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Neurology›Condition·Updated Jun 3, 2026·v1

Migraine Headache

Migraine is a chronic, heritable neurovascular disorder driven by CGRP-mediated activation of the trigeminovascular system. Management focuses on early acute intervention with triptans or gepants and preventive therapy for frequent attacks using beta-blockers, anticonvulsants, or CGRP-targeted monoclonal antibodies.

High Evidence246 references·8,682 words·35 min read·v1
NeurologyHeadacheCGRPTriptansChronic Migraine

Quick Reference

RxDrug of choiceSumatriptan (Acute); Propranolol or Topiramate (Preventive)
AltAlternativesRimegepant (Gepant), Lasmiditan (Ditan), CGRP Monoclonal Antibodies
⊘AvoidTriptans and Ergotamines in patients with CAD, stroke, or uncontrolled hypertension
DxTest of choiceClinical diagnosis (ICHD-3); MRI only for 'red flags'
ScKey scoreMIDAS (Migraine Disability Assessment) or HIT-6
→When to referRefractory to 2+ preventives, chronic migraine, or diagnostic uncertainty (e.g., hemiplegic features)
Migraine is a disabling neurovascular disease best managed by early stratified acute treatment and proactive CGRP-targeted or traditional prophylaxis.
Migraine is a chronic neurovascular disorder and the second leading cause of disability worldwide, particularly affecting women in their peak productive years. It is characterized by paroxysmal, debilitating headache episodes often accompanied by autonomic dysfunction, nausea, and sensory hypersensitivity. The pathophysiology centers on the activation of the trigeminovascular system and the release of [[calcitonin gene-related peptide]] (CGRP), which drives neurogenic inflammation and pain. Diagnosis is strictly clinical, utilizing the ICHD-3 criteria to differentiate primary migraine from secondary mimics. Management has been revolutionized by CGRP-targeted therapies, including monoclonal antibodies and gepants, which offer high specificity and improved safety profiles compared to legacy treatments. Effective care requires a dual strategy: stratified acute intervention to restore function and early initiation of prophylaxis to prevent chronification and medication overuse.

Overview and Recommendations

Background

  • •Migraine — a complex neurovascular syndrome — affects approximately 1 in 7 people globally and remains the primary cause of disability among women aged 15–49 years, carrying immense socioeconomic stakes due to lost productivity and work-family conflict.
  • •The trigeminovascular system serves as the central molecular axis of the disorder; its activation triggers the release of potent vasoactive neuropeptides, primarily and substance P, which induce dural vasodilation and neurogenic inflammation.
  • • (CSD), often described as a 'brain tsunami,' is the electrophysiological substrate of the migraine aura, involving a wave of neuronal depolarization that activates trigeminal nociceptors and may even drive migraine without aura in 'silent' cortical regions.
  • •Classification is primarily frequency-based, distinguishing between episodic migraine (less than 15 headache days per month) and (15 or more days per month for at least three months), with the latter often associated with central sensitization and medication overuse.
  • •Genetic heritability is high, ranging from monogenic forms like (mutations in CACNA1A, ATP1A2, or SCN1A) to common polygenic variants involving over 120 identified risk loci related to vascular development and glutamatergic signaling.
  • •Prognostic stakes are significant, as migraine with aura is an independent risk factor for ischemic stroke, a risk that is further potentiated by smoking, hypertension, and the use of combined oral contraceptives.

Evaluation

  • •Suspect migraine in any patient presenting with recurrent, moderate-to-severe, pulsating headaches that last 4 to 72 hours and are aggravated by routine physical activity.
  • •Apply the ICHD-3 diagnostic criteria: the patient must have at least five lifetime attacks (two if aura is present) featuring nausea, vomiting, , or in addition to the characteristic pain profile.
  • •Ask specifically about the four clinical phases: the prodrome (yawning, neck stiffness, food cravings), the aura (reversible visual or sensory deficits), the headache phase, and the postdrome (the 'migraine hangover' of cognitive clouding).
  • •Characterize the aura carefully; typical migraine aura develops gradually over at least 5 minutes and lasts no more than 60 minutes, helping to distinguish it from the sudden onset of a (TIA).
  • •Screen for 'red flags' using the SNOOP10 mnemonic, paying close attention to systemic symptoms, neurological deficits, sudden 'thunderclap' onset, or new-onset headaches in patients over age 50.
  • •Examine the patient for signs of cutaneous , such as pain when brushing hair or wearing glasses, which serves as a clinical marker for central sensitization and an increased risk of chronification.
  • •Order a brain MRI only if the patient presents with atypical features, such as a strictly unilateral headache that never switches sides, a prolonged aura lasting more than a week, or a significant change in their established headache pattern.
  • •Evaluate for in patients reporting episodic vertigo or motion sensitivity, even in the absence of a concurrent headache, as this is the most common cause of spontaneous episodic vertigo.
  • •Assess for by quantifying the monthly use of acute treatments; thresholds for concern include 10 or more days of triptans/opioids or 15 or more days of simple NSAIDs per month.
  • •Utilize validated disability scales like the Migraine Disability Assessment ( ) or the Headache Impact Test (HIT-6) to establish a baseline and guide the necessity for preventive therapy.

Management

  • •Initiate acute treatment at the earliest sign of symptoms, ideally during the prodrome or at the first onset of pain, to maximize the likelihood of achieving a pain-free state within two hours.
  • •Administer simple analgesics for mild-to-moderate attacks: 400–800 mg, sodium 500–1100 mg, or 650–1000 mg are effective first-line options.
  • •Utilize triptans (5-HT1B/1D agonists) for moderate-to-severe attacks: 50–100 mg PO or 6 mg SC is the gold standard, though SC administration is preferred for rapid onset or severe nausea.
  • •Transition to gepants for patients with cardiovascular contraindications to triptans or those who fail standard therapy: 75 mg ODT or 50–100 mg are effective and carry a lower risk of medication overuse.
  • •Prescribe 50–200 mg (a 5-HT1F agonist) for patients requiring a non-vasoconstrictive option, but advise the patient not to drive for at least 24 hours after a dose due to potential dizziness.
  • •Manage (attacks >72 hours) with aggressive rescue therapy, such as IV 30 mg, IV 10 mg, or IV dihydroergotamine (DHE) 1 mg.
  • •Offer preventive therapy to any patient with 4 or more migraine days per month or those whose attacks cause significant life disruption despite acute treatment.
  • •Start first-line oral preventives at low doses and titrate over 4–8 weeks: 40–160 mg/day, 50–100 mg/day, or 10–50 mg/day (especially if comorbid insomnia is present).
  • •Consider 16 mg/day as a first-line preventive option due to its superior tolerability profile compared to traditional beta-blockers or anticonvulsants.
  • •Escalate to CGRP monoclonal antibodies for refractory cases: 70–140 mg SC monthly, 225 mg SC monthly, or 120 mg SC monthly (after a 240 mg loading dose).
  • •Utilize IV 100–300 mg every 12 weeks for patients requiring rapid preventive onset or those who prefer infrequent clinical administration.
  • •Administer (Botox) 155–200 U via the PREEMPT protocol (31–40 injection sites) every 12 weeks specifically for the management of chronic migraine.
  • •Perform a (GONB) using 2% lidocaine and 40–80 mg of methylprednisolone for acute rescue in the emergency department or as a 'bridge' to long-term prevention.
  • •Recommend evidence-based nutraceuticals for patients preferring 'natural' options: oxide 400–600 mg/day, (Vitamin B2) 400 mg/day, and Coenzyme Q10 300 mg/day.
  • •Integrate non-pharmacological behavioral therapies, such as (CBT) and biofeedback, which can reduce attack frequency by 30–50% by modulating autonomic arousal.
  • •Avoid the routine use of opioids and butalbital-containing compounds, as these significantly increase the risk of chronification and are less effective than migraine-specific therapies.
  • •Refer to a headache specialist if the patient fails two or more classes of preventives, has a rare variant like hemiplegic migraine, or requires advanced procedural interventions.

Board Review — High Yield

  • •Scintillating scotomata — The most common visual aura, characterized by a flickering zig-zag pattern that expands over minutes.
  • •CGRP — The primary neuropeptide mediator of migraine pain and the target of 'gepants' and monoclonal antibodies.
  • •4 to 72 hours — The diagnostic duration threshold for an untreated migraine attack in adults.
  • •Topiramate — A first-line preventive often associated with paresthesias, cognitive 'word-finding' difficulties, and weight loss.
  • •Status Migrainosus — A debilitating migraine attack lasting longer than 72 hours, often requiring IV rescue therapy.
  • •PFO (Patent Foramen Ovale) — A cardiac anomaly with a higher prevalence in patients who experience migraine with aura.
  • •Allodynia — Pain resulting from a non-painful stimulus (e.g., hair brushing), indicating central sensitization.
  • •Alice in Wonderland Syndrome — A rare pediatric migraine aura involving metamorphopsia (distortions in body image or object size).

Deep Dive — Evidence Details

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