Vestibular Migraine
Vestibular migraine (VM) is the most common cause of recurrent spontaneous episodic vertigo, affecting approximately 1% of the general population with a strong female predominance (F:M ratio ~3–5:1). Despite its prevalence, VM remains significantly underdiagnosed because vertigo episodes frequently occur independent of headache — vertigo may be the sole manifestation in up to 30% of attacks. The formalization of diagnostic criteria by the Bárány Society and the International Headache Society in 2012 provided a much-needed framework for recognition and study. For neurologists, understanding VM is essential not only because it is so common, but because it overlaps clinically with Ménière disease, BPPV, and persistent postural-perceptual dizziness (PPPD), requiring a careful approach to distinguish among these entities and guide appropriate treatment.
Bottom Line
- Most common cause of recurrent episodic vertigo: Affects ~1% of the population; lifetime prevalence of vestibular symptoms in migraineurs is 25–35%
- Diagnosis is clinical: Based on Bárány Society/IHS 2012 criteria — at least 5 episodes of vestibular symptoms (5 min to 72 h), history of migraine, and ≥50% of episodes with migrainous features
- Vertigo may be the ONLY symptom: Headache is absent in up to 30% of attacks; do not require concurrent headache for diagnosis
- Key overlap with Ménière disease: ~30% of patients meet criteria for both conditions; hearing loss pattern and aural fullness help differentiate
- Treatment mirrors migraine: Preventive agents (topiramate, venlafaxine, propranolol, amitriptyline, candesartan), lifestyle modification, and vestibular rehabilitation; CGRP monoclonal antibodies show emerging promise
- Chronic condition with favorable prognosis: Most patients respond to preventive treatment, though some develop persistent dizziness overlapping with PPPD
Epidemiology
- Prevalence: ~1% of the general population; 10–12% of patients seen in dizziness clinics; prevalence increases to 9–11% among patients presenting to neurology clinics with recurrent vertigo
- Sex distribution: Female predominance (F:M ratio approximately 3–5:1), consistent with migraine overall; the sex ratio may be even more skewed in clinical populations
- Age of onset: Can occur at any age; mean onset in the 30s–40s; may begin years after the onset of migraine headaches or even after headaches have diminished; bimodal distribution with a second peak in the perimenopausal years
- Relationship to migraine: 25–35% of migraineurs experience vestibular symptoms during their lifetime; vestibular migraine may represent the most common cause of spontaneous episodic vertigo across all age groups
- Diagnostic delay: Mean delay from symptom onset to diagnosis is 5–8 years in many series; patients frequently receive alternative diagnoses (BPPV, Ménière disease, anxiety) before VM is recognized
- Pediatric population: "Benign paroxysmal vertigo of childhood" is considered a migraine precursor and appears in the ICHD-3 classification; motion sickness in childhood is strongly associated with later development of both migraine and VM
- Comorbidities: Anxiety disorders (40–60%), depression (20–40%), motion sickness (50–70%), BPPV (higher recurrence rates than general population), and PPPD (develops as a secondary complication in 10–20%)
- Genetics: Strong familial aggregation; first-degree relatives of VM patients have a 3–5 fold increased risk of both migraine and vestibular symptoms; likely polygenic inheritance with some overlap with CACNA1A (episodic ataxia type 2) and ATP1A2 (familial hemiplegic migraine) pathways
Pathophysiology
The pathophysiology of vestibular migraine is incompletely understood but involves convergent mechanisms linking the trigeminovascular system with central and peripheral vestibular processing.
Proposed Mechanisms
- Cortical spreading depression (CSD): CSD affecting the vestibular cortex (parieto-insular vestibular cortex, temporoparietal junction) may directly produce vertigo; animal models show CSD can propagate to brainstem vestibular nuclei
- Trigemino-vascular activation: Release of CGRP, substance P, and other neuropeptides from trigeminal afferents innervating the inner ear vasculature may alter labyrinthine function, producing both peripheral and central vestibular symptoms
- Central sensitization: Repeated activation leads to enhanced excitability of vestibular nuclei and cortical vestibular areas, potentially explaining interictal motion sensitivity and chronic dizziness
- Serotonergic modulation: Serotonin (5-HT) receptors are densely expressed in vestibular nuclei; fluctuations in serotonin levels during migraine cycles may directly affect vestibular processing
- Ion channel dysfunction: Shared genetic links with episodic ataxia type 2 (CACNA1A variants) support a channelopathy component in some patients
- Peripheral labyrinthine involvement: Transient vasospasm or neurogenic inflammation of the inner ear via trigeminal innervation may explain hearing symptoms and overlap with Ménière disease
Why Vertigo Can Occur Without Headache
- Cortical spreading depression may propagate to vestibular cortex without activating the trigeminovascular pain pathway
- The threshold for vestibular symptoms may be lower than the threshold for headache in some patients
- CGRP-mediated inner ear effects can occur independently of meningeal pain activation
- In many patients, vestibular symptoms become the predominant migraine manifestation as they age, while headaches diminish — a pattern analogous to "acephalgic migraine" with visual aura
Diagnostic Criteria
Bárány Society / IHS Consensus Criteria (2012)
The 2012 consensus criteria, published jointly by the Bárány Society and the International Headache Society and included in the ICHD-3 appendix, define two diagnostic levels:
| Criterion | Definite Vestibular Migraine | Probable Vestibular Migraine |
|---|---|---|
| A. Episodes | ≥5 episodes of vestibular symptoms of moderate or severe intensity | ≥5 episodes of vestibular symptoms of moderate or severe intensity |
| B. Migraine history | Current or past history of migraine with or without aura (ICHD criteria) | Only ONE of criteria C or D (migraine features or migraine history) is required |
| C. Migrainous features | ≥50% of vestibular episodes have ≥1 migrainous feature: headache (migrainous qualities), photophobia, phonophobia, visual aura | Only ONE of criteria C or D is required |
| D. Duration | Vestibular symptoms lasting 5 min to 72 hours | Same |
| E. Exclusion | Not better accounted for by another vestibular or ICHD diagnosis | Same |
Vestibular Symptom Types (per Criteria)
- Spontaneous vertigo: Including internal vertigo (false sensation of self-motion) and external vertigo (false sensation of visual environment spinning or flowing)
- Positional vertigo: Occurring after head position change — distinguished from BPPV by duration, associated migrainous features, and absence of characteristic BPPV nystagmus
- Visually induced vertigo: Triggered by complex or moving visual stimuli (grocery store aisles, scrolling screens, traffic)
- Head motion–induced vertigo: Vertigo provoked by head movement
- Head motion–induced dizziness with nausea: Dizziness (non-spinning) with nausea during head movement
Diagnostic Pitfalls
- Do not require headache during vertigo: Migrainous features are needed in ≥50% of episodes, but headache may be absent in any given attack
- Remote migraine history counts: A patient whose migraine headaches resolved years ago still meets criterion B
- Symptom duration can be highly variable: Some patients report episodes lasting seconds (often positional) while others have attacks lasting days; the 5 min–72 h range encompasses the majority
- Probable VM is clinically significant: Patients meeting probable criteria should still be offered treatment, as many progress to definite VM over time
Clinical Features
Attack Characteristics
- Vertigo type: Most commonly spontaneous rotational vertigo; may also manifest as rocking/swaying, tilting sensation, or non-spinning dizziness
- Duration: Highly variable — seconds (positional triggers), minutes to hours (most common), up to 72 hours; median attack duration is 4–72 hours in most series
- Frequency: Ranges from rare (few per year) to frequent (several per month); median frequency is approximately monthly
- Headache: Concurrent migrainous headache in ~50–70% of attacks; headache may precede, accompany, or follow vertigo
- Associated migraine features: Photophobia (most common), phonophobia, osmophobia, visual aura (in ~15%), nausea (often severe, more prominent than in typical migraine without vertigo)
- Auditory symptoms: Aural fullness, tinnitus, and mild hearing fluctuation reported in up to 40% of patients; hearing loss is typically mild and non-progressive (unlike Ménière disease)
- Motion sensitivity: Prominent during and between attacks; patients often avoid head movement, riding in vehicles, or environments with complex visual motion
Interictal Findings
- Motion sensitivity: Persistent low-grade motion intolerance between attacks in many patients; often reported as the most bothersome chronic symptom
- Visual vertigo: Worsening with complex visual environments (supermarkets, driving, screens, escalators); reflects visual-vestibular mismatch and central sensitization
- Postural instability: Mild balance impairment on tandem gait or foam Romberg between attacks; may be subclinical but measurable on posturography
- Examination: Usually normal between attacks; may show mild positional nystagmus, subtle saccadic smooth pursuit, or gaze-evoked nystagmus during or shortly after attacks
- Vestibular testing between attacks: VNG/caloric testing shows mild unilateral weakness in 10–20%; vHIT is typically normal; VEMPs may show subtle asymmetries; these findings do not change diagnosis but may support it in borderline cases
Vestibular Testing Findings in VM
| Test | Typical Findings in VM | Clinical Significance |
|---|---|---|
| Audiometry | Normal or mild bilateral high-frequency SNHL | Important to distinguish from Ménière (no progressive low-frequency loss) |
| VNG / Caloric | Normal in 70–80%; mild unilateral weakness in 10–20% | Caloric-vHIT dissociation may be present (abnormal caloric, normal vHIT) |
| vHIT | Usually normal between attacks | May show reduced gain during or immediately after attacks |
| VEMPs | Variable; subtle asymmetries possible | Not diagnostic; may show altered thresholds during attacks |
| Posturography | Visual preference pattern; increased sway on conditions 5–6 | Reflects visual-vestibular mismatch and over-reliance on visual input |
Overlap with Ménière Disease
Approximately 30% of patients with vestibular migraine meet diagnostic criteria for Ménière disease, and the reverse overlap is also significant. This comorbidity represents one of the most challenging diagnostic dilemmas in neuro-otology.
| Feature | Vestibular Migraine | Ménière Disease |
|---|---|---|
| Hearing loss | Absent or mild, non-progressive, often bilateral | Low-frequency sensorineural, progressive, unilateral (initially) |
| Aural fullness | May occur; bilateral, variable | Prominent; typically ipsilateral, preceding attacks |
| Tinnitus | Bilateral, fluctuating, often absent | Unilateral, low-pitched roaring, preceding attacks |
| Attack duration | Variable (seconds to 72 h) | 20 min to 12 h (typically 2–4 h) |
| Migraine features | Present in ≥50% of attacks | May occur (migraine is more common in Ménière patients) |
| Audiometry | Normal or mild high-frequency loss | Low-frequency sensorineural hearing loss (fluctuating early, progressive) |
| Triggers | Typical migraine triggers (sleep deprivation, stress, dietary, hormonal) | Salt intake, stress (less specific) |
| Response to migraine preventives | Good | Variable (may help if comorbid migraine) |
Practical Approach to VM vs. Ménière Overlap
- Obtain audiometry in all patients with recurrent vertigo — documented low-frequency SNHL favors Ménière disease
- Longitudinal follow-up is essential — the diagnostic picture may clarify over months to years
- If overlap criteria are met, treat both conditions empirically: migraine preventives PLUS low-salt diet
- Consider electrocochleography (ECoG) if Ménière is suspected — elevated SP/AP ratio supports endolymphatic hydrops
- MRI with 3D-FLAIR after intratympanic gadolinium can directly visualize endolymphatic hydrops (research tool, increasingly available clinically)
Differential Diagnosis
| Condition | Key Distinguishing Features | Duration |
|---|---|---|
| BPPV | Positional vertigo with characteristic nystagmus on Dix-Hallpike; no migrainous features; self-limited; responds to repositioning maneuvers | Seconds per episode |
| Ménière disease | Low-frequency hearing loss, unilateral aural fullness, roaring tinnitus | 20 min–12 h |
| PPPD | Chronic (≥3 months) non-spinning dizziness/unsteadiness; worsened by upright posture, motion, and complex visual stimuli; may develop after VM | Continuous (fluctuating) |
| Vestibular paroxysmia | Very brief attacks (seconds to 1–2 min), high frequency (≥30/day possible); neurovascular compression of CN8; responds to carbamazepine | Seconds to minutes |
| Anxiety-related dizziness | Dizziness with anxiety/panic; may coexist with VM; hyperventilation-provoked; no spontaneous rotational vertigo | Minutes to hours |
| Episodic ataxia type 2 | Episodic vertigo/ataxia with interictal nystagmus; CACNA1A mutation; responds to acetazolamide | Hours to days |
Diagnostic Workup
Vestibular migraine is a clinical diagnosis. There is no confirmatory biomarker or test. The workup is directed at excluding alternative diagnoses.
Recommended Investigations
- Audiometry: Should be obtained in all patients; typically normal or shows mild bilateral high-frequency sensorineural loss; significant low-frequency loss suggests Ménière disease
- MRI brain with IAC protocol: Indicated to exclude posterior fossa structural lesions (vestibular schwannoma, Chiari malformation, MS plaques); gadolinium-enhanced MRI if vestibular schwannoma is suspected
- Vestibular function testing (VNG/caloric/vHIT): Not required for diagnosis; may show mild abnormalities (reduced caloric response in up to 20%, subtle oculomotor findings) that do not change management but may support diagnosis
- Blood work: TSH, CBC, metabolic panel as clinically indicated to exclude systemic causes of dizziness
When to Investigate Further
- Unilateral hearing loss or progressive hearing decline → MRI with IAC protocol and audiometry
- Persistent neurologic signs between attacks → MRI brain to exclude MS, posterior fossa lesion
- Atypical features (new onset after age 50, persistent direction-changing nystagmus, focal neurologic deficits) → broader workup including vascular imaging
- Failure to respond to standard migraine preventive therapy → reconsider diagnosis; repeat audiometry; consider vestibular function testing
Treatment
Acute Treatment
- Triptans: May be effective if taken early in the attack, particularly when headache accompanies vertigo; limited evidence specifically for VM (rizatriptan showed benefit in one small RCT); less effective for isolated vestibular attacks without headache
- Vestibular suppressants: Meclizine, dimenhydrinate, or promethazine for symptomatic relief during acute attacks; should be limited to ≤3 days to avoid delaying vestibular compensation
- Antiemetics: Ondansetron, metoclopramide, or prochlorperazine for associated nausea; prochlorperazine also has vestibular suppressant properties
- Benzodiazepines: Low-dose diazepam (2–5 mg) or lorazepam (0.5–1 mg) for severe acute attacks; reserve for occasional use only
Preventive Treatment
Preventive therapy is indicated when attacks are frequent (≥2–3/month), disabling, or significantly impair quality of life. Evidence is largely extrapolated from migraine trials, with limited VM-specific RCT data.
| Agent | Typical Dose | Evidence / Notes |
|---|---|---|
| Venlafaxine | 37.5–150 mg/day | Retrospective evidence suggests high efficacy for VM; also helps comorbid anxiety/PPPD |
| Topiramate | 50–100 mg/day | One small RCT showed significant reduction in VM frequency and severity |
| Propranolol | 40–160 mg/day | Well-established migraine preventive; retrospective data support VM efficacy |
| Amitriptyline | 10–75 mg at bedtime | Useful when comorbid insomnia or chronic daily headache; start low, titrate slowly |
| Candesartan | 8–16 mg/day | RCT evidence for migraine prevention; clinical experience supports VM use; well-tolerated |
| Flunarizine | 5–10 mg at bedtime | Calcium channel blocker with vestibular effects; commonly used in Europe; not available in the US |
| CGRP monoclonal antibodies | Standard migraine dosing | Emerging evidence: case series and retrospective studies show benefit for VM; RCTs underway; consider for refractory patients |
| Valproate | 500–1000 mg/day | Effective migraine preventive; use with caution (teratogenicity, weight gain); limited VM-specific data |
Lifestyle Modification
- Sleep hygiene: Regular sleep schedule, adequate duration (7–8 hours); sleep deprivation is a potent trigger
- Exercise: Regular aerobic exercise (30+ minutes, 5 days/week) reduces migraine frequency; should be introduced gradually in patients with motion sensitivity
- Trigger avoidance: Common triggers include sleep deprivation, stress, caffeine (excess or withdrawal), alcohol (especially red wine), dehydration, skipped meals, hormonal fluctuations, weather changes, and visual triggers
- Dietary modifications: Consistent meal timing; adequate hydration; avoidance of identified dietary triggers; evidence for restrictive "migraine diets" is limited
Vestibular Rehabilitation
- Indication: Persistent interictal dizziness, motion sensitivity, visual vertigo, and postural instability
- Approach: Habituation exercises for motion sensitivity, gaze stabilization exercises, balance training; delivered by specialized vestibular physical therapists
- Evidence: Randomized studies demonstrate benefit in reducing dizziness handicap in VM patients, particularly those with interictal symptoms
- Timing: Best initiated once attack frequency is reduced by preventive therapy; severe interictal symptoms can be addressed concurrently
- Specific components:
- Habituation: graded exposure to provocative movements and visual stimuli
- Gaze stabilization: VOR ×1 and ×2 exercises to improve gaze stability during head movement
- Balance training: progressive challenges to static and dynamic balance (foam, tandem stance, perturbation)
- Optokinetic desensitization: exposure to moving visual patterns to reduce visual vertigo
- Expected outcomes: 60–80% of patients report meaningful improvement in interictal symptoms and dizziness handicap scores with consistent 8–12 weeks of therapy
Cognitive Behavioral Therapy (CBT)
- Increasingly recognized as a useful adjunct in VM, particularly when comorbid anxiety amplifies dizziness perception and avoidance behavior
- Targets catastrophizing about vertigo, avoidance of triggers, and the bidirectional relationship between anxiety and vestibular symptoms
- May be combined with vestibular rehabilitation ("integrated vestibular rehabilitation and CBT") for patients with significant psychogenic overlay
- Evidence is strongest when VM overlaps with PPPD, where behavioral and cognitive factors perpetuate chronic symptoms
Practical Treatment Algorithm
- Step 1: Confirm diagnosis (Bárány Society/IHS criteria); educate patient about the migraine-vertigo connection
- Step 2: Lifestyle modification (sleep, exercise, trigger avoidance) for ALL patients
- Step 3: If attacks are frequent/disabling, start preventive medication — choose based on comorbidities (venlafaxine if anxiety/PPPD; propranolol if hypertension; amitriptyline if insomnia; topiramate if overweight)
- Step 4: Provide acute rescue medication (triptan ± antiemetic) and vestibular suppressant for severe attacks
- Step 5: Refer for vestibular rehabilitation if persistent interictal symptoms
- Step 6: If refractory to 2–3 preventive trials, consider CGRP monoclonal antibodies, combination preventive therapy, or re-evaluation of diagnosis
Prognosis and Long-Term Outcomes
- Chronic relapsing condition: VM persists over decades in most patients; attack frequency may fluctuate with hormonal changes, stress, and aging
- Treatment response: 50–75% of patients achieve meaningful reduction in attack frequency and severity with preventive therapy
- Evolution to PPPD: A subset of patients develop persistent postural-perceptual dizziness as a secondary process, characterized by chronic non-spinning dizziness, visual vertigo, and motion sensitivity; this requires specific treatment (SSRI/SNRI + vestibular rehabilitation + CBT)
- Hearing outcomes: Unlike Ménière disease, significant progressive hearing loss is not a feature of VM; mild audiometric changes may occur but are rarely clinically significant
- Quality of life: VM causes substantial disability during attacks and chronic impairment in daily function; effective treatment significantly improves quality of life metrics
Special Populations
Pediatric Vestibular Migraine
- Benign paroxysmal vertigo of childhood: Recurrent brief (minutes to hours) attacks of vertigo in young children (typically 2–6 years), often with pallor, nausea, and unsteadiness; considered a migraine precursor (ICHD-3); most children develop typical migraine later
- Adolescent VM: Criteria and treatment as in adults; lifestyle modification and magnesium supplementation are first-line; amitriptyline or topiramate for refractory cases
Vestibular Migraine in the Elderly
- Late-onset VM can present diagnostic challenges as headache component may be minimal or absent
- Must exclude posterior circulation TIA and stroke in elderly patients with new episodic vertigo
- Drug selection must account for polypharmacy, fall risk, and cardiovascular comorbidities
Vestibular Migraine and Hormonal Influences
- Menstrual and perimenopausal exacerbation is common; hormonal fluctuations are key triggers
- Pregnancy may improve or worsen VM; treatment options are limited (propranolol is relatively safe; avoid valproate and topiramate)
- Oral contraceptives may worsen VM in some patients, particularly those with aura
- Menstrual VM: predictable attacks timed to the late luteal or early menstrual phase; consider short-term triptan prophylaxis during the vulnerable window
- Perimenopause: hormonal instability may trigger a flare in both migraine headache and vestibular symptoms; HRT effects on VM are variable and unpredictable
Vestibular Migraine and BPPV
- BPPV is more common in migraineurs than in the general population (relative risk ~2–3 fold)
- VM patients with BPPV have higher recurrence rates after repositioning maneuvers than non-migraine BPPV patients
- Migraine preventive therapy may reduce BPPV recurrence in this population
- Positional vertigo in VM should be differentiated from BPPV — VM positional vertigo typically lacks the classic BPPV nystagmus pattern (upbeat-torsional, fatiguing) and may have atypical duration or associated migrainous features
Vestibular Migraine and PPPD
- PPPD (persistent postural-perceptual dizziness) develops as a secondary complication in 10–20% of VM patients
- Characterized by chronic (≥3 months) non-spinning dizziness/unsteadiness, worsened by upright posture, active or passive motion, and complex visual stimuli
- The transition from episodic VM to chronic PPPD may be mediated by anxiety, avoidance behavior, and maladaptive central compensation
- Treatment of VM-related PPPD requires a multimodal approach: SSRI/SNRI (sertraline or venlafaxine), vestibular rehabilitation, and CBT; migraine preventives alone are insufficient
- Early identification and treatment of VM may prevent PPPD development
Patient Education and Counseling
- Explain the migraine-vertigo connection: Many patients are skeptical that their vertigo is "just migraine"; explain that the same brain mechanisms that cause migraine headache also affect the balance centers, and that this is a well-defined medical condition with established diagnostic criteria
- Set realistic expectations: VM is a chronic condition; the goal is to reduce attack frequency and severity, not necessarily to eliminate all episodes; most patients achieve 50–75% improvement with treatment
- Encourage adherence to preventive therapy: Preventive medications need 6–8 weeks at therapeutic dose to show full effect; premature discontinuation is the most common reason for treatment "failure"
- Headache diary or vertigo diary: Tracking episodes with associated features, triggers, and treatments helps confirm the diagnosis over time and guides treatment adjustments
- Address comorbid anxiety: Anxiety is both a trigger and consequence of VM; reassure patients that the vestibular symptoms are real (not "in their head") while addressing the anxiety-vertigo cycle
- Driving and occupational implications: During acute attacks, patients should not drive or operate machinery; between attacks, most patients can resume normal activities; vestibular rehabilitation can improve confidence and functional capacity
Emerging Research and Future Directions
- CGRP monoclonal antibodies: Erenumab, fremanezumab, galcanezumab, and eptinezumab are approved for migraine prevention; retrospective series and case reports suggest benefit for vestibular migraine, but dedicated RCTs are needed and are underway as of 2024–2025
- CGRP receptor antagonists (gepants): Rimegepant and ubrogepant may serve as both acute and preventive options for VM; their ability to block CGRP signaling directly at the trigeminal-vestibular interface is theoretically attractive
- Biomarkers: CGRP levels during and between attacks, vestibular-evoked myogenic potential changes during attacks, and functional MRI of vestibular cortex activation are being investigated as potential diagnostic biomarkers for VM
- Genetic studies: Genome-wide association studies (GWAS) are identifying common variants associated with both migraine and vestibular symptoms; understanding shared genetic architecture may lead to targeted therapies
- Neuromodulation: Non-invasive vagus nerve stimulation (nVNS) and transcranial direct current stimulation (tDCS) targeting vestibular cortex are in early-phase investigation for VM
- MRI hydrops imaging: Gadolinium-enhanced 3D-FLAIR MRI can visualize endolymphatic hydrops; this may eventually help differentiate VM from Ménière disease in cases of diagnostic overlap
Key Takeaways for Clinical Practice
- VM is common, disabling, and underdiagnosed — a migraine history plus episodic vertigo should trigger consideration of this diagnosis
- The diagnosis is clinical; invest time in history-taking rather than extensive testing
- Educate patients that vertigo IS migraine — many patients do not believe vertigo and migraine are connected
- Treatment is the same as migraine: lifestyle, preventive medication, acute rescue, and vestibular rehabilitation for interictal symptoms
- Monitor for evolution to PPPD, which requires additional therapeutic strategies
- Audiometry is the most important ancillary test — primarily to exclude Ménière disease
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