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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