap headache (sudden, severe, peaks within a minute), headache with fever and neck stiffness, headache after head injury, headache with new neurological symptoms (weakness, confusion, vision loss), or a new headache pattern after age 50. These may indicate a serious secondary cause such as subarachnoid hemorrhage, meningitis, or mass lesion.

◆ Sources & Verification

This reference is aligned with public clinical guidance from the American Headache Society (AHS), the American Academy of Neurology (AAN), the National Institute of Neurological Disorders and Stroke (NIH), and the U.S. Food and Drug Administration's BeSafeRx program. Drug-label information draws on the National Library of Medicine's DailyMed database and MedlinePlus. Headache classification follows the ICHD-3 criteria. Pharmacy verification follows the NABP VIPPS program.

Migraine is not a bad headache. It is a 72-hour neurological event with a forecast you can learn to read.